Journa C A L I F O R N I A
D E N TA L
May 2022 Allergic Manifestations Informed Consent in Older Adults Glycemic Index Management
A S S O C I AT I O N
WHEN SUGAR IS NOT SO SWEET
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Vol 50
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C D A J O U R N A L , V O L 5 0 , Nº 5
d e pa r t m e n t s
237 Associate Editor/Empowering Ourselves and Others 241 Impressions 292 RM Matters/Invest in Interviewing To Reduce Risk of Bad Hires
297 Regulatory Compliance/Cal/OSHA Citations of Dental Practices
299 Tech Trends
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245 Allergic Manifestations in the Oral Cavity This article aims to enumerate various types of hypersensitivity reactions based on algorithmic approach. Usha Dayanarayana, MDS; Shilpa Padar Shastry, MDS; Chetan Shankar, MDS; Naveen Kumar N, MDS; Rama Murthy TK, MDS; and Mahesh BS, MDS C.E. Credit
257 Informed Consent in the Older Adult Population: A Mixed-Methods Study This pilot study investigates how to adequately inform older patients and to secure their informed consent for dental implant treatment as well as to gather information on their perceptions of dentistry. Katherine Lambert, BS; Grace Yasewicz, BS; Garrett Finney, BS; Thomas Meuser, PhD; Regula Robnett, PhD; and Yang Kang, DDM, PhD
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Management of the Glycemic Index Through Periodontal Management With Pharmacological Agents This review focuses on current literature exploring the management of periodontitis through pharmacological agents and nonsurgical treatment to regulate the glycemic index in Type 2 diabetes mellitus patients. Christian Pretto, DDS; Joshua Tordjman, DDS; and Aviv Ouanounou, BSc, MSc, DDS
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When Sugar Is Not So Sweet This toolkit is a brief guide that includes simple visuals and messages dental providers can use to talk with patients about reducing and eliminating sugar-sweetened beverage (SSB) consumption to reduce dental decay and other associated chronic diseases. The California Department of Public Health, Office of Oral Health
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D E N TA L
Volume 50 Number 5 May 2022
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Journal of the California Dental Association Editorial Board Charles N. Bertolami, DDS, DMedSc, Herman Robert Fox dean, NYU College of Dentistry, New York Steven W. Friedrichsen, DDS, professor and dean, Western University of Health Sciences College of Dental Medicine, Pomona, Calif. Mina Habibian, DMD, MSc, PhD, associate professor of clinical dentistry, Herman Ostrow School of Dentistry of USC, Los Angeles Robert Handysides, DDS, dean and associate professor, department of endodontics, Loma Linda University School of Dentistry, Loma Linda, Calif. Bradley Henson, DDS, PhD , associate dean for research and biomedical sciences and associate professor, Western University of Health Sciences College of Dental Medicine, Pomona, Calif. Paul Krebsbach, DDS, PhD, dean and professor, section of periodontics, University of California, Los Angeles, School of Dentistry Jayanth Kumar, DDS, MPH, state dental director, Sacramento, Calif. Lucinda J. Lyon, BSDH, DDS, EdD, associate dean, oral health education, University of the Pacific, Arthur A. Dugoni School of Dentistry, San Francisco Nader A. Nadershahi, DDS, MBA, EdD, dean, University of the Pacific, Arthur A. Dugoni School of Dentistry, San Francisco Francisco Ramos-Gomez, DDS, MS, MPH, professor, section of pediatric dentistry and director, UCLA Center for Children’s Oral Health, University of California, Los Angeles, School of Dentistry Michael Reddy, DMD, DMSc, dean, University of California, San Francisco, School of Dentistry
The Journal of the California Dental Association is published under the supervision of CDA’s editorial staff. Neither the editorial staff, the editor, nor the association are responsible for any expression of opinion or statement of fact, all of which are published solely on the authority of the author whose name is indicated. The association reserves the right to illustrate, reduce, revise or reject any manuscript submitted. Articles are considered for publication on condition that they are contributed solely to the Journal of the California Dental Association. The association does not assume liability for the content of advertisements, nor do advertisements constitute endorsement or approval of advertised products or services.
Avishai Sadan, DMD, dean, Herman Ostrow School of Dentistry of USC, Los Angeles
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Harold Slavkin, DDS, dean and professor emeritus, division of biomedical sciences, Center for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry of USC, Los Angeles
Assoc. Editor
C D A J O U R N A L , V O L 5 0 , Nº 5
Empowering Ourselves and Others Marisa Kawata Watanabe, DDS, MS
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istory, law, music, economics, business administration, and then there was me — molecular and cell biology. I grew up surrounded not by dentistry, discussions about navigating that crafty MB2 or spending time in the dental office, but instead found myself helping with paralegal activities in a law office, playing sports and volunteering in the community. Like some (or maybe a few) of you, beyond dental visits, my exposure to the dental field was limited up until college. It was at University of California, Berkeley, where my civic and social responsibilities collided, where I learned about health disparities and inequities among populations and communities and discovered that dentistry expands beyond private practice delivery systems. The notion of social responsibility has long been considered economic and professional obligations in dentistry. Without searching the phrase in a web browser, or dare I say, opening an actual dictionary, we can infer by separating each word that there is an innate responsibility we take on toward all society once we receive our diploma and are called “doctor.” The recently published 2021 U.S. surgeon general report entitled “Oral Health in America: Advances and Challenges” noted that despite over 20 years since the last U.S. surgeon general’s report in 2000, data currently reflect that the number of health disparities, especially among low socioeconomic populations, has continued through the present day.1 Furthermore, the 2021 U.S. surgeon general report documented that Americans living in chronic poverty,
I believe that as oral health providers, we can incorporate both civic and social responsibilities into our profession.
