Ohd erosion 2013 gb

New Concepts in Caries and Erosion

Oral Health Dialogue Scientific Journal for Oral Health

Oral Health Inequalities Tooth Wear and Dental Erosion Caries: From Risk Assessment in Children to Role of Saliva and Reversal of Early Lesions New Opportunity in the Treatment of Hypomineralized Molars

Imprint/Content/Editorial

Editorial

Publisher: Colgate-Palmolive Europe SARL European Division Bärbel Kiene, M. Sc. Biochemistry 13–15 Cours de Rive · 1204 Geneva · Switzerland www.colgate.com

Dear Colleagues, This issue of the Oral Health Dialogue focuses on two important oral health problems that present diverging trends; caries is on continuous decline while the prevalence of erosion has increased during the last decades.

Design: eye-con Medienagentur Lechenicher Str. 29 · 50374 Erftstadt · Germany

Interestingly, dental erosion and dental caries have a common etiology but are differentiated by the source of the acid. In the case of dental caries, acids are of microbial origin; for erosion, they come from food and beverages or regurgitation from the stomach. In both cases, tooth mineral goes through repeated phases of demineralisation and remineralisation throughout the day and a net loss of minerals over time leads to the clinical symptoms. The differences between dental caries and erosion are further elaborated in an overview in this issue.

The opinions of the authors do not always have to correspond to those of the publisher.

Reprinting and publication of extracts is permitted if the reference is quoted.

Caries risk assessment in children is the basic component in the decision-making for adequate prevention and management of dental caries. The “best clinical practice” for this process is suggested in this issue.

Saliva is a key component in the host response to demineralisation and this is also discussed in detail.

Another paper deals with therapeutic options for the treatment of dental caries which are best initiated in the early stages of lesion development (white spots).

A targeted modulation of local factors and the use of dental products can successfully reverse such lesions.

Scanning electron micrograph of the stannousrich layer deposited on an enamel specimen worn in situ, a result of regular application of elmex EROSION PROTECTION dental rinse.

Content Oral Health Inequalities: A Challenge for the Dental Team Prof. Dr. David M. Williams, London, Great Britain

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Caries Risk Assessment in Kids Prof. Dr. Svante Twetman, Copenhagen, Denmark

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Evidence-Based Data on the Effect of Saliva on Caries Dr. Panos Mitropoulos and Dr. Christos Rahiotis, Athens, Greece

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How to Stop and Reverse Initial Carious Lesions in Permanent Teeth Dr. Effie Pappa and Prof. Dr. Afrodite Kakaboura, Athens, Greece What Distinguishes Erosive Hard Tooth Structure Defects from Dental Caries?

Prof. Dr. Thomas Attin, Zürich, Switzerland

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I hope you will enjoy reading this selection of interesting articles, authored by international experts in these clinical areas.

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15 17

Risk Factors and Guidelines for Risk Assessment Dr. Annette Wiegand, University of Zürich, Switzerland

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Sincerely Svante Twetman

Prevalence of Tooth Wear Prof. David Bartlett, London, Great Britain

New Possibilities in the Treatment of Sensitive Hypomineralised Molars in Children Dr. Lene Esmark and Dr. PhD Tanja S. Borch (Colgate-Palmolive A/S)

The problem of dental erosion has risen significantly in the last decade. Some of the erosions appears to occur very rapidly and especially when modulated by attrition and abrasion of the softened enamel and dentine. In this issue, the prevalence of dental erosion is discussed and also risk factors and approaches to risk assessment. Finally, the use of Colgate® Sensitive Pro Relief™ in the management of MIH (Molar Incisor Hypomineralisation) is also addressed.

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Oral Health Inequalities: A Challenge for the Dental Team Prof. Dr. David M. Williams, University of London, Great Britain

Introduction Good oral health is fundamental to overall health and wellbeing. And poor oral health impairs people’s quality of life, their ability to interact with others, to attend school, and to work. Those impacts in turn have adverse effects on psychological and social wellbeing, on economic productivity and national development.

Impaired oral health is a major public health issue for high-income countries and it is a severe and growing problem for low-to-middle income countries. Furthermore, major inequalities in oral health exist both within and between countries. This is an unacceptable state of affairs, given what we know about how to prevent the major oral diseases of dental caries, periodontal disease, oral infections and oral cancer. This article will explore why impaired oral health persists and consider what should be done to address both the burden of oral disease and the inequalities that exist.

The burden of oral disease Dental caries is one of the commonest chronic diseases (Pitts et al. 2011). The US Surgeon General asserted, “What amounts to a silent epidemic of dental diseases is affecting some population groups. This burden of disease restricts activities in schools, work and home, and often significantly diminishes the quality of life” (Department of Health and Human Services 2000).

Over 50 million school hours a year are lost because of dental-related disease in the US, with children from lowincome families twelve times more likely to miss days at school than those from higher income families (Adams & Marano 1995). The effects of caries are even more marked in low and middle-income countries, where ineffective prevention and limited access to dental treatment mean that much of the demand for care remains unmet.

Periodontal disease is a significant public health problem among adults. An important recent study in the United States has asserted that periodontal disease is much more prevalent than had previously been assumed. Eke et al. (2012) estimated that the prevalence among adults aged over 30 years in the US reaches 47 %, with 64 % of adults over 65 years having moderate to severe periodontal disease. Good prevalence data are lacking for low and middle-income countries, but it is reasonable to assume that figures will be at least as high as these results from the US.

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Oral cancer is the eighth most common cancer worldwide and the commonest cancer among men in Southeast Asia (Johnsons et al. 2011). Tobacco is a major risk factor for oral cancer, as well as for cancers of other body sites, and alcohol is also an important risk factor.

Not only do dental diseases cause considerable suffering, but also the global cost of dental care is enormous (Beaglehole et al. 2009). The provision of dental care in industrialised countries accounts for between 3 % to 12.5 % of health expenditure, which puts dental care among the top four or five expenditure heads.

Even low-income countries like Sri Lanka spend 3.5 % of the health budget on public services dental care services (Beaglehole et al. 2009). It is disturbing that, in spite of this major investment in dental care, oral disease still remains such a major problem on a global scale and it is important to understand why this is the case.

Why is oral disease still a major problem?

We have experienced considerable improvements in oral health in most high-income countries in recent years. But despite these improvements in population oral health, marked oral health inequalities persist, mirroring the situation with wider general health (Watt 2005). One of the principal reasons for the persistence of oral disease as a major public health challenge is the failure to implement effectively what is known about prevention and the reasons for this need to be understood and addressed. The major shortcoming of current approaches to prevention is the failure to understand the importance of the social determinants of health, with too much reliance being placed on dental health education directed at people adopting healthier lifestyles and avoiding unhealthy ones. Indeed, it has been stated that most dental health education approaches are theoretically flawed (Watt 2005). The World Dental Federation FDI Vision 2020 states, “Historically, the approach to oral health has thus far overwhelmingly focused on treatment, more than on disease prevention and oral health promotion. This approach however has limitations” (FDI 2012). Instead of focusing on the prevention of avoidable disease tackling the causes of dental disease, there has been a disproportionate reliance on the use of interventionist approaches. A system focused primarily on treatment of disease is not effective in controlling chronic diseases; it is not economically sustainable; and it is not ethically responsible.

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A radical reorientation in our thinking is needed if we are to achieve sustainable improvements in oral health and a reduction in the inequalities in oral health that have been described above. It is time to start thinking about oral health in the same way that the medical profession is viewing general health. The focus of oral health care systems on treatment rather than health promotion in industrialised countries is very similar to the way our medical colleagues have tried in the past to deal with the major non-communicable diseases, such as chronic obstructive pulmonary disease; cancer; diabetes; heart disease and stroke. If we are to meet the challenge of the global burden of oral disease and inequality in health, we are going to need to stop thinking about individual diseases in isolation and start thinking about them in the same way that the wider health community is dealing with non-communicable disease.

Social determinants of health – the importance for oral health The social determinants of health are the circumstances in which people are born, grow, live, work, and age (Marmot et al. 2008). The life chances of people differ greatly depending on where they are born and raised. The Commission on the Social Determinants of Health (CSDH 2008) stated that the poorest people have the highest levels of illness and premature mortality, but that poor health is not confined to those who are worst off. At all levels of income, health and illness follow a social gradient: the lower the socioeconomic position, the worse the health. Marmot and colleagues have further asserted that the social gradient of health in individual countries and the major inequalities between countries are caused by the unequal distribution of power, income, goods, and services, globally and nationally. These structural determinants and conditions of daily life constitute the social determinants of health (Marmot et al. 2008). The consequence of such findings is that, if major reductions in health inequality are to be achieved, the structural determinants of health need to be addressed. This has profound implications for approaches to the non-communicable diseases that are the major global health challenge of the twenty-first century.

There is good evidence that major reductions in caries and periodontal disease in high-income countries have resulted from the wide availability of fluoridated toothpaste, and changes in behaviours and social change. Furthermore, there has been considerable progress in the prevention of chronic diseases – including oral diseases – using the common risk factor approach (Watt & Sheiham 2012), which addresses risks including bad diet, tobacco use, excessive alcohol consumption, lack of exercise and lack of control. So it is reasonable to ask “What evidence is there that oral diseases follow a social gradient, in common with the other non-communicable diseases, and how good is the evidence that the social determinants oral health play a

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role in the causation of oral disease?” The answers have profound implications for our approach to improving oral health for all at a global level.

It has long been recognised that the poorest oral health is found among the socially disadvantaged (Locker 2000). However there is now strong evidence to show that the major oral diseases are socially patterned, sharing the same social determinants as the major noncommunicable diseases, and that there is a gradient of risk for oral diseases across all socioeconomic groups.

Watt and Sheiham (2012) have stated that “oral diseases, as is the case with other health outcomes, are socially patterned across the entire social hierarchy.”

Watt (2007) has argued cogently that, if we are to address the challenge of poor oral health based on the evidence we now possess, we need a paradigm shift away from the current predominant biomedical and behavioral ‘downstream’ approach to oral health towards one that addresses the underlying social determinants of oral health, using a combination of complementary public health strategies. Watt is particularly critical of approaches to health promotion based on lifestyle interventions that fail to appreciate the fundamental underlying importance of social determinants, showing not only that the results of such approaches are disappointing, but also that they actually increase health inequalities. He argues strongly for the adoption of ‘upstream’ integrated interventions that address the determinants of health; that emphasise the importance of promoting and maintaining good oral and general health. Such an approach calls for oral health programs to be integrated into other health interventions using a common risk factor approach.

