Dental CPD Now DCP's Edition 2017 by Professional Dentistry

PROFESSIONAL DENTISTRY PRESENTS...

DENTAL CPD NOW 2017 Edition

DCPâ&#x20AC;&#x2122;S EDITION

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Alignment, Bleaching and Veneers to Correct Big and Unsightly Front Teeth, by Anoop Maini

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The Use of Botulinum Toxin Type A to Reduce the Appearance of Fine Lines and Wrinkles in the Forehead, Frown and Eyes, by Dr Harry Singh

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VISIT: cpd.professionaldentistry.co.uk for the list of topics covered

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Contents...

1 Cleaning instruments............................................................................ 10

7 What are the risk factors for oral cancer?..................................... 82

Introduction.......................................................................................... 10 General requirements for cleaning methods................................... 12 Automated cleaning: washer-disinfectors....................................... 14 Using a washer-disinfector.................................................................. 16 Records................................................................................................. 18 Considerations for cleaning handpieces......................................... 18 Automated cleaning: ultrasonic cleaning....................................... 20 Ultrasonic cleaning procedure.......................................................... 22 Manual cleaning................................................................................. 24 Cleaning procedure summary.......................................................... 26

8 Complaints handling and patient protection.............................. 92

2 Radiation doses and risks in dental practice............................... 28

Radiation damage.............................................................................. 28 Radiation dose..................................................................................... 30 Factors influencing effective dose.................................................... 32 Intraoral radiography.......................................................................... 34 Panoramic and cephalometric radiography.................................. 35 Cone beam computed tomography............................................... 35 The risks.................................................................................................. 36 Table 1................................................................................................... 40

Asthma attack..................................................................................... 42 Signs and symptoms............................................................................ 44 Prevention............................................................................................ 44 Causes.................................................................................................. 46 Management....................................................................................... 46 Inhaled foreign body.......................................................................... 48 Signs and symptoms............................................................................ 50 Managment......................................................................................... 50 Prevention............................................................................................ 54 Dislodging an object from the airway.............................................. 54

4 Employment issues in dental practice........................................... 56

Hypoglycaemia................................................................................... 100 Clinical scenario.................................................................................. 100 Causes.................................................................................................. 100 Signs and symptoms............................................................................ 100 Prevention............................................................................................ 101 Management....................................................................................... 101 Background information..................................................................... 102 Hyperglycaemia.................................................................................. 103 Steroid insufficiency (Addisonian crisis)............................................. 103 Clinical scenario.................................................................................. 103 Causes.................................................................................................. 103 Signs and symptoms............................................................................ 104 Prevention............................................................................................ 104 Steroid cover........................................................................................ 104 Management....................................................................................... 104 Background information..................................................................... 105

10 Domestic violence: Summarised from The Management of Abuse: A Resource Manual for the Dental Team....................................... 106

The origins of British employment law................................................ 56 Enforcement......................................................................................... 58 County Courts...................................................................................... 59 Employment contracts....................................................................... 60 Disciplinary and Grievances Procedures.......................................... 62 Disciplinary policy and practice........................................................ 63 Potential outcomes............................................................................. 65

5 Child protection – what you need to do if you’re worried about a child............... 66 Assessing a child.................................................................................. 66 Colleagues to consult......................................................................... 67 Making a referral................................................................................. 67 Informing the child and parents........................................................ 67 Coping with the aftermath................................................................ 69 Information sharing and confidentiality............................................ 70 Ethical guidance................................................................................. 70 Consent ............................................................................................... 70 Assessing the needs of children who have been abused.............. 71 Diagrams and clinical photographs................................................. 72 Table 1................................................................................................... 72

What is domestic violence?............................................................... 107 Management....................................................................................... 108 Recognising the signs.......................................................................... 108 Talking to the patient ......................................................................... 108 Provide treatment for injuries or refer as appropriate..................... 108 Assessing risk......................................................................................... 108 Record keeping................................................................................... 109 Referrals................................................................................................ 109 Table 1................................................................................................... 110 Table 2................................................................................................... 110 Table 3................................................................................................... 112

11 Communication and the dental team: assertiveness without aggression..................................................... 114

6 White lesions............................................................................................. 74

Complaints handling........................................................................... 92 Guidance............................................................................................. 92 Raise concerns if patients are at risk................................................. 95 Guidance............................................................................................. 95

9 Medical emergencies: hypoglycaemia, hyperglycaemia and steroid insufficiency...................................................................... 100

3 Medical emergencies: asthma attack and inhaled body.................................................... 42

What are the known modifiable risk factors for oral cancer?........ 82 Alcohol.................................................................................................. 84 Tobacco and alcohol......................................................................... 85 Betel and similar chewing habits....................................................... 86 What are the environmental factors in oral cancer?..................... 88 What are the other known risk factors?............................................ 89 Socio-economic deprivation............................................................. 90 Table 1................................................................................................... 91

Furred tongue...................................................................................... 75 Congenital causes of white lesions................................................... 75 Inflammatory causes of white lesions................................................ 76 Non-infective causes.......................................................................... 77 Key points for patients......................................................................... 80 Table 1. Causes of oral white lesions................................................. 81

Basic rights............................................................................................ 115 Techniques for assertiveness.................................................................117 Sticking to your guns........................................................................... 118 Don’t be undermined............................................................................119 Making the most of criticism............................................................... 119 Valid criticism...........................................................................................119 Invalid criticism/put-down.................................................................. 120 Last thoughts............................................................................................121

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Contents...

12 Protective functions of saliva............................................................. 122

16 Dentoalveolar infection........................................................................ 148

Microorganisms in whole saliva......................................................... 122 Transmission of micro-organisms by saliva contacts....................... 124 Growth of bacteria in saliva............................................................... 125 Salivary components in oral biofilms................................................. 126

13 Cognitive Behavioural Therapy in dental anxiety...................... 128

Overview.............................................................................................. 131 A guide to typical Cognitive Behaviour therapy sessions.............. 132 What is CBT?......................................................................................... 132 How does CBT work?........................................................................... 133 Engagement in CBT............................................................................. 133 Level of dental anxiety....................................................................... 133

14 Common conditions that cause neurological and sensory impairment........................................................... 134

Multiple sclerosis................................................................................... 134 Myasthenia gravis................................................................................ 135 Motor neurone disease....................................................................... 136 Guillain-Barré syndrome...................................................................... 136 Cerebrovascular accident................................................................. 137 Bells Palsy.............................................................................................. 138 Trigeminal neuralgia............................................................................ 139 Parkinson’s disease.............................................................................. 139

17 Fluorosis reviewed.................................................................................. 158

15 A guide to understanding and managing herpes simplex virus in dental practice......................................... 142

Oral microflora..................................................................................... 148 Dentoalveolar abscesses................................................................... 149 Clinical features of infection.............................................................. 149 Microbiology........................................................................................ 150 Management....................................................................................... 151 Complications...................................................................................... 152 Ludwig’s angina.................................................................................. 153 Cavernous sinus thrombosis............................................................... 153 Osteomyelitis........................................................................................ 153 Mediastinitis.......................................................................................... 153 Septic shock......................................................................................... 154 Conclusion............................................................................................ 154 Table 1................................................................................................... 155 Table 2................................................................................................... 155 Table 3................................................................................................... 156 Table 4................................................................................................... 156 Table 5................................................................................................... 156

How does fluoride prevent dental caries?....................................... 158 How does fluoride cause dental fluorosis?....................................... 159 How can fluoride be used to maximise benefit and minimise risk?................................................................................ 160 What does dental fluorosis look like?................................................ 161 Treatment of dental fluorosis.............................................................. 162

18 Smokeless tobacco use in the UK.................................................... 164

Primary HSV-1 infection....................................................................... 142 Secondary HSV - 1 infection............................................................... 143 Herpes labialis (cold sores)................................................................. 143 Oral ulceration..................................................................................... 144 Asymptomatic shedding.................................................................... 144 Managing a patient with HSV infection........................................... 144 General Principles................................................................................ 144 Primary HSV-1 infection....................................................................... 144 Herpes labialis...................................................................................... 145 Oral ulceration..................................................................................... 146 Summary............................................................................................... 146 Guidance for the dental team.......................................................... 147

Smokeless tobacco............................................................................. 164 Smokeless tobacco in the UK............................................................. 165 Oral cancer.......................................................................................... 166 The role of professionals...................................................................... 167 The role of dental professionals......................................................... 167 Conclusions.......................................................................................... 168

19 Dental erosion – a continuing concern.......................................... 170

History and aetiology.......................................................................... 171 Medical considerations...................................................................... 171 Monitoring erosion – putty techniques.............................................. 172 Treatment possibilities.......................................................................... 173 Table 1................................................................................................... 175 Table 2................................................................................................... 175

20 Lasers in general dental practice.................................................... 176

The concept of laser ‘best practice’................................................ 176 Lasers in the practice.......................................................................... 177 Which laser? ........................................................................................ 178 Low level (‘soft’) lasers........................................................................ 178 Surgical (hard) lasers........................................................................... 179 Soft tissue procedures......................................................................... 179 Hard tissue procedures....................................................................... 180

Make this CPD Verifiable

CPD CERTIFIED

Turn to page 181 to find out how 6

PROFESSIONAL DENTISTRY PRESENTS

Aesthetics Now A PROFESSIONAL DENTISTRY CPD E-PUBLICATION EVERYTHING YOU NEED TO KNOW ABOUT AESTHETIC DENTISTRY, FROM THE PROFESSION’S LEADING AUTHORS.

6 hours CPD for only £59+VAT WHY USE THIS CPD E-PUBLICATION? •

Quality content written by the profession’s leading authors

•

Easy to use online interface – quiz and certificate provided for each article!

•

Works on your computer, phone or tablet

ALSO AVAILABLE:

IMPLANTS NOW

6 CPD Hours only £59+VAT

THE FOLLOWING TOPICS ARE COVERED:

DIGITAL DENTISTRY

•

Alignment, Bleaching and Veneers to Correct Big and Unsightly Front Teeth, by Anoop Maini

6 CPD Hours only £59+VAT

•

The Use of Botulinum Toxin Type A to Reduce the Appearance of Fine Lines and Wrinkles in the Forehead, Frown and Eyes, by Dr Harry Singh

DENTAL CPD NOW

•

Composite Resins in Anterior Aesthetics, by Arun Darbar

• Interdisciplinary Smile Design with Personality, by Oliver Harman •

Interdisciplinary Success, by Neil Gerrard

•

The Gold Standard for Single Tooth Replacement, by David Bloom

21 CPD Hours starting from £39+VAT (Multi-year subscription available)

VISIT: cpd.professionaldentistry.co.uk for the list of topics covered

TO BOOK... ► Call 01332 226590 ► Or visit cpdportal.professionaldentistry.co.uk 7

Question time

Dental professionals have been required to have professional indemnity by the GDC for many years, but it is now also a legal requirement to have adequate indemnity arrangements in place. Leo Briggs, Deputy Head of the Dental Defence Union answers some common questions about dental indemnity.

The DDU and other dental defence organisations describe themselves as mutual organisations. What does this mean and why should it make any difference?

The DDU is the specialist dental division of the Medical Defence Union, a not-for-profit mutual established in 1885. Being a mutual means we are owned and funded by our members who can vote on resolutions at our Annual General Meeting. Unlike a commercial provider, we have no shareholders and we are not seeking to maximise profits in order to pay an annual dividend. Our funds, time and efforts are wholly directed to guiding, supporting and defending our members.

Why is the cost of indemnity rising?

We understand members’ frustration when they are asked to pay an increasing amount for their annual subscription, especially if they have not received a claim (or are not yet aware of one). We are conscious that our subscriptions should be set at a reasonable level for all our members but we must also ensure there is enough money in the mutual fund to meet future claims and legal expenses. The sad fact is that the number of claims against our dental professional members has increased by an average of 10% per annum in the last five years. Meanwhile, compensation and legal costs have also risen sharply. In 2015 the DDU settled 11 claims exceeding £100,000 compared to just two such claims in 2006. Claimant legal costs have also increased – almost always being far in excess of our own - and we commonly have to pay more to patients’ lawyers than the patient themselves.

What is the DDU doing about the rising cost?

The affordability of indemnity is an acute concern. The only way to tackle the rising costs in the long term is to address the main reason for those costs through legal reform, such as by making the fees claimant’s lawyers can charge in personal injury cases more proportionate to the damages patients receive. We are active in raising these concerns with policy makers.

What is discretionary indemnity?

The DDU is not an insurance company and claims are paid out of a pool of member-owned funds carefully administered by our Board of Management – ‘at their discretion’. We exist solely for our members and the Board has a legal obligation, when making decisions about assistance, to act fairly, in the interests of our members and in accordance with our Memorandum and Articles of Association. What’s more, unlike a rigid policy of insurance, discretion also enables us to be flexible and responsive to the needs of members – there is no ‘small print’ buried in a long list of exclusions. With our discretionary indemnity there are also no limits on the size of claims we can indemnity or excesses to pay.

What else does a dental professional get for being a member of a dental defence organisation?

Membership of a defence organisation offers much more than financial assistance when things go wrong. For example, the benefits of DDU membership include 24-hour access to expert dento-legal advice from trained dental professionals who understand the challenges you face. We offer legal support at the GDC and with performance, disciplinary and even criminal investigations and hearings relating to your clinical work; help with press enquiries; and CPD. You can find out more about the benefits of DDU membership at www.theddu.com

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Chapter 1

Cleaning instruments

Make this CPD Verifiable Turn to page 181 to find out how

The Department of Healthâ&#x20AC;&#x2122;s document, Decontamination Health Technical Memorandum 01-05: Decontamination in primary care dental practices, often better known by its shorthand name HMM 01-05 gives the guiding principles and details of the requirements for cross-infection control in dental practices. Here we review Section 3 of the document which gives advice to dentists and practice staff cleaning instruments.

Introduction 3.1 The principal methods of cleaning reusable dental instruments currently available are: cleaning using a washer-disinfector; manual combined with ultrasonic cleaning; manual. 3.2 Effective cleaning of instruments is an essential prerequisite before sterilization and will reduce the risk of transmission of infectious agents. Wherever possible, cleaning should be undertaken using an automated and validated washerdisinfector in preference to manual cleaning, as a washer disinfector includes a disinfection stage that renders instruments safe for handling and inspection. 3.3 Manual cleaning, governed by an appropriate protocol, is acceptable within the essential-quality requirements framework. Within the best-practice framework, however, manual cleaning should be considered only where the manufacturer specifies that the device is not compatible with automated processes (including ultrasonic cleaning) or when the washer-disinfector is temporarily unavailable (for example for repair or validation). Exceptionally, where local experience indicates that pre-washing may be helpful (for example in the removal of tenacious dental materials), such action may be appropriate before automated cleaning. 3.4 New instruments should be cleaned and sterilized before using for the first time, unless supplied as sterile.

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3.5 Instruments cleaned as soon as possible after use may be more easily cleaned than those left for a number of hours before reprocessing. Where this is not possible, water immersion or the use of a foam spray or gel intended to maintain a moist or humid environment are thought useful in aiding subsequent decontamination. Long periods of wet storage should, however, be avoided. 3.6 When working with substances that can harden on instruments (for example cements), the instruments should be cleaned immediately. Instruments that cannot be cleaned should be discarded. 3.7 Where recommended by the manufacturer, instruments and equipment that consist of more than one component should be dismantled to allow each part to be adequately cleaned. Members of the dental team should be appropriately trained to ensure competence in dismantling, cleaning, sterilizing and reassembling of instruments. Amalgam carriers are an example of instrumentation requiring his approach.

General requirements for cleaning methods 3.8 Where possible, refer to manufacturersâ&#x20AC;&#x2122; instructions relating to instruments, dental equipment, cleaning devices and cleaning solutions. 3.9 Whenever possible, cleaning should be undertaken using an automated and validated process in preference to manual cleaning. Manual cleaning should be considered where manufacturersâ&#x20AC;&#x2122; instructions specify that the device is not compatible with automated processes. 3.10 Ensure that instruments can be cleaned using a method available to the practice. 3.11 Validation is the means by which an entire process is verified, tested and documented, with the ability to be consistently reproducible. Ensure that ultrasonic and washer-disinfector cleaning procedures used in the practice are validated. This is to demonstrate that all instruments and equipment cleaned by these methods are reliably and consistently cleaned using predetermined and reproducible conditions.

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3.12 Technical details for validation standards and procedures are provided in Section 3. The assistance of decontamination specialists will be necessary from time to time in order to ensure that equipment and procedures remain valid in engineering terms.

Automated cleaning: washer-disinfectors 3.13 The fitting and plumbing of washer-disinfectors must comply with the requirements of the Water Supply (Water Fittings) Regulations 1999. Further details can be found on the WRAS website (http:// www.wras.co.uk). Each stage of the decontamination process should contribute to the reduction of bioburden on the device being reprocessed. Using a washer-disinfector is the preferred method for cleaning dental instruments because it offers the best option for the control and reproducibility of cleaning; in addition, the cleaning process can be validated under European Norms (ENs). 3.14 Washer-disinfectors are used to carry out the processes of cleaning and disinfection consecutively in an automated cycle. A typical washer-disinfector cycle for instruments includes the following five stages: •

Flush – removes ‘difficult’ gross contamination, including blood, tissue debris,

bone fragments and other ﬂuid and solid debris. Latest standards indicate that a water temperature of less than 45oC is used to prevent protein coagulation and fixing of soil to the instrument. •

Wash – removes any remaining soil. Mechanical and chemical processes

loosen and break up contamination adhering to the instrument surface. Detergents used in this process must be specified by the manufacturer as suitable for use in a washer-disinfector and compatible with the quality of water used. Detergents should also be compatible with the instruments being processed to avoid instrument degradation including discoloration, staining, corrosion and pitting. •

Rinse – removes detergent used during the cleaning process. This stage

can contain several sub-stages. The quality of water to be used for this stage is an important consideration in terms of ensuring a clean unmarked product after sterilization. Advice should be taken from manufacturers with respect to the compatibility of the hardness or quality of the water supply with the equipment and detergents used.

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Help your patients spread the cost of their regular hygiene treatments with Denplan Hygiene Plan. The plan is a simple, non insurance based payment plan to fully utilise experienced hygienists and help patients achieve better oral health. You’ll benefit from regular income and patients that attend more regularly*, while your patients enjoy that ‘just cleaned’ feeling without worrying about the cost. And as a Denplan member you’ll also receive the full range of clinical, business and marketing support that comes as standard with Denplan membership. To find out more call 0800 169 9962 or visit www.denplan.co.uk/hygiene *Payment plan patients are the most likely to visit their dentist at least every six months (92%) compared to private patients who pay as they go (50%). Source: Denplan/YouGov Survey, January 2016. Online survey of 5,152 UK adults. All respondents who are regular attenders that pay privately, who have a dental payment plan or pay fee per-item: 822.

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CAM2049 01-17

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15 CAM2049 Hygiene Plan FPA Professional Dentistry Mag 01-17.indd 1

01/02/2017 08:05

Note: Some systems with a water capacity and delivery rate especially suited to use in this and other dental applications are available. The supply arrangements will frequently include a comprehensive package such that water is supplied as a service. •

Thermal disinfection – the temperature of the load is raised and held at

the pre-set disinfection temperature for the required disinfection holding time:

for example, 80oC for 10 minutes; or 90oC for 1 minute.

•

Drying – Purges the load and chamber with heated air to remove residual

moisture.

Using a washer-disinfector 3.15 For details of all operational aspects of using a washer-disinfector, follow the manufacturer’s instructions. This will include details of both the water quality/type to be used and directions on the detergents and/or disinfectants recommended for use with the device. These instructions form part of the European norm (EN) requirements for CE (Conformité Européenne) marking and are considered to be part of the regulated product. 3.16 Ensure that staff are trained in the correct operation of a washer-disinfector, including how to perform daily tests and housekeeping tasks. Records of training and the achievements of staff should be maintained. 3.17 It is crucial to load a washer-disinfector correctly, as incorrectly loaded instruments will not be cleaned effectively. Therefore, follow an instrument-loading procedure that has been shown to achieve effective cleaning in the washerdisinfector used in the practice. To do this: •

do not overload instrument carriers or overlap instruments

•

open instrument hinges and joints fully

•

attach instruments that require irrigation to the irrigation system correctly,

ensuring filters are in place if required (for example for handpieces, if specified

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3.18 After cleaning, inspect instruments for cleanliness and check for any wear or damage before sterilization. (The use of a simple magnifying device with task lighting will improve the value of this part of the process.) The satisfactory completion of this step means that these instruments may be clearly designated as ready for sterilization.

Records 3.19 Washer-disinfector logbooks and records should be kept by the designated “user” – an identified member of the practice staff. Cycle parameters should be recorded together with details of routine testing and maintenance of the equipment used. The use of automated data-loggers or interfaced small computer-based recording systems is acceptable, provided the records are kept securely and replicated. It is recommended that records be maintained for not less than two years.

Considerations for cleaning handpieces 3.20 Check with the handpiece manufacturer that a washer-disinfector can be used to clean the handpieces. 3.21 Certain types of washer-disinfector can be adapted to clean handpieces, and these can be validated independently as being effective. 3.22 Where a handpiece manufacturer does not recommend a washer-disinfector for cleaning the handpiece, use of a dedicated handpiece-cleaning machine may be considered. This uses a pressurised system to clean and lubricate handpieces. However, unlike a washer-disinfector, it does not disinfect. 3.23 Always consult the washer-disinfector manufacturer for operating details (for example whether filters are required) and running costs before purchase. 3.24 Washer-disinfectors might remove all lubricants during the cleaning cycle; therefore, handpieces might require further lubrication after cleaning. Follow the handpiece manufacturer’s recommendations for lubrication. Using a washer-disinfector is the preferred method for cleaning dental instruments because it offers the best option for the control and reproducibility of cleaning.

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Note 1. Some washer-disinfectors that have a handpiece irrigation system require that a special filter be fitted to protect the internal mechanism of the handpiece from extraneous debris during the operating cycle. These filters need to be replaced at regular intervals in accordance with the manufacturer’s instructions. 2. There are machines that both clean and sterilize dental handpieces. At present it is not possible to validate the cleaning cycle of these devices using accepted criteria. However, due to the use of a vacuum sterilization cycle (Type S) there is an advantage of this process over using a Type N sterilizer.

Automated cleaning: ultrasonic cleaning 3.25 Evidence on the effectiveness of ultrasonic cleaning gives support to its use in dentistry. However, it is important to ensure that the water/fluid is maintained, cleaned and changed at suitable intervals. The bath should also be kept free of dirt released in the cleaning process. Good maintenance is also essential. The appearance of instruments following ultrasonic cleaning should be checked to ensure that the process is operating effectively. 3.26 Ultrasonic cleaning in a well-maintained machine enhances removal of debris. Thus, although a washer-disinfector is preferred and should be incorporated into new plans or upgrades, an ultrasonic cleaner can be used as a cleaning method – including being used as an extra cleaning stage prior to an automated washerdisinfector process. This may be particularly helpful for instruments with hinges and/or intricate parts. 3.27 To enable consistent cleaning of instruments, follow the manufacturer’s operating instructions and ensure that all staff use a specified and documented operating procedure. 3.28 The use of ultrasonic cleaners to clean dental handpieces should not be undertaken without confirmation from the manufacturer that the devices are compatible. 3.29 The ultrasonic cleaner should be tested according to the manufacturer’s instructions or, in the absence of these, quarterly.

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Ultrasonic cleaning procedure 3.30 The following procedures should be followed: a. Instruments should be brieﬂy immersed in cold water (with detergent) to remove some of the blood and other visible soil before ultrasonic cleaning. Care should be taken to minimise aerosol production in this process and to safeguard against inoculation injury. The use of a purpose-designed container with sealing lid is recommended. b. Follow the manufacturer’s recommendations for the safe operating procedure of the ultrasonic cleaner and follow the points outlined below regarding loading and unloading the cleaner. c. Ensure that joints or hinges are opened fully and instruments that need taking apart are fully disassembled before they are immersed in the solution. d. Place instruments in a suspended basket and fully immerse in the cleaning solution, ensuring that all surfaces are in contact with the solution. The solution should be made up in accordance with the manufacturer’s instructions. e. Do not overload the basket or overlap instruments, because this results in poor cleaning and can cause wear to the instruments. f. Do not place instruments on the floor of the ultrasonic cleaner, because this results in poor cleaning and excessive instrument movement, which can damage the instruments. g. To avoid damage to delicate instruments, a modified basket or tray system might also be necessary depending on operational requirements. h. Set the timer to the correct setting as per the ultrasonic cleaner manufacturer’s instructions. Close the lid and do not open until the cycle is complete. j. After the cycle is complete, drain the basket of instruments before rinsing. k. Change the solution when it becomes heavily contaminated or otherwise at the end of every clinical session, because the build-up of debris will reduce the effectiveness of cleaning. Ensure that staff are aware of the need to assess when a

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change of solution is necessary as advised in the operational requirements. m. After ultrasonic cleaning, rinse and inspect instruments for cleanliness, and where possible check for any wear or damage before sterilization. 3.31 Instruments cleaned in an ultrasonic cleaner (or by hand) should be rinsed thoroughly to remove residual soil and detergents. A dedicated sink or bowl (separate from the one used for the original wash) should be used, and the instruments immersed in satisfactory potable water or, where this is not available, in RO or distilled water. Wash-hand basins should not be used. (This step may be omitted if the local policy and procedure involves the use of a washer-disinfector as the next stage in the decontamination process.) Note Hard-water contamination of wet instruments, which then go on to sterilization, can compromise the proper function of a small steam sterilizer. Advice should be sought from the manufacturers. When potable water is used, a water softener device may be needed. 3.32 Instruments should be sterilized as soon as possible after cleaning to avoid air-drying (which can result in corrosion and/or microbial growth). For instruments processed in a vacuum sterilizer, before being wrapped, instruments should be dried using a disposable non-linting cloth.

Manual cleaning 3.33 In principle, manual cleaning is the simplest method to set up, but it is hard to validate because it is difficult to ensure that it is carried out effectively on each occasion. 3.34 Compared with other cleaning methods, manual cleaning presents a greater risk of inoculation injury to staff. However, despite the limitations of manual cleaning, it is important for each practice to have the facilities, documented procedures and trained staff to carry out manual cleaning as a backup for when other methods are not appropriate. 3.35 For dental services that are working to the best practice requirements outlined in this document, manual cleaning (acceptable under the essential quality requirements) should only be used for equipment that cannot be cleaned by automated methods. 3.36 This method should have systems in place to avoid recontamination of cleaninstruments.

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3.37 An effective system for manual cleaning should be put in place and all staff should follow an agreed written procedure. A visual inspection for cleanliness, wear and damage should be carried out. 3.38 Consider routinely using an automated method (for example a washerdisinfector). Aim to phase-in instruments that can be cleaned in a washer-disinfector. Avoid instrument damage. 3.39 Most dental instruments are made of high-quality materials designed to minimise corrosion if reprocessed correctly. The corrosion resistance is based on their alloy composition and structure, which forms a protective passivation layer on the surface. The ability of the instruments to resist corrosion depends on the quality and thickness of this layer. 3.40 It is important to avoid damage to the passivation layer during cleaning. Accordingly, methods such as the use of wire brushes, which may give rise to surface abrasion, should be avoided. 3.41 Any instruments that have rust spots should be removed.

Cleaning procedure summary 3.42 Effective cleaning of dental instruments before sterilization is of the utmost importance to reduce the risk of transmission of infectious agents. 3.43 Research suggests that instruments cleaned as soon as possible after use are more easily cleaned than those left for a number of hours before reprocessing. 3.44 Instruments should be transferred from the point of use to the decontamination areas as soon as is practical to ensure that processing takes place as soon as possible after use. Evidence indicates that keeping instruments moist after use and prior to decontamination improves protein removal and overall decontamination outcomes. 3.45 It should be noted that certain solutions are corrosive to stainless steel instruments and will cause pitting and then rusting if allowed to remain on instruments for any length of time.