including populations from specific racial and ethnic minority groups, continue to show the greatest burden of disease.1 I found myself wondering, what are ways to further support system-level changes, inspire the future workforce, work collaboratively with our private and community providers as well as educational institutions and advocate for health equity? National, state and local frameworks have provided clear goals and objectives, so why has the level of health disparities remained similar to 20 years ago,1 and how do we push the needle beyond equality toward equity and, eventually, justice for all people? The 2021 U.S. surgeon general report made a call to action loud and clear, focusing on policy changes addressing social, economic and other systemic inequities, interprofessional collaborative practice among all health care professionals and increasing diversity of the future dental workforce while reassessing dental student loan debt for the next generation of oral health providers.1 With approximately 65 million people in the U.S. currently residing across 6,837 dental Health Professional Shortage Areas (dental HPSAs), an additional 11,320 oral health providers are needed to fulfill the lack of oral health care in these dental HPSAs.2 In California alone, 501 dental HPSAs
exist, the largest number of all 50 states.2 By marrying both federal and state incentivization programs, future and current dentists can apply for scholarships and grants that not only help to navigate and incentivize providers to work in dental HPSAs or practices accepting Medicaid dental, but also support reducing student indebtedness. But as a practitioner or a graduating dental student interested in pursuing one of these scholarships and grants, where can one turn to for a centralized scholarship/grant bank? Currently, social media, publications and word of mouth are the main sources of information dissemination and navigating the search process can be daunting. Fortunately, both the California Dental Association3 and the American Dental Education Association4 list opportunities such as the state California Department of Health Care Services CalHealthCares loan repayment program and the federal National Health Scholarship Corps loan repayment program for interested practitioners. These opportunities can be found via a simple search engine keyword query. With almost all dental students graduating with educational debt and current dentists still holding student loans, programs and scholarships to explore and address student loans will M AY 2 0 2 2
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ASSOC . EDITOR C D A J O U R N A L , V O L 5 0 , Nº 5
also draw oral health providers to medically underserved communities. Beyond encouraging future and current dental providers to practice in medically underserved communities, local dentists and private practices have also supported addressing barriers caused by economic and social determinants in their own communities. Returning to the original question — how can private practice and community health centers work collaboratively? — the Centers for Medicare and Medicaid Services developed one method through a federal regulation in 2011 that allows federally qualified health centers (FQHCs) to contract with private dental offices for referred delivery of oral health care services.1 Also at the federal level, the Health Resources and Services Administration continues to award infrastructure grant dollars to FQHCs to expand or enhance their current oral health services, including collaborative partnerships with private practices.1 By working in partnership and pooling resources, FQHCs have been able to increase their oral health capacity through the infrastructure expansion and together increase accessibility to dental services in and around surrounding communities.1 In addition to establishing formalized partnerships, private and community practitioners have also joined together for community events, including offering space to host one-day or weekend health day events and volunteering at events such as CDA Cares. The Healthy People 2030 objectives highlighting oral health needs as one of the disparate health conditions require the participation and support of entities outside of the oral health profession. Legislators, community and dental organizations, public health departments, promotoras, educational institutions and, most
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importantly, the community along with health care professionals must create a symbiotic relationship to achieve oral health equity. By bridging the gap between primary care and oral health providers, we can further address other areas of systemic health such as obesity, diabetes and other health conditions listed in Healthy People 2030.5 For example, FQHCs and private practices, in addition to oral health services, provide a bidirectional partnership with the FQHC providing a medical home for patients of the private practice who lack medical care due to being under- or uninsured. Interprofessional collaborative practice beyond interdisciplinary integration in the dental field to build relationships between community and private practitioners will further support the 2021 U.S. surgeon general report’s call to action. Though my exposure to dentistry may have been limited during my growing years, my family introduced philanthropic work and service early on. As a member of a local Optimist Club, from age 5 through high school, whose mission focuses on promoting “an active interest in community affairs, to work for fellowship among all people and to aid and encourage the development of youth,” I believe that as oral health providers, we can incorporate both civic and social responsibilities into our profession. By doing so, not only will we encourage a dental workforce to explore and consider providing service in medically underserved communities, but we will also play a pivotal role in improving the health of our local communities, state and nation. There were gains since the 2000 U.S. surgeon general report, such as implementation of creative programs, data collections and developments. But most importantly, the impact seen 20 years later is that far more sustainable work needs to be done to address the health disparities and
inequities that exist.1 I encourage all dental professionals to take an opportunity to volunteer, mentor a predental or dental student or a new grad and explore different delivery systems that increase access to care and foster oral and overall health equity for all. n RE F E RE N C E S 1. U.S. Department of Health and Human Services, National Institutes of Health, National Institute of Dental and Craniofacial Research. Oral Health in America: Advances and Challenges. 2. U.S. Department of Health and Human Services, HRSA Data Warehouse; 2022. Shortage Areas as of March 1, 2022. Accessed March 1, 2022. 3. California Dental Association. Student Loan Repayment Grant. Accessed March 1, 2022. 4. American Dental Education Association. State and Federal Loan Forgiveness Programs as of 2019. Accessed March 1, 2022. 5. U.S. Department of Health and Human Services, Office of Disease Prevention and Health Promotion. Oral Conditions as of Nov. 4, 2021. Accessed March 1, 2022.
Marisa Kawata Watanabe, DDS, MS, is a professor and associate dean for community partnerships and access to care at the Western University of Health Sciences, College of Dental Medicine. She currently serves on the board of the Medicaid|Medicare|CHIP Services Dental Association as the academic director and is the chair of the Los Angeles County Department, Oral Health Program Community Oral Health Improvement Plan, Workforce Development and Capacity Workgroup.
C D A J O U R N A L , V O L 5 0 , Nº 4
The Journal welcomes letters We reserve the right to edit all communications. Letters should discuss an item published in the Journal within the last two months or matters of general interest to our readership. Letters must be no more than 500 words and cite no more than five references. No illustrations will be accepted. Letters should be submitted at editorialmanager.com/ jcaldentassoc. By sending the letter, the author certifies that neither the letter nor one with substantially similar content under the writer’s authorship has been published or is being considered for publication elsewhere, and the author acknowledges and agrees that the letter and all rights with regard to the letter become the property of CDA.
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C D A J O U R N A L , V O L 5 0 , Nº 5
Less Antibiotic Use in Dentistry Did Not Increase Endocarditis Sweden is one of the few countries that has removed the dental health recommendation to give prophylactic antibiotics to people at a higher risk of infection of infective endocarditis (IE). Since the recommendation was removed in 2012, there has been no increase in this disease, according to a registry study from Karolinska Institutet published in the journal Clinical Infectious Diseases. IE is a rare but life-threatening disease caused by bacterial infection of the heart valves that affects some 500 people a year in Sweden. Individuals with congenital heart disease, prosthetic heart valves or previous endocarditis are at higher risk of infection. The registry study encompassed 76,762 high-risk individuals and 396,048 individuals at a low risk of infective endocarditis, who were monitored from 2008 to 2018 with the help of the Medical Birth Registry, the National Patient Register and the Swedish Endocarditis Registry. Cox proportional hazard models were performed to calculate adjusted ratios of oral streptococcal IE before and after October 2012 between high-risk individuals and references. The study found no increased incidence of oral streptococcal IE among high-risk individuals during the five years after the cessation, compared with before. Hazard rate ratios were 15.4 before and 20.7 after October 2012 for prevalent highrisk individuals. Corresponding ratios for incident high-risk individuals were 66.8 and 44.6. Point estimates for interaction with time period were 1.4 and 0.8 for prevalent and incident high-risk individuals, respectively. “We can only see small, statistically nonsignificant variations in morbidity, nothing that indicates a rise in this infection in the risk group since 2012,” said the study’s corresponding author Niko Vähäsarja, MDS, a dentist and doctoral student in the department of dental medicine at Karolinska Institutet. “Our study therefore supports the change in recommendation.” The recommendation was supplemented in 2016 with an instruction to consider prophylactic antibiotic treatment if prescribed by the patient’s doctor. It is unclear how this addition has influenced the prescription of antibiotics by dentists. After the change in recommendation in 2012, prescriptions of amoxicillin in dentistry declined by approximately 40%. However, the study is unable to demonstrate that this was an effect of the amended recommendation, as amoxicillin has other uses in dental medicine. “The next step is to examine which dental procedures the individuals in the risk group underwent during the 2008-2018 period, since this is information we lack and it could add to our knowledge of what is to date a poorly studied issue,” said Dr. Vähäsarja. “This and the study we’ve just published could inform similar recommendation changes in other countries, resulting in a reduction in antibiotic use.” n
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IMPRESSIONS C D A J O U R N A L , V O L 5 0 , Nº 5
New Dental Tool Prototype Spots Acidic Conditions of Teeth Von Mises stress plots for mean inclinations at both bruxing positions at the most lateral position (t = 0.25) during laterotrusive bruxing to the left side; axes orientations shown for first row are the same for all subsequent rows. (Credit: Sagl B, et al. Licensed under Creative Commons CC BY-NC 4.0.)