From theory to practical action Reducing the burden of non-communicable disease is now recognised as one of the great challenges facing society on a global scale. The Political Declaration of the High-level Meeting of the United Nations (UN) General Assembly on the Prevention and Control of Non-communicable Diseases in September 2011 acknowledged that the growing global burden of noncommunicable diseases constitutes one of the major challenges for development in the twenty-first century, undermining social and economic development throughout the world, and threatening the achievement of internationally agreed development goals (United Nations 2011). In one of the most important statements made about the burden of oral disease, the declaration also recognised “that renal, oral and eye diseases pose a major health burden for many countries and that these diseases share common risk factors and can benefit from common responses to non-communicable diseases”. The UN declaration presents both a challenge and an opportunity for the oral health community to take action to reduce the burden of oral disease and reduce inequalities. The challenge is formidable and we are not likely to deal with it effectively in isolation.

However, the UN has offered recommendations for a way forward and we should seize the opportunity.

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It is acknowledged that social injustice is killing people on a large scale and that it is imperative that public health efforts to reduce health inequalities are redoubled. However, it is argued that if these are to be more effective then a more sophisticated understanding of the barriers to progress will be needed (Popay, Whitehead & Hunter 2010). It is now equally clear that social injustice will also need to be addressed if we are to meet the growing challenges of poor oral health and inequalities.

The time is now right to develop a new model for oral health care, which considers oral health as an integral part of general health and addresses the needs and demands of populations and includes an integrated public health approach to tackle the social determinants of chronic diseases.

There are five practical actions that dentistry can take now: W We should identify key gaps in knowledge and target priority areas, recognizing that priorities will differ between global regions.

W We must work to implement what we know to be effective health promotion approaches to tackle the determinants of health, through a combination of upstream, midstream and downstream measures.

W We need to recognise the importance of partnership across disciplines; to get out of our dental silo and become advocates for better oral health and general health. It is vital that oral health researchers and practitioners become engaged in wider discussions about the determinants of health and health improvement. Dental practitioners will have a significant role in dental public health policy development by becoming health advocates (FDI 2011).

W We also need to recognise the power of civil society to effect change. A major element of the partnership described above will need to include working actively and responsively with our communities.

Acknowledgements I am grateful to Professors Richard Watt and Aubrey Sheiham for their constructive comments on early versions of this paper. The International Association for Dental Research (IADR) has identified the challenge of reducing oral health inequalities as a major strategic research priority; the support of the IADR Board for this initiative is gratefully acknowledged.

Prof. Dr. David M. Williams Bart’s and The London School of Medicine and Dentistry Queen Mary · University of London Turner Street · London E1 2AD · Great Britain

W We should argue for the integration of oral health messages into all health promotion strategies. The Adelaide Statement on Health in All Policies (World Health Organization 2010) outlines the need for a new social contract between all levels of government – local, regional, national and international, to advance human development, sustainability and equity, as well as to improve health outcomes.

There is a powerful case for the inclusion of oral health in future declarations.

Professor David Williams Professor Williams is Professor of Global Oral Health at Bart’s and The London School of Medicine and Dentistry, Queen Mary University of London. Previously he was Dean of the Faculty of Medicine, Health and Life Sciences and Professor of Pathology at the University of Southampton between 2004 –10 and then Vice Provost between 2010 –11.

He was President of the International Association for Dental Research (IADR) between 2009 –10, having previously been President of the British Society for Dental Research and the Pan European Federation of the IADR. He was the Chair of the Dentistry Panel in the 2008 UK Research Assessment Exercise. His research has focused previously on the oral mucosa in health and disease, with a focus on immune-mediated disease. He has published over 100 scientific papers, two textbooks and contributed numerous book chapters.

When he was President of the IADR, Professor Williams was the driving force behind the Global Oral Health Inequalities Research Agenda initiative. This initiative sets out the research agenda to generate the evidence for a strategy that will reduce inequalities in oral health within a generation. It is a call to action for the oral and wider health research communities; policy makers and funders of research; those involved in education and workforce development; and those engaged in the development of policy and the delivery of care.

He is also a Non Executive Director of South Central Ambulance Service NHS Foundation Trust.

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Caries Risk Assessment in Kids Prof. Dr. Svante Twetman, University of Copenhagen, Denmark

Introduction Caries risk assessment (CRA) denotes the clinical process of establishing the probability for an individual patient to develop new enamel or dentin lesions over the near future. The term is sometimes mixed up with caries prediction which is the scientific/statistical modeling of factors related to caries development in populations and expressed as predictive values, such as sensitivity and specificity. The obtained values are however only representative under conditions of that specific investigation but such findings are nevertheless often extrapolated to the practitioner’s situation. A CRA in the clinic can just be proven right or wrong; the paradox is that the educated and skilled clinician, making a correct assessment with subsequent adequate and effective management, will eventually turn out “wrong”.

As caries is a biofilm-mediated multi-factorial disease, it is generally understood that a comprehensive risk assessment should be based on a range of risk factors and risk indicators associated with the condition, balanced against a range of protective factors the patient may be exposed to. Thus, multiple models based on socio-economy, behavior, general health, diet, oral hygiene, clinical observations and past caries experience have been proposed, and especially for preschool children. The child is commonly grouped into one of several fixed risk categories (e.g. low risk, moderate risk, high risk). Narrative and systematic reviews have concluded that the best single predictor for more caries is previous caries experience (Powell 1998; Twetman & Fontana 2009). This is however far from optimal in the new era of early intervention, non-operative and minimal invasive caries management. Although there are hundreds of various factors and indicators associated with childhood caries in cross-sectional studies (Harris et al. 2004), risk variables or models must be validated in prospective clinical cohort trials in order to disclose a causal relationship (Table 1).

Why? Caries risk assessment is the basic component in the decision-making process for adequate prevention and management of dental caries and for determination of individual recall intervals. A high risk calls for shorter intervals for follow-up. CRA is however not only about finding children with high caries risk. A significant proportion of patients who regularly attend general dental practice have repeat examinations without any need for treatment. Thus, it would be desirable to screen out these children to concentrate the resources on those with greatest need.

When?

The question when a CRA should be carried out is not thoroughly studied. Studies in preschool and schoolchildren indicate that approximately 50 % of all children change their risk category over a 1– 2 year period, for better or for worse (Holgerson et al. 2009; Petersson et al. 2010). A firm recommendation is that all children should be risk assessed at their first dental visit and then regularly, at least every second year.

There also certain periods in life that may call for an increased attention to caries risk; before the eruption of the first permanent molars, before onset of fixed orthodontic appliances and at onset of chronic conditions, such as diabetes or asthma.

How? From the literature it comes clear that there are no clearly superior methods to assess caries risk and the evidence on for existing models is limited. It is however possible to identify three main avenues; 1) business as usual, 2) use of structured schemes or models, and 3) computer-based programs. Unfortunately, the first approach seems to be prevailing.

Variable

Number of trials with significant association to caries development

Low level of education (mother)

n=6

(13 %)

Low socio-economy (family)

n=6

(13 %)

Immigrant background

n=5

(11 %)

Frequent sweet intake, sweet drink in baby bottle

n = 20

(44 %)

Irregular non-daily tooth brushing (low fluoride exposure)

n =12

(27 %)

Early signs of caries (intial or cavity)

n = 24

(53 %)

Visible plaque or gingivitis

n=9

(20 %)

Mutans streptococci in saliva

n =16

(36 %)

High counts of salivary lactobacilli

n=6

(13 %)

Table 1: Baseline variables significantly associated with caries development in preschool children in 45 prospective trials published between 1994 and 2012

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Business as usual – It is highly likely that most dentists perform any kind of informal non-structured risk assessment in connection with the dental examination but this is difficult to handle from an evidence point of view. Clinical experience, knowledge and tradition are probably important parts of this process. According to a questionnaire among US and Scandinavian dentists, 73 % reported any kind of CRA among children, while only 14 % used a special form (Riley 3 rd et al.

2010). Current oral hygiene, decreased salivary flow, and the presence of active caries were rated as the most important factors that were taken into account. In Scandinavia, an analysis of dental records indicated that dentists and dental hygienists based their risk assessment in children on the past caries situation in the vast majority of the patients (Sarmadi et al. 2009). However, as the documentation generally was poor, this does not rule out the possibility that the gut feeling or other immaterial factors might have influenced the scoring.

Obviously, there is considerable variability in dentist’s views concerning the importance of specific caries risk factors and only weak evidence that caries risk assessment is a driving force for preventive treatment.

ly income and caries experience, transmission related behavior, dietary factors and health beliefs has been emphasized by Fontana and co-workers (Fontana et al.

2011a; 2011b). Another model comprising ten demographic variables [exposure to fluoridation in the municipal water supply, environmental smoke exposure, race, age, locale (metropolitan vs. rural), tobacco use, Body Mass Index, insurance status, sex, and sealant application] has been validated for future caries in a public health setting (Ditmyer et al. 2011). It was concluded that the model could be used by school nurses/nurse practitioners, health educators, and physicians for screening of risk patients. It is however also important to keep it simple when a single risk factor is enough. For example, a dry mouth child with less than 0.1 ml of stimulated saliva per minute is always at caries risk and the use of more sophisticated models is overkill. Examples of evidence-based recommendations for single predictors are shown in Table 2. A strong recommendation is that any clinical sign of demineralization on smooth, occlusal and proximal tooth surfaces should be taken as a signal for the implementation of preventive action.

Structured protocols – Several organizations have incorporated evidence from the literature into daily dental practice by constructing more or less complex caries risk assessment models for different age groups of patients. This has led to guidelines which aim to act as a framework for the categorization of risk level, treatment decision-making and determination of individual recall intervals. Examples are the Carifree and CAMBRA protocols. Separate assessment forms are available for use by dental providers for patients age 0 to 5 years (Ramos-Gomez et al. 2007) and patients age 6 through adult (Featherstone et al. 2007). Similarly, separate risk assessment protocols for the primary, mixed and permanent dentitions, based on clinical findings, have been suggested for first visit and recall patients in general practice (Evans & Dennison 2009).

Computer-based programs – Cariogram is a free download software program designed to calculate “the chance to avoid new caries lesions in the near future” (Bratthall & Hänset-Petersson 2005). The interaction of ten different caries risk factors is taken into account and the caries risk profile of the individual patient is graphically illustrated. In prospective trials, Cariogram has been validated in schoolchildren with moderate to good performance (Hänsel-Petersson et al. 2002; Campus et al. 2012), while it was found less useful in preschool children (Holgerson et al. 2009). It is important to underline that the accuracy and predictive power of computer-based risk assessment may not be improved compared with for example past caries alone.