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Chapter 2

Radiation doses and risks in dental practice

Make this CPD Verifiable

Nicholas Drage and Anne Walker FGDP Online Standards Programme

Turn to page 181 to find out how

Radiography is an invaluable tool for the clinician, providing information that is impossible to obtain by clinical examination alone. Of all the x-ray examinations carried out in the UK, around 26% are taken by general dental practitioners. In 2008, it was estimated that 20.5 million dental radiographs were taken by dentists in NHS and private practice, and of these 2.7 million were panoramic radiographs. Consequently dentists, equipment manufacturers, medical physics experts and radiation protection advisers need to work to keep radiation doses and risks as low as reasonably practicable. If selection criteria are used properly, the collective dose to the population is reduced, since unnecessary or unproductive x-ray examinations are eliminated. X-rays are a type of electromagnetic (EM) radiation. EM radiation also includes visible light, radiowaves, microwaves, cosmic radiation and several other varieties of ‘rays’. All can be considered as ‘packets’ of energy, called photons, which have wave properties, most importantly a wavelength and frequency. X-rays are shortwavelength, high-frequency EM radiation. The importance of this is that high frequency means high energy. When x-rays hit atoms this energy can be transferred, causing ionisation of the atoms.

Radiation damage An x-ray beam consists of millions of high-energy photons. These can damage molecules by ionisation of atoms, but damage to the DNA in the chromosomes is of particular importance. Most DNA damage is successfully repaired, but rarely a portion of a chromosome may be permanently altered (a mutation). This may lead to uncontrolled cell replication, ultimately leading to the formation of a tumour. The latent period between exposure to x-rays and diagnosis of a tumour may be many years. The probability of a tumour being produced is related to the radiation dose, so knowledge of the doses delivered is important. Such effects where the magnitude of the risk is related to dose can be considered as ‘chance’ (stochastic)

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effects. For these effects there is no clear evidence of the existence of a safe level of radiation dose, i.e. it is currently assumed that any level of dose could lead to tumour induction. However, the lower the radiation dose, the lower the risk of radiationinduced tumours. There is strong, well-documented epidemiological evidence that exposure to radiation at doses above some tens of millisieverts is associated with an increased risk of cancer. Studies have shown increased cancer risk associated with CT scans in childhood and raised levels of exposure to background radiation. Dose levels associated with dental radiology are even smaller; however, a number of epidemiological studies have provided evidence of a possible increased risk of brain, salivary gland and thyroid tumours related to dental radiography. Another stochastic effect is that of heritable damage seen in the children of irradiated parents. As the radiation dose to the reproductive organs is so low in dental examinations, the risk of heritable effects is negligible. There are other known damaging effects of radiation, such as skin erythema, hair loss and effects on fertility, that definitely have threshold doses below which they will not occur. As dental radiography would never exceed these thresholds which are some thousands of millisieverts, except in extraordinary circumstances, these tissue reactions or deterministic effects are given no further consideration. Cataract formation was, until recently, believed to have a similar threshold; however, the evidence has indicated a threshold of about 500 mSv, a factor of three lower than previously thought. This level is still well above that observed in dental radiography, but risk of cataract induction could become a concern if many repeated cone beam computed tomography (CBCT) or CT examinations which included the orbits were undertaken.

Radiation dose The term â&#x20AC;&#x2DC;doseâ&#x20AC;&#x2122; is widely used but often misunderstood. There are three common terms used to describe dose: absorbed dose, equivalent dose and effective dose. Absorbed dose (D) Of the three dose quantities, this is the only one that can be directly measured. The absorbed dose is the mean energy imparted to a unit mass of matter (e.g. tissue) by the ionising radiation. The units of measurement are joules per kilogram (J/kg), which are called grays (Gy).

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Equivalent dose (HT) Some types of ionising radiation are more damaging to tissue than others. This is taken into account when making dose calculations by weighting the absorbed dose depending on the type of radiation used. For instance, alpha particles will potentially cause much more biological damage than x-rays for the same absorbed dose, and so they are given a weighting 20 times that of x-ray photons. For dental radiography, which only uses x-rays, the absorbed dose and the equivalent dose are numerically the same. Equivalent dose is still measured in J/kg, but its unit is given the special name of sievert (Sv). Effective dose (E) Different tissues of the body are more susceptible to the effects of ionising radiation than others. This is taken into account when calculating the effective dose. The International Commission on Radiological Protection (ICRP) has published revised tissue weighting factors for the most radiosensitive tissues of the body. The modifications were introduced mainly on the basis of new epidemiological evidence of cancer induction in the survivors of the Japanese atomic bombs. The main changes relevant to the calculation of effective dose from dental radiography are the addition of the salivary glands as an individual weighted tissue and the inclusion of the oral mucosa in the remainder tissues. Consequently, effective doses calculated using the current ICRP recommendations for dental exposures are significantly higher than using the previous weighting factors. Therefore, caution must be taken when trying to compare effective doses calculated using different weighting factors. In dentistry, the effective dose is often small, so it is more appropriate to use subunits such as the millisievert (mSv) which is one thousandth of a Sv, or the microsievert (μSv), which is one millionth of a Sv.

Factors influencing effective dose The radiation dose delivered for a specific imaging requirement can be determined by a range of factors, some related to the equipment type and design, others to the operator’s use of the equipment. They can be grouped into three categories: •

The sensitivity of the image receptor – using a high-speed (i.e. more sensitive)

system will reduce the dose required

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•

The area exposed to the primary beam – reducing the volume exposed and

ensuring that more sensitive organs are in areas of lower dose will limit the

effective dose

•

The exposure factors selected – selecting equipment settings that give lower

dose while maintaining adequate image quality.

Correct selection of equipment and technique can significantly reduce the patient dose. However, dose should not be reduced to such a level that the image quality is not adequate for the clinical purpose. There is a balance between radiation dose and image quality, and the operator must be trained to understand how the factors interact to optimise the imaging process.

Intraoral radiography It is recommended that intraoral dental x-ray equipment should have the following design features: •

Equipment should operate at a voltage between 60–70kV

•

Constant potential units are preferred to generators with pulsating waveforms

•

The beam must be adequately filtered using an appropriate thickness of

aluminium •

An open-ended spacer cone should be used in conjunction with rectangular

collimation •

A long focus-to-skin distance should be used (200mm for sets operating

between 60–70 kV)

•

A range of available exposure times of sufficiently fine graduations to

produce optimally exposed radiographs over the full range of possible patient sizes, anatomical views and speeds of imaging system. In addition, a sensitive image detector system should be used, such as F-speed film or a digital detector. The use of modern equipment combined with good technique and sensitive detectors can make a tenfold difference to the effective dose.

A national review of dose in dental practice in the UK found that the average dose for an adult molar setting had decreased by 57% since 1999 as a result of the adoption of new equipment and more sensitive image detectors. A number of studies have compared doses in digital and film intraoral radiography in which the dose reduction offered by digital over conventional film ranged between 20â&#x20AC;&#x201C;70%. In addition, owing to the greater range of dose that will give acceptable images, care must be taken to use the level of dose that will give an acceptable image as opposed to the best image, which is likely to be at a significantly higher dose.

Panoramic and cephalometric radiography There are also marked differences in the doses associated with different panoramic machines, primarily related to the speed of the detector and the selection of beam sizes available. Modern film screen systems have speeds very similar to current digital detectors, and it is unlikely that the introduction of digital technology will see the same dose reduction in either panoramic or cephalometric radiography as is currently being experienced in intraoral radiography.

Cone beam computed tomography CBCT is the most significant development in dental and maxillofacial imaging in recent years. The first commercially available machine on the market was introduced in the late 1990s, and there are now a large number of manufacturers producing CBCT machines. High-resolution, three-dimensional images of teeth and jaws are produced. Consequently, there are several applications of CBCT in dentistry including endodontics, orthodontic diagnosis and the assessment of the jaw prior to implant placement. The SEDENTEXCT group has produced evidence-based referral criteria to clarify those clinical situations in which CBCT may be useful. CBCT units are significantly cheaper than medical CT machines and have a much smaller footprint. These features, combined with the potential for increased diagnostic yield, make these systems attractive to dentists working outside the hospital sector. The effective dose from CBCT is dependent on many factors, with one of the main ones being the volume of tissue irradiated. The volume of tissue that is irradiated is often referred to as the field of view (FoV). Comparison of effective dose with

respect to FoV size is shown in Table 1. There is a marked range in the effective doses in each category because of differences in the equipment being used, including the detector type and the scanning parameters selected (tube current, voltage and time of exposure, including the number of projections obtained). In addition, for small FoV scanners the dose varies depending on the region of the jaw being scanned. Some machines allow a choice of exposure factors and offer a wide choice of FoVs, while on other units these features are either fixed or there is a limited choice. These factors must be one of the prime considerations when considering buying such a unit. It is important that the exposure factors and FoV are optimised to the clinical question being investigated. There is no need for the routine use of lead aprons for patients undergoing CBCT examinations. However, there is some evidence to support the use of a thyroid shield for CBCT, as this may reduce the effective dose by up to 40%. If a thyroid shield is used, it must be positioned carefully so as not to cause artefacts on the images or obscure areas of interest. The effective dose from medical CT is generally higher than that from CBCT. However, scanning parameters can be optimised to reduce the dose considerably, with the advantage that softâ&#x20AC;&#x201C;tissue differentiation is still possible even with low exposure factors.

The risks It is useful to understand the magnitude of the risk associated with dental radiography when considering the justification of individual dental exposures and the effect of dental exposures on the whole population. Risk factors are regularly published and are constantly being refined as new data become available and more sophisticated modelling is undertaken. As discussed above, the risk associated with dental radiography is primarily that of cancer induction. A publication by the UK Health Protection Agency proposes the use of a total lifetime cancer induction risk factor for an average 30-to-39-year-old of 6.8% per Sv for men and 5.5% per Sv for women for radiography of the head. Another way of expressing this is to say that there is a 1 in 15,000 (for men) and 1 in 18,000 (for women) risk of a cancer being induced for every 1mSv effective dose received from dental radiography. Risk is age-dependent, being highest for the young and lowest for the elderly. The tissues of younger people are more radiosensitive and their prospective life span is

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likely to exceed the latent period. For the very elderly, life expectancy will be less than the latency period, which can be anything from five years upwards and the risk could be considered negligible. In general, young children are at about two to three times the risk of develop radiation-induced cancer than adults in their thirties for the same effective dose, hence the importance of using specific paediatric exposure protocols when radiographing children to ensure that the dose is minimised. There is often considerable concern about radiography during pregnancy because of possible risk to the foetus. In dental radiography, it is unusual for an x-ray beam to be pointed at the abdomen (only for vertex occlusal radiographs, which are rarely indicated) and, in those cases where radiography is essential, abdominal lead protection should be used when a foetus lies in the primary beam. For all other dental radiographic views, including panoramic and CBCT examinations, there is no requirement to delay radiography until after the birth. However, as the subject of radiography during pregnancy is emotive, it is recommended that practitioners offer pregnant patients the option of delaying non-urgent radiography. Table 1 gives typical doses for radiographic examinations of teeth and jaws, including dental radiographic techniques likely to be used in primary dental care. The doses have been calculated either using the current ICRP recommendations or, in those studies that predate these recommendations, those ones that include weighting factors for the salivary glands. Effective doses are calculated for a reference patient and there are many uncertainties in the calculations. Risk estimates for an individual based on the calculated effective dose may be higher or lower by a factor of five. For this reason, risk has been split into broad categories to indicate the health detriment. The risk from dental radiography falls into the lowest risk category. Even the risk from medical CT of the jaws is considered very low. However low the risk from the examination, it is imperative that each radiographic exposure is fully justified and the doses optimised to reduce the detrimental effects to the lowest possible level. categories to indicate the health detriment. The risk from dental radiography falls into the lowest risk category. Even the risk from medical CT of the jaws is considered very low. However low the risk from the examination, it is imperative that each radiographic exposure is fully justified and the doses optimised to reduce the detrimental effects to the lowest possible level.

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Table 1 Effective doses for traditional dental 1: Effective doses for traditional dental radiography, CBCT and CT examinations

Radiographic technique

Effective dose (μSv)

Intraoral radiograph

0.3–21.6

(bitewing/periapical) Panoramic radiograph

2.7–38

Lateral cephalometric radiograph

2.2–14

CBCT (small field of view*)

11–214

CBCT (medium field of view**)

18–674

CBCT (large field of view***)

60–510.6

CBCT (extended field of view****)

30–1025

CT scan (mandible)

250–1410

CT Scan (mandible and maxilla)

430–860

* The height of cylindrical volume or spherical diameter of the volume ≤ 5cm ** The height of cylindrical volume or spherical diameter of the volume > 5cm and ≤ 10cm. *** The height of cylindrical volume or spherical diameter of the volume > 10cm and ≤15cm **** The height of cylindrical volume or spherical diameter of the volume > 15cm

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Chapter 3

Medical emergencies: asthma attack & inhaled body By M H Thornhill, M N Pemberton & G J Atherton

Make this CPD Verifiable Turn to page 181 to find out how

There are a variety of situations in practice which precipitate a medical emergency, two of which are an acute asthma attack and the circumstance of an inhaled foreign body.

Asthma attack The reported incidence of asthma is increasing both in the UK and worldwide. Most people with asthma are atopic and have a tendency to suffer with eczema, hayfever, rhinitis, and other allergies. Contact with a sensitiser causes inflammation and narrowing of the airways resulting in the asthma symptoms of difficulty in breathing (mainly on expiration), wheezing, chest tightness and cough. Such effects can be measured with a peak flow meter. Acute asthmatic attacks can be triggered by environmental allergens, exercise and respiratory viral infections. Attacks can be fatal and should be treated promptly.

Figure 1

Figure 2

In general, less than 20% of people presenting to an emergency department with asthma are actually admitted to hospital and of these, fewer than 10% require mechanical ventilation. A systematic review has indicated that delivering an inhaled bronchodilator via a spacer device can be as effective as using a nebuliser in the treatment of an acute asthmatic attack (Figure 1). In developing countries, commercially produced spacers are generally unavailable or too expensive. This has led to efficacy testing of home-made devices. A 500ml plastic soft-drink bottle with a hole cut in its base for the metered dose inhaler to be inserted, and the bottle 42

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opening used as a mouthpiece has been found to be as efficient as a conventional spacer (Figure 2). A polystyrene drinks cup converted for use as a spacer was found to be less efficient, although still able to produce clinically important improvement. All plastic spacers have an electrostatic surface charge that reduces their efficiency. This can be overcome by priming the spacer with several puffs of bronchodilator or rinsing in detergent before use.

Signs and symptoms •

Breathlessness and a tight chest

•

Wheezing on expiration

•

Accessory muscles of respiration in action

Features of an acute severe attack •

Inability to complete a sentence in one breath

•

Respiratory rate greater than 25 per minute

•

Heart rate greater than 110 per minute

Features of life threatening asthma •

Exhaustion, confusion

•

Feeble respiratory effort or cyanosis

•

Heart rate less than 50 per minute

Prevention The best means of prevention are to avoid anxiety, pain and known allergens. Ensure that the patient has had their normal prophylactic medication and has their bronchodilator readily available. If a nebuliser is not available a similar effect can be obtained by administering 4-6 puffs of a bronchodilator into a large volume spacer and getting the patient to inhale through the spacer. This can be repeated every 10 minutes if necessary. A makeshift large volume spacer can be formed by administering the bronchodilator through a hole in the base of a large disposable cup or 500ml soft drink bottle that the patient holds to their mouth.

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Causes Exposure to an allergen, anxiety, cold, exercise or infection can precipitate an acute asthmatic attack in a patient predisposed to bronchospasm. Most attacks come on rapidly (within 30 minutes) and occur in patients with a known history. An acute asthma attack should not be taken lightly; if a patient fails to respond to treatment, they should be referred to hospital.

Management •

Keep the patient sitting upright - laying them flat will increase breathlessness

•

Encourage them to use the bronchodilator they normally use

•

Offer a salbutamol inhaler if they do not have their own available

•

If available administer 4-6 activations from a salbutamol inhaler via a large –

volume spacer device

•

Give oxygen

•

Patients requiring additional doses of inhaled bronchodilator to control

their asthma should be referred to their general medical practitioner for further assessment of their asthma control (Note: Bronchodilator inhalers are blue, steroid inhalers are brown). If the patient continues to be distressed or develops features of severe or life threatening asthma) •

Call for an ambulance

•

Give nebulised salbutamol 5mg (Ventolin®) with oxygen, or continue to give

4-6 activations from a salbutamol inhaler via a large-volume spacer device

•

Give oxygen If the asthma is life threatening or part of an anaphylactic attack

•

Give 0.5mL of 1:1,000 (500μg) adrenaline (epinephrine) i/m

Inhaled foreign body Inhalation of a foreign body such as a tooth, inlay, crown or reamer is an everpresent risk in dentistry. An object lodged in the upper airways may cause respiratory obstruction. Smaller objects may be inhaled into the lower airways where, if left, may result in a lung abscess. Judging by the paucity of discussion of this subject in the literature, this type of event, although common, only rarely causes serious problems. The use of a rubber dam and tethering of fine hand instruments is advisable. Take extra care with those patients who may have a reduced gag reflex, such as those under sedation, who are more at risk of swallowing or inhaling an object. Positioning of the patient may be a factor; some believe that treating patients while they are supine decreases the risk of aspiration or swallowing, while others believe that this increases the likelihood of these events occurring. There are reports of objects passing into the trachea without eliciting a cough or any other symptom suggesting inhalation. The effect of a foreign object passing into the oropharynx depends on its size and shape and where it ends up. A sharp metallic object could theoretically pierce the lining mucosa at any point of its journey either into the respiratory or gastro-intestinal (GI) tracts and cause a mediastinal or abdominal infection. A pneumothorax may result if the lung wall is pierced. It may become impacted in the oropharynx; an object large enough to block the opening to the trachea may obstruct the airway and cause the patient to choke. If the object enters the respiratory tract it will lodge in the bronchial tree and it is important that it is retrieved as quickly as possible. The intense inflammatory response provoked by the object will make removal by brochoscopy much more difficult if there is delay, and surgical removal may then become necessary. If the object passes down the oesophagus into the stomach, more than likely it will pass uneventfully through the gastro-intestinal (GI) tract. Sharp objects, such as reamers, tend to pass through the intestines with the sharp end trailing in the centre of the faeces once they reach the transverse colon. Bloody stools or abdominal pain suggest perforation of the gut wall. Many authorities suggest chest and abdominal radiographs to locate the object and, if it is in the GI tract, serial radiographs to monitor its passage. However, in the absence of symptoms, some may think repeated irradiation of the abdomen and reproductive systems, especially in growing patients, to be excessive. Results from a British survey suggest that objects passing beyond reach into the oropharynx are approximately 30 times more likely

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to be swallowed than inhaled. According to a review of the Japanese literature, the majority of dental foreign objects swallowed or inhaled were dentures and the majority of instruments ‘lost’ during dental treatment were reamers.

Signs and symptoms Upper airways obstruction •

An object lodged in the upper airway will stimulate a cough reflex

•

If the patient is choking, the object is large enough to cause respiratory

obstruction •

The patient may grasp their throat

If the object blocks the airway completely they will be silent, unable to breathe or speak •

The skin will become cyanosed; this is especially evident in the lips

•

They will make exaggerated efforts to take breath

•

Eventually they will lose consciousness

Lower airways obstruction •

The patient may be totally unaware that they have inhaled anything

Management If the patient is not choking or having difficulty breathing, check if the object is still in their mouth or clothing If the object cannot be found or is known to have fallen into the throat: •

If the patient is supine, do not allow them to sit up but place the dental chair

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may be retrieved Rolling the patient into the recovery position and encouraging them to cough may also help. If the object cannot be retrieved: •

Explain what has happened

•

Refer to a hospital accident and emergency department for further

assessment (chest and abdominal radiographs may be taken – a further sample of the lost object shown to the accident and emergency doctor can help with assessment and radiographic identification) •

If the object is found to be in the gastrointestinal tract (i.e., to have been

swallowed), it is normally left to pass per rectum

•

If the object is found to be in the respiratory tract, removal may require

endoscopy or thoracic surgery.

If the object is larger and is causing breathing difficulties or choking •

Encourage the patient to cough forcefully to dislodge the object

•

Lean the patient forward and give up to five sharp blows between the

shoulder blades

•

If this does not dislodge the object, give up to five abdominal thrusts

•

If this fails, recheck the mouth and remove any obstruction and continue to

alternate five back blows with five abdominal thrusts.

If the patient becomes unconscious •

Lay them flat

•

Commence CPR

Note. The pressure generated in the chest by performing chest compressions may also help to dislodge the foreign body.

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Prevention Such events are far easier to prevent than to treat and the use of a rubber dam will prevent all but the most bizarre incidents. An efficient high volume aspirator is also useful in aiding retrieval of any object dropped in the mouth. Be especially careful when trying-in crowns or inlays or using small instruments in the mouth, ensure that burs are properly secured in the handpiece.

Dislodging an object from the airway Back blows Lean the patient forward, for example over a chair, so that when the obstructing object is dislodged it is ejected from the mouth rather than going further down the airway. Use the heel of your hand to give up to five sharp blows between the shoulder blades (Figure 3). Abdominal thrusts (Heimlich Manoeuvre) Form a fist with one hand and grip it with the other hand while encircling the patient with your arms from behind; your arms should be positioned just below the patientâ&#x20AC;&#x2122;s ribs (Figure 4). Pull upwards and towards you, delivering a firm, upward, inward thrust to the patientâ&#x20AC;&#x2122;s diaphragm to expel air and the object from the chest. At any time the patient may become unconscious. Unconsciousness may relax the muscles around the larynx and allow air to pass into the lungs.

Figure 3

Figure 4

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Chapter 4

Employment issues in dental practice Glenys Bridges Adapted from Dental practice management

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This article looks at the background of employment law and considers contracts of employment, disciplinary and grievance procedures and the Equality Act 2010. As employment law is a rapidly evolving aspect of practice management this article looks at the underpinning principles, official bodies and broad themes. When required for policy building or taking remedial action, the finer detail should be gathered from legal advisors, or from the range of government websites which will be introduced throughout this article. It is important to note that Scottish law can differ from English law. The information here applies to English law.

The origins of British employment law The origins of British law can be traced back to 1066 and the Norman Conquest when feudal barons used trial by ordeal techniques. Records show that in 1215 the Church intervened to stop this practice and introduced trial by jury. In the 1400s the legal system began to evolve its modern shape when travelling judges on tours known as Assizes were introduced. In 1972 the Crown (Criminal) and County (Civil) Courts Systems currently in place were introduced and in the 1970s the Tribunal system was introduced to make the law more accessible. When Britain joined the European Community, under the terms of the Treaty of Rome, we became subject to European Union (EU) rules and regulations and the authority of the European Court of Justice (ECJ), which legislates through: •

Regulations: Immediately binding upon member states

•

Directives:

Binding but member states choose how

and when to introduce them

•

Binding on the state to which they directly apply.

Decisions:

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Britain is subject to European Directives relating to Employment Law in respect of: •

Equal Pay

•

Employee’s Rights

•

Health and Safety

•

Freedom of movement for workers from member country to country

•

Equality and Human Rights.

How this may differ following the UK exit from the EU (Brexit) remains to be determined.

Enforcement There are a number of bodies with responsible for enforcing employment law these are: Employment Tribunals (ET) The Tribunals system was set up in 1974 to deal with the majority of Employment Law actions. Tribunals make the law more accessible to the population in general, hearing applications, sometimes called ‘complaints’ and appeals about employment matters such as: •

Unfair dismissal

• Redundancy • Equality • Pay •

Terms and conditions of employment.

Tribunals are similar to courts in many ways, although less formal. Claims are heard by a Panel in the Employment Tribunal’s offices. A tribunal panel generally has three members, the Chairman, who is legally qualified and appointed by the Lord Chancellor, plus two lay members appointed by the Secretary of State for Trade and Industry. They will be people with experience of resolving work related problems. The time limits for Employment Tribunal are shorter than for the courts. Applications must be made within three months of the end of the employment, or from when the complaint occurred. Unlike in the courts, at tribunals the parties cannot be ordered to pay costs for the other party, unless the tribunal considers that one party has behaved unreasonably. 58

County Courts Civil (non criminal) cases are brought through the County Courts. This can include breach of contract, damages and wrongful dismissal cases. Anyone taking Employment Law action for claims in excess of £50K, or where damages need to be assessed must apply to the County Court, where proceedings are more complicated and costly than in an Employment Tribunal. Employment Relations Directorate (ERD) Over recent years Employment Law has placed an increasing emphasis on social and political correctness. This has prompted guidance and directives from Europe and as a result the red tape with which businesses have needed to contend has increased. To help businesses work within the law the Government has created the Department for Business, Energy and Industrial Strategy to provide simplified information policy and legislation related to: •

European directives

•

Representation in areas of employment rights

•

Employment relations

•

Hours of work The ERD has operational responsibility for:

•

Payment of redundancy and insolvency claims

•

An employment agency standards inspectorate

•

Monitoring on pay and advice on pay

•

The arbitration service ACAS.

The ERD can be found on the government website bis.gov.uk ACAS - Advisory, Conciliation and Arbitration Service Founded in 1974, ACAS is a publicly funded body run by a council of 12 members from businesses, unions and the independent sector. ACAS employs about 800 people throughout England, Scotland and Wales and is structured into 11 main regions, plus a Head Office in London.

The Aim of ACAS is the prevention and resolution of problems in the workplace by: •

Providing telephone help lines providing free information to anyone with a

work problem. This information is supported by an extensive range of publications and an informative website •

Resolving problems

•

ACAS’s focus remains on prevention and the promotion of good practice.

The Advisory Service works with hundreds of companies every year to develop a joint approach to problem solving •

Settling employee complaints. Over 100,000 each year apply to Employment

Tribunals 71% of these are sorted out at pre-tribunal stages through ACAS •

Education. ACAS run workshops and seminars on Employment Law subjects.

Employment contracts The employment contract is central to employment law; a contract of employment is an agreement between employer and employee and forms the basis of the employment relationship. A contract of employment is an agreement between an employer and an employee setting out the rights and duties of both parties in the ‘terms’ of contract. The contract does not have to be in writing, but employees are entitled to a written statement of the main terms within two months of starting work. The contract is made as soon as a job offer is accepted, and both sides are then bound by its terms until it is properly ended (usually by giving notice) or, until the terms are changed (usually by mutual agreement). Employment rights are dependent upon whether the employment status is classed as an ‘employee’, ‘worker’ or ‘self-employed’. This depends on the type of contract you have with your employer. The contract of employment should specify: •

Date on which contract is given

•

Names of parties

•

Date of employment

•

Wages - including overtime/calculation of bonuses

•

Intervals at which wages will be paid

•

Hours of work

•

Holiday entitlement and what happens on leaving

•

Job title and/or description

•

Place of work

•

Notice requirements.

In addition, information must be given about: •

Sick pay

•

Pension scheme

•

Duration of employment if temporary.

It is advisable for employment information to be supported by a staff handbook in which the relevant details are set out. The following information must be communicated to all staff members: •

Grievance and Disciplinary Procedure

•

Reclaiming training costs

•

Confidentiality

•

Restrictive covenants

•

Maternity Leave

•

Sickness Policy

•

Notification of absence and evidence of incapacity requirements

•

Any other benefits.

In addition to the contract of employment it is also useful for the practice to have a staff handbook which includes: •

Grievance and Disciplinary Procedures

•

Arrangements for reclaiming of training costs, or not

•

Defined standards for confidentiality

•

Any restricted covenants agreed at the time of employment

•

Arrangements for maternity leave

•

Sickness policy - in-line with notification of absence and evidence of

incapacity requirements

•

Any other benefits the practice is allowing staff over and above its legal

requirements.

There are many more additions which the handbook can contain, such as: equal opportunities policy, telephone protocols, complaints procedure and uniform requirements. The handbook should be tailor made to meet the businesses needs and must be clear, accessible and understood by all dental team members.

Disciplinary and Grievances Procedures The ACAS Code of Practice Disciplinary and Grievance Procedures It is crucially important for this code to be followed: an employment tribunal will adjust any awards made by up to 25% for unreasonable failure to comply. Legislation setting out disciplinary and grievance procedures seeks to provide a clear and transparent framework for dealing with difficulties which can arise from either the employer’s or employee’s perspective. They standardise how everybody in similar circumstances is treated and ensure fair and reasonably interactions. Practice managers should consult and follow the ACAS Code of Practice for handling disciplinary and grievance issues as outlined below. Disciplinary procedures are needed: •

So employees know what is expected of them in terms of standards of

performance or conduct (and the likely consequences of continued failure to meet these standards) •

To identify obstacles to individuals achieving the required standards (for

example training needs, lack of clarity of job requirements, additional support needed) and take appropriate action •

As an opportunity to agree suitable goals and timescales for improvement in

an individual’s performance or conduct •

To try to resolve matters without recourse to an employment tribunal

•

As a point of reference for an employment tribunal should someone make a

complaint about the way they have been dismissed. Grievance procedures are needed: •

To provide individuals with a course of action should they have a complaint

(which they are unable to resolve through regular communication with their line manager) •

To provide points of contact and timescales to resolve issues of concern

•

To try to resolve matters without recourse to an employment tribunal.