Nocturnal Bruxism Can Damage Temporomandibular Joints A study conducted at the University Clinic of Dentistry of the Medical University of Vienna and led by Benedikt Sagl, PhD, found that certain tooth shapes and tooth locations could lead to temporomandibular joint problems as a result of bruxism. The research findings were recently published in the Journal of Advanced Research. The research was based on the theory that specific combinations of tooth shape and tooth location during grinding have an influence on the mechanical load on the temporomandibular joint and can thus be considered a risk factor for TMJ disorders. The studies were performed using a state-of-the-art computer model of the masticatory region, which examined the interaction of two factors that coincide in bruxism. The first factor is the shape of the affected tooth, more precisely the angle of inclination of the dental cusp that is in contact with its opposite number during grinding. The second factor is the location of the wear facet during a dynamic grinding motion. The study simulated the effects of lateral grinding on the first molar and on the canine with six different wear-facet inclinations, resulting in a total of 12 simulated scenarios. 242
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A new study by University of Washington researchers has shown that a dental tool they created can measure the acidity built up by the bacteria in plaque that leads to cavities. The study was published in February in IEEE Transactions on Biomedical Engineering. The O-pH system is a prototype optical device that emits an LED light and measures the reactions of that light, the fluorescence, with an FDA-approved chemical dye applied to teeth. The O-pH then produces a numerical reading of the pH, or acidity, of the plaque covering those teeth. Knowing how acidic the plaque is can tell dentists and patients what area of a tooth is most at risk of developing a cavity. To test their device, the researchers recruited 30 patients between the ages of 10 and 18, with a median age of 15, in the UW School of Dentistry’s Center for Pediatric Dentistry. The test is noninvasive. While the dye is applied to the teeth, a probe at the end of a length of cord transmits and collects light while hovering over the surface of a tooth. The collected light travels back to a central box that provides a pH reading. The conditions on the patients’ teeth were read several times before and after sugar rinses and other condition changes, such as pre- and post-professional dental cleaning. The research team reported that one limitation to their study was being unable to consistently measure the same location on each tooth during each phase of testing. To address this limitation, in particular, the researchers are evolving their device to a version that produces images for dentists that instantly show the exact location of high acidity, where the next cavity may occur. O-pH in operation at a dental clinic. Inset figure shows a closer look of the device inside the mouth. The tip of the probe used to transmit and collect light is hovering over the occlusal surface of the subject. (Credit: University of Washington and IEEE Xplore/Creative Commons.)
“Our results show that both the inclination and location of the wear facets have an influence on the strength of the mechanical load on the temporomandibular joint. However, it would appear that the decisive factor is the steepness of the grinding facet,” Dr. Sagl said. “The flatter the tooth, the higher the loading on the joint and therefore the higher the risk of a TMJ disorder.” Conversely, if the dental
cusps involved in bruxism have a steeper angle of inclination, the calculated joint loading was lower, even with the same bruxing force. Further research will now be conducted, coupled with clinical investigations, to establish whether this finding can be incorporated into the development of therapeutic interventions for sleep bruxism.
C D A J O U R N A L , V O L 5 0 , Nº 5
Study Reveals How Vaping Alters Oral Health A series of new studies by researchers at the NYU College of Dentistry highlights how e-cigarettes alter oral health and may be contributing to gum disease. The latest study, published in mBio, finds that e-cigarette users have a unique oral microbiome that is less healthy than nonsmokers but potentially healthier than cigarette smokers. The study measures
worsening gum disease over time. The researchers studied the oral health of 84 adults from three groups: cigarette smokers, e-cigarette users and people who have never smoked. Gum disease was assessed through two dental exams six months apart, during which plaque samples were taken to analyze the bacteria present. All participants had some gum disease at
Some Oral Bacteria Linked With Hypertension in Older Women Some oral bacteria were associated with the development of hypertension in postmenopausal women, according to the Buffalo Osteoporosis and Periodontal Disease Study published in the Journal of the American Heart Association. Researchers evaluated data for 1,215 postmenopausal women (average age 63 at study enrollment, between 1997 and 2001) in the Buffalo Osteoporosis and Periodontal Disease Study in Buffalo, New York. At study enrollment, researchers recorded blood pressure and collected oral plaque from below the gumline. They also noted medication use and medical and lifestyle histories to assess if there is a link between oral bacteria and hypertension in older women. At study enrollment, about 35% (429) of the study participants had normal blood pressure readings below 120/80 mm Hg, with no use of blood pressure medication. Nearly 24% (306) of participants had elevated blood pressure readings above 120/80 mm Hg with no medication use. About 40% (480) of participants were categorized as having prevalent treated hypertension. Researchers identified 245 unique strains of bacteria in the plaque samples. Nearly one-third of the women who did not have hypertension or were not being treated for hypertension at the beginning of the study were diagnosed with high blood pressure during the follow-up period, which was an average of 10 years. The analysis found 10 bacteria were associated with a 10% to 16% higher risk of developing high blood pressure. Five other kinds of bacteria were associated with a 9% to 18% lower hypertension risk. These results were consistent even after considering demographic, clinical and lifestyle factors also influence the development of high blood pressure.
the start of the study, with cigarette smokers having the most severe disease, followed by e-cigarette users. After six months, the researchers observed that gum disease had worsened in some participants in each group, including several e-cigarette users. Additionally, in a study of the same participants published in Frontiers in Oral Health, the research team found that clinical attachment loss was significantly worse only in the e-cigarette smokers, not nonsmokers and cigarette smokers, after six months. The researchers then analyzed the bacteria found in the plaque samples and determined that e-cigarette users have a different oral microbiome from smokers and nonsmokers. While all groups shared roughly a fifth of the types of bacteria, the bacterial makeup for e-cigarette users had strikingly more in common with cigarette smokers than nonsmokers. Several types of bacteria, including Selenomonas, Leptotrichia and Saccharibacteria, were abundant in both smokers and vapers compared to nonsmokers. Several other bacteria, including Fusobacterium and Bacteroidales, were particularly dominant in the mouths of e-cigarette users. When plaque samples were gathered and analyzed in the six-month followup, the researchers found greater diversity in bacteria for all groups studied, yet each group maintained its own distinct microbiome.