The advantage is that the risk profile is didactic and useful for motivational interviews. Suggestions for preventive action linked to the individual profile are offered which may enhance patient’s understanding.

Furthermore, CRA can be made by dental personnel with different experience and background education with improved documentation in the dental records.

The use of risk models has generally proven more accurate for children than using few or single factors.

The importance of a structured interview to unveil fami-

Variable

Age group

Recommendation

Past/active caries

All ages

strong

Prediction models

Preschool, schoolchildren

strong

Diet sugar intake

All ages

weak

Bacterial tests

All ages

weak

Visible plaque/oral hygiene

Toddlers

weak

Fluoride exposure

Preschool children

weak

Post-eruptive age, 2–3 years

Young permanent teeth

strong

Saliva flow rate and buffer capacity

All ages

expert opinion

Table 2: Single risk factors for caries risk assessment. Grading of recommendations according to the Scottish Dental Clinical Effectiveness Program: Strong = Recommendation supported by strong evidence with limited bias; Weak = Recommendation supported by weak evidence with some potential for bias; Expert opinion = Recommendation based on expert opinion.

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It has been argued that the downside with the Cariogram is that the program is complex and requires costly and time-consuming laboratory tests. The Cariogram can be used without salivary tests but with a marked reduction in the combined sensitivity and specificity (Petersson et al. 2010). Without doubt, the use of guidelines, structured forms, models or computerbased programs in caries risk assessment must be regarded as “best clinical practice” since they provided structure to the clinical work and aid patient motivation.

Accuracy of caries risk assessment The accuracy of the informal, “intuitive” businessas-usual concept is not known but more surprisingly, even few of the structured protocols are validated in prospective trials. Based on five predictive studies of moderate quality, the probability to identify the risk for future caries was highest in preschool children with a mean sensitivity and specificity of 80 % and 79 %, respectively (SBU 2007). This means that the risk assessment actually was correct in eight out of ten children.

The corresponding mean values for schoolchildren and teenagers were 61% and 82 % (SBU 2007). These values must be regarded as acceptable, in the light of the complex caries etiology. Interestingly, CRA was generally slightly more effective in selecting children at low risk than finding those with high caries risk. The best precision so far was reached in a recent trial from Singapore in which a combined sensitivity and specificity of 180 % was achieved when a questionnaire, oral examination and biological (saliva) tests were combined to predict one-year caries increment in preschool children (Gao et al. 2010).

Conclusions Risk-based clinical decision-making for caries management in everyday clinical practice should be based on the best available evidence while taking into account the dentist’s knowledge and expertise and focusing on the needs and desires of the patient. The lack of a perfect method is not an excuse to avoid CRA. Best clinical practice is to use any of the objective, easyto-use, multiple risk assessment tools that have been developed during the last few years. Evidence suggests that past and current caries is far from ideal but the most important single risk component for more caries.

Thus, any early sign of likely active demineralization on smooth, occlusal and proximal tooth surfaces should be taken as a signal for the implementation of secondary prevention.

Based on a symposium held at EAPD in Strasbourg, June 2012 Prof. Dr. Svante Twetman Institute of Odontology, Faculty of Health and Medical Sciences · University of Copenhagen Nørre Allé 20 · DK-2200 Copenhagen N · Denmark

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Evidence-Based Data on the Effect of Saliva on Caries Dr. Panos Mitropoulos1 and Dr. Christos Rahiotis 2 1

DDS, Master in Operative Dentistry, Faculty of Dentistry, University of Athens, Greece 2 Lecturer, Operative Dentistry, Faculty of Dentistry, University of Athens, Greece

Introduction Saliva is a biological fluid of major importance because of its multiple roles in the functioning of the oral cavity and in the general maintenance of health.

Saliva’s multiple functions include hard and soft tissues lubrication, facilitation of mastication, speech and digestion while at the same time preventing injuries.

Saliva also acts as a preventive mechanism against carious lesions, erosion, attrition and mechanical wear of dental hard tissues (Nauntofte et al. 2003).

Saliva formation is regulated through the autonomic nervous system. Stimuli relating to mastication, olfaction and taste may alter saliva production, while health problems and medication intake may affect total saliva volume (Mazariegos et al. 1984; Edgar 1990).

Saliva is a hypotonic fluid of 99 % water consisting of electrolytes, proteins, mucins, immunoglobulins, urea, bicarbonate and phosphoric acid ions. Constituents of saliva are related to buffering capacity, antimicrobial action and remineralisation process (Humphrey & Williamson 2001).

Saliva and caries The influence of saliva on the caries process is fundamental. Flow rates and clearance, pH and buffer capacity, calcium phosphate homeostasis and effects on bacterial metabolism, adsorption to oral tissues and elimination from the oral cavity are all obvious manifestations of the saliva/caries interaction. In general, people with a low salivary flow rate are particularly susceptible to caries because of the loss of many protective effects of saliva, which are described below.

Salivary clearance Salivary clearance refers to the ability of saliva to clear all kinds of substances remaining in the oral cavity following the completion of mastication cycle. The rate of clearance varies markedly at different oral sites and is fastest lingual to the mandibular incisors and slowest on the buccal surfaces of the teeth. Saliva is responsible for sugar clearance from the mouth and for acid clearance from dental plaque, which depends primarily on the velocity of the salivary film flowing over the plaque.

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Again, this varies markedly according to the site, the velocity is highest in the same locations where sugar clearance is fastest. These two factors seem to explain why smooth-surface caries is more prevalent on buccal than on lingual surfaces.

The saliva produced in the absence of any stimulation is referred as unstimulated flow rate. The presence of gustatory, olfactory or mechanical stimuli leads to the increase of saliva flow rate, known as stimulated flow rate (Schneyer & Levin 1955; Dawes & Wood 1973).

The production of saliva is affected by medication intake, hormones level fluctuation, stress and psychological state, hydration level, age and gender. In addition, the amount of saliva produced is subject to variation during the day, known as circadian circle. It also varies according to the season and at different stages of life. Although, setting a threshold for normal saliva flow rate in any state of stimulation can prove a difficult task, unstimulated flow rate less than 0.1ml/min is known as hyposalivation. In a stimulated state, the presence of mechanical stimulus such as chewing can result in a flow rate of 3.15 – 4.94 ml/min, while an acidic stimulus can increase the flow rate up to 7 ml/min. Actually, stimulated and non-stimulated flow rate are positively correlated (Watanabe & Dawes 1988a; 1988b).

Although different methods have been applied in various studies for the assessment of saliva flow rate, the use of sophisticated equipment and methodology make their adoption in everyday clinical practice impractical. A more easily applied method for assessing the non-stimulated flow rate includes the evaluation of minor salivary glands located in the labial surface of the lower lip. After drying the surface with gauze, the clinician calculates the time necessary for a saliva drop to form (Fig. 1). This method constitutes an arbitrary measure of non-stimulated saliva flow rate – any time less than 1 minute is considered as normal flow rate, while time exceeding 1 min indicates low flow rate.

Several clinical signs are common in cases of hyposalivation, including loss of the glossy sheen usually observed in oral mucosa, while the tongue dorsum and the lips present fissuring and lobulation. Salivary glands can present swelling, but do not excrete saliva during mechanical stimulation with milking motions. In cases of severe hyposalivation, carious lesions are expected in unusual tooth sites (i.e labial and incisal surfaces) with a higher progression rate.

The assessment of saliva flow is useful in order to monitor the effect of ongoing medical treatments in the oral cavity, including the effects of drugs and radiotherapy on salivary glands. However, the effect of hyposalivation is mostly validated through clinical observation, without having studies that set a threshold on how much saliva is enough to avoid high caries occurrence. On the contrary, several studies fail to prove the impact of salivary flow on caries occurrence.

Indeed, in individual cases a drop in salivary flow rate may be indicative of high caries risk (Tenovuo 1997).

Therefore, it seems more useful to assess salivary flow rate at regular intervals and to be vigilant for any major alterations in the recorded data. However, the clinician should keep in mind that the data collected is useful only as a reference for future validation of saliva flow and is not indicative of high caries risk.

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Fig. 1: Non-stimulated flow rate assessment

For the assessment of stimulated flow rate, chairside commercial kits are available. The patient is instructed to chew a paraffin cube included in the kit and to expectorate at regular intervals into a volumetric cup for a predetermined time (Fig. 2). The flow rate is classified as normal or low according to the volume of saliva.

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The available scientific data fail to support a correlation between saliva flow and caries status. No relationship has been proved between stimulated flow rate and caries clinical indexes in studies including different

Calculating buffering capacity is a challenging task because of the complex mechanism involved in acid neutralisation. Laboratory techniques are available for assessment of buffering ability, whilst several chair-side kits are available and intended for clinical application.

Studies present diverging results regarding agreement of laboratory and chair side techniques. In several studies, however, chair-side kits are considered a clinically reliable solution for this task (Maldupa et al. 2011; Cheaib et al. 2012).

Fig. 2: Paraffin cube (left) and volumetric cup (right) used for stimulated flow rate assessment

age groups for coronal (Russell et al. 1990; Mazengo et al. 1996; Gabris et al. 1999) and for root caries (Lundgren et al. 1998). Additionally, a study examining both stimulated and non-stimulated flow rate found no correlation between clinical indexes DMFT and DMFS or caries activity (Varma et al. 2008). Thus, more sensitive indicators of caries status need to be used, possibly combining in vivo demineralisation/remineralisation models and other indicators of caries activity, together with regular, standardised and comprehensive salivary collection.

However, the most important question to answer, however, is whether measuring buffering ability is useful in explaining caries incidence or predicting caries progression. In this specific area, scientific data is rather scarce; buffering capacity assessment in stimulation state does not prove useful in predicting high caries risk patients (Coogan et al. 2008). Additionally, this saliva parameter does not correlate with several indices of caries incidence or activity (Varma et al. 2008). This could be attributed to the over-simplification involved in determining the role of buffering systems in acid neutralisation. Examination of saliva collected under stimulation presents several disadvantages as, the real impact of the carbonic acid/bicarbonate system fails to be measured and the proteins are denatured when carbon dioxide is diffused into the atmosphere. In addition the effectiveness of the protein buffering system in preventing hard tissue demineralisation depends on the concentration of macromolecules, which varies in different locations in the oral cavity. It seems reasonable to expect that pH fluctuations in plaque do not relate to the results of stimulated-state saliva buffering ability assessment kits. Nevertheless, examination of the impact of buffering systems in plaque covering teeth surfaces is not currently applicable.