Disciplinary policy and practice There are two main areas where a disciplinary system may be used: capability and performance, and conduct. Capability/performance Capability issues may arise because an employee does not have adequate training, or is unable to do the work to a satisfactory standard for another reason. An employer must try to identify the reason and give appropriate support, before taking disciplinary action. An individual who is unable to do their job because of ill-health may also fall into this category. In these instances an employee should be dealt with sympathetically and offered support. However, unacceptable levels of absence could still result in the employer making use of warnings. Conduct Employee misconduct could range from continued lateness, failure to follow a reasonable management instruction, abuse of the organisation’s computer system or Internet access, bullying behaviour or creating a hostile work environment, through to theft, fighting and committing criminal offences. The graver offences may constitute gross misconduct. In all cases, an employer should follow the recommendations in the ACAS Code. Stages of the process If action is to be taken, it should observe at least the following three stages: • Letter • Meeting • Appeal. There must always be a full and fair investigation to determine the facts and to decide if further action is necessary. The ACAS Code recommends at least these three steps, however in some cases a second meeting stage may be appropriate. When matters begin to escalate be sure to keep good records of all interactions, you will need to produce these records should a case be taken to an employment tribunal. Your records should include:

•

All meetings minutes

• Emails •

Attendance notes

•

Notes of telephone calls

•

Copies of correspondence etc.

Disciplinary interviews Managers should be trained and supported so that they are able to carry out disciplinary meetings which: •

Ensure all the facts are investigated in advance (including consulting the

individual’s personal file for relevant information) and plan how the meeting is to be approached •

Make sure the employee knows from the letter inviting them to the meeting

why they have been asked to attend and that they have a right to have a companion present •

Make sure the individual has reasonable notice, ideally more than 72 hours,

and that they have a chance to arrange an appropriate representative if they wish •

Provide appropriate statements from people involved in advance of the

meeting, together with any key information you intend to rely on •

Make sure another member of management can be there to take detailed

notes and help conduct the interview •

Never pre-judge the outcome of the interview before hearing the employee’s

perspective •

Start the interview by stating the complaint to the employee and referring to

appropriate statements from people involved •

Give the employee ample opportunity to put forward their side of the story

and call any supporting witnesses •

Employers can also call witnesses, but they can only be in the room for the

relevant part of the interview, not the duration •

Make use of adjournments: always take a break to consider and obtain any

extra information you need before reaching your decision. Adjournments can be useful if things become heated or people are upset during the interview •

Deliver the decision (and give reasons, taking into account any mitigating

circumstances), confirm review periods and ensure you give details of how to appeal •

Confirm the decision in writing.

It is important that everyone involved in disciplinary action understands the importance of following the correct procedure as even if the case against an employee seems proven, they can still be deemed to have been treated unfairly if the correct procedures are not followed. Workers are entitled to be accompanied by a work colleague or trade union official at formal disciplinary and grievance interviews. It would be good practice for an employer to offer this at any investigatory meeting. Employers do not have to allow family members, or lawyers to accompany but can allow this if they wish.

Potential outcomes No action - After the meeting, the employer may decide that no action is necessary. For example, if an employee was unclear about what was expected from them and they agree to try to resolve the issue via additional support or counselling. Warnings - Alternatively, the employer may decide to give the employee a warning. An organisation’s policy should outline exactly what warnings will be given, but the following are examples of warnings and organisation may use: •

Verbal/ oral warning (ACAS no longer recommends this stage as part of a

formal procedure but, for cases of minor misconduct, this will often be a reasonable method to prevent a problem escalating) •

First written warning/improvement notice (PIP)

•

Final written warning.

Employers should specific a ‘life’ for formal disciplinary warnings after which they are disregarded for disciplinary purposes. Typical timescales suggested in the A nonstatutory guidance for the types of warning are: •

First written warning – 6 months

•

Final written warning – 1 year.

It may be appropriate for a warning to continue to be regarded for a longer period, provided the timescale was specified in the organisation’s disciplinary policy from the outset. The time period employers select for warnings to remain current, and the penalties imposed, must be reasonable in all circumstances. For example, they must take into account the nature of the misconduct, the employee’s disciplinary record and be consistent with penalties imposed in similar cases.

Chapter 5

Child protection – what you need to do if you’re worried about a child

Make this CPD Verifiable Turn to page 181 to find out how

Adapted from Child protection and the dental team by Jenny Harris et al.

Assessing a child History and examination As with all aspects of dentistry, assessing a child with an injury or with possible signs of abuse or neglect starts with a thorough history. As well as getting details from the child and carer of any injury or presenting complaint, it is important to consider aspects of the past dental history, wider medical history and of the family and social circumstances. Particular aspects of the presentation may in themselves raise some concerns and should be carefully evaluated. These would include, for example, a delay in the presentation, discrepancies between the history and examination findings or previous concerns about the child or siblings. A full dental examination should be carried out, noting in particular any dental, oral or facial injuries, their site, extent and any specific patterns. It is important also to note the general appearance of the child, their state of hygiene, whether they appear to be growing well or are ‘failing to thrive’, their demeanour and interaction with their parents or carers and others. Look particularly for signs of ‘frozen watchfulness’ where the child seems to take in everything going on, but in a detached, wary or fearful manner. Questions to ask yourself A list of questions to ask yourself in such circumstances can be kept in the surgery to act as a prompt and are based on the actions in Table 1. Within electronic patient records these could be incorporated into a custom screen. Talking to the child It is good practice to ask the child about the cause of any injuries and to allow them to talk if they volunteer information about abuse. You should avoid asking leading questions and should respond calmly and kindly with a non-judgmental attitude. A child who makes a disclosure of abuse should always be taken seriously. If requested to keep a secret, you should not do so but should explain that you may have to share information, but will explain with whom and when it will be shared.

The most important thing to remember if you are faced with a child who may have been abused is that you do not need to manage this on your own. It is also important to remember that your first duty is to the child and that you have the responsibility for dealing with any injury or dental needs. No child should be left untreated or in pain because of underlying concerns about abuse.

Colleagues to consult The first stage if you have any concerns should always be to discuss this with an appropriate colleague or someone else you can trust. This may be an experienced dentist, a senior dental nurse, a paediatrician, child protection nurse or a social worker. In the salaried primary dental care services close working relationships often exist with health visitors and school nurses, some of whom are highly experienced in child protection and may be a source of helpful advice.

Making a referral If, having discussed it with an appropriate colleague, you remain concerned, then you should make a referral to your local social services. The practice should already have identified where and how to contact your social services team. Referrals should be made by telephone, so that you can directly discuss your concerns, and should be followed up in writing within 48 hours. Your letter should clearly document the facts of the case and include an explicit statement of why you are concerned. The telephone discussion should be clearly recorded, documenting what was said, what decisions were made and an unambiguous action plan. ‘I used to think it wasn’t my business to interfere – but now I see that my phone call could be the first link in the chain to put the family in touch with the support they need’ A dental therapist, speaking after a child protection training session

Informing the child and parents It is good practice to explain your concerns to the child and parents, inform them of your intention to refer and seek their consent. Research shows that being open and honest from the start results in better outcomes for children. There are certain exceptions and reasonable judgement must be made in each case. Usually you should not discuss your concerns with the parents in the following circumstances,

where: • Discussion might put the child at greater risk • Discussion would impede a police investigation or social work enquiry • Sexual abuse by a family member, or organised or multiple abuse is suspected • Fabricated or induced illness is suspected; • Parents or carers are being violent or abusive, and discussion would place you or others at risk • It is not possible to contact parents or carers without causing undue delay in making the referral. Informal advice could be taken first without disclosing the child’s name. Further discussion of information sharing and confidentiality follows later. ‘I know I did the right thing in referring him, but what was so difficult was the feeling that I’d gone behind their backs and didn’t discuss it with the family first. I think things have changed for the better now you’re advised to explain your concerns to the parents first. Of course it wouldn’t be easy, but I’m convinced that’s the best way to do it’ A dentist reflecting on a child protection referral she had made some years ago Useful guidance can be obtained from your ‘LSCB/ACPC Procedures’. If not already supplied to your practice, a copy of this informative document should be available from your local social services department or online if they have a website (go to www.dfes.gov.uk/acpc and follow links or, if a link is not available, use your preferred search engine to find the website for your LSCB/ACPC). Many practitioners worry that by making a referral to social services, they will initiate a process that will quickly get out of hand, and end up with severe and drastic action being taken to remove the child and punish the family. This is a misperception that does not reflect current practice in the UK. Less than 50% of children investigated for possible abuse end up being placed on child protection registers. It is estimated that fewer than 1% of children referred to social services for possible abuse end up in judicial proceedings. When a child is referred to social services on suspicion of abuse, the duty social worker will note details of the child and family and the concerns that are being raised. The social work team manager will then convene a strategy discussion (often by telephone) with a senior member of the police child protection team. This happens within one working day and often involves a paediatrician or other

health professional. The purpose of this strategy discussion is to share information and decide on how best to manage the referral, taking note of the concerns that have been raised. They may decide that a social worker will visit the family to carry out an initial assessment or initiate a joint investigation with the police. If the concerns are minor, or the family is already known to other professionals, it may be appropriate for those professionals to take the lead in supporting and working with the family, rather than continuing down a child protection route. In extreme cases, where there is the risk of immediate harm to the child, legal action may be required through an emergency protection order or police powers of protection. In those cases where the initial assessment identifies ongoing concerns and risks, a multiagency case conference may be held. Parents are normally invited to these conferences. At the conference, all those present are given an opportunity to share information about the child and family, including any concerns they may have. The conference chair then summarises any identified risks to the child, along with any factors that may be serving to protect the child or support the family. An action plan is then agreed with the family in order to provide support and ensure the safety of the child. This plan will include a decision on whether the child’s name should be placed on the child protection register – a decision that is then reviewed at a further case conference after three months and at any subsequent conferences that may be held, until such time as the child is felt to be no longer at risk of significant harm. At any stage in this process, it may be necessary to take legal action to protect the child, but this would only be where it has been shown that the child cannot be protected without recourse to such action. Further details of the process are discussed in the Department of Health booklet ‘What To Do If You’re Worried a Child is Being Abused’.

Coping with the aftermath It is quite normal to have some anxiety about the consequences of making a child protection referral. This may include fears about potential adverse consequences for the child or family, or repercussions on the dental practice or yourself. Talking it through, or ‘debriefing’, with an experienced colleague may be helpful or you may wish to seek independent confidential counselling. This may be available through your local occupational health department or child protection named nurse ‘I still think this is a really difficult thing for us, working in a small town where everyone knows everyone else’ A dental practice owner

â&#x20AC;&#x2DC;I had some sleepless nights after I referred the little girl. I wondered whether I had done the right thing. It helped to talk to someone who had seen this kind of thing beforeâ&#x20AC;&#x2122; A dental nurse

Information sharing and confidentiality Whenever a child in this country dies as a result of abuse, local agencies are required to undertake a serious case review to look at the case and any lessons that might be learned from it. One consistent theme comes out in all these case reviews; a failure of communication between professionals involved with the child. If we are ever going to protect children from abuse, it is crucial that we learn to communicate with each other and share information. As dental professionals seeing a child, we have information about the child that no other professional will have. We have a responsibility to share that information appropriately. Where you have identified concerns, you should highlight those to the social worker to whom you are referring the child, backing those concerns up in writing. In other situations you may be asked to provide information for the purposes of an initial assessment or as a contribution to a case conference.

Ethical guidance Practitioners are often anxious about the legal or ethical restrictions on sharing information, particularly with other agencies. You should be aware of the law and should comply with the principles of current ethical guidance for the dental team. These do not provide an absolute barrier to information sharing. However, the amount of information shared should be proportionate to your level of concern about the child. You should be prepared to exercise your judgment. A failure to pass on information that might prevent a tragedy could expose you to criticism in the same way as an unjustified disclosure.

Consent In most situations, it will be appropriate to share any concerns you have identified with the family and to obtain their consent to sharing information with others. However, as considered above, there may be situations where to discuss your concerns with the family could put the child at greater risk or may put you or your staff at risk. In practice, such situations are rare. Restrictions on sharing information are embodied in the common law duty of confidence, the Human Rights Act 1998

and the Data Protection Act 1998. Within these frameworks there is provision for sharing information where: •

Those likely to be affected consent, or

•

The public interest in safeguarding the child’s welfare overrides the need to

keep the information confidential, or

•

Disclosure is required under a court order or other legal obligation.

Therefore, if you have concerns about a child’s welfare, and you consider the sharing of information to be important in safeguarding that child, you should consider sharing that information even if you are unable to gain parental consent to do so. Sources of further guidance include the defence organisations (Dental Defence Union, Dental Protection Limited, MDDUS or others). Defence organisations welcome enquiries from practitioners in any and every situation and can provide immediate advice and legal assistance if necessary.

Assessing the needs of children who have been abused Children who have been subject to abuse or neglect need a full assessment of their health and developmental needs. This process is coordinated by social services and may require input from a range of professionals. You may be called upon to assess the dental health, oral injuries and unmet dental needs of such children, whether existing patients of your practice or new. In such circumstances the social worker should have obtained consent for dental examination from the parent, alternatively the courts may order an assessment to be carried out. If consent is not available, seek the advice of an experienced colleague or defence organisation before proceeding. Particular attention should be paid to the following: •

Oral examination and assessment of dental health and oral hygiene

•

Documentation of any injuries and interpretation in the light of any history

given and the developmental stage of the child

•

Records of previous dental attendance and treatment (which may provide a

positive indicator of appropriate care)

•

Treatment required, in your opinion, and how it could be carried out.

All assessments should be thoroughly documented, dated and signed. You may be required to provide a written report for social services, or in criminal or civil proceedings a statement that may be placed before the courts.

Any situation where a child has been harmed as a result of abuse or neglect potentially involves a criminal offence against that child. The responsibility for carrying out any criminal investigation rests with the police, usually the local police child protection team. Other agencies have a responsibility to cooperate with the police in their investigations. Comprehensive, contemporaneous and accurate record keeping is essential to this process. You may be requested to assist the police by providing a statement, copies of records or by carrying out particular forensic examinations or tests where you are qualified to do so. You need to obtain consent and should consider taking advice from your defence organisation in all such situations.

Diagrams and clinical photographs When you examine a child, you should consider whether your notes should include a diagram of your findings or be supplemented by clinical photographs. Diagrams and photographs should be clearly labelled with the childâ&#x20AC;&#x2122;s identity and the date and time marked. They should be referred to in the clinical notes. Diagrams should be annotated with descriptions and measurements of any injuries. Other than for medical record purposes, it is not the role of the dental team to attempt to take photographs of forensic quality. There are very precise requirements for such photographs. A rigid, right-angled measuring scale must be incorporated and multiple views may be required when marks involve different parts of curved body surfaces.

Table 1 HISTORY: FEATURES OF CONCERN Changing or inconsistent history Developmentally inappropriate (does not fit with the age of the child) Delay in presentation Previous concerns, including siblings EXAMINATION Dental examination Injuries (site, extent, patterns) General appearance (growth, hygiene)

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Chapter 6 White lesions

Make this CPD Verifiable

By Professor Crispian Scully, Dr Jane Luker & Dr David Felix Adapted from Oral medicine – update for the dental team

Turn to page 181 to find out how

Truly white oral lesions appear white usually because they are keratotic (composed of thickened keratin, which looks white when wet) or may consist of collections of debris (materia alba), or necrotic epithelium (such as after a burn), or fungi (such as candidosis). These can typically be wiped off the mucosa with a gauze swab.

Figure 1

Figure 2

Other lesions, which cannot be wiped off, also appear white usually because they are composed of thickened keratin (Figure 1). A few rare conditions that are congenital, such as white sponge naevus present in this way, but most white lesions are acquired and many were formerly known as ‘leukoplakia’, a term causing misunderstanding and confusion. The World Health Organisation originally defined leukoplakia as a ‘white patch or plaque that cannot be characterised clinically or pathologically as any other disease’, therefore specifically excluding defined clinicopathologic entities such as candidosis, lichen planus (LP) and white sponge naevus, but still incorporating white lesions caused by friction or other trauma, and offering no comment on the presence of dysplasia. A subsequent international seminar defined leukoplakia more precisely as: ‘…a whitish patch or plaque that cannot be characterized clinically or pathologically as any other disease and which is not associated with any physical or chemical causative agent except the use of tobacco’. 74

There is a range of causes of white lesions (Table 1), but morphological features and site may also give a guide to the diagnosis. For example, focal lesions are often caused by keratoses; multifocal lesions are common in thrush (pseudomembranous candidosis) and in LP; striated lesions are typical of LP; and diffuse white areas are seen in the buccal mucosa in leukoedema and some LP, in the palate in stomatitis nicotina and at any site in keratoses. White lesions are usually painless but this may not be the case in burns, candidosis, LP, or lupus erythematosus. Local causes of white lesions are debris, burns (from heat, chemicals such as mouthwashes), grafts and scars may appear pale or white. Materia alba can usually easily be wiped off with a gauze.

Furred tongue Tongue coating is common, particularly in edentulous adults on a soft, non-abrasive diet, people with poor oral hygiene, and those who are fasting or have febrile diseases. The coating appears more obvious in xerostomia. The coating consists of epithelial, food and microbial debris and the tongue is the main reservoir of some micro-organisms, such as Candida albicans and some Streptococci, and the various anaerobes implicated in oral malodour. In diagnosis, the history is important to exclude a congenital or hereditary cause of a white lesion. The clinical appearances usually strongly suggest the diagnosis: biopsy is only required if the white lesion does not scrape away from the mucosa with a gauze. Treatment is of the underlying cause where this can be identified.

Congenital causes of white lesions Fordyce spots Some common whitish conditions, notably Fordyce granules (ectopic sebaceous glands), are really yellowish, but may cause diagnostic confusion. This condition is entirely benign and does not require any further intervention, though there is some evidence they may become more prominent in hereditary nonpolyposis colorectal cancer.

Leukoedema Leukoedema is a common benign congenital whitish-grey filmy appearance of the mucosa, seen especially in the buccal mucosae bilaterally in people of African or Asian descent. Diagnosis is clinical; the white appearance disappears if the mucosa is stretched. No treatment is available or required. Inherited dyskeratoses Inherited disorders of keratin are rare, but may be diagnosed, especially if there is a positive family history or other associated features, such as lesions on other mucosae, or skin appendages such as the nails. White sponge naevus, the commonest of the inherited dyskeratoses, is an autosomal dominant condition with variable expression and a high degree of penetrance. It generally presents during childhood and is characterised by thickened, folded white patches, most commonly affecting the buccal mucosae. Other mucosal sites in the mouth may be involved and some patients may have similar lesions affecting genital and rectal mucosa. Since the other dyskeratoses may have wider implications and, in particular the risk of malignant transformation, specialist care is indicated.

Inflammatory causes of white lesions Infections White lesions which can result from infections include candidosis (Figure 2), hairy leukoplakia caused by Epstein-Barr virus, warts and papillomas (caused by human papillomaviruses), and the mucous patches and leukoplakia of syphilis. Specialist care is usually indicated. Candidosis (candidiasis; moniliasis) The importance of Candida has increased greatly, particularly as the HIV pandemic extends, since this common commensal can become opportunistic if local ecology changes, or the host immune defences fail. Candida albicans is the most common cause but occasionally other species may be implicated. Some 50% of the normal healthy population harbour (carry) C albicans as a normal oral commensal, particularly on the posterior dorsum of the tongue, and are termed Candida carriers. Candidal carriage is more common in smokers and people who wear oral appliances.

Candidosis is the state when C albicans causes lesions and these can be mainly white lesions or candidal leukoplakia in which hyphal forms are common, or red lesions (denture-induced stomatitis, median rhomboid glossitis, erythematous candidosis), in which yeast forms predominate, and which may be symptomless though antibiotic stomatitis and angular cheilitis can cause soreness. Circumstances that cause susceptibility to candidosis include local factors influencing oral immunity or ecology, or systemic immune defects, or a combination of more than one factor. The diagnosis of candidosis is primarily clinical but a Gram-stained smear (looking for hyphae), a microbiological swab or oral rinse for culture may help to confirm the diagnosis. Possible predisposing causes should be looked for and dealt with, if possible. Topical polyene antifungals, such as nystatin or amphotericin or imidazoles, such as miconazole or fluconazole, are often indicated.

Non-infective causes Lichen planus (LP) is a very common cause of oral white lesions. It affects up to 2% of the adult population. Accordingly, most dental practitioners will have patients afflicted with LP. It is the main skin disease that can present with oral white lesions but lupus erythematosus can present similarly. Up to 44% of patients with oral lichen planus will have skin lesions and more than 70% of patients with skin lesions will have co-incident oral lesions. It usually affects people between the ages of 30 and 65 and there is a slight female predisposition, and is an inflammatory autoimmune-type of disease. However, it differs from classic autoimmune disorders in having no defined autoantibodies, and only rarely being associated with other autoimmune diseases. There is also no definitive immunogenetic basis yet established for LP and familial cases are rare. Many patients afflicted with LP have a conscientious type of personality with obsessive-compulsive traits and suffer mild chronic anxiety, suggesting neuroimmunological mechanisms may be at play. Stress has been held to be important in LP: patients have a tendency to be anxious and depressed, but of course the chronic discomfort may partially explain some cases in which this association has been documented.

Pathologically, there is a local cell-mediated immunological response characterised by a dense T-lymphocyte inflammatory cell infiltrate in the upper lamina propria causing cell death (apoptosis) in the basal epithelium, probably caused by the production of cytokines such as tumour-necrosis factor alpha (TNF-γ) and interferon gamma (IFN-α). The antigen responsible for this immune response is unclear but lesions very similar to LP, termed lichenoid lesions, are sometimes caused by: •

Dental restorative materials (mainly amalgam and gold)

•

Drugs (non-steroidal anti-inflammatory agents, antihypertensive agents,

antimalarials, and many other drugs)

•

Chronic graft-versus-host disease seen in bone marrow (haemopoietic stem

cell) transplant patients

•

Infection with hepatitis C virus (in some populations such as those from

southern Europe and Japan)

•

A variety of other systemic disorders such as hypertension and diabetes

(probably a reaction to the drugs used).

Lichen planus can affect stratified squamous epithelium of the skin, the oral mucosa and genitalia. Oral LP may present a number of different clinical pictures including: •

Papular (white papules)

•

Reticular (a network of raised white lines or striae)

•

Plaque-like (simulating leucoplakia)

•

Atrophic (red atrophic areas, simulating erythroplasia)

•

Mixed atrophic/erosive form.

LP is one of the most common causes of desquamative gingivitis; erosions are less common, but persistent, irregular and painful, with a yellowish slough. White lesions of LP are often asymptomatic, but there may be soreness if there are atrophic areas or erosions. LP typically results in lesions, which are usually in the posterior buccal mucosa bilaterally, but the tongue or gingivae are other sites commonly affected. On the skin, lichen planus frequently presents as a flat-topped purple polygonal and pruritic papular rash most often seen on the front (flexor surface) of the wrists in which lesions are often crossed by fine white lines called Wickham’s striae. Nail lesions may also be seen and oral LP may be accompanied by vulvovaginal lesions (the vulvovaginal-gingival syndrome).

Often, the onset of LP is slow, taking months to reach its peak. It usually clears from the skin within 18 months but in a few people persists for many years. Oral lesions often persist. There is no sign or test to indicate which patients will develop only oral, or oral and extra-oral lesions of LP. Non-reticular oral LP in particular has a small malignant potential, probably of the order of 1%. LP is often fairly obviously diagnosed from the clinical features but, since it can closely simulate other conditions such as: lupus erythematosus, chronic ulcerative stomatitis, Keratosis or even carcinoma. Biopsy and histopathological examination of lesional tissue, occasionally aided by direct immunostaining, is often indicated. Removal of the affected area does not necessarily remove the problem, therefore, the best management is usually to ensure the mouth is checked by a healthcare professional at least at 6-monthly intervals. While treatment of LP is not always necessary, unless there are symptoms, predisposing factors should be corrected: •

It may be wise to consider removal of dental amalgams if the lesions are

closely related to these, or unilateral, but tests such as patch tests will

not reliably indicate which patients will benefit from this. Accordingly,

empirical replacement of amalgam restorations may be indicated.

•

If drugs are implicated, the physician should be consulted as to the possibility

of changing drug therapy.

•

If there is HCV infection, this should be managed by a general physician.

•

Improvement in oral hygiene may result in some subjective benefit;

chlorhexidine or triclosan mouthwashes may help. Symptoms can often be

controlled, usually with topical corticosteroids or sometimes with tacrolimus.

•

If there is severe or extensive oral involvement, if LP fails to respond to topical

medications, or if there are extra-oral lesions, specialist referral may

be indicated.

•

Patients with non-reticular lichen planus should be monitored to exclude

development of carcinoma. Tobacco and alcohol use should be minimised.

Key points for patients •

This is a common condition

•

The cause is unknown

•

Children do not usually inherit it from parents

•

It is not thought to be infectious

•

It is sometimes related to diabetes, drugs, dental fillings, or other conditions

•

It sometimes affects the skin, hair, nails or genitals

•

Blood tests and biopsy may be required

•

The condition tends to persist in the mouth but it can be controlled

•

Most lichen planus is benign but some forms may rarely, after years, lead

to a tumour;

Therefore, the best management is usually to: Avoid habits such as use of tobacco, alcohol or betel (and, for lips, sun-exposure) Have a healthy diet rich in fresh fruit and vegetables Have your mouth checked by a healthcare professional at least at 6-monthly interval Changes that might suggest a tumour is developing could include any of the following persisting more than 3 weeks: a sore on the lip or in the mouth that does not heal; a lump on the lip or in the mouth or throat; a white or red patch on the gums, tongue, or lining of the mouth; unusual bleeding, pain, or numbness in the mouth. Websites and patient information http://www.bcd.tamhsc.edu/outreach/lichen/index http://www.aad.org/pamphlets/lichen.html

Table 1. Causes of oral white lesions Local causes Materia alba and furred tongue (debris from poor oral hygiene) Burns Keratoses Frictional keratosis (and cheek/lip biting) Smoker’s keratosis Snuff-dipper’s keratosis Skin grafts Scars Congenital Fordyce spots Leukoedema Inherited dyskeratoses (rare, eg white sponge naevus, dyskeratosis congenita, Darier’s disease) Inflammatory Infective Fungal (eg pseudomembranous and hyperplastic candidosis) Viral Hairy leukoplakia (Epstein-Barr virus) Human papillomavirus infections Bacterial (eg syphilitic mucous patches and keratosis) Non-infective Lichen planus Lupus erythematosus Neoplastic and possibly pre-neoplastic Leukoplakia Keratoses Carcinoma

Chapter 7

What are the risk factors for oral cancer? Professor Crispian Scully CBE Professor Emeritus, UCL, London & Mr Nicholas Kalavrezos Maxillofacial & Reconstructive Surgeon of The Head, Face & Neck University College London Hospital & The Harley Street Clinic.

The International Agency for Research on Cancer (IARC) and the World Cancer Research Fund/American Institute for Cancer Research (WCRF/ AICR) are the gold standard in cancer epidemiology, and their conclusions about oral cancer risk factors are shown in Table 1.

What are the known modifiable risk factors for oral cancer? Most of the lifestyle (modifiable) cancer risk factors;

•

Are addictive

•

Affect other body systems

•

Cause other health problems

•

Are often multiple habits

•

Have spread by migration.

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Tobacco is a major hazard to health and promotes many diseases, particularly heart disease, lung disease, and cancers of the lung, oesophagus, mouth and bladder. Tobacco smoke contains nicotine, which is highly addictive and is absorbed readily from the lungs on smoking and also when tobacco is chewed. Nicotine withdrawal results in excessive anger, hostility and aggression. Tobacco is a potent risk factor for oral cancer. All forms of tobacco both smoked and smokeless are carcinogenic. There is for oral cancer a: â&#x20AC;˘

20-fold higher risk in heavy smokers (dark tobacco is worst)

â&#x20AC;˘

Strong dose-response relationship.