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IT’S A VERB.
oral allergic reactions C D A J O U R N A L , V O L 5 0 , Nº 4
Allergic Manifestations in the Oral Cavity Usha Dayanarayana, MDS; Shilpa Padar Shastry, MDS; Chetan Shankar, MDS; Naveen Kumar N, MDS; Rama Murthy TK, MDS; and Mahesh BS, MDS
abstract Background: Allergic reactions in the oral cavity can be triggered by a wide range of common allergens, dental materials and medications that can cause oral and systemic clinical manifestations. Diverse symptoms and signs of allergic reactions in the oral cavity mimic other common diseases, making diagnosis difficult. Hence, early diagnosis and management are necessary to reduce the risk of serious complications. Types of articles reviewed: This review was performed by compiling information available from various popular search engines on the internet, in textbooks and in bibliographic databases such as Google Scholar, PubMed (Medline) and Scopus. Results: This article aims to enumerate various types of hypersensitivity reactions based on algorithmic approach. The duration, recurrent nature, morphology, location and systemic symptoms that are useful in evaluating etiology, signs and symptoms of allergic reactions in the oral cavity are discussed. Practical implications: In general, a detailed history of the patient’s diet, drugs and systemic features is essential for correct diagnosis and management of their condition. This review updates the dentist to understand and enhance their knowledge for better diagnosis and treatment. Keywords: Allergens, allergies, allergic reaction, oral manifestations, hypersensitivity reactions
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oral allergic reactions C D A J O U R N A L , V O L 5 0 , Nº 5
AUTHORS Usha Dayanarayana, MDS, is a senior lecturer in the department of oral medicine and radiology at the Vydehi Institute of Dental Sciences and Research Center in Bengaluru, India. Conflict of Interest Disclosure: None reported.
Naveen Kumar N, MDS, is a senior lecturer in the department of oral medicine and radiology at the Vydehi Institute of Dental Sciences and Research Center in Bengaluru, India. Conflict of Interest Disclosure: None reported.
Shilpa Padar Shastry, MDS, is a reader in the department of oral medicine and radiology at the Vydehi Institute of Dental Sciences and Research Center in Bengaluru, India. Conflict of Interest Disclosure: None reported.
Rama Murthy TK, MDS, is a professor and the head of the department of oral medicine and radiology at the Vydehi Institute of Dental Sciences and Research Center in Bengaluru, India. Conflict of Interest Disclosure: None reported.
Chetan Shankar, MDS, is a professor and the head of the department of orthodontics at the Vydehi Institute of Dental Sciences and Research Center in Bengaluru, India. Conflict of Interest Disclosure: None reported.
Mahesh BS, MDS, is a reader in the department of oral medicine and radiology at the Vydehi Institute of Dental Sciences and Research Center in Bengaluru, India. Conflict of Interest Disclosure: None reported.
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llergy is defined as a hypersensitive state acquired through exposure to a particular allergen. Reexposure to the allergen produces a heightened capacity for reaction.1 Contact with the allergen can be through the skin, the oral mucosa, the eyes, lung inhalation, swallowing or injecting. The phenomenon of allergy was discovered in 1906 by Clemens von Pirquet.2 The word allergy comes from the Greek words “allos” meaning other and “ergos” meaning work. The human oral mucosa is often subjected to a wide spectrum of foreign agents, including hot or cold foods, acidic or alkaline substances, spicy foods, drugs, microorganisms, cosmetics, metals in utensils, dental materials, toothpaste, tobacco and alcohol taken through the mouth. Allergic reactions to such agents can manifest in diverse ways. Allergic reactions are an inappropriate immune response to a normally harmless substance. The immune system, which includes antibodies, white blood cells, mast cells, complement proteins and other substances, normally defends the body against foreign substances called antigens. However, certain antigens (called allergens) can stimulate the immune system to exaggerate, which can cause harm in susceptible people. The result is an allergic reaction. Some people are allergic to only one substance while others are allergic to many. Incidence of allergic or hypersensitivity reaction is difficult to ascertain, as many allergic reactions go unreported. However, Tannol et al. (2018)3 suggested 15% of the world’s population will be affected by a type of allergic reaction during their lifetime. European data estimated that 0.3% of the population will be troubled by anaphylaxis at some point in their lives. In the U.S, 1 in 3,000 inpatients annually experience a severe allergic reaction. Worldwide epidemiological data of anaphylaxis are scant and remain unavailable in many countries.4
Additionally, articles with a compilation of allergic manifestations affecting the oral cavity are few. As dentists, we must be aware of different types of oral features of hypersensitivity reactions for timely diagnosis and management. Hence, this article aims to bring together different allergic manifestations of the oral cavity, their clinical expressions, types, oral manifestations, various allergens and management.
Methods of Literature Search
This review was performed by compiling information available from various search engines on the internet, in textbooks and in bibliographic databases such as Google Scholar, PubMed (Medline) and Scopus. We also analyzed the cross references of these articles and included them if necessary. The duration of included articles was from 1982 to 2021, and only those articles published in English were included for this review. Keywords used for the search were “allergy,” “hypersensitivity reactions,” “oral manifestation,” “dental materials,” “allergens” and combinations of these words. A total of 58 articles that fulfilled our criteria were included in this review
Classification
Based on the time required for a sensitized host to develop clinical reactions on reexposure to the antigen, hypersensitivity reactions are divided into two types: 1) immediate hypersensitivity reaction — B cell or antibody mediated (anaphylaxis, atopy, antibody-mediated cell damage, Arthus phenomenon, serum sickness) and 2) delayed hypersensitivity reaction — T cell-mediated (infection type, contact dermatitis type).5 Another classification followed for allergy and hypersensitivity is Coombs and Gell’s classification6 (TABLE 1). Common allergens and dental allergens are
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TABLE 1
Allergic Manifestations in the Oral Cavity (According to Coombs and Gell) Type I
Type II
Type III
Type IV
Synonyms
Immediate/anaphylactic
Cytotoxic or cell-stimulating
Immune complex or toxic complex disease
Delayed or cell-mediated hypersensitivity
Immunoglobulins involved
IgE
IgG/IgM
IgG/IgM
–
Cells involved
Mast cells or basophils
Host cell Neutrophils Complements T cells
Complement Neutrophils
T cells Macrophages
Pathogenesis
Following sensitization, crosslinking of antibodies by antigen occurs. This results in the degranulation of immune cells.
The host cell is considered as foreign, antibody binds to the target cell leading to complement activation and destruction of the cell.
Antigen-antibody immune complex activates complement system resulting in the attraction of neutrophils at the site.
Antigen-presenting cell activates T cell-mediated reactions.