Saliva pH Buffering capacity

(Fig. 3)

The role of saliva in acid elimination is assisted through its three distinct buffering systems – the carbonic acid/bicarbonate, phosphate and protein systems (Nauntofte et al. 2003).

Commercially available chair side tests allow the calculation of salivary pH, either on stimulated or nonstimulated status (Fig. 4). The reasoning behind the development of this diagnostic tool is that low pH values favour the loss of mineral elements from hard dental tissues linked with caries progression.

Fig. 3: Buffering ability assessment tab (left) compared with the index included in the chair-side kit (right) Fig. 4: Non-stimulated saliva pH assessment

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The scientific data on the usefulness of this diagnostic tool are not adequate. In a study by Varma et al. non-stimulated saliva pH value was negatively correlated to the number of incipient carious lesions and the total number of lesions (Varma et al. 2008). On the other hand, regarding saliva pH in stimulation status, the scientific data are contradictory, since both, positive and negative correlation between saliva pH value and caries status have been reported (Crossner & Holm 1977; Johansson et al. 1992).

Antimicrobial action Human saliva secretes immunoglobulin IgA, which plays a critical role since it obstructs S. mutans colonisation in the pellicle. Certain diseases, such as selective IgA immunodeficiency, should provide a unique model for the evaluation of the role of slgA in the colonisation of streptococcus mutans. However, even these results are contradictory, and increased, decreased, or lack of correlation between IgA deficiency and caries susceptibility have all been reported (Tenovuo 1998).

Lysozyme degrades the bacterial cell wall. Lactoferrin has a bacteriostatic effect. Peroxidase systems have both an antimicrobial and a protective action (Edgar 1990). Agglutinins aggregate residual unattached bacteria to larger formations (Nauntofte et al.

2003).

The multiple interactions among the antimicrobial proteins do not allow comparing them in terms of anticariogenic impact – the various proteins present synergistic action leading to maximization of their effect.

Summary Human saliva is a complex mixture of inorganic and organic components. The biochemical and physicochemical properties of saliva contribute to the numerous functions of saliva.

The protective role of saliva against caries is demonstrated by the rampant caries seen in human subjects with marked hypo-salivation. Anti-caries properties of saliva include salivary clearance, buffering capacity and antimicrobial ability. It is important for the clinician to identify the saliva flow in their patients.

However, the clinician must keep in mind that the caries process is a complex phenomenon involving internal defense factors, such as saliva, tooth surface morphology, general health, and nutritional and hormonal status, and a number of external factors such as diet, the microbial flora colonising the teeth, oral hygiene and fluoride availability. In conclusion, no solid relationship between individual saliva characteristics and caries progression has been established – in either in vitro or in vivo investigations.

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How to Stop and Reverse Initial Carious Lesions in Permanent Teeth Dr. Effie Pappa1 and Prof. Afrodite Kakaboura 2 1

DDS, Master in Operative Dentistry, Faculty of Dentistry, University of Athens, Greece

2

Professor, Operative Dentistry, Faculty of Dentistry, University of Athens, Greece

Current approach in caries concepts In recent decades, the focus of treatment of dental caries has shifted from a restorative approach to a therapeutic one. Caries is nowadays considered to be a disease continuum ranging from subclinical demineralisation and extending to gross cavitated lesions, rather than a disease identified at the threshold of restorative intervention (Pitts 2011). It is now widely acknowledged that, throughout the day, the tooth surface is subjected to cycles of demineralisation and remineralisation, as part of a dynamic physiological process. Under acidic conditions, when demineralisation prevails over remineralization, caries lesions will take place, whereas when remineralisation predominates over demineralization, carious lesions can be reversed or arrested. A wide range of therapeutic procedures can be applied to favour remineralisation, depending on the stage in the caries process and on the rate of progression of a lesion (Featherstone 2004).

Meanwhile, considerable changes in oral health profile have been observed during the last decade, resulting in fewer lesions per person and a slower rate of progression from the early enamel defect to cavitation level.

The above are considered to be complementary characteristics so that minimal therapeutic interventions may achieve a favourable outcome (Sheiham & Sabbah, 2010).

Initial carious lesions Diagnosis of caries can be considered as a threestep procedure, involving the detection of the lesion, followed by an assessment of the extent and the activity of the lesion (Ekstrand 2001). Caries risk assessment also plays an important role in decision making, since it highlights the imminent risk of getting new lesions in near future. The first sign of a carious lesion is a slight change in the translucency and microporosity of the enamel, which is obvious when the tissue is dried for a short period. If demineralisation challenges continue, the microporosity will increase, leading to a further reduction of the refractive index of the enamel. Such carious lesions are observed even when the surface is wet and/or covered with saliva. White spot lesions, which require air drying, are most likely to be limited to

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the outer half of the enamel. The depth of a white or brown spot lesion, which is obvious without air drying, is located somewhere between the inner halfof the enamel and the outer third of the dentin. Localised enamel breakdown with no visible dentin, represents a more advanced stage of dental caries and indicates that the histological depth of the lesion extends to the middle third of the dentin. According to the ICDAS II criteria, which incorporate concepts from the research conducted by Ekstrand et al. (1995, 1997) and other caries detection systems (Ismail 2004), initial carious lesions are coded with digits 01 and 02 respectively, depending on whether the change in surface translucency is evident when dry or wet. These systems indicate that measurement of non-cavitated carious lesions in enamel or dentin can be based on visual topography at the surface level. Clinically, even lesions characterized as 03 according to the ICDAS II criteria – without cavitation but with a histological lesion extending beyond the dental-enamel junction – are considered to be initial lesions and are treated accordingly.

Numerous factors, including the extent, activity and location of the lesion, as well as a patient’s caries risk profile, influence the choice of therapy. The range of treatments available to a professional to tackle initial lesions, consists of a variety of fluoride compounds available in dentifrices, mouthwashes, varnishes and gels for topical fluoridation, remineralising agents such as CPP-ACP (casein phosphopeptide-amorphous calcium phosphate), sealants and, more recently, resin infiltration materials.

Management of initial coronal carious lesions Smooth surfaces (Fig. 1) Treatment modalities for initial carious lesions follow the concept of minimal intervention, using non-invasive techniques and remineralization procedures, depending on the individual’s caries susceptibility. For patients with a low caries risk, preventive routine care is emphasised in order to arrest non-cavitated smooth surface carious lesions. This regimen includes daily oral hygiene (tooth brushing twice a day, use of fluoride a)

toothpaste and interdental flossing), dietary advice as required and patient motivation.

Individuals with a moderate to high risk of caries can be actively provided with preventive care, which includes the standard regimens listed above, plus remineralisation treatment with the use of fluoride or alternative b) remineralising agents (CPP-ACP), as well as behavioral modifications and frequent follow-up. For non-cavitated smooth surface carious lesions in a moderate or high caries-risk patient, the appropriate fluoride regimen would be either topical application of a fluoride varnish containing 5 % NaF for 20 days, or topical application of CPP-ACP for the same period, using a brush at the site of the lesion. In addition, the patient should use a fluoridated toothpaste twice daily containing NaF or MFP or SnF2 (1,000 –1,500 ppm F), and a fluoride mouthrinse once daily every day, containing 0.05 % NaF. When the lesions are located on the proximal surface, dental floss or interdental brushes are used to apply fluoride varnish or other remineralising agents at the specific area. It should be emphasised that such non-cavitated carious lesions need to be monitored regularly, to ensure that preventive treatment is effective and that the lesions are not progressing (Griffin 2007, Sonbul 2010).

For adults highly susceptible to caries – such as patients undergoing orthodontic treatment or patients with hyposalivation, both professionally applied and self applied topical fluoride treatments are recommended. The first professional fluoride therapy visit should consist of the application of a high-concentration agent (either a 1.23 % APF gel for four minutes in a tray or a 5 % NaF varnish) to be applied four times per year. Self applied fluoride therapy should consist of the daily 5minute application of 1.1% NaF (5,000 ppm F) in a custom-fitted tray. A daily 0.05 % NaF rinse for 1 minute may be a less effective alternative for those who cannot tolerate a tray delivery (Zantner 2006, Chambers 2009).

The adherence of fluoride varnishes is their main advantage since they permit prolonged fluoride exposure and uptake. Helfenstein and Steiner (1994), in a meta-analysis of the efficacy of fluoride, using very rigid criteria for inclusion of data, found a mean caries reduction of 38 % for fluoride varnishes. Similarly, in a comprehensive review of evidence-based literature, Bader et al. (2001) reported incomplete evidence for the efficacy of most measures currently used for caries prevention, with the exception of fluoride varnishes.

Fig. 1: Incipient carious lesion (white spot) at the labial surface of lateral incisor (a) and at the proximal surface of the molar (b)

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New Concepts in Caries and Erosion

Remineralising agents such as CPP-ACP have been shown to localise and stabilise calcium and phosphate ions at the tooth surface in a bioavailable form. CPPOral Health Dialogue

New Concepts in Caries and Erosion

ACP promotes remineralisation of enamel subsurface lesions in situ, and has been shown to restore the opaque, white appearance of the lesions (Reynolds 2008). In the presence of fluoride, it contributes to the formation of fluorapatite deep below the dental subsurface (Reynolds 2008). In post-orthodontic patients with white spot lesions, the use of this remineralising agent, in addition to fluoride toothpaste and mouthrinse, promoted a significant regression in initial lesions (Bailey 2009).

Recently, caries infiltration has been introduced as a new technique that fills the non-cavitated pores of an early lesion with a low-viscosity resin by capillary action, creating a barrier that impedes further bacterial diffusion and lesion progression (Meyer-Lueckel 2008). In cases of white spot lesions in the asthetic zone, this method seems to reduce opacity, creating a proper blending with the natural teeth. Resin infiltration is indicated for lesions located in smooth and proximal surfaces. The protective effect of infiltration against caries for proximal lesions is validated by recent studies conducted in young adults (Paris 2010) and children (Ekstrand 2010).

eruptive fluoride exposure is more effective than topical fluoride in such cases. Pre-eruptively, ingested fluoride is incorporated into the developing enamel hydroxyapatite crystal, which results in the reduction of enamel solubility (Newbrun 2001; Pickett 2011).