Tobacco also predisposes to cancers of the larynx, pharynx, lung, oesophagus, stomach, colon, liver, and breast as well as other diseases (e.g. heart diseases, bronchitis). Smoking cessation on the other hand leads to a fall in oral cancer risk; by one to four years after smoking cessation the risk of oral cancer is 35% lower than that of a current smoker, and by 20 years or more after cessation the risk is reduced to that of a never-smoker. The extent of oropharynx/hypopharynx cancer risk reduces by around half by 5-9 years of smoking cessation, and is almost that of a neversmoker by 20 years. People who have only smoked pipes or cigars, rather than cigarettes, also have an increased risk of mouth, pharynx and larynx cancers. People who smoke bidi (a type of hand rolled cigarette used by some south Asians) have around three times the risk of oral cancer compared with bidi never-smokers. People who smoke a hookah (waterpipe, hubble-bubble, narghile, arghila, qalyan, or shisha) â&#x20AC;&#x201C; have a raised risk of mouth and lung cancers. Smokeless tobacco can also increase cancer risk while people exposed to second hand smoke at home or in the workplace have a small increase in their risk of mouth or oropharyngeal cancer.

Alcohol Alcohol (ethanol or ethyl alcohol) may be carcinogenic via various mechanisms but an important route is by its oxidization to acetaldehyde (a carcinogen) by enzymes (alcohol dehydrogenases; ADHs). There is for oral cancer a â&#x20AC;˘

20-fold risk with heavy alcohol drinkers (spirits are the worst)

â&#x20AC;˘

Strong dose-response relationship.

Alcohol use also predisposes to: â&#x20AC;˘

Cancers of the stomach, colon, liver, and breast

â&#x20AC;˘

Other diseases.

IARC and WCRF/AIRC classify alcohol as a cause of mouth, tonsil and pharynx cancers. A large Cancer Research UK study found that about a third of cancers of the mouth and throat (30%) were caused by drinking alcohol. The more alcohol a person drinks, and the greater number of years they drink for, the higher the risk. Every 1.5 units consumed per day increases the risk of mouth and pharyngeal cancer by 35% in men and 9% in women; every 6 units daily increases the risk more than threefold (223% and 231% increase for men and women respectively). Overall, regular alcohol drinkers have around two-and-a-half times (155% increase) the risk of mouth and pharyngeal cancer, compared with nondrinkers and occasional drinkers. Heavy drinking (6 or more units per day) increases the risk of mouth and pharyngeal cancer more than fivefold (440%). Risk of a secondary primary tumour in the upper aerodigestive tract (UADT) is increased by 9% for every 1.25 units of alcohol consumed per day. Some studies have suggested that mouthwashes with a high alcohol content could increase the risk of oral cancer but other studies have found that this is not the case.

Tobacco and alcohol Tobacco and alcohol use are independent risk factors for oral cancer and tongue cancer but these lifestyle habits often co-exist of course and they interact and contribute to a multiplicative carcinogenic effect. Heavy tobacco smokers have a 20-fold greater risk; heavy alcohol drinkers a 5-fold greater risk and those who do both have a 50-fold greater risk.

Betel and similar chewing habits Chewing tobacco or betel quid is common in parts of Asia and in some immigrant groups.

The International Agency for Research on Cancer (IARC) recognised that betel (which contains the stimulant arecoline) chewed as quid (with or without tobacco) is carcinogenic to humans. Betel quid substitutes also contain both carcinogens and genotoxic agents which have a role in oral cancer. Chewing betel quid is an independent risk factor for developing oral cancer. Betel may cause oral submucous fibrosis and cancer. Betel quid alone (with no tobacco) increases the risk of oral cancer in tobacco non-smokers by around threeand-a-half times, and in those who neither smoke nor drink alcohol by around 15 times. Betel quid with tobacco increases the risk of oral cancer in those who neither smoke nor drink by around seven times. People who smoke tobacco, drink alcohol and chew betel have over 30 times the oral cancer risk compared with those who abstain from these habits. Various other chewing habits, usually combinations that contain tobacco, are used in different cultures (e.g., Khat, Shammah, Toombak).

Microorganisms Many patients with OSCC have poor oral health, with carious teeth and periodontitis. The use of tobacco and alcohol are confounding factors difficult to control in epidemiological studies, but periodontal disease has been shown to increase the

statistical risk for cancer. Among young people (under the age of 45 years) with oral cancer, up to 25% appear not to have had any exposure to the major known risk factors such as tobacco, alcohol or betel. Other factors known to be involved in OSCC include solar irradiation in lip cancers. Immunodeficient patients may also develop oral potentially malignant and malignant neoplasms. Besides these factors, infections such as poor oral hygiene, periodontal disease, chronic candidosis, and virus infections link statistically with OSCC. Human papillomavirus (HPV) infection is also increasingly implicated - particularly in oropharyngeal cancer. HPV-related tumours tend to be seen in younger patients, in the fauces, and have usually a better prognosis. HPV-positive oropharyngeal cancers are associated with oral sex and marijhuana use; high-risk (oncogenic) HPV subtypes have been identified in a significant fraction of oropharyngeal tumours, including HPV 16, 18, 31, and 33. HPVs can be transmitted by close contact between skin and/or mucosae, and risk factors for infection include; •

Early onset of sexual activity

•

Unknown sexual partners

•

Multiple sexual partners

•

Lack of condom use.

HPV can be passed on during sexual contact and most sexually active adults will be infected with at least one type of HPV at some time during their life. Greater numbers of sexual partners, early age of first sexual intercourse, and high-risk sexual behaviour are emerging as risk factors for HPV-related disease independent of tobacco and alcohol abuse. Nevertheless, smoking also increases the risk of HPV infection in the mouth. HPV infection of the mouth is more common in men than in women. For many people, the virus causes no harm and goes away without treatment. Only a small percentage of people with HPV develop oropharyngeal cancer. Most sexually active adults become infected with high-risk (cancer-promoting or oncogenic) HPV types such as HPV-16 and HPV-18 at some stage - but most patients (90%) clear the HPV infection spontaneously within 2 years. There are more than 100 different types of HPV, some types are called the wart virus, because they cause warts on the genital area or skin. HPV of all types can be transmitted between the mouth and anogenital region, and there are associations demonstrated between oral and anogenital cancers. The risk of HPV infection in the mouth and throat is linked to certain sexual

behaviours, such as open mouth kissing and oral sex. The risk increases with the number of sexual partners a person has. Risk factors for oropharyngeal cancer include a high lifetime number of oral-sex partners (six or more) or vaginal-sex partners (26+). People with a higher number of past sex partners (particularly oral sex partners), or who started having sex at a younger age, have an increased risk of oropharyngeal, tonsil, and base of tongue cancers. Persistent HPV infection can cause cancer. HPVs play a role in some anogenital cancers, including cancers of the: •

Cervix

• Anus •

Vulva

• Vagina • Penis. Oral cancer is also increased in: •

Patients with anogenital cancer

•

Patients with cervical cancer

•

Partners of women with cervical cancer.

The oropharyngeal cancer HPV prevalence rate appears to have increased over time, reaching over 70% in data from 2005 onwards. The HPV vaccines now administered to young people in an effort to prevent cervical cancer afford protection against other HPV-related lesions, including oral lesions, but there is no hard evidence yet, as to a significant protective effect against oral cancer. A study of 5,840 sexually active women in Costa Rica (ages 18-25 years) showed however, that mouthwash samples after four years found that only one woman after HPV vaccine was infected with HPV whereas 15 women after a placebo vaccine were infected.

What are the environmental factors in oral cancer? The effects of environmental factors such as ionizing radiation, ultraviolet light or air pollution (wood stoves; fossil fuels; volatile carcinogenic compounds formed during cooking) are ill-defined but they may act via the production of free radicals that elicit DNA mutations.

What are the other known risk factors? Radiation: Skin cancers are relatively common on the face and neck, and lip cancer is an issue mainly in older men exposed over long periods to sunlight, as these areas are often exposed to ultraviolet light (UV). Both the sun and tanning beds give off UV rays which can cause skin cancers in unprotected skin. Chemicals and dusts: Occupations with an increased risk of oral cancer mostly involve blue collar workers. Diseases: People who have had mouth or oropharyngeal cancer have an increased risk of getting a second one. Women have a higher risk of a second oral cancer than men. People who have had some other types of cancer also have an increased risk of oral cancer and these include: •

Cancer of the oesophagus

•

Lung cancer

•

Squamous cell skin cancer

•

Cervical, anal or genital cancer in women

•

Cancer of the rectum in men.

Dietary defects: A diet high in animal fats and low in fresh fruit and vegetables may increase the risk of developing head and neck cancer. Immune defects: HIV/AIDS Meta-analyses have shown people with HIV/AIDS have around double the risk of mouth, oropharyngeal and pharyngeal cancers, compared with the general population. Immunosuppression: Several large cohort studies and a meta-analysis have shown that organ transplant patients (who of course are chronically immunosuppressed) have between 1746 times an increased risk of lip cancer and 2-5 times increased risk of mouth and pharyngeal cancers, compared with the general population.

Socio-economic deprivation: Socio-economic deprivation has been linked to an increased risk of oral cancer, but many other explanations (e.g. habits, oral health, diet, nutrition) may be responsible. What factors may reduce oral cancer risk? Diet: WCRF/AICR classifies consumption of non-starchy vegetables and fruits (not salted or pickled), and foods containing carotenoids, as possibly protective against mouth, pharynx and larynx cancers. People with the highest fruit intake have around half the risk of head and neck cancer and each portion of fruit consumed per day around halves the risk of oral cancer, as does each portion of vegetables. A significant protective effect of diet against oral cancer has generally been shown in persons who consume beta-caroteneâ&#x20AC;&#x201C;rich vegetables and citric fruits. People who have ever-used vitamin C supplements have a 24% reduced risk of head and neck cancer, and ever-users of calcium supplements have a 36% reduced risk. Exercise: Recreational physical activity is associated with a 26-47% reduction in oral cancer risk, and a 33-42% reduction in pharyngeal cancer risk.

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Table 1. IARC and WCRF/AICR Evaluations of Mouth and Head and Neck Cancer Risk Factors

Increases risk (‘sufficient’ or ‘convincing’ evidence) •

Alcoholic beverages (oral cavity, tonsil, pharynx)

•

Betel quid with tobacco (oral cavity, tonsil, pharynx)

•

Betel quid without tobacco (oral cavity)

•

Human papillomavirus type 16 (oral cavity, tonsil, pharynx)

•

Tobacco, smokeless (oral cavity)

•

Tobacco smoking (oral cavity, tonsil, pharynx, nasopharynx)

•

X-radiation, gamma-radiation (salivary gland)

•

Epstein-Barr virus (nasopharynx)

•

Formaldehyde (nasopharynx)

•

Salted fish, Chinese-style (nasopharynx)

•

Wood dust (nasopharynx)

May increase risk (‘limited’ or ‘probable’ evidence) •

Hydrochlorothiazide (lip)

•

Solar radiation (lip)

•

Human papillomavirus type 18 (oral cavity)

•

Radioiodines, including Iodine-131 (salivary gland)

•

Asbestos (all forms) (pharynx)

•

Mate drinking, hot (pharynx)

•

Printing processes (pharynx)

•

Tobacco smoke, secondhand (pharynx)

May decrease risk (‘limited’ or ‘probable’ evidence) •

Non-starchy vegetables (not salted or pickled) (mouth, pharynx and larynx)

•

Fruits (not salted or pickled) (mouth, pharynx and larynx)

•

Foods containing carotenoids (mouth, pharynx and larynx)

Chapter 8

Complaints handling & patient protection

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Stressed as important by the General Dental Council (GDC) to the extent that ethics and complaints handling is a recommended CPD subject area, we look at the GDC Standards for the Dental Team document (Section 5) in complaints handling and in raising concerns if patients are at risk (Section 8).

Complaints handling Patients expect: Their concerns or complaints to be acknowledged, listened to and dealt with promptly. You must: 5.1 Make sure that there is an effective complaints procedure readily available for patients to use, and follow that procedure at all times. 5.2 Respect a patient’s right to complain. 5.3 Give patients who complain a prompt and constructive response.

Guidance 5.1.1 It is part of your responsibility as a dental professional to deal with complaints properly and professionally. You must: •

Ensure that there is an effective written complaints procedure

where you work;

•

Follow the complaints procedure at all times

•

Respond to complaints within the time limits set out in the procedure

•

Provide a constructive response to the complaint.

5.1.2 You should make sure that everyone (dental professionals, other staff and patients) knows about the complaints procedure and understands how it works. If you are an employer, or you manage a team, you must ensure that all staff are trained in handling complaints. 5.1.3 If you work for a practice that provides NHS (or equivalent health service) treatment, or if you work in a hospital, you should follow the procedure set down by that organisation. 5.1.4 If you work in private practice, including private practice owned by a dental body corporate, you should make sure that it has a procedure which sets similar standards and time limits to the NHS (or equivalent health service) procedure. 5.1.5 You should make sure that your complaints procedure: •

Is displayed where patients can see it -

patients should not have to ask for a copy

•

Is clearly written in plain language and is available in other formats if needed

•

Is easy for patients to understand and follow

•

Provides information on other independent organisations that

patients can contact to raise concerns

•

Allows you to deal with complaints promptly and efficiently

•

Allows you to investigate complaints in a full and fair way

•

Explains the possible outcomes

•

Allows information that can be used to improve services to pass back to your

practice management or equivalent

•

Respects patients’ confidentiality.

5.1.6 Complaints can be an opportunity to improve your service. You should analyse any complaints that you receive to help you improve the service you offer, and share lessons learnt from complaints with all team members. 5.1.7 You should keep a written record of all complaints together with your responses. This record should be separate from your patient records so that patients are not discouraged from making a complaint. You should use your record of complaints to monitor your performance in handling complaints and identify any areas that need to be improved.

5.2.1 You should not react defensively to complaints. You should listen carefully to patients who complain and involve them fully in the complaints process. You should find out what outcome patients want from their complaint. 5.3.1 You should give the patient a copy of the complaints procedure when you acknowledge their complaint so that they understand the stages involved and the timescales. 5.3.2 You should deal with complaints in a calm and constructive way and in line with the complaints procedure. 5.3.3 You should aim to resolve complaints as efficiently, effectively and politely as possible. 5.3.4 You must respond to complaints within the time limits set out in your complaints procedure. 5.3.5 If you need more time to investigate a complaint, you should tell the patient when you will respond. 5.3.6 If there are exceptional circumstances which mean that the complaint cannot be resolved within the usual timescale, you should give the patient regular updates (at least every 10 days) on progress. 5.3.7 You should try to deal with all the points raised in the complaint and, where possible, offer a solution for each one. 5.3.8 You should offer an apology and a practical solution where appropriate. 5.3.9 If a complaint is justified, you should offer a fair solution. This may include offering to put things right at your own expense if you have made a mistake. 5.3.10 You should respond to the patient in writing, setting out your findings and any practical solutions you are prepared to offer. Make sure that the letter is clear, deals with the patientâ&#x20AC;&#x2122;s concerns and is easy for them to understand. 5.3.11 If the patient is not satisfied despite your best efforts to resolve their complaint, you should tell them about other avenues that are open to them, such as the relevant Ombudsman for health service complaints or the Dental Complaints Service for complaints about private dental treatment. 94

Raise concerns if patients are at risk Patients expect: That the dental team will act promptly to protect their safety if there are concerns about the health, performance or behaviour of a dental professional or the environment where treatment is provided. That a dental professional will raise any concerns about the welfare of vulnerable patients. You must: 8.1 Always put patients’ safety first. 8.2 Act promptly if patients or colleagues are at risk and take measures to protect them. 8.3 Make sure if you employ, manage or lead a team that you encourage and support a culture where staff can raise concerns openly and without fear of reprisal. 8.4 Make sure if you employ, manage or lead a team that there is an effective procedure in place for raising concerns, that the procedure is readily available to all staff and that it is followed at all times. 8.5 Take appropriate action if you have concerns about the possible abuse of children or vulnerable adults.

Guidance 8.1.1 You must raise any concern that patients might be at risk due to: •

The health, behaviour

or professional performance of a colleague

•

Any aspect of the environment where treatment is provided

•

Someone asking you to do something that you think conflicts with your duties

to put patients’ interests first and act to protect them.

You must raise a concern even if you are not in a position to control or influence your working environment. Your duty to raise concerns overrides any personal and professional loyalties or concerns you might have (for example, seeming disloyal or being treated differently

by your colleagues or managers). 8.1.2 You must not enter into any contract or agreement with your employer or contracting body which contains a ‘gagging clause’ that would prevent you from raising concerns about patient safety or restrict what you could say when raising a concern. 8.2.1 You must act on concerns promptly. Acting quickly may mean that poor practice is identified and tackled without there being a serious risk to patient safety. If you are not sure whether the issue that worries you amounts to a concern that you should raise, think about what might happen in the short or longer term if you did not mention the issue. If in doubt, you must raise your concern. 8.2.2 You should not have to prove your concern for it to be investigated. If the investigation shows that there was no problem, the fact that you raised the concern should not be held against you as long as you were justified in raising the concern. Remember that you must put patients’ interests first and act to protect them. If you fail to do so by not raising a concern, your own registration could be at risk. 8.2.3 Where possible, you should raise concerns first with your employer or manager. However, it may not always be appropriate or possible to raise concerns with them, particularly if they are the source of your concern. 8.2.4 If it is not appropriate to raise your concern with your employer or manager, or if they fail to act on your concern, you must raise your concerns with your local commissioner of health or with the appropriate body from the following: •

The Care Quality Commission

•

Healthcare Inspectorate Wales

•

The Regulation and Quality Improvement Authority

•

Healthcare Improvement Scotland.

You can also get advice from your defence organisation or professional association.

8.2.5 If you think that the public and patients need to be protected from a dental professional registered with the GDC, you must refer your concern to us. This may be appropriate when: •

Taking action at a local level is not practical; or

•

Action at a local level has failed; or

•

The problem is so severe that the GDC clearly needs to be involved (for

example, issues of indecency, violence, dishonesty,

serious crime or illegal practice); or

•

There is a genuine fear of victimisation or deliberate concealment; or

•

You believe a registrant may not be fit to practise because of his or her health,

performance or conduct.

8.2.6 You must refer concerns about other healthcare professionals to the relevant regulator. 8.3.1 You must promote a culture of openness in the workplace so that staff feel able to raise concerns. 8.3.2 You should embed this culture into your policies and procedures, beginning with staff training and induction. 8.3.3 You should encourage all staff, including temporary staff, staff on different sites and locums, to raise concerns about the safety of patients, including the risks that may be posed by colleagues, premises, equipment or practice policies. 8.3.4 You must not offer staff contracts which contain a ‘gagging clause’ that would prevent them from raising concerns about patient safety or restrict what they could say when raising a concern. 8.4.1 You must make sure there are written procedures in place to enable staff members to raise concerns. This means: •

Being aware of and adhering to current laws and regulations

•

Supporting staff members who raise concerns

•

Taking steps to tackle any shortfalls in the standards and performance of staff

•

Having systems in place for supporting staff who may be having problems with

their health, behaviour or professional performance.

8.4.2 When a member of your team has raised a concern, you must: •

Take the concerns seriously

•

Maintain confidentiality when appropriate

•

Investigate promptly and properly and make

an unbiased assessment of the concern

•

Keep the staff member who raised the concern advised of progress,

explaining any action taken or reasons for not taking action; and

•

Ensure that you monitor the action you take to solve the problem.

8.5.1 You must raise any concerns you may have about the possible abuse or neglect of children or vulnerable adults. You must know who to contact for further advice and how to refer concerns to an appropriate authority such as your local social services department. 8.5.2 You must find out about local procedures for the protection of children and vulnerable adults. You must follow these procedures if you suspect that a child or vulnerable adult might be at risk because of abuse or neglect. See www.gdc-uk.org

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Chapter 9

Medical emergencies: hypoglycaemia, hyperglycaemia and steroid insufficiency

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By M H Thornhill, M N Pemberton and G J Atherton

Hypoglycaemia Clinical scenario Diane Jones, a 30-year-old insulin dependent diabetic, is attending your practice this morning for some routine restorative work. She got up late this morning and, while she gave herself her normal dose of insulin, in the rush to get her children to school, she ate only half a slice of toast. At the practice, your current patient’s extraction has turned into a difficult surgical and you are running late. In the waiting room, Mrs. Jones becomes anxious and confused. She is sweating and her hands are trembling. She asks for a sugary drink but collapses in the waiting room before this can be provided. This patient is having a hypoglycaemic episode. what would you do next?

Causes Hypoglycaemia most often occurs in a known ‘type I’ (insulin dependent) diabetic who has taken a normal dose of insulin but failed to eat adequately or at the right time. As a result, the blood glucose levels fall to a low level (hypoglycaemia) and the brain is starved of glucose. First line emergency treatment of diabetics is therefore aimed at increasing blood glucose levels.

Signs and symptoms In a known diabetic, the following suggest hypoglycaemia - especially if a meal is known to have been missed: •

Increasing drowsiness

•

Disorientation and confusion

•

Excitability or aggressiveness

•

Slurred speech.

100

The sympathetic nervous system may be activated in an attempt to release more glucose. Consequently, autonomic symptoms include: • Shaking • Sweating • Palpitations •

Anxiety and pallor.

Hypoglycaemia can be quickly confirmed by measuring the blood glucose using an automated blood glucose measuring device, if this is available. A diabetic may carry their own test system with them. Normal blood glucose is in the range 3.9 – 6.2 mmol/L. Cognitive dysfunction develops at a glucose concentration around 3mmol/L and autonomic symptoms at around 2mmol/L.

Prevention Give patients appointments early in a session, ensure that they are treated on time and not kept waiting. Avoid treating at mealtimes. Enquire whether they have had their normal food and insulin intake. If not, give a sugary drink prior to commencing any treatment (even now, many patients mistakenly believe that they need to starve prior to a local anaesthetic).

Management If conscious, give glucose or sugar orally as either: •

50g glucose dissolved in water to make a drink

•

GlucoGel® - a gel preparation which contains glucose

•

Lucozade® or another soft drink (not the ‘diet’ variety)

•

Dextrosol® tablets or at least four sugar lumps.

If impaired consciousness, give: •

Glucagon 1mg by i/m injection

•

If glucagon is unavailable or contra-indicated by hepatic glycogen

depletion, 50ml of 20% sterile glucose (or 25ml of 50% sterile glucose)

by slow i/v injection can be given instead if available

•

Lay the patient in the recovery position.

A hypoglycaemic patient will recover rapidly with the glucagon regimen, although it may take 5-10 minutes to work. Notes: Sugar (sucrose, a combination of glucose and fructose) takes longer to act

101

than glucose. Glucagon, given by intramuscular injection, is simple and safe to use. It is a hormone which breaks down glycogen stores in the liver; however, it may take some minutes to work and it requires the patient to have adequate glucose stores. Rarely, it can be ineffective in protracted hypoglycaemia or if hepatic glycogen stores are depleted such as in anorexic patients or alcoholics: 50ml of 20% glucose solution given intravenously will produce a rapid response. Alternatively, 25ml of 50% glucose solution may be given. However, the more concentrated the solution the more viscous it is and the more difficult it is to inject. Viscous glucose solutions are best administered through a large bore (white) needle into a large vein in the antecubital fossa. Once fully conscious, the patient should be given a drink containing glucose and some food containing carbohydrate. In simple cases, the patient may go home if they are fully recovered and accompanied. They should not drive. If hypoglycaemia has been caused by an oral antidiabetic drug, the patient should be admitted to hospital. If recovery is not rapid: •

If possible, re-check blood glucose to ensure that the level has risen to above

5.0 mmol per litre, in conjunction with an improvement

in the patient’s mental state

•

Consider other causes of collapse

•

Call for an ambulance

•

Check airway and circulation – start basic life support if necessary.

Remember that diabetics may also faint or suffer from other types of medical emergency. They have an increased risk of a myocardial infarction or stroke as atherosclerosis is a common complication of longstanding diabetes.

Background information Diabetes mellitus is a common disease characterised by raised blood glucose levels and affects tens of millions of people worldwide. Blood glucose levels are regulated primarily by the release of insulin from the pancreatic islet cells; its action is to lower blood glucose. Diabetes mellitus results either from failure of insulin production (type I, insulin dependent diabetes) or from a relative insensitivity of the tissues to the effects of insulin (type II, insulin independent diabetes). Type II diabetes is becoming more common with the increase in obesity in western populations and is now reported in juveniles. There is considerable variation in the severity of the signs and symptoms of hypoglycaemia between diabetics and sometimes the symptoms will not be recognised by the patient, requiring relatives and dental team members to be alert to the warning signs. Several important studies published in the last

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decade have confirmed that careful glycaemic control in diabetics results in delay and possibly even prevention of the long-term complications of diabetes. with this knowledge, it is likely that poorly controlled non-insulin dependent diabetics will increasingly be treated with insulin, while insulin dependent diabetics will be encouraged to adopt tighter glycaemic control. As control becomes tighter, the potential for hypoglycaemic episodes increases and thus diabetics and their dental practitioners are increasingly likely to encounter such episodes.

Hyperglycaemia In an undiagnosed diabetic, or a diabetic who fails to take their treatment, blood glucose levels may rise to high levels (hyperglycaemia). Although this can result in coma, it is of much slower onset than hypoglycaemic coma and is unlikely to present in the dental surgery. In any case, it is better to assume that a diabetic in difficulty is suffering a hypoglycaemic episode and treat it as such. Giving glucose to a hypoglycaemic diabetic will save their life and will not seriously worsen the prognosis of a hyperglycaemic one. â&#x20AC;&#x192;

Steroid insufficiency (Addisonian crisis) Clinical scenario Alison Jackson is a 30-year-old printer. On her medical history form she lists Addisonâ&#x20AC;&#x2122;s disease, for which she takes hydrocortisone and fludrocortisone. She is attending your practice today for surgical removal of a wisdom tooth under local anaesthetic. Her previous appointment, when the tooth removal was discussed, had been rushed as you were running late. As a result, she was not sure if you were going to use local or general anaesthetic and she has starved herself this morning and not taken her regular medication. On her arrival today you forgot to check her medical history and ten minutes into bone removal, she becomes unconscious. what would you do next?

Causes The natural production of adrenocortical steroids is increased at times of physiological stress and is important in maintaining blood pressure and blood glucose levels. In Addisonâ&#x20AC;&#x2122;s disease (primary hypoadrenocorticism) there is adrenal atrophy, often the result of auto-antibodies to the adrenal cortex, and failure of adrenocortical production of cortisol and aldosterone. More commonly, steroid insufficiency is the result of long-term systemic steroid therapy. Systemic steroids inhibit adrenocorticotrophic hormone (ACTH) production

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by the pituitary gland. Without ACTH stimulation, the adrenal cortex atrophies and may eventually become incapable of producing an increase in cortisol production at times of stress. With prolonged use of topical or inhaled steroids, there may be sufficient systemic absorption to cause adrenal insufficiency. It is worth enquiring of the patient’s doctor or hospital specialist if this is likely. In general, the longer the course of steroid treatment and the higher the dose used, the more likely the adrenal response to stress will be suppressed.

Signs and symptoms • Pallor •

Rapid, weak or impalpable pulse

•

Loss of consciousness

•

Rapidly falling blood pressure

•

Failure to regain consciousness when laid flat.

Prevention Always check the medical history and give steroid cover to any patients undergoing surgery or another stressful procedure who have been on a long-term course of steroids during the previous 12 months. Steroid cover should also be considered for patients who have been on long term high dose steroid therapy within the last two years and need to undergo anything more than minor surgery. Patients taking systemic steroids should carry a steroid card with them detailing their treatment.

Steroid cover For minor surgery (e.g. biopsy or single extraction): •

Double normal oral steroid dose on the morning of the procedure, or give

•

50mg hydrocortisone i/m 30 mins before, or i/v immediately before the

procedure. For major surgery or trauma (e.g. maxillofacial surgery): •

50mg hydrocortisone i/m 30 mins before, or i/v immediately before the

procedure and then 6 hourly for up to 72 hours.

Management •

Lay the patient flat and raise their legs

•

Open the airway

•

Give oxygen

•

Call an ambulance for urgent transfer to hospital

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•

If available, while awaiting an ambulance, give 100mg hydrocortisone sodium

succinate i/v (or i/m). Repeat if necessary

•

Monitor the patient carefully

•

Consider other possible causes of collapse.