Examples of allergic manifestations
Anaphylaxis Angioedema Food allergy Oral allergic syndrome True latex allergy
Autoimmune reactions like pemphigus
Serum sickness Arthus reaction Systemic lupus erythematosus
Lichenoid reaction Contact stomatitis Stomatitis cheilitis Perioral dermatitis Erythema multiforme Fixed drug eruption Allergic to dental material
TABLE 2
Common and Dental Allergens Causing Allergic Manifestations in the Oral Cavity Common allergens
Common dental allergens
Drugs, food products, plant pollens, insect stings, animal products, animal hairs, tobacco chewing, etc. Dental preparations
Dentifrices Oral hygiene products: toothpaste, mouthwashes and dental floss Denture powders
Dental materials
Rubber dam, latex gloves Vulcanite Acrylic Metal alloy base: nickel, chromium, cobalt, titanium, tantalum and niobium Dental amalgam Impression compound, coloring agents and preservatives
Dental therapeutic agents
Alcohol, iodides, phenols and volatile oil
listed in TABLE 2. A compilation of clinical/oral manifestations of allergic reactions affecting the oral cavity is cited in TABLE 3.
Anaphylaxis
Anaphylaxis is defined as “a serious allergic reaction that is rapid in onset and may cause death.”7 It is a severe immediate-type systemic
generalized hypersensitivity reaction affecting multiple organ systems that can lead to acute, life-threatening respiratory failure, bronchospasm, cyanosis, hypotension and shock. It is an immunoglobulin (IgE) mediated process that leads to mast cells and basophil activation resulting in the sudden release of a large amount of histamine and, later, leukotrienes,8
tumor necrosis factor and various cytokines leading to the allergic response. Most anaphylaxis is triggered by food (peanuts, tree nuts, shellfish and fish, cow’s milk, eggs and wheat), medications (most commonly penicillin and other antibiotics) or insect venoms.9 In children, food allergy is the most common cause and is responsible for about 80% of anaphylactic reactions; whereas in adults, it accounts for up to 20% to 30%10,11 of cases. Venom- and drug-induced anaphylaxis are more common in adults. The onset of anaphylaxis is a generalized systemic reaction involving at least two organ systems. Respiratory (obstruction) and cutaneous (urticaria, angioedema, erythema, pruritus), cutaneous and cardiovascular (hypotension, dizziness, syncope, tachycardia) or cutaneous and gastrointestinal (nausea, vomiting, abdominal pain, diarrhea). Signs and symptoms of anaphylaxis are unpredictable and may vary from patient to patient and from one reaction to another. M AY 2 0 2 2
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TABLE 3
Compilation of Clinical/Oral Manifestations of Allergic Reactions Affecting the Oral Cavity Allergic reactions/ types
Clinical/oral manifestations
Etiology
Locations
Angioedema Type I
Diffuse edematous swelling of soft tissues commonly involving the subcutaneous tissue and submucosal connective tissues due to vascular leakage. Usually seen in the perioral and periorbital areas.
Food, drugs, radiologic contrast media and latex gloves
Face, lips, chin, eyes, tongue, pharynx, larynx
Oral/pollen allergy syndrome
Contact allergic reaction that occurs upon contact of the mouth and throat with raw fruits or vegetables. Swelling and itchiness of the mouth, lips, tongue and soft palate.
Proteins found in some fruits, vegetables, nuts and spices and are very similar to those found in pollen lead to cross-reactivity.
Lips, mouth, face, tongue, throat
Reticular white patches, papules, plaques, erosions or ulceration; unilateral lesions related with a dental restoration; lesions resolve on withdrawal of the etiologic agent.
Dental materials, flavoring agents, drugs and tobacco chewing
Lesions restricted to the areas of contact with dental materials
Variety of signs and symptoms includes stomatitis, cheilitis, gingivitis, perioral dermatitis, burning mouth syndrome, lichenoid reaction and orofacial granulomatosis
Restorative materials, mercury-based products, nickel sulfate, cobalt chloride gold, zinc, bonding agents, composites, ethereal oils, silicone and polyester impression materials, oral hygiene products, flavoring agents
Inflammation of the entire oral mucosa, e.g. mouthwash toothpaste, drugs
Stomatitis cheilitis Type IV
Inflammation of lips erythema, burning sensation, swelling associated with pain to the formation of vesicles, fissures, sloughing, ulceration and crusting
Cosmetics products, flavoring agents, preservatives, mouthwashes, toothpaste
Lips
Recurrent aphthous stomatitis Type IV
Recurrent single or multiple, small, round or ovoid shallow ulcers with regular margins, having a yellow or gray base and surrounded by erythematous haloes noted in the oral cavity
Drugs, food, hormonal changes, stress, trauma, infections
Labial mucosa, buccal mucosa, floor of the mouth, lips, soft palate
Perioral dermatitis Type IV
Facial rash, inflammatory papules that tend to occur around the mouth
Multiple environmental exposures topical nasal steroids, toothpaste, flavoring agents, hormonal factors, cosmetic products
Perioral region
Erythema multiforme Type IV
Affect both the skin and mucous membranes. It presents as irregular oral ulcers with diffuse erythema and target lesions (flat round red dark circles with the purple-gray center) of the skin
Drugs, NSAIDS, penicillin, sulfonamides, barbiturates, infections, immunotherapy
Oral mucosa, genital mucosa, ocular mucosa, erosions or bullae encrustation seen on lips
Drugs, barbiturates, beta-blockers, dapsone, NSAIDs, phenazone derivatives, thiazide derivatives, phenolphthalein, sulphonamides, tetracyclines, antihistamine-levocetirizine
Labial mucosa, lips, hard palate, tongue
Type I Lichenoid reactions Type IV
Contact stomatitis Type IV
Fixed drug reactions The presentation can range from bullous Type IV to erosive, hyperpigmented, pruritic or erythematous lesions
Treatment
Acute treatment of anaphylaxis begins with a rapid assessment of the airway, breathing and circulation followed by the immediate administration of epinephrine. The recommended dose of epinephrine for 248
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Buccal mucosa lateral border of the tongue
anaphylaxis is 0.01 mg/kg body weight up to a maximum dose of 0.5 mg (0.5 ml) administered intramuscularly every five to 15 minutes as necessary.12,13 If resuscitation using intramuscular epinephrine is ineffective, intravenous epinephrine may be required. Oxygen
Localized lesions adjacent to dental restoration, orthodontic wires, dental prosthesis
therapy is recommended for those with prolonged reactions. Intravenous crystalloid solutions (IV fluids) volume replacement should be provided in massive fluid shifts, which occur rapidly in anaphylaxis leading to hypotension due to increased vascular permeability.
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TABLE 4
Clinical Details of Various Allergic Reactions Manifested in the Oral Cavity Age/Sex
History
Clinical Features
Treatment Given
Figure
26/M
Diffuse swelling of lower lip for three days; history of eating mushroom three days ago
Diffuse enlargement of right lower lip crossing midline, slightly tender, soft in consistency and overlying mucosa appeared stretched
Antihistamine for a week with avoidance of allergen in the future
Figure 1
41/M
Burning sensation in the left side of the mouth for three months
Red patch with whitish striae seen adjacent to mandibular left first molar tooth region with amalgam restoration in the same tooth.