Management of initial root carious lesions Root surfaces become vulnerable to caries attack only in adulthood, and the risk increases with age. Agerelated conditions often contribute to the increase in the prevalence of root caries, such as recession of gingival tissue, decreased salivary flow and changes in the composition of the saliva. Initial root carious lesions present opacity or discolouration, that is not accompanied by cavity formation, but they also refer to lesions where the depth of cavity does not exceed 0.5 mm, according to ICDAS II clinical criteria (Fig. 3).

Pits and fissures (Fig. 2) In recent years, the proportion of occlusal caries has increased relative to proximal and smooth-surface caries. The occlusal molar surfaces are the most common sites of caries attack and these surfaces seem to be least affected by the advantages of fluoride (Rozier 2001).

Fig. 3: Root caries with formation of cavity which can be arrested

Fig. 2: Initial pit and fissure caries at the occlusal surface of the premolars

Special assessment and management is required at these sites, as diagnosis is less reliable at pit and fissure tooth surfaces. For early carious lesions located in enamel with intact outer surfaces, observation of the lesions and re-evaluation at the annual dental check-up examination is recommended for patients with a low caries risk. For patients with moderate or high caries risk, application of sealant is the indicated therapy, in order to achieve an immediate bactericidal effect and to create a barrier against further demineralisation.

Although, the role of fluoride seems to have minimal effect on those surfaces, it has been reported that preOral Health Dialogue

Patients with root carious lesions, irrespective of caries risk, are advised to brush twice daily using 5,000 ppm fluoridated dentifrice. Randomised clinical trials have shown that the additional use of mouthrinse with 0.02 % NaF, once daily, significantly reduces the extent and depth of initial root lesions, by comparison with the use of a placebo solution. When a highly fluoridated dentifrice is not used -depending on a patient’s susceptibility to caries – the topical fluoride application of 0.5 % NaF varnish, 1– 4 times/year is recommended (Fure 2009; Lynch 2000; Tan 2010).

Conclusion The modern concept of a dynamic nature of the caries process, where lesion progression can be arrested at any stage of the procedure, supports the significance of clinically assessing caries activity status and implementing the proper treatment according to a patient’s disease susceptibility (Table 1). This is particularly essential in the case of non-cavitated lesions, since they may become arrested due to alterations in the local environment, as a result of a reverse in the equilibrium of the demineralisation-remineralisation process provided by the essential materials and techniques.

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Caries risk

Tooth Surfaces Buccal/Lingual

Proximal

Occlusal

Root

Pit and Fissures Low

W

Daily oral hygiene

W

Daily oral hygiene

W

Patient motivation

W

W

Patient motivation

W

Patient motivation

W

Recall every 12 months

W

W

Recall every 12 months

W

Emphasis in inter-

Mouth rinse with 0.02 % NaF once daily

W

dental areas W

Daily oral hygiene

Recall every 12 months

Use of 5,000 ppm fluoridated dentifrice daily or 0.5% NaF varnish, once a year

Moderate

Recall every 12 months

W

Standard regimen

W

Standard regimen

W

Standard regimen

W

Daily oral hygiene

W

Fluoride varnish 5 % or

W

Fluoride varnish 5 % or

W

Sealant application

W

Mouth rinse with

CPP-ACP daily / 20 days

CPP-ACP daily/ 20

W

Recall every 6 months

Fluoride mouth rinse

days-application with

0.05 % NaF

inter-dental brush / floss

W

W

High

W

Recall every 6 months

W

0.02 % NaF once daily W

Use of 5,000 ppm fluoridated dentifrice

Fluoride mouth rinse

daily or 0.5 % NaF

0.05% NaF

varnish twice a year

W

Recall every 6 months

W

Recall every 6 months

W

Standard regimen

W

Standard regimen

W

Standard regimen

W

Daily oral hygiene

W

Fluoride varnish 5 % or

W

Fluoride varnish 5 % or

W

Sealant application

W

Mouth rinse with

CPP-ACP daily / 20 days

CPP-ACP daily / 20

W

Recall every 3 months

Fluoride mouth rinse

days-application with

0.05 % NaF and/or

inter-dental brush / floss

W

caries infiltration W

W

Recall every 3 months

Fluoridated toothpaste 5,000 ppm daily or

Fluoride mouth rinse

0.5 % NaF varnish

0.05 % NaF and /or

four times a year

caries infiltration W

0.02 % NaF once daily W

W

Recall every 3 months

Recall every 3 months

Table 1: Guidelines for the management of the initial tooth carious lesions

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What Distinguishes Erosive Hard Tooth Structure Defects from Dental Caries?

Prof. Dr. Thomas Attin, University of ZĂźrich, Switzerland A high calcium and/or phosphate content and the presence of fluoride reduce the erosive potential of a noxa of this type (Attin et al. 2003; Caglar et al. 2006).

The protons released by the acids react with the carbonate and/or phosphate of the enamel apatites, thus destabilise the enamel crystals and result in the dissolution of dental mineral (Featherstone & Lussi 2006). The calcium and phosphate thus dissolved is released into the surrounding solution and is so to speak swallowed.

Etiology of dental erosion and caries Erosion is defined as the superficial loss of hard tooth structure caused by chemical processes, which occurs without the involvement of microorganisms (Imfeld 1996). Erosion develops under the influence of acids or chelator substances, which may be extrinsic (e.g. dietary) or intrinsic (e.g. gastric acid) in origin. The loss of hard tooth structure associated with this often occurs as a key-shaped, non-discoloured, flat indentation with rounded margins. Depending on the etiology, the lesion can be observed on both oral and also vestibular free dental surfaces. In rare cases the lesions can also lie subgingivally (Balanko & Jordan 1990).

o n p atie nt

si d

e

rs o n nutr itio

id ns

Fig. 1 gives an overview of the various Emp loy ment factors which can affect the development of erosion. Thus acidic foods with a high buffer capacity, a low pH value or a high proportion of free, titratable acid can facilitate the development of erosion. It is perfectly possible for the pH value of some foodstuffs, especially of acidic beverages, to lie in the range of pH 2.2 (Lussi et al. 2005).

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e

ow

c to

Kn

its

Fa

le d

Ha b

ge

h alt

Beh av

Fa

rs o t c

He

io

ur

It should also be borne in mind that saliva normally represents a solution supersaturated with apatite (i.e. calcium/phosphate). This supersaturation depends amongst factors upon the calcium, phosphate and fluoride content of the saliva, and on the pH value. The Etiological complex in relation to the development critical surrounding pH value, below which subsaturaof erosion (following Lussi et al. 2005) tion of the saliva with hard tooth structure and thus a tendency to the dissolution of dental mineral occurs, is approx. 5.5 for enamel and approx. 6.5 for dentine.

After 1% citric acid is drunk, the pH level on the surfan i g r b i ng Up ce of the tooth can drop as low as pH 3 (Millward et al. 1997). The fall in the pH level caused by the erosive noxa results in subsaturation in relation to the various apatite forms of the tooth and thus facilitates the dissolution Eating-/drinking habits of calcium and phosphate. Thus a twice daily erosive attack of 90 seconds with Tooth cleaning Reflux/bulimia a soft drink (pH 2.9; without brushing) results in a loss of dental enamel at Medication Soft tissue least 1 Âľm in thickness within 21 days (Attin et al. 2001). In addition to this Saliva Time Pellicle direct acid attack, certain acids (including citric acid, lactic acid, tarTooth Tooth taric acid, oxalic acid) can bind calAcid type (pK) Adhesion cium in a chelate complex and thus exacerbate the subsaturation of the pH Phosphate surrounding milieu with calcium, but can also precipitate on the surface of Buffering Fluoride the enamel (Hannig et al. 2005). Such a precipitate can definitely have a tempoCalcium rary protective effect.

Dental caries is caused by acids which are produced by bacteria which adhere in the dental biofilm (plaque) on the surface of the tooth. Some of the acids produced from low-molecular polysaccharides are weak acids, such as lactic acid, acetic acid or propionic acid. This bacterial metabolic activity lowers the pH value in the dental plaque e.g. after the introduction of a sucrose solution for a period of approx. 15 minutes from originally approx. pH 7 to up to pH 4 (Imfeld 1983). The acids already dissociated in the plaque cause signs of interprismatic dissolution on the surface of the enamel (Arends &

New Concepts in Caries and Erosion

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New Concepts in Caries and Erosion

Christoffersen 1986). This early initial lesion is comparable with the appearance of erosion. A concentration gradient also develops, with the result that the weak acids diffuse into the dental enamel and dissociate there (Hellwig et al. 2007). The released H+ ions attack the enamel crystals, so that the mineral components of the hard tooth structure are dissolved. These components then diffuse in the interprismatic aqueous sheath of the enamel in accordance with their concentration gradient in the direction of the surface of the tooth.

However at the surface of the tooth the diffusion rate and the concentration gradient decline. There is therefore a precipitation of calcium and phosphate and the new formation of crystals.

This creates a so-called pseudo-intact surface layer on the initial caries lesion. This layer is more porous than healthy enamel and therefore makes it easier for acids to continue to migrate to the dental enamel. If this pseudo-intact layer is destroyed, microorganisms can penetrate into the dentine. The organic parts in the enamel and dentine are also destroyed by proteolytic enzymes of the bacteria. The result of this is that necrosis develops in the dentine. In addition the defence activity of the odontoblasts results in further zone formation in the dentine altered by carious changes, such as for example dead tracts, sclerotic dentine etc.

Histomorphology of erosion damage and caries In enamel erosion the resulting surface loss can be clearly seen in the histological specimen (Fig. 2).

Underneath this is an enamel zone, which is demineralised and softened and which can be easily removed under mechanical influence (Attin et al. 1997). This means that the total acid damage is composed of the layer completely lost and the softened layer still remaining. This zone is approx. 500 nm after the effect of hydrochloric acid with pH 2.3 (Wiegand et al. 2007).

The depth of this demineralisation depends on the type of acid applied and the duration of the exposure time.

However, in longer acid reaction times, this zone, which is hardly resistant to abrasion, is not significantly thicker in every case (Lippert et al. 2004). Nevertheless the total acid damage increases in longer exposure times, as the thickness of the layer completely lost increases.

In the scanning microscope view the surface of the enamel erosion appears as an etched area with the prismatic structure clearly visible (Fig. 3).

Fig. 3: Scanning microscopic image of surface of tooth after erosion

In erosion in the dentine there is likewise a dissolution of the mineral and a softening of the surface.

However the collagen of the dentine is generally not attacked by the short-acting acid (Ganss et al. 2004).