Background information Among the body’s responses to surgery are an increase in plasma concentrations of adrenocorticotrophic hormone (ACTH) and cortisol. After minor surgery the increase is minimal in most people. However, the ability to respond is totally lost in those who have had an adrenalectomy and in some patients with Addison’s disease. In patients taking oral corticosteroids, the ability to respond to surgery is suppressed. The corticosteroid dose below which adrenal suppression is unlikely to occur is difficult to predict but suppression has not been reported with doses below 5mg of prednisolone a day. Various perioperative corticosteroid replacement regimes have been proposed for use in general surgery and these have frequently been adopted for use in oral surgery. The traditional regime followed the initial reports of fatal perioperative adrenal suppression in the 1950s and involved high dose corticosteroid cover. whilst such regimes have had few adverse effects, concerns have been raised that such high dose regimes are unnecessary and may impair wound healing, cause an increased susceptibility to infection and cause disruption of control in insulindependent diabetics. In recent years, several small studies investigating adrenal function in patients undergoing surgery have been undertaken. These involved patients on daily oral doses of 10mg prednisolone or less, and found no evidence of adrenocorticosteroid insufficiency. As a result, a more recent alternative approach to corticosteroid replacement for general surgery takes into account the dose and duration of maintenance corticosteroid therapy, and the nature of the surgery. These regimes involve far lower doses of steroid cover than previously given. There are no definitive guidelines for oral surgery in patients taking oral corticosteroids, but the physiological stress involved is likely to be no more severe than minor general surgical operations. In the few documented cases of apparent adrenal crisis during dental surgery, several additional factors have been identified which could have increased the risk of developing hypotension. These include the use of general anaesthetic, multiple extractions, oral infection and hypovolaemia. It is therefore unlikely that a routine extraction under local anaesthetic in a patient taking low dose systemic corticosteroids will precipitate an adrenal crisis. The difficulty in performing prospective randomised studies however, means that a consensus on this issue is still being developed.

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Chapter 10

Domestic violence: Summarised from the Management of Abuse: A Resource Manual for the Dental Team By Elizabeth Bower

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â&#x20AC;&#x192; Domestic violence is a violation of fundamental human rights. In Britain, it is a crime, with serious and long term consequences for the health and well-being of victims. Historically, domestic violence was considered a private family matter and until the 1970s, there was silence about the issue and virtually no assistance for victims. Since then, vigorous campaigning by womenâ&#x20AC;&#x2122;s groups has raised awareness and placed it firmly on the public agenda. A raft of policy and legislative changes enacted by successive British governments has encouraged the issue to be taken more seriously by the police and other professional bodies, in addition to the more obvious aim of providing protection for victims. In an era where domestic violence is regarded as seriously as other forms of violent behaviour, it is hard to believe that it was not until 1993 that the United Nations formally recognised womenâ&#x20AC;&#x2122;s rights as human rights, and violence against women as a human rights abuse. Domestic violence can affect men, but the majority of violence in the home is the abuse of women. Therefore, in discussing this issue, we have adopted a convention of identifying the victim as a woman. This should not dissuade health care professionals from investigating possible abuse in men as necessary. The NHS has a particular contribution to make to the multi-agency team of the police, social services and other statutory and voluntary agencies in tackling domestic violence. Health care staff have a role to play in identifying, assessing and responding to domestic violence, not just because of the impact of domestic violence on health, but because health services are sometimes the only point of contact for victims with professionals who can recognise and intervene in their situation. This particularly applies to victims who are restricted in their movements by an abusive partner, or who do not wish to become involved with the police and the criminal justice system. Patients are often seen more frequently in dental practices than other health agencies, thereby allowing greater opportunity for scrutiny and detection.

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In recognition of this, the Department of Health has issued a resource manual to guide health care professionals and managers in developing multi-agency partnerships with the police, social services and other statutory and voluntary sector agencies. The manual provides information to help raise awareness of domestic violence amongst health care practitioners, and suggests approaches for assisting victims. This article draws heavily on the resource manual in order to guide the dental team in formulating a practice policy on the management of domestic violence that is in line with current government policy. ‘What did I do in the 80s? I walked into doors. I got up off the floor. I became an alcoholic. I discovered that I was poor, that I’d no right to the hope I’d started out with. I was going nowhere, straight there. Trapped in a house that would never be mine. With a husband who fed on my pain. Watching my children going nowhere with me; the cruellest thing of the lot. No hope to give them. They saw him throw me across the kitchen. They saw him put a knife to my throat. Their father; my husband.’ Victim of domestic violence

What is domestic violence? Domestic violence refers to: ‘a wide range of physical, sexual, emotional and financial abuse of people who are, or have been, intimate partners’ (Department of Health). Although domestic violence can take place in any intimate relationship, including same-sex relationships, the vast majority of domestic violence and the most severe and chronic incidents are perpetrated by men against women. The need to maintain control and power over the victim is a common factor motivating perpetrators of domestic violence, although the perpetrators often do not perceive their behaviour in such terms. Abusive partners are likely to deny and cover up their behaviour, and may appear quite different in public to their demeanour at home. Isolated incidents of domestic violence are the exception rather than the norm. The abusive behaviour can be seen as forming part of a coercive pattern of controlling behaviour which usually escalates over time, and is made worse by the victim attempting to leave the situation, or being assertive. There is no set pattern for the abuse which is often unpredictable and irregular and it is important to note that whilst domestic violence is often considered synonymous with physical and sexual violence, the definition also includes emotional and financial abuse.

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Management It is likely that all dental practices have regular contact with patients whose health and well-being is damaged by domestic violence. It is not safe to assume that another agency is providing support to the patient, or preventing further abuse. The dental surgery may be seen as less stigmatising than some other clinics, giving members of the dental team an opportunity to respond to victims of domestic violence who have not had the courage to disclose the problem to other agencies. It is the responsibility of the GDP who has examined the victim to ensure that appropriate action is taken (Table 1).

Recognising the signs Victims of domestic violence may often seek help for other complaints rather than the actual violence itself. Table 2 lists signs which may suggest the possibility of abuse. None of the signs is pathognomic of abuse; rather it is often the combination of several features of a situation that raises the possibility of domestic violence.

Talking to the patient It can be extremely difficult to broach the subject of domestic violence. Fear of offending the patient, fear of opening up an issue which will explode out of control, lack of time, and uncertainty as to how to deal with such a situation, are just a few reasons which prevent health professionals asking about domestic violence. It is recommended that a few general indirect questions are asked initially to establish a rapport with the patient before using appropriate direct questions as prompts (Table 3).

Provide treatment for injuries or refer as appropriate It is important that the patient receives appropriate care for any injuries. If the GDP feels competent to treat the oral injuries, treatment should be initiated. Referrals to appropriate specialist departments should be made if the problems or injuries are more severe.

Assessing risk It is important to establish whether the patient is at imminent risk of serious harm or even death. The patientâ&#x20AC;&#x2122;s feelings and beliefs about the situation are central to the assessment. Making a safety assessment also involves considering whether the violence has increased in intensity, frequency and severity. The type of behaviour of the perpetrator is also crucial, such as a history of physically harming children, threats to harm or abduct children, and abusive behaviour whilst intoxicated. A patientâ&#x20AC;&#x2122;s

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past attempts to get help from statutory and voluntary agencies should also be taken into consideration, as should the patient’s response to the abuse, such as selfharm or suicide attempts/threats. The availability of support from family and friends should also be discussed. If it is believed that any children in the household are at risk of abuse, child protection guidelines must be adhered to.

Record keeping It is important that the history, examination and any treatment provided are documented in as much detail as possible. Records should be contemporaneous. Documenting injuries includes details of site, shape, size, colour, swelling, and any distinguishing features. Body maps are recommended to illustrate physical injuries. Clinical photos should be taken where appropriate, with written consent. Details of discussions about domestic violence, and information given, should be recorded. The records should also detail the basis for any concerns about children in the household, decisions made, and the reasons for those decisions. Consent to disclosure should also be documented. It is possible that a GDP may be required to discuss the case at a later stage in a court hearing, or at a child protection conference and comprehensive records are crucial. All records must be kept confidentially, and the dental team must ensure that they are not accidentally seen by another family member, or a member of the public, for example, on a computer terminal in the reception area.

Referrals It is important that the patient’s consent is obtained before disclosing abuse to another agency, and the patient should be party to, and have the opportunity to, see any information written about them. There are two situations when a disclosure to the police or social services can be made without consent: •

If the adult is believed to be at risk of death or serious harm

•

If a child in the household is believed to be at risk of significant harm.

Whilst both the police and social services would provide assistance in this situation, social services would normally be the initial point of contact where the victim’s children are at risk of significant harm, and the police would normally be contacted when the victim has no children, or his/her children are not at risk. Information can also be shared without consent if it is required under a court order or another legal obligation. However, where possible, consent should be sought from the patient and any other victims if they are capable of giving consent. Any decisions to disclose information without consent should only be made after discussion with senior

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colleagues (such as a senior partner in the practice, the designated trainer of a foundation dentist, or preferably a local consultant), and a defence organisation. Telephone referrals to social services should be followed up in writing within 48 hours. It is vital to ensure that a disclosure will not put the patient or any associated children in the household at increased risk of violence. If the domestic violence is not considered to fall into the two high risk categories listed above, it would be usual for the dentist and team to provide helpful information for the patient, such as details of voluntary agencies, the national domestic violence helpline, and sources of legal advice. It is not the role of the dentist or team to give advice to the patient. Referrals to specialist services regarding mental health problems, and drug and alcohol dependency would normally be made via the patient’s GP with his/her consent.

Table 1 Role of the dental team in the management of domestic violence • Recognise the signs of domestic violence • Respect what the victim says and be sympathetic • Provide treatment for oro-facial injuries and refer for treatment if necessary • Assess risk to victim • Assess risk to children in household • Keep comprehensive records • Give helpful information not advice • Make other appropriate referrals • Support and follow-up

Table 2 Signs of domestic violence General • Appointments often missed • Frequent appointments are made for vague complaints/chronic pain • Poor compliance with treatment regimens • Financial difficulties (may be due to financial restrictions imposed by partner)

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History • Injuries are inconsistent with explanations given • Delay in presentation for treatment of injuries Behaviour of patient • Appears passive or afraid of partner • Remains quiet while partner responds to questions • Withdrawn/detached • Anxious • Poor eye contact • Closed body position/holding head down • Patient minimises injuries Behaviour of partner • Partner always accompanies patient to surgery • Strongly assertive and demanding • Coercive and controlling behaviour • Offensive or intimidating behaviour • Excessive love and concern towards patient • Possessive and jealous towards patient • Answers questions addressed to patient • Minimises the injury or chief complaint Psychological indicators • History of psychiatric illness • History of alcohol/drug dependency • Signs and symptoms of depression or anxiety • History of self-harm • Poor self-care Physical indicators • Lacerations or bruising to the head or face • Fractured teeth/missing teeth • Facial fractures • Bruises or cuts to the ear (rarely accidental) • Patterns of injuries (e.g. slap mark, pinch mark, bite mark) • Scarring of the face and lips • Hair loss • Oral lesions of sexually transmitted diseases • Bruising of hard or soft palate • Evidence of previous injuries

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Table 3 Talking to a patient who may have experienced domestic violence • See the patient on his/her own. The presence of a partner or another relative could place the patient in greater danger. Discussion should also not take place in the presence of children • Ensure privacy. The consultation should take place in a room in which you cannot be overheard • Consider the need for an interpreter. This person should be an independent, professional interpreter, not someone from the family • Ensure a nurse or other team member is present at all times during the history and examination • Listen carefully. Often requests for help are veiled and the patient may talk around the subject before getting to the point • Believe what he/she says and say so • Reassure the patient that they were right to tell you about the domestic violence. • Be sympathetic and non-judgemental. The patient must not be made to feel that they are to blame for what has happened • Let the patient talk at his/her own pace. Disclosure can be very difficult • Respect confidentiality. But also explain the limitations of your confidentiality should child protection issues arise • Consider the welfare of any children. If it is believed that children are at risk, child protection guidelines must be adhered to • Be constructive. Give information on local support groups, help lines etc. • Consider whether your intervention will leave the patient and any associated children in greater danger • Respect the patient’s autonomy.

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Chapter 11

Communication & the dental team: assertiveness without aggression

Make this CPD Verifiable Turn to page 181 to find out how

Professor Liz Kay, Foundation Dean Peninsula Dental School

Every now and then situations may arise in the surgery that require a member of the dental team to deal with a patient in an assertive manner. A word of caution: assertive is NOT a synonym for aggressive and, no matter how angry, frustrated or out of control you might feel, aggression will always be counter-productive and is likely to increase, rather than reduce, the feelings of tension. Assertiveness does not mean being hard-nosed, bullying, self-centred or hostile. It is also not something that only the shy and retiring should know about. Those of us who are naturally ‘bolshy’ can benefit enormously from learning to be assertive, as aggression and energy can become more productively used if the principles of assertiveness are adhered to. The need to be assertive stems from the power relations that often exist between two individuals. Almost invariably, when one person is dealing with another, one of the two parties has more power, or a higher status than the other. In fact, we become so used to this arrangement (parent-child, teacher-pupil, dentist-patient, employeremployee) that we forget that power need not be divided so unequally. It is not necessary for interactions between individuals to be based on the ‘top-dog’ and ‘under-dog’, powerful and powerless principle. There is a middle path and it is this principle of equality which is the key to assertiveness and successful communication, especially under difficult circumstances. Assertiveness involves standing up for legitimate rights and communicating our needs, wants, feelings and beliefs in direct, honest and appropriate ways without violating the rights of others. The hallmark of being assertive is that each party in an exchange can pass on messages about what they think, how they feel and how they see the situation without dominating or degrading the other individual. From this definition, it is clear that, for a dental team to function well, both for and with patients, assertiveness from all (especially the patients) is required and should be encouraged.

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To be an assertive dental professional, two types of respect are needed. Firstly, respect for oneself and secondly (but just as importantly) respect for others. This recognition of the rights of others is important as, contrary to popular opinion, assertiveness is not a means of getting what one wants, or controlling or manipulating others. The goal, when being assertive and encouraging others in the surgery to do so, is simply open and direct communication and that is the reason for the inclusion of the subject in this text. The aim is to ensure that both partiesâ&#x20AC;&#x2122; needs are at least partially met. Thus, others have as much right to be assertive as you do (although not aggressive). Below are some examples that have occurred in dental surgeries. They are chosen to illustrate the different forms which assertiveness can take.

Basic rights It is sensible here to consider some basic rights applicable to all people. It is helpful in difficult situations, which require non-aggressive assertion, to remember these rights. 1. Despite any role which you take on (as part of the dental team, or as wife, mother, father, employee) it is important to remind yourself that you also have a right to have, and to state, your personal needs and priorities. This does not imply that you no longer have to honour the responsibilities inherent in your daily life but that you have needs that are separate from those of the people around you. 2. Your knowledge, expertise and capabilities give you a right to be treated as an equal. Some patients cast the dental team as people whose role is all-powerful, whilst others regard health workers as beings whose only responsibility is to serve their needs. As a member of a dental team, you are neither of these things. Respect your own intelligence and common sense but do not allow yourself to assume you have either more, or less, of either of these attributes than the patients who visit the surgery. 3. You have a right to feel what you feel and to express yourself. Often, by explaining your feelings in a reasoned and appropriate way, you will feel less urge to shout, scream, walk out or cry. If you suppress how you feel, for example, about the way in which children are treated in the surgery, because you believe that you will be judged as being over sentimental, or â&#x20AC;&#x2DC;softâ&#x20AC;&#x2122;, you will become upset. Even if your values are different from the rest of the team, you still have a right to respect and express your own judgements.

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4. You have a right to make your own choices. You do not have to justify your actions. For example, a dentist who decides to take a postgraduate qualification may feel that the decision must be justified by such comments as “because it will be a practice builder” or “because it will help me to undertake new types of treatment”. No further justification than “because I want to” is needed. 5. Making mistakes is acceptable. People sometimes do silly stupid things. This does not mean that the person is silly or stupid. When you make a mistake or things do not go as planned, it does not indicate that there is an intrinsic flaw in your being or personality. The ability to admit to ourselves when we make mistakes, without it destroying our belief in ourselves, is crucially important to our ability to behave and communicate assertively. 6. You can change your mind. Refusing to alter a plan of action and proceeding with a commitment you are unhappy with can be a reflection that you made a decision for the wrong reasons. If you change your mind about something, it is not an indication that you are a whimsical butterfly, incapable of making decisions. 7. Often we feel shame and embarrassment when we do not understand something. It is important for those who wish to learn to become more assertive, to realise that you can no more be expected to know everything about everything than you can expect to be perfect! You are not being ridiculous if you ask for more information or a repeated explanation. 8. Everyone has a right to ask for what they want. Patients have a right to ask it of the dental team and, equally, the dental team has a right to ask it of patients. The same rules apply within the dental team. For example, the dentist has a right to ask for extra help from the staff if he needs it. Equally, dental nurses have a right to ask dentists to write legibly if their scrawl is making their job difficult. 9. A very important right is to decline responsibility for others. This does not mean that patients’ welfare does not come first, but simply that, because the team have built a relationship with a patient, this does not mean that they have to take on the responsibility for the patient’s overall well-being. It is important for each of the team to set limits concerning which of their patients’ needs should be put before their own, and which should not. For example, although the team might decide that it is their responsibility to offer emergency care at the end of a busy day to a child in pain, they cannot offer an open-all-hours service for people who simply wish their dental care to fit with their own convenience.

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10. Lastly, and perhaps most importantly, none of us is dependent on others for approval. We cannot expect all patients to think we are fabulous. The need to be liked and approved of is extremely powerful but it is important, if assertive behaviour is to be the norm in the surgery, to learn that the world will not come to an end if you are not accepted and approved of by everyone, all of the time.

Techniques for assertiveness There are three major skills that you need to enable you to be assertive. •

It is vital that you are DIRECT and SPECIFIC about what you want or feel

•

Stick to your guns! If necessary, repeat your statement about what you want/

feel, over and over again.

•

Look out for ways in which people might try to undermine your assertiveness. If

you are not aware of these tactics, you will be sidetracked.

Specificity This is the art of stating precisely what you want to say, without any frills or furbelows! Frequently, we ‘dress up’ what we wish to say with unnecessary and extra words. This is particularly likely when feelings of anxiety are high, usually the times when we most need to be assertive. Patient

“I’m very sorry, I’m always getting dates muddled,

but I won’t be able to come for my appointment next week.”

Here the patient simply wishes to let you know that he cannot attend for an appointment. Why did he not simply say “I can’t make my appointment on the 24th.”? The key to being specific is to decide exactly what it is that you want to express and stick to that single point without clouding the issue by adding other information. Using preambles and circumlocution only serves to weaken your statement. It also prevents the listener from understanding quickly what you want. You are much more likely to get what you want if you are direct and specific. It is insufficient to assume that people (even those who are closest to us) will automatically understand us and empathise with our feelings. It is easier for people to respond to explicit requests, than to hints, sighs or complaints.

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People (especially anxious patients) are not telepathic - you must therefore give clear statements of what is required.

Sticking to your guns Once you have determined what you wish to say and have found a way of making your statement clearly, specifically and directly, you must then stick to it. Even if your statement is met by a torrent of abuse, or a request is met by a blank refusal, you will need to repeat what you have said, without getting angry or raising your voice. Simply keep saying what you wish to say until you get a response and you believe the other party to have understood you. Although anger may be one reaction you might receive, the other person, in order to deflect you from your point and thereby avoid respecting your wishes, may use other tactics. The commonest of these are: •

Manipulative comment

•

Irrelevant logic

•

Argumentative bait.

Receptionist

“Mr. Smith, we sent you an account last month and it has still not

been settled”.

Mr. Smith

“Oh yes, I was away on holiday last month.” (Irrelevant logic)

Receptionist

“I hope you had a nice time but the account

must be settled, Mr. Smith.”

Mr. Smith

“You lot, always after money, ripping us all off you are.”

(Argumentative bait)

Receptionist

“Since the work in your mouth is complete,

you must settle your bill, Mr. Smith”.

Mr. Smith

“Well I’m bringing my wife in for treatment next week.

Another customer for you.” (Manipulative comment)

Receptionist

“We’ll be starting a new account then,

but this one must be settled today.”

Mr. Smith grumpily pulls out his credit card.

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Note that, where possible, the receptionist commented on the patient’s statement. It is important that you do not simply keep saying the same thing over and over again, without acknowledging or responding to the other person. If you sound like a record that has stuck, you will not be assertive, but at the same time you should not allow yourself to be sidetracked.

Don’t be undermined Although you need to indicate that you have heard what the other person has said, it is important not to lose track of your point. You must maintain your statement.

“You may never have paid this much before,

but the account must be settled.”

“I understand that you wish to come on a Saturday,

but there are no free appointments that day.”

Making the most of criticism There will be times during your working life when you will be criticised. Sometimes this will be justifiable criticism and on other occasions criticisms are no more than insults, designed to aggravate you. To deal with criticism assertively, we first need to distinguish between criticism which is valid, criticism which is invalid and the simple put-down, insult or ‘wind-up’.

Valid criticism Imagine that you know that you have arrived late, done a job badly, forgotten to pass on a message. If your action (or lack of it) is commented upon, you need to take it on the chin. There is fact in what is being said and you were the person involved. But, it is not necessary to dissolve into abject and grovelling apology, nor is it productive to be cross. The most assertive way in which valid criticism can be dealt with is acknowledging the truth in what the critic says. “Yes, it was me who forgot to send those impressions to the lab.” and, if you truly are sorry, an apology can be added. However, if someone criticises you for something you rather like about yourself, you should not apologise. If someone criticises you for holding up the smooth running of the surgery by chatting too long to your patients, if you rather like your relationship with them, don’t say:

“Yes, I know, I talk too much, I’m ever so sorry.”

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but be assertive by acknowledging the valid criticism but at the same time by being honest.

“Yes, I do talk a lot to them all,

but I like it, I think it helps them to relax here.”

Invalid criticism/put-down If someone says something that is not true, the fact that they have said it does not make it any more accurate. If someone makes an invalid criticism of you, you need to grasp the bull by the horns and refute the comment absolutely.

“That is untrue.”

“That isn’t right.”

“I don’t accept that.”

For example: Patient

“The work you’ve done in my mouth is shoddy.

It’s not up to standard.”

Dentist

“I do not accept that at all.

My work is always of the highest standard.”

Whatever reply this response engenders, remember to stick to your guns and repeat as often as you wish, that you do not accept the criticism. Acknowledging why the criticism has been made, even though it is not true, may also be useful. Nurse

“You’re always moaning at me or being horrid.”

Dentist

“That is not true. I get bossy when I’m stressed,

but I’m not always horrid.”

Always begin with refuting the statement. Don’t give your explanation first as it may come out sounding like an excuse. Patient

“You’ve messed it up. You sent me a card saying

Friday and here I am and there’s no dentist.”

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Receptionist

“But I always put a record in the book when I

send out a card. I haven’t messed it up.”

A more assertive response would be:

“That’s not right. I always put a record in

the book when I send a card.”

Last thoughts In essence, the ability to be assertive is based in self-esteem and it therefore enables us to relate to others in an entirely new way. It is very important that assertiveness does not become confused with selfishness. Assertiveness requires that we consider how others are affected by our remarks and that we consider their wants and needs whilst at the same time remaining honest about ours. Assertiveness can improve your relationships with everyone around you because if all are assertive, then everything is clear and everyone is honest. Repeatedly practising the skills of assertiveness in the dental surgery will make the whole concept become more and more important. Instead of feeling confident about handling certain specific situations, you will become generally more confident and assertive. Adopting assertiveness techniques leads to being more open and more relaxed, exactly the ambience that promotes good communication. Changing a dental practice into one where equality reigns and direct, honest communication occurs at all times is an enormous challenge and will take hard work and commitment, but is definitely worthwhile for both staff and patients.

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Chapter 12

Protective functions of saliva Eva J. Helmerhorst

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Human saliva not only lubricates oral tissues, making oral functions such as swallowing and speaking possible, but it also protects teeth and mucosal surfaces in many ways. The main protective factor is the constant flow of saliva from the mouth into the gut, and this ‘flushing effect’ transfers, for example, food debris as well as many endogenous and exogenous agents into the gut. These comprise both oral and exogenous, often noxious, microorganisms. Some of the exogenous bacteria and viruses as well as food-borne mutagens are detoxified or killed by innate components of human saliva. Also, some members of the commensal oral microflora and many of its harmful metabolic products are inhibited or neutralised by salivary components. Thus a proper amount of saliva, with its antimicrobial agents, is a requirement for a healthy balance between host defence and microbial attack in the human mouth.

Microorganisms in whole saliva The human mouth is almost perfect for bacterial growth because bacteria appreciate its temperature, its humidity, the large surface areas for attachment, and various nutrients (growth-stimulating effects) presented through saliva. This perfect environment is made possible by the constant presence of saliva, which dissolves the nutrients and also provides some substances, for example amino acids and endogenous carbohydrates, for bacterial growth. Saliva is sterile when it enters the oral cavity through the glandular excretory ducts. Once released into the mouth, mixing occurs of the glandular secretions with the non-exocrine components in saliva, together forming what is called ‘whole saliva’, a non-sterile fluid containing a wide variety of microorganisms. Commensal microorganisms as well as epithelial cells are shed from various oral surfaces where endogenous bacteria are attached and where they multiply to be detached into whole saliva, for example during chewing.

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The major sites of origin are tooth surfaces (dental plaque, oral biofilms), tongue surface and tonsils. However, microorganisms exist over the entire intraoral surface area. Gingival, periodontal, tonsillar or mucosal inflammations may increase both the number of species and the total number of salivary microorganisms remarkably. It must be emphasised that while microorganisms may multiply in saliva, the salivary flow rate is higher than oral bacterial doubling times, such that newly formed cells are removed by swallowing more quickly than they are generated by cell division. Therefore, the salivary microflora is primarily a reflection of the overall composition of the attached microflora in the mouth. Considering the multitude of microbial species, the large surface areas and other growth-supporting properties in this salivamoistened environment, it is not surprising that the number of micro-organisms in whole saliva is high. It has been estimated that each millilitre of whole saliva (oral fluid) contains 108-109 microorganisms and the amount of bacteria swallowed per day is in the range of 1-3 g! Based on these facts, it is very understandable that clearance of bacteria from the mouth into the gut is essential to prevent microbial overgrowth in the mouth â&#x20AC;&#x201C; which often exists in cases of hyposalivation. In a healthy situation a dynamic equilibrium exists between oral microorganisms and us. It has been estimated that oral bacteria multiply once in approximately 3-4 hours, which emphasises the need of salivary clearance of microbial cells into the gut. The microorganisms harboured in the oral cavity have been characterised by culture- dependent approaches and more recently by culture-independent molecular methods based on 16S rDNA sequencing. The oral microbiome was the first human body-associated microbiome to be characterised in great detail. More than 800 different oral taxa belonging to 13 different phyla have been identified. Over 92% of these taxa group into five phyla: Firmicutes (42%), Proteobacteria (20%), Bacteroidetes (13%), Actinobacteria (11%) and Spirochaetes (6%). The numbers of taxa that account for 90%, 95% and 99% of microbial biomass in the oral cavity are approximately 259, 413 and 875 taxa, respectively. Streptococci are the most abundant species in the mouth, followed by members of the genera Abiotrophia, Gemella and Granulicatella. Besides microbe identification, the 16S rDNA technology has also provided new ways of microbe visualisation through Fluorescence In Situ Hybridization (FISH). Bacteria in typical brush-like structures, previously observed in dental plaque, have now been speciated. In these organised aggregates bacteria from the Cytophaga-Flabobacterium-Bacteroides (CFB) cluster (most likely T. forsythia) and F. nucleatum are arranged perpendicularly around lactobacilli, forming the fine test tube brush-like appearances. In dispersed dental plaque, species of Veilonella, Prevotella and Actinomyces are most frequently

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engaged in interactions with other species. Defining bacterial interactions and unravelling the biofilm architecture at the species level are important steps forward allowing the design of strategies to interfere specifically with such associations as a means of plaque control. In this context, it must be noted that bacterial colonisation is not necessarily disadvantageous to the host when it concerns commensal microbes that in fact may prevent, by occupying docking sites, colonisation with more harmful bacteria, a process known as colonisation resistance.