Patient was prescribed topical corticosteroids and amalgam restoration replacement
Figure 2
45/M
History of tobacco placement in his right lower vestibule
near mandibular right canine, first and second premolar tooth region where quid placement; nontender and nonscrapable in nature
Patient was advised to quit the Figure 3 tobacco habit along with antioxidants
11/M
Ulcer in the right side of the mouth; history of similar ulcers elsewhere in the mouth which heals and recurs with the frequency of 2-3 ulcers in a month.
An ulcer was shallow oval, tender, with surrounding erythema present with respect to mandibular right deciduous first molar tooth region
Patient was symptomatically treated with topical anesthetics and multivitamins
50/M
Lesions on his lips and mouth. He gave a history of urinary tract infection, which was prescribed with antibiotics and diclofenac sodium.
Encrustation with erythematous erosions and epithelial tags was found with respect to the upper and lower lip; bleeding lesions were found with respect to the lower labial mucosa
Figure 5 He was symptomatically treated with topical anesthesia, topical corticosteroids and avoidance of the drug or removal of the offending drug
61/M
Complains of ill-fitting dentures
Diffuse multiple pinpoint erythema found on the palate confined to denture-bearing region
Patient was prescribed antifungal medication and refabrication of denture
immunopathogenesis very similar to that of allergic asthma and rhinitis in response to ordinary exposure to the allergen, usually proteins.15
Arthus Reaction
FIGURE 1. Angioedema: Diffuse edematous swelling of the lower lip.
Inhaled beta 2-agonists (for patients experiencing bronchospasm) and antihistamines (for control of cutaneous symptoms) can also be useful. Intramuscular or intravenous administration of methylprednisolone is considered in severe cases.14
Atopy
Atopy is a familial tendency to produce IgE-mediated disease that affects the skin and has an
An Arthus reaction is a localized reaction that occurs at the site of an injection when a small quantity of antigen is injected into the skin. The reaction occurs in the presence of a high level of circulating antibodies due to repeated injection. This is characterized by marked edema and pain and swelling at the site of injection beginning several hours after immunization. It is self-limiting; severity and frequency can be reduced by spacing out the injections.16,17
Serum Sickness
Serum sickness is a type III systemic hypersensitivity reaction that results from the injection of a heterologous or foreign protein or serum. The
Figure 4
Figure 6
circulating immune complex infiltrates the blood vessels and tissues causing increased vascular permeability leading to an inflammatory process such as vasculitis and arthritis. Certain medications like penicillin and nonsteroidal anti-inflammatory drugs produce clinically similar serum sickness-like reactions. These reactions typically occur one to three weeks after exposure to the drug but may occur as early as one to 24 hours afterward.18
Angioedema
Angioedema is diffuse edematous swelling of soft tissues commonly involving the subcutaneous tissue and submucosal connective tissues due to vascular leakage (FIGURE 1, TABLE 4). It results in death when the gastrointestinal or respiratory tract is involved. Allergic angioedema is due to mast cell degranulation, which leads to histamine release and M AY 2 0 2 2
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FIGURE 2 . Lichenoid reaction: Erythematous lesions with whitish striae on buccal mucosa adjacent to amalgam restoration.
FIGURE 3 . Tobacco pouch keratosis: White, wrinkled, nonscrapable keratotic lesion corresponding to quid placement region.
typical manifestations that are seen commonly in Ig-E-mediated type I hypersensitivity reactions caused by drugs, foods (especially eggs, mussels, milk, shellfish and nuts),19 cosmetics, topical medications and even dental rubber dams. It can also result from physical stimuli such as heat, cold, exercise, emotional stress, solar exposure and significant vibration. Angioedema manifests as a soft, nontender, diffuse edematous swelling with relatively rapid onset that may be solitary or multiple. It most commonly involves the face around the lips, chin, eyes, tongue, pharynx and larynx. The symptoms appear rapidly, within one to two hours of exposure to the allergens. The eyes may be swollen shut and the lips extremely puffy. The enlargement usually resolves within 24 to 72 hours, but some cases persist for several days. Avoidance of the allergen and the use of antihistamines may prevent future attacks. Chronic cases require steroid therapy, which generally provides a good response. In cases where the allergic attack is 250
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progressing toward airway obstruction, epinephrine may be lifesaving.
Lichenoid Reactions
Lichenoid reactions have been associated with numerous drugs including antihypertensives, antimicrobials, anxiolytics, NSAIDs and oral hypoglycemic agents. They are also associated with tobacco chewing and dental materials such as amalgam, gold, casting alloys and flavoring agents. Clinically, a lichenoid reaction exhibits similar patterns of reactions as those seen in oral lichen planus (OLP), that is papules, reticulum, plaque type, erythema and ulcers. The most distinguishing feature between OLP and lichenoid contact reaction (LCR) is the site and extension of the lesions. Lesions are usually restricted to the areas where there is regular contact with dental materials. The most common sites are the buccal mucosa and the border of the tongue. Gingiva, the floor of the mouth, the dorsum of the tongue and palatal mucosa are the least affected sites.20,21 Most LCRs are nonsymptomatic. In some cases, the patient may experience an uneasy burning sensation when erythematous or ulcerative lesions are present (FIGURE 2, TABLE 4). When in contact with composite restorations of the anterior teeth, LCRs are observed in both upper and lower lip mucosa.22 Most types of LCR resolve after removal of the restoration that is in direct contact with the lesion followed by replacement of biocompatible dental materials.
Tobacco Chewing
Arya S et al. (2017)23 observed quid-induced lichenoid oral lesions among betel quid chewers. This lesion consisted of white, linear, wavy,
parallel, nonelevated streaks that could not be scraped off (FIGURE 3, TABLE 4). The fine lesion did not overlap or crisscross as in a lichen planus. The lesion, found at the site of betel quid placement, has the proposed term “betel quid lichenoid lesion.”22 There may be complete lesion regression if the user ceases betel quid chewing.
Contact Stomatitis
A contact stomatitis is a type of allergic reaction on the oral mucosa that can occur in a localized area or can be polymorphic as a consequence of repeated contact with many causative agents like mercury-based products, nickel sulfate, cobalt chloride and gold, bonding agents (composites), ethereal oils, silicone and polyester impression materials.24 The oral manifestations of contact allergy are gingivitis, stomatitis, cheilitis, perioral dermatitis, burning mouth syndrome, lichenoid reaction and orofacial granulomatosis.25 The treatment for contact stomatitis is avoidance of the allergen. When the contact stomatitis is due to a dental restoration or an orthodontic wire, replacement of the restoration may be considered. If it is due to a flavoring or preservative in food or a dental hygiene product, the patient should be advised to stop eating the food or using the product. The lesions usually disappear once the allergen is removed. Topical application of corticosteroids is indicated in persistent severe or chronic cases.