Thus for example in an attack with hydrochloric acid, two zones develop in the eroded dentine: 1. a completely demineralised zone with an exposed organic section, and 2. a partially demineralised zone, to which the healthy dentine below is attached. After repeated attacks with hydrochloric acid (pH 1.6) each of these zones is approx. 50 Âľm thick (Schlueter et al. 2007b). It is the subject of discussion as to whether the exposed collagen on the surface provides protection for the dentine below from further acid damage or from mechanical influences (Schlueter et al. 2007a).

Histologically speaking, the initial enamel caries (Fig. 4), in which there is as yet no cavitation, presents as a multilayered lesion, which can be up to 150 – 200 ¾m deep (Silverstone 1975). In the polarisation microscope, depending on the imbibition medium, up to 4 zones can be seen: 1. a superficial, pseudo-intact layer, 2. the lesion body lying below it, 3. a dark zone, and 4. a translucent zone near the healthy dentine. The pore volume in the respective layers varies in size.

In the first and third zone it is approx. 5 % and in the lesion body approx. 25 %. Healthy enamel has a pore volume of approx. 0.1%. Crystallographic studies have shown that the first and third zone develop as a result of remineralization processes (see above). The situation is reversed in the second and fourth zone, in which demineralisation processes give rise to the typical picture.

The increase in pore volume on the surface is clear in the specimen.

Fig. 2: Polarisation micrograph specimen of enamel erosion

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New Concepts in Caries and Erosion

Prevalence of Tooth Wear Prof. David Bartlett, BDS, PhD, MRD, FDS, FDSRCS, London, Great Britain

Introduction

Fig. 4: Polarisation micrograph specimen of dental caries

Dentine caries also presents as a multilayer lesion (Fig. 5). Its layering is determined on the one hand by the proteolytic activity and acid production of the migrating bacteria, and on the other hand by the defence activity of the pulp-dentine complex. Without treatment the dentine lesion progresses and then usually reaches the pulp.

Fig. 5: Scanning microscopic image of dental enamel surface with initial caries

Erosion is therefore primarily a surface phenomenon, even if a certain depth effect can be observed in the enamel and in the dentine in particular. The acid attack results in centripetal substance loss. The carious lesion, along with various surface symptoms, is primarily a depth phenomenon, in which demineralization of the inorganic components and/or degradation of the organic components dominate below a partially intact surface.

Prof. Dr. Thomas Attin Klinik für Präventivzahnmedizin, Parodontologie und Kariologie · Universität Zürich Plattenstrasse 11 · 8032 Zürich · Switzerland

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We often hear that tooth wear and erosion are becoming more prevalent – but what exactly does it mean? Firstly, there are some issues around definitions and how different countries interpret them. It is clear that acid erosion is a consequence of non-bacterial dissolution of enamel and dentine, attrition is tooth-to-tooth wear and abrasion is tooth against another surface (Smith & Knight 1984a). What is not so clear is how you assess a particular tooth and then classify the type of tooth wear from the appearance of the lesion. This has important consequences particularly when trying to compare the prevalence data from different countries.

In North America the role of erosion in tooth wear is not as well understood or appreciated as it is in Europe (Bartlett et al. 1999). Even within Europe the interpretation of erosive tooth wear differs. Some countries will include the cervical wear lesions as fundamentally erosive whereas others might consider abrasion more important. This in itself is not a problem provided that any measure used to evaluate tooth wear does not discriminate between the etiology. However, there are a number of indices measuring specific tooth sites or surfaces, for example palatal surfaces of upper incisors and occlusal surfaces of lower molars, and using them to give data on prevalence.

The only reliable way to measure changes to teeth in large populations are tooth wear indices. Most indices use changes to the anatomical appearance of teeth to record the amount of wear. Some indices measure tooth wear on every surface of every tooth (Smith & Knight 1984b), some use selected sites (O’Brien 1993) and others use specific surfaces (Dahl et al. 1989). Other studies have reported the prevalence of erosion rather than tooth wear (Johansson et al. 1993). The difficulty lies in making a diagnosis of the etiology and then using an index which does not record other causes of tooth wear. Most importantly, it is clinically very challenging to diagnose the etiology from the appearance of a lesion without a comprehensive dietary and dental history (Kidd & Smith 1993; Bartlett & Smith 2000). In most cases changes to the anatomy of teeth from tooth wear is a combination of erosion, abrasion and attrition and it is difficult to assess which component is most important. It is generally safer not to be specific and use an index to record change and then use the results to allow analysis of risk factors to identify the cause.

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New Concepts in Caries and Erosion

Another important question is what is exactly meant by prevalence. The oxford dictionary definition is “widespread; of wide extent or occurrence; in general use or acceptance” but in terms of tooth wear what does this actually mean? The prevalence of dental caries is usually measured using the parameters “decayed, missing, filled teeth” (DMFT). The prevalence of the disease can then be compared between different countries and geographical regions provided the same assessment of caries is used by all. Although the prevalence of filled teeth may suggest an outcome of decay there are other reasons why teeth are restored, for instance, worn teeth. Despite the complexities with the DMFT the same universal agreement does not exist for tooth wear and erosion.

What is an important assessment which measures prevalence of tooth wear and erosion? Is it the percentage of exposed dentine surfaces or the most commonly worn tooth or tooth site? An obvious possibility might be the percentage of exposed dentine in a population. Provided researchers use similar or comparable indices there is a possibility that the prevalences can be compared.

The Smith & Knight tooth wear index (TWI) has been used extensively by different researchers around the world and is perhaps the most widely used index.

The index is a way of recording changes to the anatomical structure of teeth and is evaluated on each tooth and is independent of the etiology. Teeth are divided into four sites: cervical, buccal, occlusal/ incisal and lingual/palatal. Other indices also record the degree and severity of dentine exposure so it should be possible to break down the more complex indices to simpler ones so that comparisons can be made. A new index has recently been developed which is simple and possible to use for re-analysis of tooth wear scores. The basic erosion wear index (BEWE) has the potential for widespread up take by different researchers.

Knowing the percentage of dentine exposure in a given population may be useful but it also ignores the impact of tooth wear on enamel. For dentine to become exposed the enamel overlying it must also have been lost. Many indices focus the outcome of the recording on the degree of involvement of dentine and often ignore the effect on enamel. From a preventative concept the aim must be to prevent wear of enamel and therefore some recognition of the damage to enamel should be considered. However, changes to the enamel surface from tooth wear or erosion can be more difficult to distinguish from a normal appearance.

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New Concepts in Caries and Erosion

Over the past 20 years there have been a number of studies evaluating the prevalence of tooth wear in different populations. By far the majority of prevalence studies have been reported on children and adolescents as these groups are easier to investigate and recruit. Studies on adults on the other hand tend to be less common because of the difficulty of recruitment. One convenient adult study population are military personnel and there have been a number of studies investigating this particular group (Johansson et al. 1996). One of the first studies conducted on adults recruited subjects from general dental practice but used a ratio to record the severity of wear and unfortunately most subsequent studies have not used the same technique.

Prevalence of tooth wear and erosion in the deciduous dentition Most of the studies on tooth wear in children have been reported from Europe (Jones & Nunn 1995; Al-Malik et al. 2002; Wiegand et al. 2006; Millward et al. 1994) investigated 178 4-year-old children from Birmingham, Great Britain, and reported that as high as 17 % showed involvement of dentine exposure. The results from this study are amongst the highest levels reported by any geographical region. The authors reported that almost half the subjects showed some sign of tooth wear and the most commonly affected tooth surface was the palatal/lingual of the maxillary incisors. When such high levels of wear are observed the outcome could almost be considered normal.

Another study on 987 pre-school children conducted in Saudia Arabia reported 31% showed some evidence of tooth wear with 13 % having dentine exposure. However, in this study the measurements were restricted to the primary maxillary incisors.

A larger study in China on 1,949 children aged 3–5-years-old reported that only 5.7 % showed signs of wear (Luo et al. 2005). It is difficult to understand why the geographical areas showed such a difference but it may reflect socio-economic state of the nations.

Prevalence of tooth wear and erosion in adolescents There have been considerably more studies undertaken in the mixed dentition of children at school. Like that in the deciduous dentition the larger studies often use selected teeth and selected sites to provide an estimation of the condition as a whole. One group of researchers measured erosive wear on study models/casts of 1,000 11-year-olds and reported up

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New Concepts in Caries and Erosion

to 70 % of tooth surfaces and 26.4 % with advanced lesions high incidence of erosive wear (Ganss et al.

2001). A smaller sample reported the results from 210 11–14-year-olds and observed less destruction with less than 2 % with dentine exposure (Bartlett et al.

1998).

The difference between the studies was that dentine involvement was used by the latter as a measure of advancement whereas the shape and depth of the lesion was used by the former. Another significant difference between the studies was that the most commonly worn surface in the study reported by Bartlett et al. was the palatal surfaces whilst Ganss et al. reported the occlusal and incisal surfaces. The reason for this difference again is not clear. There may be geographical differences between populations but within Europe that may be difficult to understand.

Another possibility is that researchers are using differently focused indices. If one group is recording erosion they may not be recording the effects of abrasion or attrition. To fully appreciate the effect of tooth wear in a given population the impact of changes to the tooth surface as a result of non cariogenic causes needs to be recorded. Once done the etiology may be considered.

The larger studies mostly report the impact of tooth wear on specific sites. Truin et al. (2005) reported the prevalence of erosion in a group of 12-yearold children in the Hague, the Netherlands. Their examination was limited to the palatal surfaces of the incisors and canines and the occlusal surfaces of first molars. Wear was observed on 59.7 % of the subjects with 2.7 % having dentine involvement. Milosevic et al. (1994) reported 30 % exposed of dentine in 1,035 14-year-olds in Liverpool, Great Britain. There study included all tooth surfaces and observed the most commonly affected surface was the incisal edges of upper and lower incisors. A study by the same group using multifocus selection recruitment showed even a higher prevalence of dentine exposure approaching 50 % (Bardsley et al. 2004).

These results have been supported by other studies in England. Al Dlaigan et al. (2001) reported 51% of subjects with dentine exposure but only 2 % with severe levels. Dugmore et al. (2004) reported much lower levels of dentine involvement with only 2 % from 1,753 12-year-olds. It is difficult to understand why such wide variation in dentine exposure is observed in so many different studies. Many subsequent studies have excluded the incisal surfaces from any comparative analysis. Perhaps the most important figure to remember is that severe dentine exposure remains around 2 % in most studies.