Transmission of micro-organisms by saliva contacts The first microorganisms colonise infants’ oral cavities immediately after delivery and the quality of flora during the first days of life is rather similar to that of the mother’s vaginal flora. However, increasing exposure to external sources widens the number of species and increases the total quantity of oral microorganisms – of course, depending on the available species. The most important source of transmission into the baby’s mouth is his/her mother. There are a number of ways by which mothers (and also other family members) can supply new microorganisms into the infant’s developing oral flora. These include cleaning the pacifier (dummy) in the mother’s own mouth before giving it to the baby, tasting the food in her own mouth before feeding the baby, and kissing the baby on the lips. It would be of no concern if the mother’s own (oral) health is qualitatively good and she does not carry abundant cariogenic microorganisms in her own saliva. A typical example of this salivary transmission of cariogenic species is the group of mutans streptococci. Mothers with high salivary counts of mutans streptococci often infect their children’s dentitions via salivary contacts by the age of 1-2 years and reliable scientific evidence shows that the earlier and the more abundant the transmission of mutans streptococci to the baby’s dentition, the higher is the caries incidence in later childhood. This information is clinically highly relevant, since chair-side test methods can be used to screen mothers (or other family members/ caretakers) with high salivary counts of mutans streptococci. High numbers can be reduced temporarily with e.g. chlorhexidine or xylitol to prevent, or at least delay and diminish, the salivary transmission of these harmful bacteria from mothers to their babies. Strong evidence also exists that periodontal pathogens, mainly anaerobic bacteria, are transferred via salivary contacts from person-to-person, often already by preschool age. More familiar infections from saliva are, for example, viruses – such as herpes simplex type 1, Epstein-Barr virus (‘kissing disease’) and influenza viruses.

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Growth of bacteria in saliva Saliva not only inhibits but also selectively supports the growth of certain bacterial species. This has been proven by studies of humans (and animals) who have received their nutrition by stomach tube (gavage) but who still harbour large numbers of microorganisms in their mouth. This is mainly due to the presence of saliva-borne glycoproteins, which provide carbohydrates, proteins and amino acids for bacteria. However, the microbial flora in these cases is usually low in lactobacilli, mutans streptococci and yeasts but their numbers increase as soon as oral intake of fermentable sugars is frequent. In the salivary ecosystem the microorganisms first metabolise glycoprotein-derived carbohydrates and later the proteins. Individual species grow in different types of saliva but in most cases submandibular/sublingual secretions rich in mucins are the best growth medium. To be able to grow in saliva, bacteria need to produce glycosidases and/or proteases to get nutrients to survive without external supply. Mucins are mucoglycoproteins containing protein cores with a number of attached oligosaccharide side chains. There are two mucins in saliva, high molecular weight mucin glycoprotein 1 (MUC5B, previously designated MG1) and lower molecular weight mucin glycoprotein 2 (MUC7, formerly MG2). They are products of different cell populations within the submandibular, sublingual and minor salivary glands. Among salivary streptococci there is large variation in their ability to grow in the presence of mucins and this difference is related to their capacity to hydrolyse oligosaccharide side chains by glycosidases. These enzymes are seldom found in mutans streptococci. Because mucins form an integral part of biofilms on tooth surfaces, the relative proportion of various streptococci reflects the amount of mucins in salivary pellicles, i.e. early colonisers â&#x20AC;&#x201C; such as S. oralis (formerly S. mitior), S. mitis and S. sanguinis â&#x20AC;&#x201C; are dominant in early dental plaque rich in mucins. Saliva alone, without an external source of fermentable sugars, selects for a non-cariogenic microflora with low levels of mutans streptococci. S. mutans and S. sanguinis both possess proteolytic activity which enables them to use the nitrogen sources in saliva. Urea and free amino acids in saliva may serve as substrates for ammonia production by salivary microorganisms; ammonia is the major base in dental plaque. S. sanguinis can also digest arginine peptides to release arginine, which is a good source of ammonia production in the vicinity of tooth surfaces. Thus, salivary energy sources for different bacteria produce different components, which partly determine the microbial composition of oral biofilms.

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Salivary components in oral biofilms In the mouth, salivary glycoproteins are found either as a mucosal film, or on the tooth surfaces as the acquired enamel pellicle. The acquired enamel pellicle is a cell-free proteinaceous layer formed immediately after tooth enamel is exposed to saliva. The adsorption of salivary proteins onto enamel is a specific process; the composition of pellicle differs significantly from the overall protein composition of glandular secretions or whole saliva. Pellicle precursor proteins primarily constitute phosphorylated salivary proteins with demonstrated high affinity for hydroxyapatite, i.e. acidic proline-rich proteins, statherin, histatin 1 and cystatin. Besides phosphoproteins, dental pellicle also contains glycosylated proteins such as mucins, amylase, and sIgA. Protein compositional analysis of dental pellicle has been hampered by the small amounts of this integument that can be harvested from the tooth surface. One of the techniques to collect pellicle uses PVDF membranes soaked in sodium bicarbonate buffer. With the advent of mass spectrometry it has become feasible to identify proteins at sub-Âľg levels and to simultaneously identify proteins in complex mixtures, such as in oral specimens. Shot gun proteomics approaches have catalogued over 2,000 proteins in human saliva, with 20% representing cytoplasmic cell-derived components. Substantially fewer proteins, 130, have been documented in the acquired enamel pellicle, consistent with the selective adsorption concept. The pellicle and the attached biofilm are dynamic structures. Attachment, growth, removal and reattachment of bacteria may occur at the same time. Because of its significant content of salivary glycoproteins and its rapid rate of formation on cleaned tooth surfaces, pellicle can be considered as a renewable lubricant, which helps to protect the teeth from attrition and abrasion. In addition, protective functions of pellicle pertain to maintenance of mineral homeostasis by protection of demineralisation and facilitation of remineralisation. Indeed, acidic PRPs, as well as lipocalin, cystatin SN and cystatin S are more abundant in dental pellicle obtained from caries-free subjects than in pellicle from individuals with high levels of decayed, missing or filled teeth (DMFT). On the other hand, amylase, immunoglobulin A and lactoferrin are correlated with high DMFT levels. Relationships between oral disease and proteins in the dental pellicle may be explained by the direct protective functions of pellicle proteins towards enamel.

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Alternatively, or additionally, the oral disease relationship can be attributed to differences in the levels of cariogenic bacteria that are attached to the pellicle structure. Pellicle serves as a layer to which oral bacteria bind. As such, pellicle influences early bacterial colonisation of the tooth surface and may even determine the composition of the ultimate bacterial biofilm formed. Thus, dental pellicle may dictate, to some extent, the composition of dental plaque. This interesting concept has not been proven in vivo yet, but with the available proteomics and 16S rDNA technologies it is anticipated that pellicle signatures will be identified that are associated with ‘good’ or ‘bad’ biofilms.

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Chapter 13

Cognitive Behavioural Therapy in dental anxiety Adapted from Cognitive Behavioural Therapy for adults with dental anxiety: a toolkit, Tim Newton et al

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Anxiety is the term used to describe feelings of apprehension, dread and uneasiness and is a ‘vague, unpleasant feeling accompanied by a premonition that something undesirable is about to happen’. The term ‘phobia’ is reserved for a marked and specific fear that is excessive or unreasonable in which the anxiety-provoking situation is avoided and this avoidance interferes with the person’s daily life for at least 6 months. Anxiety has three components – physiological (e.g. increased heart rate, sweating, raised blood pressure, palpitations, breathlessness), behavioural (e.g. avoidance of the anxiety-provoking situation or escape from the situation) and cognitive (e.g. thoughts about the situation, reduced ability to concentrate or to remember). Dental anxiety has been defined as, ‘an abnormal fear or dread of visiting the dentist for preventive care or therapy and unwarranted anxiety over dental procedures’. The prevalence of dental anxiety is high with about 40% of adults being afraid to visit the dentist, 20% being highly anxious or fearful of visiting the dentist and 5% are thought to avoid dental treatment because of their anxiety. These figures do not appear to have changed over the last 40 years despite the improvements in dental treatment methods and increased knowledge in how fear and anxiety might be alleviated and managed. Dental phobia has been found to be the most prevalent phobia in adults and can lead people to postpone visiting the dentist, cancel or miss their appointments, or not visit a dentist at all. As regular and appropriate dental care improves peoples’ chances of having a healthy mouth and retaining their teeth into older age, it is vitally important that health professionals attempt to tackle the problem of dental anxiety. Indeed, dental anxiety and the resultant avoidance of dental treatment has been shown to have a number of detrimental effects on physical health (untreated gum disease and tooth decay leading to tooth loss), function (poor chewing and eating), social interaction and quality of life including disturbed sleep, reduced concentration at work and feelings of embarrassment, shame and misunderstanding. There are a number of theories as to how dental anxiety can arise.

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In reality it is likely that multiple factors act in combination and in different ways to initiate and maintain feelings of anxiety. For instance, dental anxiety may arise due to learning from previous unpleasant experiences (classical conditioning). Indeed, many people who are dentally anxious have experienced traumatic events at the dentist earlier in their life. Fear of dentistry and the reaction of avoidance may be maintained by operant conditioning. Mowrerâ&#x20AC;&#x2122;s two-factor theory (classical conditioning and operant conditioning acting in combination) suggested that when an object or situation becomes feared, this stimulates motivation to avoid the object or situation in order to reduce the feelings of fear. Reductions in fear that occur from avoidance act to reinforce future avoidance. However, this two-factor theory does not offer a complete explanation of the development and maintenance of dental anxiety as many people who have experienced a traumatic event do not become anxious about dentistry and some people who are anxious cannot remember a traumatic event. Another possible way of developing dental anxiety is to learn from others. For example, children may learn to be fearful of dentists via their parents, siblings, friends or other family members. Mothers whose dental anxiety is high are more likely to have children who are anxious about visiting their dentist and demonstrate negative behaviour in the dental chair compared to mothers who are not anxious. Dental anxiety may also develop from negative experiences in other settings. For example, someone who is anxious about giving blood may also become anxious about receiving dental injections. A further theory as to the cause of dental anxiety is that we are born with a predisposition or â&#x20AC;&#x2DC;preparednessâ&#x20AC;&#x2122; to be anxious about certain situations and objects that leave us susceptible to harm. Cognitions also play a key role in the development and maintenance of dental anxiety. It has been suggested that key cognitions surrounding uncontrollability, unpredictability, dangerousness and disgust create a feeling of vulnerability that in turn leads to dental anxiety. Within the UK at present, the majority of individuals with dental fear or phobia are currently managed through conscious sedation or general anaesthesia. However, a recent meta-analysis indicated that psychological interventions for dental phobia, most notably graded exposure to the feared stimulus, significantly reduced self-reported dental anxiety and increased dental attendance, with medium to large effect sizes. Thirty-eight behavioural treatment studies were reviewed and found to result in large reductions in dental fear and that 77% of subjects were seeing the dentist regularly after four years or more. Thus it appears that psychological approaches to the treatment of dental anxiety are a potential alternative or adjunct to sedation and general anaesthesia.

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Cognitive Behaviour Therapy (CBT) is an example of a brief psychological therapy with proven effectiveness. CBT, a talking therapy, is a synthesis of Behaviour Therapy and Cognitive Therapy. Behaviour Therapy posits all behaviour as the result of simple Stimulus-Response connections, with maladaptive behaviour in particular resulting from learnt, faulty or inappropriate Stimulus-Response connections. The Behavioural Therapist therefore, aims to assist the client in learning more adaptive Stimulus-Response patterns. Behavioural therapies include learning relaxation skills, conducting mini-experiments and systematic desensitisation (constructing a hierarchy of situations that elicit varying and increasing degrees of anxiety or fear and then progressing through the hierarchy in a relaxed, non-anxious state Cognitive therapy on the other hand, is based primarily in the analysis of people’s cognitions (e.g. thoughts, beliefs, interpretations). The idea here is that the way people think about events, plays a central role in their emotions (e.g. anxiety) and physiological responses (e.g. excessive perspiration) and pave the way to establishing and maintaining unhelpful behaviours (e.g. avoidance). Cognitive therapy, therefore aims to facilitate a new understanding (cognitive restructuring) that the feared stimuli are unlikely to be dangerous and in turn that avoidance or other safety behaviours are not required. By merging behavioural therapies and cognitive therapy, CBT uses both behaviour modification techniques and cognitive restructuring procedures to change maladaptive beliefs and behaviours. An important principle underlying CBT is its focus on the ‘here and now’ as what started a problem is often not the same as what is keeping it going. In contrast to other psychotherapies, CBT is a shortterm therapy, with treatment typically lasting 6 to 10 sessions. There are additional characteristics of CBT which set it apart from other therapies. These include the collaborative nature of CBT, its structured approach and asking clients to complete homework. In terms of the collaborative nature of CBT, the therapist and client work together rather than the therapist being the expert. In this way the therapist teaches the client the CBT model and encourages and assists the client to apply this to their problems. In this way CBT encourages clients to become their own therapist. CBT takes a structured approach therapy whereby the CBT therapist approaches each session in a structured manner with a planned agenda. Sessions involve assessment, collaborative goal setting, presenting and reviewing formulations (i.e. working hypotheses about the client’s problems), and receiving feedback. Homework is a key aspect of CBT as performing tasks in between sessions enables the client

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to apply CBT techniques in a more natural environment and put what has been learned into practice. The efficacy of CBT for a range of psychological problems is now well established, most notably for depression and anxiety related disorders (including phobias), but also for a diverse range of psychological disturbances. CBT has been reported to be “the psychological therapy with the most solid and wide evidence base for efficacy and effectiveness”. This has led to the establishment of the Increasing Access to Psychological Therapies programme from the Department of Health. The efficacy of cognitive interventions and behavioural interventions for dental anxiety has received some attention and studies indicate that both cognitive and behavioural interventions can be successful in reducing dental anxiety and increase dental attendance. These positive effects have been shown to be maintained over time.

Overview It is suggested that a typical series of CBT sessions should comprise of 10 appointments each of between 45 minutes to one hour. Patients can complete the therapy is less than 10 sessions and this is often the case. The first session will provide an introduction to the overall plan of therapy, assess the patient’s current level of fear and anxiety and set goals. The next session introduces the patient to the practice of relaxation and simple coping strategies. The remaining sessions address the cognitions associated with dental anxiety and fear using structured exercises and homework tasks, as well as undertaking systematic desensitisation tasks. In the final session the patient’s goals and achievements are reviewed. The patient completes a final assessment questionnaire and is offered a review session after 6 months’ time. The first task in each session is to set an agenda in collaboration with the patient for what will happen in that session. This then provides a structure for both the therapist and the patient and sets the scene for subsequent sessions. Each individual therapist will have preferences for starting with either the behavioural or the cognitive components, and this can also be guided by the patient’s views. Some patients will prefer to understand the thought processes behind their fear before seeking to change their behaviour, while others would rather address the practical aspects first. This is a good topic for discussion in the initial assessment appointment. Outlined below is a typical introductory session, and series of sessions using CBT techniques including systematic desensitisation. The sessions are flexible and are adapted to the needs of the individual patient and the speed at which they progress. For instance, the sessions of systematic desensitisation may in reality take several sessions to complete whereas the introduction to relaxation and distraction techniques may only take half a session.

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A guide to typical Cognitive Behaviour therapy sessions Session 1 – Assessment and Case Formulation 1. Set agenda The aim for this session is to introduce the patient to the principles and practice of CBT, to build a therapeutic rapport with the patient, to assess the patient’s level of anxiety and specific dental fears, and finally to produce an initial case formulation of the origin and maintaining factors in the patient’s fear. 2. Building Rapport The therapist should take time to establish a good rapport with the patient. Therapists will be familiar with simple techniques for establishing a good rapport from their clinical practice but they may consider discussing the patient’s success in attending for this initial assessment which may have been difficult given that it is a requirement for them to face their fears. 3. Introduction to CBT In introducing CBT you should explain the following elements; What is CBT? How does CBT work? Engagement in CBT.

What is CBT? Explain that CBT stands for Cognitive Behaviour Therapy, it has three elements, it is a therapy – which means it is about helping people overcome their difficulties, in this specific instance their fear of dental treatment. It involves both cognitive and behavioural techniques. Cognitive techniques refer to changes in the thoughts which are related to their dental fear, and this is typically done by a series of tasks involving identifying those thoughts and seeking to change them. The Behavioural techniques involve gradual exposure to the feared object. It is important to emphasise this exposure is done very gradually, and at a pace that is set by the patient in order to challenge them whilst still allowing them to feel comfortable. A useful analogy in this regard is the training for a long run, it would be unrealistic to expect a person to be able to run 26 miles within a week, but with gradual training over a long time they can increase the distance that they can run up to a point where they can achieve a marathon. To encourage confidence in the therapy, it is useful to explain to patients that CBT has been found to be effective in a range of problems but in particular, anxiety, phobias and depression. The practicalities of CBT should also be discussed, in that it is problem focussed and short term.

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How does CBT work? CBT works by changing the way you think about the feared object and by changing your behaviour towards the feared objects. The focus is on those thoughts and those behaviours which are maintaining the fear in the here and now, rather than what caused the problem. This is partly because, those factors which maintain a problem are not necessarily the same as those which started it, but also it is much more difficult to change events than the past. By gradually reintroducing you to the feared object, behavioural therapy allows you to relearn that dental treatment can be safe.

Engagement in CBT CBT requires the patient to participate actively in their own therapy, and involves â&#x20AC;&#x2DC;homeworkâ&#x20AC;&#x2122; or tasks set between sessions. The more involved the patient becomes in their homework and the tasks that are set them, the more effective the treatment is likely to be.

Level of dental anxiety The modified Dental Anxiety Scale devised by Professor Gerry Humphris is a five-point scale which has specific items relating to different aspects dental treatment all rated on a 1-5 scale. It is easy to score, you simply add up the numbers that the patient has circled and any patient scoring 19 or more is highly likely to be considered phobic of dental treatment, note that a number of patients might score below 19 but be very anxious about specific aspects of dental treatment such as local anaesthetic injections. These patients should be considered separately from the general phobia group. The specific items can also be used to identify targets for use of systematic desensitisation as they cover, the use of local anaesthetic, waiting in the waiting area, drilling, scaling and general treatment. See http://medicine.st-andrews.ac.uk/supplemental/ humphris/dentalAnxiety.htm

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Chapter 14

Common conditions that cause neurological & sensory impairment

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Adapted from Holistic Oral Care by Janet Griffiths and Steve Boyle

Neural damage can cause both motor and sensory dysfunction, and higher function may also be affected if there is cerebral involvement. Such conditions affect patients’ behaviour and care, and need to be taken into consideration by the dental team.

Multiple sclerosis Multiple sclerosis (MS) is a common and complex neurological condition that occurs as a result of degeneration of the myelin sheath and causes interruption in sensory and motor nerve transmission. MS is the most common cause of severe disability in young adults in the UK. The incidence of MS is estimated to be approximately 1.8 per 1,000. Women are more frequently affected than men in a ratio of 3:2. Diagnosis is usually between the age of 20 and 40; it relies on two occurrences of symptoms involving different areas of the nervous system, at least 2 months apart, and each lasting for at least 24 hours; diagnosis is confirmed by neurological tests. Many factors are involved in MS, but no single cause has been identified. Environmental factors such as viral or bacterial infections, a genetic predisposition to MS, family history of MS, climatic and geographic factors are all relevant. There is growing evidence to suggest that infection may play a role. There are four main types of MS: • Benign •

Relapsing/remitting

•

Secondary progressive

•

Primary progressive.

MS is a condition characterised by remission and relapse. Although some symptoms are common, there are no typical symptoms that apply to all cases. Symptoms vary from a very mild manifestation in the benign form to steadily worsening symptoms without remission in primary progressive. Symptoms vary in severity and duration, and depend upon the areas of the central nervous system affected. They include fatigue, muscle weakness, tremors, double or blurred vision, ocular or facial pain,

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auditory giddiness, sensory loss, mobility impairment due to loss of balance, sensory loss, speech and swallow impairment, bowel and sexual dysfunction. Cerebral involvement may affect memory, motivation, insight, personality, touch, hearing, vision and muscle tone. Trigeminal neurological and sensory impairment neuralgia is commonly associated with MS with a reported prevalence of up to 32%. For this reason, a dentist may be the first person to suspect a possible diagnosis of MS in younger persons. Epilepsy in people with MS is three times more common than in the general population. Symptoms and treatment of MS influence oral health, self-care and dental management. They include: chronic pain, trigeminal neuralgia, spasticity and spasm, tremor, speech disorders, dysphagia and side effects of medication. People with MS experience the same oral and dental problems as the general population. However, they may be more prone to periodontal disease and an increased risk of dental caries due to reduced ability for selfcare and the oral side-effects of medication, particularly xerostomic medication. Dietary advice, preventive measures, aids to oral hygiene and support for carers are a priority in progressive and severe MS. Dental treatment should be arranged to coincide with the periods of remission and times of least fatigue. The patient with MS is the expert in their condition and should be consulted on how he or she prefers to manage their symptoms. There has been considerable concern that exposure to mercury in dental filling materials can cause neurological disorders, and particularly MS. Although there is no scientific evidence to support this contention, it has led to demand for removal of amalgam fillings. Patients should be reassured that even the MS Society advises that there is lack of proof that mercury is a factor in MS. It is reasonable to use appropriate alternative filling materials that do not contain amalgam when fillings need to be replaced but the routine removal of amalgam fillings should be discouraged; a new awareness campaign has been set up with this objective.

Myasthenia gravis The name â&#x20AC;&#x2DC;serious muscle weaknessâ&#x20AC;&#x2122; is an accurate description of myasthenia gravis (MG), which is caused by defective neuro-transmission mechanisms. Weakness is at its worst following exercise and at the end of the day, and seriously affects the musculature of the face, neck, hands and feet. Generalised muscle weakness and fatigue affects mobility, speech, and swallowing. MG is commoner in women in

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younger age groups and in men in later life. Congenital or inherited myasthenias are rare and present in childhood. Typically, the mandible drops due to muscle weakness. Eating becomes an effort and dietary changes to facilitate mastication may result in an increased intake of soft or cariogenic food and an increase in tooth-food contact time. Oral selfcare may be tiring and difficult. Dental care when necessary should be planned to coincide with periods of least fatigue. General anaesthesia should be avoided as respiration may be depressed. With appropriate treatment, 90% of patients return to normal function. Symptom relief for MG is provided with anticholinesterases, a range of drugs that increase salivation. Atropine may be prescribed to reduce salivary secretion and counter the side-effects of high doses of anticholinesterase. Steroids also provide relief and their oral side-effects must be considered.

Motor neurone disease Motor Neurone Disease (MND) describes a group of related conditions affecting motor neurones, the brain and spinal cord. MND is a steadily progressive disabling condition. Degeneration of motor neurons leads to weakness and wasting of muscles. Symptoms depend upon the site of affected motor neurones but there is no sensory or intellectual impairment. The physical aspects of weakness and muscle paralysis are the main factors for oral health and dental management. Weakness of head and neck muscles pose a risk to the airway, create eating and swallowing difficulties, and challenges for oral care. Adequate lubrication is essential to maintain comfort.

Guillain-BarrĂŠ syndrome Guillain-BarrĂŠ syndrome (GBS), also called acute inflammatory demyelinating polyneuropathy and Landryâ&#x20AC;&#x2122;s ascending paralysis, is an inflammatory disorder of the peripheral nerves. The cause is unknown but thought to be viral in origin. GBS is characterised by rapid sudden onset of weakness and often, paralysis of arms, legs, facial and respiratory musculature. It is a common cause of rapidly acquired paralysis. Although many cases are mild, extensive paralysis is possible in severe cases and artificial ventilation may be necessary. In the acute phase, bilateral facial palsy and dysphagia may occur, with variable motor and sensory loss in limbs. Some 10-30% have a range of residual disabilities. Individual assessment at intervals during

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illness, rehabilitation and in recovery ensures that the most appropriate oral care can be provided.

Cerebrovascular accident Cerbrovascular accidents (CVA), commonly called strokes are a common cause of impairment and disability, particularly in older people. Approximately 100,000 people in England and Wales experience a first stroke each year. It is estimated that a third will die in the first year, a third will make a good recovery and a third will be left with moderate to severe disabilities. Stroke can affect all age groups; the majority are people over 55 and around 300,000 people in the UK are living with stroke related disabilities. A stroke (CVA) may be caused by haemorrhage (cerebral or subarachnoid), thrombosis or embolism. Symptoms and prognosis are dependent on the cause, affected area and extent of brain damage. Hypertension and atherosclerosis are possible precursors for haemorrhagic and thrombotic CVA. Subarachnoid haemorrhage affects any age group. In 50%, onset is characterised by a sudden and severe headache followed by rapid loss of consciousness. Physical or emotional stress are contributory factors. In 10% of cases, the cause is a congenital aneurysm in the circle of Willis. Bleeding into the cerebral ventricle is generally fatal. Approximately one third die from the first haemorrhage. Prognosis is poor but has been improved by surgical and radiological treatment. Thrombosis and embolism are the main causes of an ischaemic stroke (CVA). Thrombotic strokes may be preceded by Transient Ischaemic Attacks (TIA), â&#x20AC;&#x2DC;ministrokesâ&#x20AC;&#x2122; caused by temporary interruption to the cerebral blood supply. Onset of cerebral thrombosis is generally gradual with ill-defined symptoms. Prognosis ranges from minimal impairment to death within a week. Embolic causes of CVA are associated with atrial fibrillation and infective endocarditis, and are characterised by sudden onset associated with headache and immediate symptoms. Symptoms of CVA include weakness, loss of balance, motor and sensory loss, paralysis, speech and swallowing difficulties, and intellectual and communication impairment. Common deficits affecting communication are dysphasia, dysarthria and dyspraxia, loss of visual field due to homonymous hemianopia, and sensory inattention which can involve more than one modality. In hemipleagia, personal care may be affected by loss of use of the dominant hand. Rehabilitation involves the development of new compensatory skills. Intellectual impairment delays and

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interferes with rehabilitation. Unilateral facial paralysis mainly affects the mandible; oral hygiene may deteriorate on the affected side due to loss of neuromuscular control and food pocketing. Previously functional dentures appear to lose their fit due to loss of neuromuscular control. In some cases, dentures can be modified to compensate for this. Swallowing difficulties may increase tooth-food contact time and increase the risk of dental caries. Dietary adjustment to maintain nutritional status and facilitate safer swallowing may increase the risk of dental caries. Patients receiving parenteral nutrition are still at risk of oral disease; calculus appears to form more rapidly in tube-fed subjects compared with the non-tube fed, indicating a significant oral care need. Palatal training devices may improve the swallow reflex, although recovery and improvement may be spontaneous. Predisposing factors such diabetes may influence oral health. Thrombotic and embolic strokes are treated with anticoagulants, which affect management of dental care. Anticoagulant dosage may need to be adjusted before invasive dental treatment but the risk of lowering a patient’s INR must be weighed against the risk of thrombosis. Most patients on anticoagulant therapy can be managed without risk and without adjustment of anticoagulant dosage. Interdisciplinary assessment should be carried out as early as possible to ensure that oral factors are included in the rehabilitation programme. Minor adjustments to dentures to improve stability or compensate for paralysis are relatively simple, and can make a significant contribution to well-being. An oral care programme that takes account of assessed and changing risk factors, side-effects of medication and nutritional intake should be implemented at the point of diagnosis.

Bell’s palsy Bell’s palsy is the term for paralysis of facial muscles caused by inflammation in the stylomastoid canal. Paralysis may also develop following trauma, surgery or other serious conditions. Bell’s palsy is generally preceded by pain in the area and fairly rapid onset paralysis. It is usually unilateral and may be associated with loss of taste. With incomplete paralysis, the prognosis for full recovery is good but is less favourable in cases of complete paralysis. Permanent paralysis can cause drooling on the affected side. This may be reduced

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by fitting an intra-oral appliance to lift facial musculature or by modifying dentures; both methods having psychological benefits. Speech and swallowing may be affected. As with any cause of paralysis of oro-facial musculature, food retained on the affected side is in increased contact time with teeth, thus increasing the risk of caries and periodontal disease. Short courses of steroid therapy are beneficial.