Stomatitis (Cheilitis) Venenata
Stomatitis (cheilitis) venenata is a contact allergic reaction caused by different chemical and cosmetic substances that cause inflammation of the labia and of the entire oral mucosa. There can be pronounced
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FIGURE 5 . Erythema multiforme: Multiple erosions and encrustations noted on both upper and lower lip.
FIGURE 6 . Denture stomatitis: Multiple pinpoint erythematous lesions on the palate confined to denture bearing area.
edema with multiple forms of small erosions 0.5 mm in diameter. With chronic local irritation on the labia, exfoliative cheilitis with strong exudation can be expected.24 The treatment involves elimination of the offending allergen. The complete resolution of the lesions can take up to two weeks. Patients presenting with extensive lesions are treated with antihistamines, topical or systemic corticosteroids and mouthwashes.
Recurrent Aphthous Stomatitis
Recurrent aphthous stomatitis (RAS) is one of the most common oral mucosal diseases. Studies have shown that food ingredients contribute to some cases of RAS.26 However, an outbreak of aphthae following ingestion of certain foods or drugs by different patients has been reported so frequently that allergy must be considered a precipitating factor.27 The aphthous ulcer begins as a single or multiple superficial erosions covered by a pseudomembrane. The ulcer generally has a wellcircumscribed margin surrounded by an erythematous halo (FIGURE 4, TABLE 4). 28 The lesions are usually painful,
vary in size from 2 mm to 3 mm to over 10 mm in diameter. The most common sites of occurrence are the buccal mucosa, labial mucosa, buccal and lingual sulci, tongue, soft palate, pharynx, gingiva and all locations of labile mucosa not bound to the periosteum.27 Three clinical variations have been recognized: minor, major and herpetiforme ulcers. Minor form and herpetiforme ulcers heal without scarring in seven to12 days while the major form persists for three to six weeks.29 Topical steroids are used for treatment, and in severe cases, intralesional steroid injection or lowdose systemic steroids are prescribed.
Perioral Dermatitis
Perioral dermatitis is a unique inflammatory idiosyncratic disease of the skin affecting the circumoral area precipitated because of tartar, toothpaste, bubble gum, cosmetic products, nasal steroids, flavoring agents and hormonal factors. A study has shown that patients with oral mucosal diseases are significantly more likely to have hypersensitivity to food additives (especially benzoic acid), perfumes and flavorings (especially cinnamaldehyde).30 Treatment includes the use of metronidazole cream or gel, clindamycin lotion or gel, erythromycin gel, topical sulfur preparations and azelaic acid gel. Topical calcineurin inhibitors such as tacrolimus ointment or pimecrolimus cream can also be effective.31–33 If topical treatment is not helpful, 250 mg to 500 mg of tetracycline twice a day, 100 mg of doxycycline once or twice a day and 100 mg of minocycline once or twice a day for an eight- to 12-week tapering course can be prescribed.34,35
Erythema Multiforme
Erythema multiforme (EM) is an acute reactive mucocutaneous inflammatory and hypersensitivity reaction characterized by a skin eruption, with symmetrical erythematous edematous or bullous lesions of the skin or mucous membranes. EM is a disorder with variants ranging from self-limited, mild, exanthematous, cutaneous lesions with minimal oral involvement to a progressive, fulminating and severe disease with extensive mucocutaneous epithelial necrosis. More than half of the cases have no known cause; other causes include medications, infections, immunotherapy or illnesses.36 Drugs are responsible for 4% of EM cases and 80% of Stevens-Johnson syndrome cases. The oral lesions disappear within two weeks of drug withdrawal.37 The most common drug reaction seen in the oral cavity is caused by NSAIDs, penicillin, sulfonamides and barbiturates.38 EM primarily involves oral mucosa but subsequent attacks can produce more severe forms of EM involving the skin. At times, oral and lip ulcerations can occur without any skin target lesions (FIGURE 5, TABLE 4). Management of EM depends on the underlying etiology and the disease severity. Acute, uncomplicated erythema multiforme involves symptomatic treatment with highpotency topical corticosteroids, antihistamines, antiseptic mouthwash and anesthetic solutions.39 If drugs are the cause of erythema multiforme, then discontinuation of the offending drug is recommended. In herpes simplex virus infections, oral acyclovir is recommended to reduce the severity and duration of EM.40
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Food Allergy
Food allergy is a type of immune response triggered by eggs, peanuts, milk, shellfish, soy, tree nuts, wheat or food additives such as dyes, thickeners and preservatives. Other specific foods can cause an allergy.41 Signs and symptoms include hives, nausea, stomachache, diarrhea, shortness of breath, swelling of the airways, tingling or itching in the mouth, swelling of the lips, face, tongue and throat or other parts of the body, gastrointestinal and respiratory tracts and the cardiovascular system. Symptoms can range from mild to severe based on the amount of food necessary to trigger the allergic reaction, which varies from person to person. Reaction to food allergy usually develops within a few minutes to two hours after eating the offending food.42 Intraoral allergic reactions to food, candy and chewing gum can result from potent flavoring agents, such as cinnamon, or fresh fruits and vegetables. The lesions in the oral cavity are focal and usually develop at sites with direct and prolonged contact with the cinnamon agent. The labial and buccal mucosa and lateral tongue are most commonly affected; the floor of the mouth and the gingiva may also be involved. Once a food allergy has developed, the best way to prevent an allergic reaction is to know and avoid foods that cause signs and symptoms. In the case of accidental exposure, the treatment of choice is epinephrine administered by intramuscular injection into the lateral thigh.43 Patients with food allergies can wear medical alert bracelets or necklaces to indicate their allergy.
Oral Allergy Syndrome
A localized IgE-mediated reaction
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is also known as the pollen-food syndrome, which causes tingling and itching of the mouth and pharynx. Swelling of the lips, tongue, palate and throat along with oral pruritis and irritations sometimes associated with other allergic clinical features, including rhinoconjunctivitis, urticaria and even anaphylaxis, have been referred to as oral allergy syndrome. It seems to be precipitated by fresh foods, including apples, in people who have been sensitized to cross-reacting allergens in pollens,
A localized IgE-mediated reaction is also known as the pollen-food syndrome.
particularly birch.44 Patients with this allergy should avoid eating raw fruits and vegetables; fruits and vegetables are tolerated when they are cooked, baked or processed. Antihistamines are given to relieve the itching or mouth tingling.
Fixed Drug Reaction
A fixed drug reaction is a localized or fixed allergic reaction specific to an allergic reaction to drugs. Usually, it is a localized erosion with thick pseudomembrane mostly solitary and may involve two different sites of the oral mucosa. Localized lesions are to be expected on the hard palate mucosa, labial mucosa or the dorsum of the tongue.45,46 The lesions always appear in the same
spot after repeated contact with the antigen. Discontinuation of suspected medication and topical application of steroids resolve this condition.