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The difference between gender has been reported in a number of studies. Most studies have reported the incidence more common in males (van Rijkom et al. 2002). A recent review concluded there was an increasing trend towards increasing wear with age (Jaeggi & Lussi 2006). In addition, dietary habits, presence of gastro-oesophageal reflux and socio-economic status all affected the prevalence of erosive tooth wear.

Prevalence of tooth wear and erosion in adults Comparatively few adult studies have been reported as this probably reflects the difficulty in recruitment and selection of subjects. Children and adolescents attend school and consideration can be made for socio-economic status by using specific selection criteria. However, adults over the age of 18 years are more difficult to investigate. Institutionalised adults such as military personnel provide some opportunity but the group are a convenient sample. Johansson et al. reported the occlusal and incisal wear amongst Swedish military personnel and reported that 28 % had erosion of the maxillary teeth. Lussi et al. (1991) reported around 10 % of 391 subjects had exposed dentine. Unlike many other studies this group reported buccal/facial dentine exposure to be more frequent than palatal/lingual surfaces.

The largest study to date was on 10,827 extracted teeth and reported between 13 and 21% of teeth but the study lacks a relevance to the oral environment (Sognnaes et al. 1972). Xhonga & Valdmanis (1986) examined 527 subjects selected randomly and aged between 14 and 88 years). The authors suggested that the prevalence in the USA was around 25 % but dentine involvement was comparatively rare at 4 %. The largest clinical study in general dental practice on 1,007 adults aged from 18 to 88 reported pathological levels of wear approaching 5 %. Unlike all other studies this particular group of researchers grouped ages together and subjectively estimated the expected wear rates based on the 1,007. Those subjects with higher levels of tooth wear were assessed as having pathological levels. However, the overall figure of around 5% with higher than normal levels of tooth wear seems to compare well with other studies.

The concept of pathological levels of tooth wear has recently been discussed. Whilst it is a convenient and emotive principle the meaning is more difficult to define. Different researchers, government officials and patients will interpret the data differently depending upon their subjective view of the impact of tooth wear.

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Patients will consider low levels of exposed dentine pathological because of the impact on appearance of teeth. Whereas, government officials may have consider higher levels because of the financial implications of treating a condition that can affect up to 50 % of a population. As a result the term pathological tooth wear is not particularly helpful as it usually relates to an individual’s subjective interpretation.

Perhaps a better estimate for the impact of tooth wear and erosion in the community is the “percentage of dentine exposure”.

Conclusion Tooth wear and erosion are modern-day problems for dentistry. Patients are increasingly concerned about their appearance and generally wish to delay the aging process and this includes the impact upon teeth. There is reasonably strong evidence to suggest that tooth wear is an age related phenomenon and it is common. The implication for dentists is that early diagnosis and prevention are vital to the well being of their patients. Overwhelmingly the evidence indicates that tooth wear and erosion affect most people but fortunately only a relatively small proportion develops severe levels.

Fig. 1 shows the appearance of erosive lesions on the palatal surfaces of the upper incisors teeth. This was caused by frequent consumption of fruit based drinks.

Prof. David Bartlett Floor 25, Guy’s Dental Hospital London Bridge, London SE1 9 RT Great Britain Fig. 2: The attrition on the teeth shown here is caused by continual grinding and clenching of the teeth over many years. The forces exerted by the muscles of mastication are extremely damaging.

Fig. 3 shows a typical cervical wear lesion in the maxilla. The etiology of the lesion is uncertain with some investigators suggesting it is abrasion, other erosion whilst most consider it a combination of erosion and abrasion.

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New Concepts in Caries and Erosion

Risk Factors and Guidelines for Risk Assessment Dr. Annette Wiegand, University of Zürich, Switzerland The identification of potential risk factors for the development of dental erosions is necessary as a basis for initiating suitable prophylactic measures or causal therapy. Erosions are caused by exposure to extrinsic (e.g. beverages, foods) or intrinsic (e.g. gastric acid) acids. The extent of erosive demineralisation is modulated by various (host) factors such as salivary parameters. Besides describing the risk factors, this article considers the various general disease conditions associated with an increased incidence of erosions.

Finally, professional swimmers are also observed to have an increased risk of erosions (Centerwall et al.

1986); improperly chlorinated water (low pH) is presumably the main factor in increasing the risk of erosions (Gabai et al. 1988).

Dietary lesions are now probably the most common form of extrinsically induced erosions, and the presence of erosions on the vestibular surfaces of the front teeth of the upper jaw (Fig. 1) should therefore prompt speculation that the erosions may be of dietary origin.

Exogenous risk factors Dental erosions are frequently of dietary origin and reflect the widespread consumption of acidic foods and drinks. Increased consumption of soft drinks or sports drinks or citrus fruits, for example, can be observed especially among athletes or health conscious patients.

Patients with eating disorders often also display altered dietary patterns (e.g. high consumption of light soft drinks, intake of vinegar).

The erosiveness of a drink or food depends on the frequency and type of consumption (e.g. drinking habits such as sipping, sucking through a straw, intraoral flushing with the drink) (Zero & Lussi 2006). The erosive potential is also co-determined by the pH, content of titratable acid, and by the buffer capacity and mineral concentration of the agent (Lussi & Jaeggi 2006).

Fig. 1: Vestibular erosions of the front teeth of the upper jaw caused by extrinsic acid exposure

Endogenous risk factors

In addition to the dietary risk factors, acidic medications such as acetyl salicylic acid or vitamin C can increase the risk of dental erosions, especially if they are taken regularly and in the form of chewable tablets (Hellwig & Lussi 2006; Hannig & Albers 1993).

Endogenous erosions are induced by the frequent presence of gastric acid or acidic gastric contents in the oral cavity and are therefore observed especially in patients with bulimia or anorexia nervosa, alcohol abuse or reflux diseases (Bartlett 2006).

The formerly relatively common occupational erosions have now become a rarity, not least because of the introduction of suitable occupational safety measures. Various studies have shown, however, that – especially in the absence of such safety precautions – certain industrial workers (e.g. in munitions factories or metal plating works) are at increased risk of suffering erosions since they are exposed to increased levels of acids or acidic vapours (Wiegand & Attin 2007).

Professional wine testers, who are required to carry out wine tasting over prolonged periods, are also at an increased risk of developing dental erosions (Chikte et al. 2005).

The prevalence of eating disorders is reported as 0.5 – 3 %, with young women aged between 15 and 25 years being mainly affected. The chronic vomiting leads to erosions of the occlusal and oral tooth surfaces.

Various studies have shown that this patient population has a significantly higher incidence of non-carious dental hard substance defects (Robb et al. 1991; Milosevic & Slade 1989). Patients with eating disorders often also have oligosialia as a consequence of the general dehydration secondary to weight loss or as a side effect of psychotropic medications and which promotes the formation of erosions (see “Modifying host factors”) (Imfeld & Imfeld 2005).

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New Concepts in Caries and Erosion

Chronic alcohol abuse is also associated with frequent vomiting and can cause gastroesophageal reflux, thereby increasing the risk of developing erosive defects. Robb & Smith (1990) and Hede (1996) observed an increased prevalence of dental erosions in alcohol-dependent patients compared to healthy controls.

While eating disorders and alcohol abuse are generally observed in adolescents and/or adults, reflux diseases may already develop during childhood and give rise to erosions (Fig. 2) (Ersin et al. 2006).

Fig. 2: Erosions on deciduous teeth

Reflux-induced erosions often remain unnoticed for long periods and the patient only becomes aware of their presence when troubled by painful hypersensitivities. The severity of the reflux disease appears to correlate with the extent of the erosion (Moazzez et al. 2004; Meurman et al. 1996).

As regards the endogenously induced erosions, it should be considered that the dentist is often the first person who is in a position to make a tentative diagnosis based on the clinical presentation (erosions in palatine/lingual and occlusal localisations, Fig. 3) and should therefore, when appropriate, arrange for a further general medical diagnostic evaluation.

Modifying host factors The development of erosions is determined not only by the type, incidence and frequency of exposure to acid, but also by various modifying host factors. A particularly important role in this respect is played by the saliva. During attack by acid, the saliva exerts a protective effect on the tooth in the form of the pellicle and by diluting and neutralising the acid. After the acid attack, the saliva has a repair potential by providing minerals for incorporation in the demineralised surface (Hara et al. 2006). Various medical conditions (diseases of the salivary glands, head and neck radiotherapy, Sjögren’s syndrome, diabetes mellitus, chronic renal insufficiency) and adverse effects of certain medications (psychotropics, anticholinergics, antihistamines, antiemetics, antiparkinson drugs, drug abuse) (Tredwin et al. 2005) are associated with a reduction in salivary secretion and thus contribute to an increased risk of erosion.

Erosive loss of dental hard substance is accompanied by softening of the tooth surface, which results in decreased resistance to mechanical influences (Attin et al. 1997). Erosively demineralised enamel and dentine surfaces can then be damaged further by abrasive stimulation (e.g. brushing the teeth, mastication of food).

Excessive brushing of the teeth immediately after contact with acid or the use of a highly abrasive toothpaste can thus promote the progression of the lesion.

Risk evaluation Early diagnostic evaluation of non-carious dental hard substance defects is necessary in order to initiate suitable prophylactic measures and prevent or postpone the need for invasive treatments (e.g. filling therapy). The dentist should therefore already be alert for the presence of erosions when recording the initial findings.

A detailed medical history should be taken first to analyse potential risk factors (Table below). During this session, the patient may also be asked to complete a ‘nutrition diary’ with the aim of identifying potentially erosive foods and beverages.

The occurrence of erosions, whose clinical localisation (palatine/lingual) suggests the presence of a gastrointestinal disorder or an eating disorder requires etiological evaluation under general medical or psychological management. The function of the salivary glands should also be checked by performing a saliva test in which not only the salivary flow rate and pH but also the buffer capacity are determined.

Finally, it is recommended to document existing defects (erosion index, photographs and/or models), to allow follow-up of possible progression of the lesions.