Trigeminal neuralgia Trigeminal neuralgia (TN), also known as tic douloureux is a disorder of the fifth cranial nerve. It is characterised by intense stabbing pain across the face in areas supplied by the trigeminal nerve. Atypical TN is less common and may cause less intense, constant, dull burning or aching pain. TN is usually unilateral but sometimes experienced bilaterally. Onset is most often after the age of 50 but cases are known in children and even infants. Facial stimuli can provoke an intense attack; it is considered to be one of the most painful afflictions. Drug therapy is the initial treatment and anticonvulsants such as carbamazepine and phenytoin are the first choice. Baclofen, pimozide, oxcarbazepine, sodium valproate and clonazepam are alternatives if symptoms are not controlled. Some anti-depressants offer significant pain relief. If drug therapy is not effective, neurosurgical procedures may offer relief. The oral side-effects of medication must be considered.

Parkinsonâ&#x20AC;&#x2122;s disease Parkinsonâ&#x20AC;&#x2122;s disease (PD) is a progressive neurological condition affecting movement. It is characterised by tremor mainly affecting hands and arms, rigidity, abnormal posture, dyskinesia (involuntary movements), bradykinesia (slowness initiating and executing movement) and akathasia (muscular rigidity). Hand tremor is characterised by pill rolling and is worse at rest. Arms are rigid, flexed and held at the side; bradykinesia leads to restricted mobility. Rigidity leads to abnormal posture and restricts activity, particularly in the activities of daily living. Lack of facial expression is reflected in a mask-like appearance. Speech and communication may be affected. Intellectual impairment occurs in 30-40% of cases after 7-10 years. PD occurs most commonly in people over the age of 50 although young onset PD starts before the age of 40. Around 120,000 people in the UK have PD; approximately 10,000 people in the UK are diagnosed each year. Idiopathic Parkinsonâ&#x20AC;&#x2122;s disease is caused by a deficiency of the neurotransmitter, dopamine. Other causes of Parkinsonian symptoms include cerebrovascular disease, head injuries, encephalitis lethargica, some toxins or drugs, particularly phenothiazine and butyrophenone neuroleptics. 139

Treatment is mainly with drugs. Levodopa in combination with a dopadecarboxylase inhibitor is the treatment of choice for idiopathic Parkinson’s disease. Anticholinergic drugs relieve hand tremor at rest. Dopamine agonists (e.g. amantidine, bromocriptine, amantadine, lisuride, ropinirole and pramipexole) are prescribed when levodopa is ineffective. Facial dyskinesia, involuntary movements of the facial muscles such as pursing the lips and ‘flycatcher tongue’ are distressing side-effects of treatment. Physiotherapy and physical aids help maintain independence. Dietary intake is increasingly important to achieve optimal nutrition, address swallowing difficulties and lessen the symptoms of the disease. Oral problems associated with PD include: •

Xerostomia and root caries

•

Dysphagia and drooling

•

Neuromuscular control of dentures

•

Maintenance of oral hygiene.

Frequent intakes of high calorie dietary supplements increase the risk of dental caries. Neurological symptoms affect dental management. Drooling and pooling of saliva is associated with delayed swallow and poor posture. A physiotherapy assessment may be beneficial to improve posture and reduce drooling. Side-effects of anticholinergic medication may help reduce hypersalivation. Botulinum toxin injections into the parotid salivary gland are helpful in reducing salivation but there is a risk of producing permanent dry mouth. Burning mouth syndrome is also more common in PD. As with all progressive neurological conditions, advice and prevention at diagnosis provide the best prognosis for maintaining oral health.

140

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Chapter 15

A guide to understanding & managing herpes simplex virus in dental practice

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Approximately 70% of UK adults are infected with herpes simplex virus type I (HSV-1), the sporadic activity of which, within the orofacial tissues, may produce recurrent symptoms, in particular herpes labialis (cold sores). The presence and high infectivity of herpetic lesions has implications for the patient and for the delivery of dental care. Fluid released from the blisters contains approximately 1,000,000 HSV-1 viral units per ml, each capable of transmitting infection. Dental team members should be aware of the potential cross-infection risk and their duty to take appropriate action. HSV-1, a DNA virus, is characteristically first acquired in early childhood. Primary infection is self-limiting and resolves within ten days. However, the virus subsequently remains latent in the orofacial tissues, with the potential to reactivate causing further symptoms (secondary infection).

Primary HSV-1 infection Although most cases of primary infection are unnoticed or dismissed as teething during childhood, some individuals develop striking symptoms of vesicular bloodcrusted eruptions on the lips, widespread oral ulceration, pyrexia and cervical lymphadenopathy. Herpetic whitlow is a primary localised form of HSV-1 infection that characteristically develops in one of the fingers as a result of the virus gaining access through cuts or abrasions. Whitlow was a recognised occupational problem for members of the dental team prior to the routine wearing of gloves. This form of infection is particularly painful and may persist for many weeks. This condition should be treated with systemic antiviral therapy from a doctor.

142

Secondary HSV - 1 infection A number of factors have been recognised that predispose to reactivation of latent HSV-1. •

Emotional stress

•

Exposure to ultraviolet light

•

Exposure to cold weather

•

Physical injury

•

Dental treatment

• Flu • Menstruation • Pregnancy •

Iron deficiency

•

Immunodeficiency / suppression.

The resultant rapid multiplication of virus (200,000 times in eight hours) produces the clinical symptoms of a herpes labialis or oral ulceration.

Herpes labialis (cold sores) The classic episode of herpes labialis progresses through a series of distinct clinical stages over a period of 7 – 10 days. 1.

Tingle / burning (prodrome)

2. Erythema 3. Swelling 4.

Blister (vesicle)

5. Ulcer 6.

Crust (healing)

In addition to causing a high degree of embarrassment, herpes labialis is often extremely painful, particularly during the swelling, blister and ulcer stages.

143

Oral ulceration Reactivation of HSV – 1 may occasionally produce a localised area of ulceration, particularly in the hard palate. The ulcers resemble recurrent aphthous stomatitis but are irregular in outline and are usually preceded by a tingle or burning sensation similar to that experienced prior to herpes labialis.

Asymptomatic shedding It is becoming increasingly recognised that some individuals who have had primary infection, periodically and asymptomatically secrete HSV-1 in their saliva. This observation is important since the saliva is infectious and is probably, in part, the reason why HSV infection is so widespread in the UK population. Routine glove wearing and universal infection control procedures for all patients adequately address the risk.

Managing a patient with HSV infection General principles •

HSV – 1 is a robust, easily spread virus. Working practice must aim to reduce

the risk of spread of infection.

•

Universal infection control procedures should be employed, in particular the

wearing of gloves by clinical staff.

•

Patients should be advised on the nature of HSV-1 infection and given

appropriate advice on action that will limit the impact of the virus on their life.

•

When required, HSV-1 infection should be treated with an antiviral agent.

Primary HSV-1 infection Patients and parents (in the case of children) should be reassured about the widespread nature of HSV – 1 and warned about the risk of spread of infection to other body sites (particularly the eye) as a result of finger contact with lesions. Active treatment consists of supportive symptomatic therapy. The use of systemic antiviral therapy should be considered in those patients with severe symptoms or an underlying medical condition that is associated with a reduced immune defence.

144

Patients with primary infection usually feel generally unwell and are unlikely to wish to undergo any routine dental treatment whilst symptoms are present.

Herpes labialis Most people correctly recognise herpes labialis but a thorough history and examination are required to differentially diagnose angular cheilitis or rarely, carcinoma. Many non-specific topical preparations are available for the treatment of herpes labialis. However, use of a specific anti-viral agent is preferred. Two creams are available aciclovir (over-the-counter) and penciclovir (prescription only). Whilst early application provides maximum reduction in lesion duration, healing is enhanced by application at the blister and ulcer stage. The patient should be advised to wash hands regularly, especially after applying topical treatment, avoid finger contact, particularly if contact lens are worn and avoid intimate contact whilst the lesion is present. Individuals who have frequent recurrences should discuss the problem further with their dentist, hygienist or doctor. In addition, the patient may need to be referred to a specialist service (oral medicine or dermatology) for further investigation and the possibility of systemic antiviral prophylaxis. The presence of herpes labialis does not necessarily mean that dental treatment has to be avoided but it can be extremely painful until crusting begins and patients may wish to delay treatment at such a stage. Trauma and stretching of the lips could lead to localised virus spread. At later and less painful stages application of petroleum jelly to the lips can help reduce discomfort, permitting dental treatment. Standard infection control measures eliminate the virus from instruments and the risk of transmission by this route. Dental treatment can trigger herpes labialis and it is essential for regular sufferers to have a topical antiviral cream which contains aciclovir such as Zovirax Cold Sore Cream) to use immediately after treatment should symptoms occur.

145

Oral ulceration Reactivation of HSV-1 should be considered in association with recurrent oral ulcers in the hard palate, where it is also occasionally seen following extraction or root surface debridement of a maxillary tooth, predisposed by the trauma of the local anaesthetic infiltration. No active treatment is required but recognising HSV-1 involvement is important. Recognition is similarly important where oral ulceration is seen in HIV-positive patients or those receiving immuno-suppressive drugs, when the use of systemic antiviral agents is indicated.

Summary •

HSV-1 is extremely widespread with specific implications for the patient,

dentistry and dental care.

•

The dental team should be:

•

Able to recognise the symptoms of HSV-1 infection

•

Aware of their important role in providing advice to limit the impact of HSV-1

to patients and others.

•

The appropriate use of antiviral therapy can significantly reduce the impact

that HSV-1 has on the patient.

146

Guidance for the dental team

Guidance for the dental team Patient presents for dental treatment with herpes labialis

Ask patient about symptoms Examine to confirm herpes labialis

Painful or Blister stage

• •

Not painful or Crust stage

Give advice on HSV-1 Recommend use of topical antiviral which contains aciclovir (Zovirax)

Apply petroleum jelly to lips Carry out planned treatment

• •

No dental treatment Give patient new appointment

147

Give advice on HSV-1 Recommend use of topical antiviral which contains aciclovir for future episodes

Chapter 16

Dentoalveolar infection

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Dental teams commonly encounter dentoalveolar or periapical infections. The vast majority are treated successfully and with few long-term problems, however, some infections can quickly become systemic, unpredictable and potentially lifethreatening. The management of dentoalveolar infections is a topic of considerable interest and has local and national significance; systemic infection secondary to dentoalveolar infections accounting for an increasing percentage of dental visits to accident and emergency departments. Accurate and timely diagnosis of dentoalveolar infection, coupled with appropriate management leads to prompt resolution of symptoms with minimal discomfort and anxiety to the patient. This article outlines the clinical presentation of dentoalveolar infections, their microbiology, the appropriate management and possible complications.

Oral microflora The oral flora is a diverse collection made up of representation from all four groups of micro-organisms. However, the population is dominated by bacteria, with hundreds of species identified to date. The variety of bacterial species is a reflection of the diverse metabolic conditions that exist in the oral cavity, most notably variations in oxygen and available nutrients. The species vary from the absolute anaerobe and anaerobic to a significant number of species capable of existing in both environments (facultative anaerobes), e.g. Oral Streptococci such as S oralis.

148

Dentoalveolar abscesses Acute infections associated with the teeth and surrounding supporting structures often progress to become dentoalveolar abscesses. The aetiology of most dental abscesses is invariably due to bacterial contamination of the dental pulp as a result of caries, traumatic fractures or exposure during cavity preparation. The pulp system responds to infection either by rapid acute inflammation involving the whole pulp, which rapidly becomes necrotic, or by development of a chronic localised abscess with most of the pulp remaining viable. Pus formation occurs due to neutrophil infiltration from the blood stream and to suppuration. Once this occurs, it may develop into an acute or chronic abscess localised to the pulp, periapical tissues or spread into the surrounding tissues. Often this may result in the formation of a tracking sinus where pus extends through the overlying mucosa and skin. Sometimes, significantly, spreading infection may travel along muscle and fascial planes (Table 1), following a path of least resistance, resulting in severe soft tissue swelling and/or cellulitis. Such spread is dependent on the anatomical position of the source of infection and the local muscle attachments in relation to the adjacent tissues. Fascial space infections often spread rapidly and for some distance. These can be potentially life-threatening, causing upper airway embarrassment.

Clinical features of infection Clinically, the presentation of dentoalveolar infection depends upon the site of the infection, the virulence of the causative micro-organisms, the efficiency of local and systemic defence mechanisms of the host and the degree and mode of spread. If infection originates periapically there may be considerable pain as the inflammatory exudate and pus creates raised intraosseous pressure, stimulating local nociceptors. Eventually the pus/inflammatory exudate escapes the bone resulting in rapidly increasing soft tissue swelling but a reduced intraosseous pressure and subsequent pain reduction. The initial external swelling is largely due to local oedema, and therefore soft. However as pus forms centrally, pain levels rise accompanied by local fluctuance. For all infections of dental origin, there should be an identifiable cause and there is often a non-vital tooth, with an associated carious lesion or evidence of trauma. Swelling accumulates at sites least constrained by fascia, for example the lips and

149

eyelids although pus distribution is governed more by influences such as pressure and gravity and in many cases develops a local sinus. Other associated features include pain and enlargement of draining lymph nodes. When dentoalveolar infections spread, they may travel along interlinked planes and potential fascial spaces resulting in a number of clinical diagnostic features. For example, trismus is a common symptom of fascial plane involvement and a significant sign of masseteric space involvement. Of more significance, infections involving the lateral pharyngeal or retropharyngeal spaces are of particular concern because of the risk of respiratory obstruction and involvement of the mediastinum and its contents. The regional draining lymph nodes are usually enlarged and tender. Almost all dentoalveolar infections drain to the jugulodigastric node in the upper part of the deep cervical chain, although mandibular infections may first spread to the submandibular nodes. Dental infections have the potential to become systemic. This is marked by recognisable symptoms and signs such as pyrexia (>37.4oC), generalised malaise, tachycardia (p<100bpm), anorexia, nausea and lethargy. Such symptoms require urgent attention as there is a risk of septic shock developing.

Microbiology Microbiological studies in recent years have shown that dental abscesses are usually polymicrobial (Table 2). Obligate anaerobes (absolute requirement for anaerobic conditions) are the predominant organisms and are comprised of a variety of genre and species, dominated by gram negative rods e.g. Prevotella and gram positive cocci, e.g. Peptostreptococcus. Contemporary literature has shown that the most common species isolated from dentoalveolar abscesses are Prevotella, Porphyromonas and Fusobacterium. These bacteria possess a wealth of virulence factors e.g. gram negative bacteria and lipopolysaccarides (LPS). It is considered that these virulence factors exert synergistic effects and such interactions play an important role in the severity of infection. Other micro-organisms identified, but less likely to play a causative role include aerobic, e.g. Neisseria subflava, facultative anaerobes, e.g. Enterococcus spp, micro-aerophillic bacteria, e.g. Staphylococcus aureus, and capnophillic (CO2 dependent) species, e.g. alpha-haemolytic streptococci the most frequently found. 150

Dentists are taught to obtain specimens from dental infections to facilitate culture and identification of the associated micro-organisms. However, this probably adds little to the treatment because by the time the sensitivity results are known local treatment and antibiotics have been successful in resolving the infection. However, in more serious infections a more compulsive case may be made for identifying the causative micro-organism. Swabs or aspirates are collected under strict aseptic collection techniques as contamination with salivary or skin bacteria will render results inaccurate and confusing. The evidence for such an approach relies upon the reported cases of infections not responding to standard antibiotic approaches, requiring advice from microbiologists and subsequently changing ntibiotic prescription.

Management Most dentoalveolar infections and abscesses may be managed very successfully in the general practice environment. There is much literature on the treatment options and, whilst the general principles of treatment are universal (Table 3), the specific treatment for any given individual may vary. But the underlying concept is to remove the source of infection if at all possible. Mild dentoalveolar infection and well localised abscesses, with minimal spread of infection and without signs of systemic illness, may be treated successfully by simple local therapy. This requires the removal of the source of infection and the establishment of drainage alone. Drainage may be achieved under local anaesthesia by extraction of the tooth or by pulp extirpation and allowing pus to drain from the root canal system. More severe abscesses, especially those presenting with a palpable fluctuant soft tissue collection, will require incision and drainage, occasionally via an extraoral skin approach and placement of a surgical drain. Systemic antimicrobial treatment should not be the first-line treatment of mild dentoalveolar infection. However, where symptoms are severe or spread of the infection makes local anaesthesia or access difficult, it may be unavoidable to delay treatment, although every effort should be made to eliminate the source of infection. If patients show signs of systemic infection; fever and/or regional lymph node involvement, systemic antimicrobial treatment is advisable. It should also be considered when appropriate local treatment has been unsuccessful or the patientâ&#x20AC;&#x2122;s resistance to infection is reduced, e.g. in immunocompromised patients.

151

There is a wide choice of antibiotics, the most commonly prescribed are outlined in Table 4, and evidence-based practice requires targeted therapy to the causative organism. As outlined, studies have shown that the organisms isolated are complex polymicrobial with a predominance of anaerobic bacteria and synergistic aerobes, Prevotella, Porphyromodentinas and Fusobacterium spp. being the most common. No single antibiotic is likely to be effective against the whole range of bacterial species found in dentoalveolar abscesses; however eliminating one organism can be effective in treating the infection, because of the influence of synergism. It is common practice to commence treatment with amoxycillin, unless there are obvious contraindications. This has the advantage of broad-spectrum cover as amoxycillin has a structure which allows penetration through the gram negative cell wall and is effective against the majority of the bacteria involved. The predominance of anaerobes makes metronidazole a good choice as well. It is cheap, well tolerated and effective. In more serious infections the prescription of amoxycillin and metronidazole together, is an effective combination. Amoxycillin with clavulanic acid, developed to avoid resistance, is also effective in severe infection but has a significantly higher cost. Erythromycin may be used as an alternative for penicillin-allergic patients. However, resistance is increasingly common and clindamycin is frequently prescribed in preference. Provided that it is used for short courses there is little evidence of significant danger of antibiotic induced colitis. It is important to follow-up patients after antibiotic prescription, but every effort must be made to complete the eradication of the source of the infection. Failure to control an infection with antibiotics may occur and it is important to identify why the patient has failed to respond. This maybe due to use of an inappropriate antibiotic, inadequate dose, patient non-compliance, a substantial residual collection of pus or more importantly persistence of the cause.

Complications Well localised dentoalveolar abscesses managed appropriately have few complications and most patients will make an unremarkable recovery. However, some patients may present with a considerable systemic reaction and significant symptoms including difficulty swallowing (dysphagia) or difficulty breathing (dyspnoea). In some, especially those with an impaired immune response, local

152

measures may have failed to control the infection resulting in extensive spread. These patients require immediate referral to hospital for specialist care.

Ludwigâ&#x20AC;&#x2122;s angina Ludwigâ&#x20AC;&#x2122;s angina is a serious and life-threatening complication presenting rapidly as spreading, bilateral infection of the submandibular and sublingual spaces. This raises the floor of the mouth and tongue and causes local oedema. Its course is unpredictable and leads to airway obstruction due to paratracheal or pharyngeal oedema or the tongue blocking the pharynx. This is a surgical emergency and requires urgent transfer to a specialist unit.

Cavernous sinus thrombosis The cavernous sinuses receive venous blood from the facial veins and, in turn, empty into the inferior petrosal sinuses, then into the internal jugular veins. It is a complex web of veins that contains no valves; blood can flow in any direction depending on the prevailing pressure gradients. Any local infection may spread backwards by way of the veins to reach, and involve, one of the cavernous sinuses. If this happens, the blood in the sinus may turn to an infected clot, or thrombosis, with potentially very serious consequences, e.g. increased retrobulbar pressure signs of increased intraocular pressure e.g. decreased visual acuity. The treatment is aggressive antibiotic therapy and immediate transfer for specialist care.

Osteomyelitis This is a spreading infection of bone marrow. Osteomyelitis usually develops from a contiguous focus of infection which penetrates the cancellous bone. Conditions that reduce bone vascularity, e.g. radiotherapy or Pagetâ&#x20AC;&#x2122;s disease, may predispose to the condition. The onset of osteomyelitis is characterised by pain, mobility or death of the surrounding teeth, alteration in sensation to the local nerves. Bone resorption occurs and necrotic bone may sequestrate, weakening the bone itself. Treatment can be complex and relies upon antibiotics and possible surgical intervention.

Mediastinitis Infection may extend from the head and neck downward into the mediastinum. This is often described as descending necrotising mediastinitis because the infection uses the fascial planes in the neck to gain access to the mediastinum. It is necrotising, as the infection is often includes gas-producing organisms, is associated with a high mortality rate and is a surgical emergency. The priority of treatment is to maintain the airway.

153

Septic shock Septic shock occurs when systemic infection progresses resulting in a cascade of reactions causing the sequential release of endogenous mediators, such as cytokines, tumour necrosis factor (TNF), interleukin-1 and interleukin-2. There is severe hypotension and tissue anoxia, leading to multiple organ failure. Septic shock has a poor prognosis, despite antibiotics and supportive therapy and mortality is high.

Conclusion Most patients are effectively and safely managed in general practice with local measures alone, without the need for antibiotic treatment. The key to treating dentoalveolar abscesses is early identification of the source of infection and its subsequent removal. Pus, where evident, should be drained immediately. The use of supportive antimicrobial therapy remains an area of contention, with patients often demanding a prescription. It is essential that practitioners resist and reserve such treatment for cases where local treatment is unlikely to be successful alone; those with reduced immune response, with systemic involvement or when drainage cannot be achieved or is delayed. Whilst complications are rare if early drainage and removal of the source of infection is achieved, they are unpredictable and can rapidly become life-threatening. It is essential that all patients who have had prescription of antibiotics are reviewed to ensure resolution.

154

Table 1: Potential spaces for spreading dentoalveolar infection

Space

Clinical Feature

Sublingual

Raised floor of mouth

Submental

Firmness and pain in midline

Submandibular

Swelling beneath lower border of mandible in submandibular space Buccal swelling above lower border of mandible

Buccal

confined to cheek Submasseteric

Limitation in mouth opening

Parapharyngeal

Difficulty in swallowing

Retropharyngeal

Difficulty in swallowing and breathing +/- spread to mediastinum

Pterygoid

Limitation in mouth opening

Infratemporal Fossa

Swelling and pain over temple

Table 2: Bacteria isolated from dentoalveolar infection sites:

Strict anaerobes

Facultative Bacteria

• Bacteroides

• Streptococci

• Clostridium

• Staphylococci

• Eubacterium

• Lactobacilli

• Fusobacterium

• Eikenella

• Peptostreptococcus

• Corynebacterium

• Porphyromonas

•

Prevotella

• Veillonella

Aerobes

• Neisseria

• Propionibacterium

Microaerophillic

• Actinomyces • Gemella • Streptococci

155

Table 3 General principles of treatment: •

Removal of source of infection

•

Drainage of pus

•

Supportive chemotherapy, if appropriate

Table 4 Commonly prescribed antibiotics • Penicillin •

Amoxycillin

• Metronidazole •

Co-amoxyclav

• Erythromycin • Clindamycin

Table 5 Factors to consider in prescribing an antibiotic •

Efficacy

• Safety • Resistance •

Plasma half-life

•

Adverse effects and interactions

• Compliance • Cost

156

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Chapter 17

Fluorosis reviewed

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It is widely accepted that in the United Kingdom an increase in the availability of fluoride from oral care products is largely responsible for the dramatic reduction in dental caries seen over the last 40-50 years. The beneficial effects of fluoride were first identified in epidemiological studies more than 80 years ago when H Trendley Dean noticed that populations with dental fluorosis had lower levels of dental caries than might be expected. The dilemma of balancing the benefit of using fluoride to control dental caries, whilst at the same time minimising the risk of fluorosis, is a challenge that remains today. How to balance the risk to maximise caries benefit whilst minimising the risk of fluorosis can be best addressed by considering the modes of action of fluoride.

How does fluoride prevent dental caries? The presence of fluoride under acid conditions encourages the formation of fluorhydroxyapatite and hence remineralisation of the enamel surface. Fluorhydroxyapatite is less soluble than hydroxyapatite and thus prevents further demineralisation of tooth enamel. A less important benefit is that fluoride may also help to reduce the metabolic activity of bacteria. These benefits result from having small amounts of fluoride present in the oral environment through its topical application. The benefit of systemic exposure to fluoride and incorporation of fluoride into the developing tooth is controversial. However, if any benefit is gained from systemic exposure it is probably small compared to that gained from topical exposure. To be effective small amounts of fluoride must be present in the mouth throughout the day and particularly at the time of an acid challenge. Hence it is important that fluoride is used at a number of times throughout the day and if possible close to meal times. The effectiveness of fluoride toothpastes in preventing dental caries is primarily

158

dependent upon their concentration and if low fluoride toothpastes are used the risk of caries is increased. In contrast the amount of fluoride toothpaste applied is probably less important. This is due to the small size of the potential fluoride reservoirs in the mouth. In terms of caries benefit daily use of 0.33 g of an adult fluoride (1500 ppm F) toothpaste is likely to be more beneficial than 1 g of a low fluoride (500 ppm F) even though both result in the application of 1.5 mg of fluoride.

How does fluoride cause dental fluorosis? Fluoride affects enamel formation predominantly in the mineral deposition (maturation) phase of enamel formation. The result is a more porous mineral structure, predominantly at the surface of the enamel, giving it a whitish appearance. Dental fluorosis can only occur when the teeth are forming and the risk period depends upon the developmental stage of the different tooth groups. For the anterior teeth children are probably at risk until the age of about 8 years. In contrast to caries benefit which is primarily concentration dependent, the risk of fluorosis is influenced by the total amount of fluoride ingested i.e. both the weight used and its concentration. The amount of fluoride a child needs to ingest to risk the formation of dental fluorosis depends upon the body weight of the child and the severity of fluorosis that is considered to be important. Hence estimates of fluoride intake resulting in a risk of developing dental fluorosis range from 0.05-0.1 mg F per kg body weight. If we assume that a 5-6 year-old weighs approximately 20 kg then a daily ingestion of 1 or 2 mg of fluoride per day may be sufficient to result in mild fluorosis for some individuals. Covering the head of a toothbrush with toothpaste results in the application of approximately 0.5 to 1 g of paste. Hence for a low fluoride toothpaste (500 ppm F) toothpaste up to 0.5 mg of fluoride per brushing might be used and for an adult toothpaste (1500 ppm F) as much as 1.5 mg. Clearly not all the toothpaste is swallowed and the requirement for young children to spit out excess toothpaste slurry is clear. However, for very young children not only is the body weight less (12 kg for a 2-year-old) but their ability to spit out toothpaste is very limited. For young children it is essential that very small amounts of toothpaste (pea or smear) are used and that brushing is carefully supervised. Consideration should be given to the use of low fluoride toothpastes, particularly prior to the eruption of the deciduous molars. The most appropriate fluoride regime for a child should be based upon an assessment of the balance between the risk of fluorosis and benefit of different forms of fluoride exposure.

159

It is also important to remember that the total fluoride exposure from all sources should be considered in any risk assessment. In areas with fluoridated drinking water, or when fluoride tablets or drops are used, particular care is needed when using other fluoride oral care products such as toothpaste.

How can fluoride be used to maximise benefit and minimise risk? From the above it is clear that in order to maximise benefit and minimise risk it is important to maximise topical fluoride exposure and discourage ingestion of fluoride. To do this we must: •

Fluoride toothpaste

•

Use small amounts of toothpaste

•

Maximise the concentration of fluoride used in relation to

degree of risk of fluorosis

•

Supervise brushing for young children

•

Keep fluoride products out of the reach of young children

•

Encourage the spitting out of waste toothpaste slurry

•

Discourage rinsing with large amounts of water after brushing as this removes

fluoride from oral fluoride reservoirs and dilutes benefit

•

Brush twice daily

•

Brush around the time of an acid challenge

•

Brush before going to be at night when salivary flow rate is reduced and

fluoride levels remain elevated for longer periods.

•

Fluoride rinses

•

Use at different time to toothpaste to spread fluoride exposure times

•

Rinse thoroughly around the mouth to distribute the fluoride as effectively as

possible into fluoride reservoirs

•

Do not allow young children to use fluoride rinses due to the risk of swallowing.

•

Fluoride tablets and drops

•

Use only in high risk individuals due to the high systemic ingestion

•

Ensure that tablets are chewed and fluoride is dispersed around the mouth to

gain topical benefit.