Fig. 3: Endogenously induced erosions in the upper jaw

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New Concepts in Caries and Erosion

Diet

Incidence and frequency of consumption of erosive drinks (fruit juices, soft drinks, sports drinks, alcopops) and foods (citrus fruits, pickled gherkins, sweets, salad dressing), possibly a nutrition diary

General diseases

Gastrointestinal disorders (reflux) Eating disorders Alcohol abuse Diseases affecting salivary gland function Diseases of the salivary glands Head and neck radiotherapy Sjögren’s syndrome Diabetes mellitus Chronic renal insufficiency

Medication

Acidic medications (acetylsalicylic acid, vitamin C) Reduction of salivary secretion as a side effect of – Psychotropics – Anticholinergics – Antihistamines – Antiemetics – Antiparkinson drugs – Drug abuse

Behaviour / Environment

Occupational exposure to acid Sport (swimming pool, increased consumption of erosive sports drinks)

Medical history factors for evaluation of erosive defects Dr. Annette Wiegand Klinik für Präventivzahnmedizin, Parodontologie und Kariologie · Universität Zürich Plattenstraße 11 · 8032 Zürich · Switzerland

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New Concepts in Caries and Erosion

New Possibilities in the Treatment of Sensitive Hypomineralised Molars in Children Dr. Lene Esmark and Dr. PhD Tanja S. Borch (Colgate-Palmolive A/S)

Introduction Permanent first molars with disturbances in enamel mineralisation of unknown aetiology were first described by Swedish dentists in the 1970s. In 2001 the condition was defined and given the title molar incisor hypomineralisation (MIH). MIH is defined as a hypomineralisation of systemic origin of the permanent first molars and incisors (Weerheijm et al. 2001). One or more molars can be affected as well as permanent incisors. The more teeth that are affected the greater the risk of a more severe expression of the condition. In addition, it has been shown that half of the children with MIH-affected molars also show clinical signs of MIH on their incisors (Jälevik et al. 2001).

The MIH-affected teeth are distinguished clinically on sight by their white, beige or dark yellowish-brown opaque areas. These opaque areas are less translucent than healthy enamel. In some teeth, the enamel is so poorly mineralised that a breakdown of affected areas is seen shortly after eruption as a result of to occlusal load. This is known as post-eruptive breakdown (Weerheijm 2003).

MIH can cause a number of problems for affected children. The most common complications are caries and dentine hypersensitivity (DHS). The latter causes inadequate oral hygiene because of the discomfort suffered during brushing – therefore increasing the risk of caries. Teeth affected by MIH can be treated in a number of ways – including high-fluoride solutions and fillings – but often with limited success.

In 2009, Colgate launched Colgate ® Sensitive ProRelief™ (CSPR) based on the Pro-Argin™ technology for the treatment of dentine hypersensitivity caused by open dentine tubules. Pro-Argin™ is a patented formula consisting of 8 % arginine and insoluble calcium carbonate, that plugs and seals open dentine tubules with a calcium-rich mineral layer and thereby prevents the transmission of pain-provoking stimuli to the dental nerve (Petrou et al. 2009). The system consists of two products: Colgate ® Sensitive Pro-Relief™ Desensitising Polishing Paste and Colgate ® Sensitive Pro-Relief™ Toothpaste. Both products offer immediate and longlasting relief from dentine hypersensitivity.

Several Danish dentists and dental hygienists have treated children who suffer from severe sensitivity due to MIH with CSPR polishing paste with positive results.

Colgate-Palmolive A/S therefore asked the head of Frederiksberg’s paediatric dental service, Copenhagen area, Lene Esmark, to collect the experiences of dentists who have used Pro-Argin™ technology in the treatment of hypomineralised teeth. The purpose of this article is therefore to pass on this experience.

Materials and methods

Tooth 46 affected by MIH. Photo courtesy: Kirsten Marquard

The prevalence of MIH varies from a few per cent in China to almost 40 % in Denmark and Brazil (Wogelius et al. 2008; Soviero et al. 2009; Jälevik 2010). The etiology of MIH remains unknown, but several different factors have been proposed and examined. Recently, a research team from Sweden examined 17,000 children born between 1997 and 1999 in the South Eastern part of Sweden, as part of the ABIS project (All Babies In South East Sweden). The project showed that nutritional factors during the first six months of a baby’s life are important in establishing an individual’s risk of developing MIH (Fagrell et al. 2011).

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Three dentists from Frederiksberg’s paediatric dental service, Copenhagen area, were invited by ColgatePalmolive A/S to share their experiences of treating children with hypomineralised teeth with Colgate ® Sensitive Pro-Relief™ Desensitising Polishing Paste.

The three dentists were asked to grade the teeth according to the FDI-moderated score for hypomineralised teeth (Table 1) and whether the teeth were sensitive upon tooth brushing, eating and drinking.

FDI moderated score 0

Normal enamel

1

Hypomineralised enamel WITHOUT loss of tooth substance

2

Hypomineralised enamel WITH loss of tooth substance end exposed dentin

Table 1: FDI World Dental Federation scores for hypomineralised teeth

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New Concepts in Caries and Erosion

The degree of hypersensitivity can be measured in various ways. The method used here is known as the Schiff Cold Air Sensitivity scale, where a cold air blast on the sensitive area is used to determine the degree of sensitivity before and after treatment (Schiff et al. 1994) (see Table 2).

Schiff Cold Air Sensitivity scale 0

Subject does not respond to air stimulus

1

Subject responds to air stimulus, but does not request discontinuation of stimulus

2

Subject responds to air stimulus and requests discontinuation, or moves from stimulus

3

Subject responds to air stimulus, considers stimulus to be painful, and requests discontinuation of the stimulus

Table 2: Schiff Cold Air Sensitivity scale

The dentists applied Colgate ® Sensitive Pro-Relief™ Desensitising Polishing Paste using a rubber polishing cup, at low speed, for at least three seconds. After application on the relevant teeth, the procedure was repeated (in line with manufacturer’s instructions). After the treatment, the degree of sensitivity was registered using the Schiff Cold Air Sensitivity scale. The above procedure was repeated after one week. The third visit acted as a control four weeks after the second visit.

No treatment took place but sensitivity was measured using the Schiff Cold Air Sensitivity scale.

Children were encouraged to use Colgate ® Sensitive Pro-Relief™ Toothpaste between the visits.

Results Altogether the dentists treated 6 children (4 boys, 2 girls) with Colgate ® Sensitive Pro-Relief™ Desensitising Polishing Paste. The children were between 5 and 11 years old (average: 7.7 years). A total of 15 teeth were diagnosed as being affected by MIH – an average of 2.5 teeth per child. The average FDI moderated score was 1.8. of the 6 children, 5 had previously received other kinds of treatment, without success, for dentine hypersensitivity related to MIH. The other trial treatments included composite fillings, glass ionomer fillings, fissure sealants and Duraphat™ Varnish.

Before the treatment with Colgate ® Sensitive ProRelief™ Desensitising Polishing Paste, all children reported hypersensitivity problems when eating and drinking. Half of them experienced hypersensitivity during tooth brushing.

Two children gained only a small benefit from the treatment (patients 2 and 5). Four patients reported significant benefits from the treatment (patients 1, 3, 4 and 6) and one remarked, that he was no longer bothered by hypersensitivity, even though this cannot be established from the results (patient 2) (see Fig. 1).

Schiff Scores before and after treatment

Schiff Score

3 2,5

Patient 1

2

Patient 2

1,5

Patient 3

1

Patient 4 Patient 5

0,5

Patient 6

0 1. Before treatment

1. After treatment

2. Before treatment

2. After treatment

3. Control

Figure 1: Average Schiff Scores for each of the children before and after treatment with Colgate® Sensitive Pro-Relief™ Desensitising Polishing Paste (visits 1 and 2) and a control visit four weeks after the second visit.

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The effect of the treatment with Colgate ® Sensitive Pro-Relief™ Polishing Paste was difficult to establish since the children in some cases refused repeated air blast examination after treatment. As a result, there are missing results from the first visit for two children (patients 4 and 6) and two patients at the control visit (patients 4 and 5).

Discussion In this article we have presented six patients treated with Colgate ® Sensitive Pro-Relief™ Desensitising Polishing Paste in an attempt to relieve the symptoms of hypersensitivity in teeth affected by MIH. In most of the cases, previous attempts at treatment had been met with limited success.

The effect of treatment with Colgate ® Sensitive ProRelief™ Desensitising Polishing Paste varied. Some experienced significant pain relief, whilst others experienced little, or no, effect.

Classification of results was difficult because most children were reluctant to undergo procedures that cause pain, such as the Schiff Cold Air Sensitivity scale.

It was especially difficult to obtain cooperation from the youngest children.

Research has shown that children with MIH receive ten times more dental treatment than a group of children with clinically healthy first molars. It has also been shown that multiple treatment sessions increase the risk of dental fear and anxiety (Jälevik & Klingberg 2002).

This knowledge, taken together with the increased caries risk, underlines the importance of finding the most effective and least painful treatment for teeth affected by MIH.

Conclusion Based on the present experience with Colgate ® Sensitive Pro-Relief™ Desensitising Polishing Paste, it seems reasonable to recommend Colgate ® Sensitive Pro-Relief™ Desensitising Polishing Paste for the inoffice treatment of hypersensitive teeth affected by MIH. Since the treatment is gentle and the application is associated with less discomfort for the child compared with traditional treatments, it can be recommended as a first choice treatment when the primary focus is sensitivity.

Acknowledgement Colgate-Palmolive A/S wishes to thank former head of Frederiksberg’s paediatric dental service for children on Frederiksberg, Copenhagen area, Lene Esmark for coordinating this project and to dentists Mikaela Hagen, Kirsten Marquard and Christina Thibodeau for their passing on their experiences.

About Lene Esmark: Having graduated as a dentist in 1968 from the Dental School in Copenhagen, Lene Esmark has worked intensively in paediatric dentistry through her entire career. She is a member of the European Academy of Paediatric Dentistry (EAPD) and has, since 1973, held several positions at executive level in the Danish children’s dental care service – the last 16 years as head of Frederiksberg’s paediatric dental service, Copenhagen this covers 17,000 children and 11 clinics. Lene Esmark is a regular lecturer and examiner of dental and dental hygienist students in Denmark.

Treatment with Colgate ® Sensitive Pro-Relief™ Desensitising Polishing Paste can be carried out without air-drying, etching or other pain-provoking procedures prior to the application. Colgate ® Sensitive Pro-Relief™ Toothpaste contains the same active ingredients as the polishing paste (8 % arginine and insoluble calcium carbonate) and therefore it allows for the treatment to be repeated at home, should the hypersensitivity return.

The procedure for obtaining immediate relief by using the toothpaste is to massage a pea-sized amount on the sensitive area for one minute with a fingertip. The active ingredient, arginine, is an amino acid and a natural component of saliva and thus this treatment represents one of the mildest effective interventions against hypersensitivity.

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New Concepts in Caries and Erosion

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