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What does dental fluorosis look like? In addition to the amount of fluoride ingested, the appearance of dental fluorosis predominantly depends upon when and for how long the exposure occurred. Like other systemic conditions, such as tetracycline staining, the distribution is characteristically symmetrical around the dental arch. The presentation of fluorosis may well be different in the case of sustained low levels of fluoride exposure such as those occurring from drinking water containing fluoride and use for shorter periods, such as when fluoride tablets are used for a few years in infancy. The first signs of dental fluorosis are only visible when the teeth are carefully dried. This appearance is the result an increase in enamel porosity along the Striae of Retzius. As the degree of exposure increases, this porosity increases until these lines may be visible without drying of the teeth. It is widely accepted that for these early presentations of fluorosis the main affect is to make the teeth look whiter and in the majority of cases this is perceived to be aesthetically pleasing by most individuals. In the more the severe forms fluorosis takes on a patchy white appearance and depending on the contrast with the surrounding can become aesthetically less pleasing. At this stage the teeth may show a characteristic snow capped appearance. In the most severe cases the whole surface of the tooth can appear parchment white and due to the porosity of the enamel post eruptive loss of surface enamel can occur resulting in pitting and sometimes staining. It is often difficult, if not impossible, to distinguish fluorosis from other developmental defects of enamel. Many of the criteria usually employed to diagnose dental fluorosis rely on the fact that fluorosis is systemic in origin whereas other defects, such as those resulting from trauma, may be localised to single teeth. However, this is an oversimplification as other systemic aetiologies such as amelogenesis imperfecta can also result in symmetrically distributed developmental defects. The situation becomes even more complicated when systemic conditions such as amelogenesis imperfecta are superimposed on dental fluorosis. This being said, perhaps the two most useful signs to distinguish fluorosis from other developmental defects are the generalised and symmetrical distribution of lesions in the mouth and the colour and texture of the lesions. Fluorosis appears parchment white and as the lesions are due to surface porosity when the teeth are dried the surface enamel tends to take on a frosted appearance and the lesions become more apparent.

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Treatment of dental fluorosis Most dental fluorosis is not noticed in the general population and in the case of the more minor presentations may even be aesthetically pleasing. However, in a small number of cases restorative treatment may be required. In the most severe presentations removal of the affected surface enamel may be required and porcelain veneers may be fitted. However, other treatment options exist and these can be best understood when it is appreciated that dental fluorosis often only affects the outer surface of the enamel and is seen as an increase in surface porosity. Abrasion of the outer surface of the enamel combined with fluoride treatments to remineralise the surface enamel and reduce surface porosity may be all that is required to produce an aesthetically acceptable outcome. When staining has occurred, peroxide-based whitening systems may be useful to remove stain. In addition, this approach may also improve appearance by making the normal surface of the tooth appear whiter so that the contrast between the normal tooth enamel and the fluorosis is reduced and the tooth has a more confluent white appearance.

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Chapter 18

Smokeless tobacco use in the UK

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Oral cancer is an increasingly common cancer worldwide and epidemiological studies have shown that incidence and mortality rates have risen considerably during this time. In the UK its incidence is on a par with that for cervical cancer. It has a low survival rate when detected in its late stage, but a comparatively better prognosis if treatment is initiated during the early stages. Its incidence shows increases within industrialised as well as developing countries, such as in parts of Asia and Africa, and is being recording in progressively younger patients. A variety of factors have been identified as closely linked to oral cancers in those individuals having a genetic predisposition: these include; excess use of tobacco, of alcohol on its own and synergistically with tobacco, the use of areca nut, a deficiency of fresh fruits and vegetables, the presence of immunodeficiency or of viruses including Herpes simplex (HSV) and the Human papilloma virus (HPV). Tobacco use is a common risk factor for a range of chronic conditions as well as in relation to oral diseases. This article looks closely at the role of tobacco particularly smokeless tobacco and its relationship with oral cancer in the UK.

Smokeless tobacco Tobacco is popularly used in the form of smoking (cigarette, pipe, cigar), or is sometimes chewed or used inhaled as snuff. Tobacco chewed or used as snuff is termed â&#x20AC;&#x2DC;smokeless tobaccoâ&#x20AC;&#x2122; (ST) (Figure 1). In common with smoking, ST is implicated as an aetiological factor for oral, pharyngeal and laryngeal cancer, but it is also responsible for gingival recession, leukoplakia, delayed wound healing, nicotine addiction, increased cardiovascular mortality, and hepatic cancer. Tobaccoâ&#x20AC;&#x201C;specific Nitrosamines such as N/nitrosonornicotine (NNN), and 4-(methylnitroamino)-1-(3-pirydil)-1-butanone (NNK), are formed by nitrosation of nicotine and other tobacco alkaloids.

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WHO International Agency for Research on Cancer has concluded that, â&#x20AC;&#x153;exposure to NNN and NNK is carcinogenic to humans, on the basis of sufficient evidence from animals and strong mechanistic evidence in exposed humans. NNN and NNK are the most abundant strong carcinogens in ST; their uptake and metabolic activation in ST users has been clearly observed.â&#x20AC;? Chewing tobacco may be consumed on its own, mixed with other ingredients such as areca nut, acacia extracts, sweets etc., in betel quid, or alternatively shredded into a proprietary combination and sold as Gutka, Mawa, Zarda, Kiani, etc. ST can also be mixed with slaked lime (Niswar) and the blend placed inside the upper or lower cheek or lip and sucked slowly. These are the most common methods of tobacco consumption among people originating from the Indian Subcontinent, and Asian migrants in the UK from East Africa, where traditional values do not favour smoking by the young or by women, but where there is no such taboo against using ST. In Africa, Tombuk and Shamma are popular varieties of ST, whereas American Spit Tobacco and Swedish Snus are becoming fashionable with more affluent members of the society in the countries other than those of origin of these products. Swedish Snus is moist snuff packed in tea-bag like sachets which are stored under the upper lip and sucked.

Smokeless tobacco in the UK In the UK we have up-to-date data on tobacco use (as in smoking), made available for all four countries and broken down by age, gender and ethnicity. Comparable figures on the use of ST are not available, although a number of more localised studies have looked at the practice ST use in the UK. Surveys in England have showed that Bangladeshi women smoked less but more frequently consumed betel quid with tobacco. This traditional use of ST in the South Asian communities has also been identified in a number of other studies. Ethnic communities migrating to the UK can bring their indigenous habits with them. The use of ST is thus more prevalent in the Bangladeshi, Indian, and Pakistani ethnic minorities within the UK. Some males (Indian, Pakistani and Bangladeshi) practice both tobacco smoking and chewing habits, thus significantly increasing their risk. Many of these ST products manufactured in the Indian Subcontinent are available on the UK market, catering for South Asian communities. Products such as Gutka, Pan

165

Masala, Zarda, Niswar and Mawa are regularly advertised on South Asian satellite channels as well as in glossy magazines, endorsed by Bollywood celebrities. Members of these South Asian communities make regular visits to their countries of origin, this also exposes them to these indigenous habits. Imports into the UK of homogenised or reconstituted tobacco; tobacco extracts and essences; chewing tobacco and snuff continue and current regulations also permit people coming into Britain to bring in small quantities of ST when travelling from both a European Union (EU) country or a non EU country, for personal use. This makes ST products very easily available in the UK to those people who want to use them.

Oral cancer While, there are no reliable routine data collected for ethnic variations in oral cancer incidence, some regional studies have recorded high rates among South Asian populations. A significantly higher number of deaths from oral cancer have been recorded among males originating from the Indian Subcontinent than among the indigenous UK population. The habit of taking ST has been implicated as a precursor to smoking, since ST users are more inclined to take up smoking than those people who do not. The use of tobacco among children and youths easily produces a nicotine dependency, the risk of which is vastly underestimated by young people. More than 80% of adults, who use tobacco, started their use of tobacco before the age of 18 years. In addition, studies in the USA have identified tobacco as the first drug that children have tried before moving on to â&#x20AC;&#x2DC;harderâ&#x20AC;&#x2122; substances. While leukoplakia is widely recognised to be a potentially pre-cancerous condition, Oral Sub Mucous Fibrosis (OSF) also has the capacity to convert to a malignant state (Figure 2). OSF can be caused by regular use of areca nut, which is often combined with tobacco, for instance in a betel quid or in pan masala. Tobacco as an ingredient in some areca nut mixtures is not a causative factor for OSF, but is responsible for a higher occurrence of OSF due to increased addiction and concurrent use of areca nut.

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The role of professionals Initiatives to raise awareness of ST have been in place for some years stressing ‘holistic’ tobacco cessation, which should also include tobacco chewing in all its forms. While this is clearly important on behalf of those areas with a high proportion of residents originating from the Indian sub-continent, it is also an essential message for the general population, not least by confirming that all forms of tobacco are bad for health. Oral cancer awareness is low amongst some primary health care (PHC) professionals, yet these professionals (e.g. GPs, practice nurses etc.) are often the first ‘port of call’ for those subjects most at risk. People who smoke/chew tobacco and drink heavily are less likely to adopt other health-promoting practices, such as being regular dental attenders. Thus, these at risk individuals are least likely to visit their dentist and miss the possibility of opportunistic screening as part of the dental check. It is important to raise awareness about oral cancer among all the members of the PHC team, including the risk factors and modes of presentation. PHC team members should also encourage regular dental attendance and make appropriate referrals when individuals complain of oral mucosal conditions that fail to heal within three weeks. The time delay between a patient’s awareness of symptoms, the primary referrer’s response and formal diagnosis in a secondary/tertiary care setting is crucial. An examination of this period of delay between initial recognition of symptoms and formal diagnosis among a sample of patients recently diagnosed with head and neck cancer lead to recommendations for a special educative initiative directed at those at risk and their general practitioners.

The role of dental professionals While they may not encounter all high-risk individuals, the dental profession definitely has a key role in combating the tobacco use. Apart from supporting wider tobacco control measures like putting posters in the waiting room, oral health professionals can encourage their patients to stop using tobacco in all its forms. In reality, this may be the single most important service dentists can provide for their patients’ overall health.

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Oral lesions and altered periodontal status can help members of the dental team to identify patients who may be indulging in ST. A brief intervention using the widely recognised 4As; Ask your patient Advise your patient Assist your patient Arrange follow up. This will often result in significant health gain and, in the long term, reduce smokingrelated health-care costs to countries. Finally, ‘Assess your patient’, has also been added to the A’s list as the dental team, when taking a careful social history, can pick out the susceptible patients. A proper referral protocol should also be in place so that if a suspected lesion is found in a patient in dental practice, the patient can be seen by a specialist within two weeks of their general practitioner deciding that they needed to be seen urgently and requesting an appointment.

Conclusions •

Oral cancer has a low prevalence in the UK, but it is rising, particularly in

younger age groups. The deaths recorded due to oral cancer are on a par

with cervical cancer.

•

The availability and use of smokeless tobacco presently affects mainly

migrants from South Asian countries, but in future, if other STs are introduced as

part of a smoking cessation policy, the whole population may be affected

with the potential to increase the risk of oral cancer in susceptible

communities. •

The Government’s policy for smoking cessation should continue to be

extended to include all forms of tobacco.

•

It is essential to raise awareness of oral cancer including the risk factors

and presenting signs and symptoms among members of the PHC teams, high

risk individuals and the public at large.

•

Opportunistic cancer screening remains an important role of the dental team.

168

Figure 1 - Smokeless tobacco

Figure 2 - Oral Sub Mucous Fibrosis 169

Chapter 19

Dental erosion – a continuing concern

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With more people keeping more of their teeth for longer it is inevitable that conditions of tooth wear will increase, as indeed has been regularly reported in recent years. Additionally, changes to dietary habits with, for example, greater consumption of fruit juices and carbonated soft drinks have meant that teeth are subject to more acidic challenges than previously. We know that bacterial acids cause decay but other acids in drinks and foods or from the stomach can lead to different problems. Eroded teeth are smaller, disfigured and possibly sensitive if the enamel has been dissolved, resulting in exposed dentine. The sites most commonly affected are the occlusal surfaces of the first molars and the labial and palatal aspects of the upper teeth. Any tooth surface, however, is susceptible (Figure 1). The occurrence and site distribution vary according to occlusion, habits and salivary factors. Most patients are unaware that their occlusal and/or palatal surfaces are eroded. Therefore, the dentist should examine for the early signs of erosion. It is difficult to see loss of only the enamel surface characteristics, so that good lighting and dry teeth are important aids to diagnosis. Index teeth are the upper and lower incisors, all surfaces, and all first molars, although the occlusal surface of the lowers are more commonly affected with dentinal exposure. Cupping, an early sign, is the appearance on the cusp tip of dentine. The ‘cup’ is the rim of enamel around the exposed dentine. As erosion progresses the enamel becomes thinner and the area of exposed dentine increases in size until the cupped areas coalesce (Figure 2). Often the mesio-incisal corners of central incisors erode prior to the distal half and mid-palatally an ‘island’ of enamel is surrounded by dentine. Should the dentist diagnose erosion, the next stage is to take a history and identify aetiology.

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History and aetiology Carefully question the patient about dietary intake of acidic beverages including sports drinks and herbal tea, fresh fruit especially citrus, pickled foods and vinegar including sauces such as ketchup. Table 1 lists low pH drinks with erosive potential. The critical pH of 5.5 at which enamel demineralisation occurs in caries is also used for erosion. It should be remembered that caries is a sub-surface phenomenon with smaller crystals and greater porosity in the body of the lesion, which is beneath a distinct surface zone. Erosion, however, occurs on the tooth surface with loss of the surface and porosity extending into the newly exposed surface. This demineralised or acid softened zone is prone to wear by abrasion or attrition. Clinicians and researchers face considerable difficulty when trying to distinguish between these three types of wear and hence the popularity of the catch-all term: tooth wear.

Medical considerations A positive history of GORD (Gastro-Oesophageal Reflux Disease) is not necessary for gastric reflux to be present, as many patients have silent reflux. Ask if there is a familial history of reflux or whether the patient has gastro-intestinal disorders known to be associated with reflux (ulcers, hiatus hernia). Self-induced vomiting, as a means of weight control, is a common method of purging in the eating disorders and in certain sports. Asking a patient whether they make themselves sick is difficult and requires sensitive questioning. The response will not necessarily be truthful but it is important to identify the aetiology(ies), which contribute to dental erosion. Once this has been established, the patient can be advised to change their habit or lifestyle. The dentist should refer the patient to a gastro-enterology department if reflux is suspected or to the general medical practitioner for vomiting or other medical conditions. There is a theoretical relationship between medical problems, their medication and erosion. Nausea, vomiting and gastric disturbance are common side effects of much medication whilst other drugs can have a xerostomic effect. In older patients, polypharmacy could contribute to wear/erosion, whereas in younger subjects, use of so-called â&#x20AC;&#x2DC;recreationalâ&#x20AC;&#x2122; drugs could increase dehydration (and hence xerostomia), bruxism and the intake of carbonated drinks. Significantly more occlusal dentine is exposed in Ecstasy users compared to non-E users but incisal edge dentinal exposure is no different. Much more research is needed in order to clarify the relationship between diet, saliva, habits, general medical health, tooth wear and erosion.

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Most patients do not complain of sensitivity or functional difficulty but seek treatment when incisal edges become thin, translucent or chipped. Even if the patient presents without cosmetic deficit, it is still very important to explain the nature and progress of erosion with emphasis on the difference between plaque as the factor in caries and acids in the progress of erosion. Commercially available patient information leaflets are available or can be designed in-house. A change in lifestyle, habit or dietary intake may be all that is necessary to stop the progress of erosion. General advice to patients regarding risk reduction is shown in Table 2. A widely held belief that carbonated or sparkling water itself is erosive is not true. Carbonic acid is a very weak acid and has negligible erosive potential, although the varieties with added fruit juices and flavourings are probably not safe in this respect. Hence the advice to make your own fizzy pop as home made orangeade is likely to be less acidic than a commercially available variety. Chilled drinks are safer as the acid dissociation constant is temperature dependent with less hydrogen ion available to attack the tooth. The final recommendation to avoid acidic drinks at night time relates to the fact that there is no salivary flow at night, thus any low pH drink would be especially damaging.

Monitoring erosion â&#x20AC;&#x201C; putty technique A technique to measure and monitor the erosion and thus check on whether or not it has progressed is recommended. Study casts, photographs, erosion indices and putty indices have all been advocated. Casts are difficult to store and chip easily. Erosion indices are generally not specific for erosion but measure tooth wear and are really only designed to be used in epidemiological surveys. Intra-oral photographs are helpful but require expensive equipment. The use of a silicone putty index however, is accurate and quick. The technique involves the hand mixing of a small amount of fast set putty into a â&#x20AC;&#x2DC;sausageâ&#x20AC;&#x2122; followed by placement over the eroded teeth, usually the upper sextant or over the first molars. A stock impression tray is not needed, but if used, a polythene spacer prevents the putty sticking to the tray. Adhesive is NOT needed! At the review appointment a year later, the putty is sectioned with a scalpel labio-lingually across the most eroded tooth and inserted into the mouth. If it fits tightly, progress has not occurred and the patient can be reassured. If a gap is present, perhaps advice was not heeded and further reinforcement is needed. This, therefore, distinguishes between a condition, which is present but static or a process which is progressing/worsening. Follow-up over two years is advisable, after which, if the erosion is static the index 172

can be given to the patient for safe keeping. The index must have the date it was taken so that any subsequent dentist will know this and can judge whether any progress of the wear over a few years could be acceptable/physiological. Dentists should understand that some degree of wear is to be expected as it is age related. Clearly, what is acceptable in an 80-year-old may be unacceptable in an 18-yearold. Determining what is and what is not acceptable is difficult and relies on the dentist’s experience and knowledge. Unfortunately there are few guidelines. In general, treatment is necessary if the patient has a complaint, such as poor appearance.

Treatment possibilities Should interventionist treatment be indicated, a simple, reversible approach may be all that is required. Dental composite is the preferred restorative material as it has very good wear resistance, excellent aesthetics, can be bonded to enamel and dentine and is relatively easy to use. Importantly, composite does not dissolve in acid media unlike glass ionomer/polyalkenoates, which have little application in an eroding/wearing dentition. Another point to note is that the dentinal tubules on worn or eroded dentine surfaces are not open, even after acid etching. Most tubules are sclerosed through deposition of highly mineralised peritubular dentine as the odontoblastic process recedes. Therefore, the classic scanning electron microscope image of resin tags densely infiltrating tubules is not an accurate reflection of the resin bonded worn surface. ‘Keying’ across the dentine with a slow speed rose head bur in order to remove pellicle and plaque (rarely present) and roughen the surface is a useful technique. Acid etching with ortho-phosphoric acid for up to 30s will improve micro-mechanical adhesion of the bonding resin. Cupped and grooved surfaces have a rim of enamel, which provides a predictable bond at the margin and restoring to the level of the rim generally avoids an increase in occlusal vertical dimension. This approach offers protection to the worn surface, restoration of any chipped and translucent enamel as well as reduction in sensitivity. The composite can be replaced as and when it wears down. Some patients will grind through the composite more quickly than others because of an abrasive diet or above average masticatory loads. In conclusion, the steps needed to successfully manage the eroded dentition are: •

Examine for the early signs of erosion

•

Take a history and identify aetiology

•

Explain the nature and progress of erosion

•

Measure and monitor the erosion

•

Interventionist treatment (if indicated).

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Figure 1 - Erosion on the labial surfaces of upper incisors

Figure 2 - Cupping of molar teeth due to erosion

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Table 1 The pH of popular drinks Drink

Orange juice

3.7

Diet Cola

3.2

White wine

3.1

Herbal teas

3.1-7.1

Lime cordial

3.0

Blackcurrant juice

2.9

Lemon juice

2.7

Carbonated drinks

2.4

Table 2. General advice to patients with dental erosion • Cut down on the frequency of intake • Drink alternatives (milk, tea, water, ‘tooth friendly drinks’) • Dilute drinks or make your own ‘fizzy pop’ • Don’t swish, sip, froth or hold in mouth • Use a wide bore straw placed behind the top teeth • Chill drinks • Don’t drink at bedtime or at the night

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Chapter 20

Lasers in general dental practice

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The use of lasers in medical practice is common knowledge to all healthcare professionals. In dentistry, the first dedicated dental laser was introduced into the UK in 1990. Far from ideal, this laser represented an innovative extension by its manufacturers, from medical to dental use, that backfired somewhat, due to its restrictive use in soft tissue procedures. The word ‘laser’ (an acronym: Light Amplification by the Stimulated Emission of Radiation), conjures perceived benefits of precise therapeutic use, bordering on the magical. Certainly the marketing of laser therapy to patients would suggest such attributes. The evolution of laser use in dentistry, from anecdotal hype to recognised evidence-based, treatment-targeted discipline, has prompted a recognition by the dental profession that, to paraphrase Morton’s first anaesthetic: ‘this is no humbug!’ Used correctly, some lasers offer scope to cut or ablate soft tissue without causing bleeding or the need for sutures, while others can ablate hard dental tissue and bone. The consequence of interaction with bacterial cellular structure often renders a surgical site sterile and some lasers are used adjunctively in endodontics. The lack of tactile stimulation is an additional benefit to patients who might be fearful of the vibration of rotary dental instruments.

The concept of laser ‘best practice’ Laser therapy depends on a source of specific electro-magnetic energy, i.e. light, being absorbed by a target tissue element. Such absorbance results in energy exchange, usually heat, that effects tissue change. This change could result in water vaporisation, protein denaturation or tissue ablation and can be applied to both hard and soft tissue targets. The ‘trick’ is to match the precise, unique laser wavelength of any given machine, to the absorption coefficient of the target tissue. In this way, certain lasers can be used for soft tissue procedures, whilst others are used in cavity preparation or bone

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ablation. Matching laser wavelength to target tissue produces a definable ‘power – effect’ outcome; violation of such could result in unwanted changes, e.g. carbon production and collateral heat damage.

Lasers in the practice Market forces, beyond the scope of this article, have transformed dental practice in the UK demanding of practice principals a breadth of business acumen that would cause recent predecessors in the profession to recoil in amazement. Not content with the explosion in clinical protocols, there are numerous demands from an avaricious patient body for innovative techniques that maximise comfort and minimise intervention. Peer and public pressures exist that constitute a drain on practitioner approach to dental care, not to mention finances. Laser dentistry might seem an attractive epithet for any professional who seeks to exploit the move away from ‘drill and fill’, but the differing array of laser units and light wavelengths, together with the implicit dangers for practice and patient alike of a wrong choice, demand a level of understanding that is sufficient to make a sensible choice and avoid potential financial embarrassment. All lasers are annotated by virtue of their ‘active medium’, i.e. the source of light energy. As such, a CO2 laser employs a gas source, which when energised, releases far infra-red light (electro-magnetic) energy of a specific wavelength value. Wavelength is measured in metres, common values expressed in nanometres (10-9 metres), with the CO2 dental laser emitting at 10,600 nanometres. Other lasers available for use in the oral cavity include Neodymium Yttrium-AluminiumGarnet (Nd:YAG) at 1,064nm, Erbium YAG (2,940nm) and Erbium, Chromium Yttrium-Scandium-Gallium-Garnet (YSGG) at 2,790nm. In addition, a range of laser wavelengths, emitting in the visible to near infra-red range of 635-980nm, exist collectively as ‘diode’ lasers, whereby the light is produced by a bank of silicone chip wafers. ‘Therapeutic’ lasers for oral use can range from low-powered devices, insufficient to produce gross tissue change, but which can stimulate cellular-level change or are used in diagnostic (caries detection) procedures, to high-powered surgical lasers, capable of cutting hard and soft tissue.

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Which laser? Perhaps the best way to approach this difficult question is to review the scope of treatment being offered by a given practice or individual. Predominantly soft-tissue procedures would merit a choice of a soft-tissue laser and vice-versa. However, the heterogeneous component nature of oral tissue can allow for differing laser wavelengths to be able to beneficially interact with elements within a target tissue. In this way, an Erbium laser, which is maximally absorbed by water, will ablate hard and soft tissue, although its poor absorption in pigment would restrict its haemostatic potential in the latter. Laser-tissue interaction is a complex subject, but, in general, shorter wavelengths, such as Nd:YAG and Diode are predominately interactive with pigmented soft tissue, whereas longer wavelengths, Er:YAG, Er,Cr:YSGG and CO2 are interactive with water and hydroxyapatite. The current trend would suggest that diode lasers are popular for soft tissue use, due to their relative small size and Erbium lasers are bought because of their ability to be used in restorative dentistry.

Low level (‘soft’) lasers This group of lasers is characterised by their non-surgical action. Conversely, the low power range is thought to produce stimulatory effects within cellular structure, especially mitochondria, and accelerates the conversion of ADP to ATP. In addition, the laser energy is seen to inhibit the release of biochemical mediators associated with inflammatory response and pain. Thus, the indirect effect on injured tissue would be seen to stimulate reparative cellular groups, reduce inflammation, reduce swelling, through increased lymphatic drainage and relieve pain. Low level lasers are less expensive than surgical cutting lasers and are small and lightweight. The laser is often configured for dental use as a rigid fibre-optic probe, not dissimilar to a curing light tip. It is not uncommon to expose injured tissue repeatedly, over several days and some lasers are ‘hired’ to patients for home use. Reported uses in clinical dentistry include the following: Dentine hypersensitivity Post-extraction socket / post-trauma sites Viral infections: Herpes labialis, Herpes simplex Neuropathy: Trigeminal neuralgia, paraesthesia Apthous ulceration TMJDS Post-oncology: mucositis, dermatitis, post-surgery healing.

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Other low-level laser uses in dentistry include caries detection and photo-activated disinfection, where laser light causes the release of singlet oxygen from an applied chemical that causes bacterial cell destruction.

Surgical (hard) lasers This group of lasers is capable of delivering light energy which, when absorbed by target tissue, is predominately converted to heat. This photothermal effect causes a range of effects, consistent with temperature rise, from protein denaturation, water vaporisation through to complete ablation and, unwanted, carbon production. The range of surgical uses of any laser is dependant on the absorption coefficient of tissue components, relative to the incident laser wavelength. All surgical lasers are stand-alone units and light is delivered through optical conduits, such as quartz optic fibre and hollow waveguides. The water content of quartz limits its use to short laser wavelengths.

Soft tissue procedures Diode (810 â&#x20AC;&#x201C; 980nm) and Nd:YAG lasers, together with the KTP (532nm) laser (Potassium Titanyl Phosphate), can cut, coagulate and ablate pigmented soft tissue. The production of a tenacious coagulum that covers the cut surface prevents contamination of the wound and reduces post-operative pain and inflammation. Small blood vessels are sealed by the laser action, producing predictable haemostasis. The ability to deliver laser light through fine fibre-optics, allows for detailed and fine cutting action, which has advantages during cosmetic soft tissue procedures. Carbon dioxide lasers are used in soft tissue surgery due to the absorption of this wavelength in water. The delivery configuration of this laser for dental use prevents its use on hard dental tissue and bone, even though hydroxyapatite has very high absorption. The vaporisation of water leads to ablation of cellular structure and conductive heat effects help in providing some haemostasis. Both fine and gross surgery can be accomplished with ease.

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Hard tissue procedures The target chromophore (light absorbing tissue element) is the water contained within enamel, dentine, cementum, calculus and bone. The Er:YAG 2940nm wavelength is strongly absorbed by water molecules (H2 O) and Er,Cr:YSGG 2790nm by OH-radicals in hydroxyapatite. In both cases, the result is an explosive disruption of the mineral content and ablation of gross structure. Ablation rates using these two laser wavelengths reflect the comparative volume by composition of various hard tissues, being fastest in tissues with most water content. In addition, composite restorative materials can be easily removed with these lasers, although metal and porcelain removal is contra-indicated. The development of laser wavelengths that have prime interaction with the various chromophores found within oral tissues has enabled an evidence-based approach to the correct use of these machines in treating disease. The advantages of lasers over conventional treatment modalities may be a matter of debate, but a dentist who receives objective training and education in the use of lasers in dentistry, will be able to assess the relative risks and benefits for their patients and deliver responsible care.

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Tracks all training completed with Professional Dentistry, including E-Publications and event attendance

3-year subscription: £169+VAT 5-year subscription: £379+VAT

Print backup copies of certificates

DENTAL CPD NOW DCP’S EDITION: 21 Hours verifiable CPD only £39+VAT

Keep an online development plan

3-year subscription: £89+VAT 5-year subscription: £129+VAT

Track all training in one place, including training from other providers

IMPLANTS NOW: 6 Hours verifiable CPD only £59+VAT DIGITAL DENTISTRY: 6 Hours verifiable CPD only £59+VAT AESTHETICS NOW: 6 Hours verifiable CPD only £59+VAT

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