Stomatitis Medicamentosa — Drug Allergy
Drug allergies include a wide range of variant sensitivity reactions to numerous drugs and chemicals. Oral drug reactions often manifest as nonspecific diffuse erosions and ulcerations with or without vesicle or bulla formation,47 but they may mimic pemphigus vulgaris or lichenoid reactions. In drug-induced reactions, the relatively fragile vesicles are rarely observed at clinical examination, and most cases are characterized by irregular ulcerations with ragged borders that may coalesce to involve large areas of the mucosa.48 But in lichenoid reactions, shallow, irregular ulcerations or erosions with a peripheral border of fine keratotic striae that radiate from the center of the lesion adjacent to dental restorations are observed. Moreover, lichenoid reactions tend to be erosive and unilateral. Clinically, pemphigus lesions appear as relatively sturdy vesicles or bullae that break down into shallow ulcerations. Pressure exerted to an apparently normal area results in the formation of a new lesion. These phenomena are called Nikolsky’s sign. Diagnosis is facilitated by detailed history, clinical findings and immunohistological findings. Discontinuation of the offending agent is the treatment of choice; glycerine mouthwash, artificial saliva for xerostomia, xylocaine, benzocaine orabase for pain and antibiotics if there is infection can be administered as supportive therapy.47 Common drugs used in dentistry
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TABLE 5
Etiopathogenesis of Drugs Causing Allergic Manifestations in Oral Cavity Drugs
Etiology
Clinical manifestation
Antimicrobials
95% of penicillin is transformed into the major antigenic determinant; the penicilloyl moiety leads to hypersensitivity mediated by IgE and mastocytosis Majority of antimicrobials’ crossreactivity leads to allergic reactions
Angioedema Anaphylaxis Vesiculobullous or ulcerative mucositis Different patterns of manifestations similar to stomatitis Erythema multiforme Pemphigus Lichen planus Pemphigoid
NSAIDs
NSAIDs-induced COX-1 and COX-2 blockade results in more arachidonic acid available for lipoxygenase activity Inhibiting COX-1 diminishes the inhibitory effect of prostaglandin (PGE2) on lipoxygenase activity leads to increase leukotrienes
Immediate reactions Urticaria Angioedema Anaphylaxis Vesiculoulcerative lesions in oral cavity Nonspecific ulcerations and mucositis Xerostomia Lichen planus-like Erythema multiforme-like Aphthous-like
Opioids
Codeine mast cell degranulation and histamine release
Angioedema Xerostomia Burning sensation Candidiasis
Aspirin
Ulceration with epithelial necrosis may result from direct application
Nonspecific ulceration and mucositis Mucosa appears whitish and corrugated with erosion and ulcerations
Local anesthetics
Esters-type local anesthetics are metabolized into p-aminobenzoic acid, a substance known for its allergenicity, e.g., benzocaine, procaine, tetracaine
Anaphylaxis: urticaria/angioedema joined by respiratory symptoms or cardiovascular symptoms Involvement of two systems in any combination of mucocutaneous, respiratory, cardiovascular or gastrointestinal symptoms
True allergy can be due to preservatives and antioxidants contained in local anesthetic preparations such as parabens, metabisulfite or even latex residues from rubber stoppers and diaphragms in dental cartridges Sulfonamides antimicrobials/ sulfonylureas
Glucocorticoids
Within the structure of sulphonamides defining N1 heterocyclic ring and N4-arylamine component required for potent antimicrobial activity, they are associated with typical sulfa drug allergy Metabolites of the sulfonamide are the potential determinants of allergy
Anaphylaxis Angioedema Nonspecific ulceration and mucositis Erythema multiforme-like reactions with extensive hemorrhagic ulcerations and crusting of the labial vermilion Stevens-Johnson syndrome Toxic epidermal necrolysis
Group I: methylprednisolone, hydrocortisone seem to cross-react
Stomatitis
that cause allergic reactions, their etiopathogenesis and oral manifestations49,50 are listed in TABLE 5.
Allergic Reactions to Dental Materials Acrylic “Denture sore mouth” is the
inflammatory change of mucous membranes developing beneath the dentures. When the allergic reaction is caused by a prosthetic component material allergy, it is called prosthetic allergic stomatitis. This form rarely
occurs as an expression of contact allergy to acrylate, denture furnish, metal denture alloys and cobaltchromium pastes for denture fixation. Thereby, stomatitis lesions are found on the areas where the prosthesis base comes in contact, causing erythema, edema, vesicles, bullae, erosions and ulcerations24 (FIGURE 6). Self-cured acrylics are more frequently associated with the allergy than heat-cured ones. Most frequently, the palatal oral mucosa and maxillary ridges are involved and tissue appears bright red and edematous. Patients report soreness, dryness and burning.
Dental Amalgam
Allergy to dental amalgam has been reported in many cases. The allergy is caused by mercury leaching. This can develop over a prolonged period when the amalgam is in direct contact with the oral mucosa. The site affected has a close relationship to the amalgam filling.51 It manifests as oral lichenoid lesions related to the contact area. Thornhill et al. (2003) found that 70% of the amalgam contact hypersensitivity reactions were patch positive for amalgam or mercury.22
Latex
Allergic reactions to latex have increased in the last few years. It is still unclear whether the components of latex or the cornstarch/borax powder incorporated are responsible for it. Latex can also cause different reactions including allergic contact dermatitis (Type IV) and true latex allergy (Type I).52 Latex allergy reactions can vary from localized stomatitis to life-threatening airway compromise. Abdollahi et al. (2008) stated that latex-free environments to reduce the incidence of latex issues M AY 2 0 2 2
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relating to both the surgical team and patients need to be created.36 Alternative materials such as vinyl or nitryl should be considered whenever latex allergy is suspected.53
Nickel
Nickel is the most common metal to cause contact dermatitis. Nickel-titanium alloy used in orthodontic treatment contains around 55% of nickel, which can release enough nickel in the oral environment to elicit Type IV delayed hypersensitivity immune response.54 However, orthodontic auxiliaries made of stainless steel have lower nickel content (8%), and the nickel is bound in a crystal lattice, so it is not available to react. Nickelinduced allergy is also seen with frequent use of nickel-containing jewelry and intraoral piercings.55 Severe intraoral manifestations of nickel allergy are rare. However, diffuse erosions and ulceration are seen intraorally extending to the perioral area. Skin reactions include urticaria and eczematic reactions in the face. High-content nickeltitanium wires should be avoided in nickel-sensitive patients, as nickel-free alternatives are available and should be considered for these patients.56
Oral Hygiene Products
Flavoring agents57,58 are the main cause of allergy for toothpaste and mouthwash use and can manifest as: ■ Allergic contact cheilitis. ■ Perioral eczema due to contact allergic dermatitis. ■ Contact leukoderma and urticaria. Common allergens found in toothpaste are unspecified flavors, cocamidopropyl betaine, propylene glycol, essential oils and biological 254
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additives, parabens, peppermint, vitamin E, spearmint, grape extract, specific flavors, propolis and tea tree oil.58 After contact, the mucosa becomes remarkably inflamed and edematous. The surface appears smooth and shiny. Vesicles rupture to form small areas of erosion and ulceration, which may become extensive. Lips will have a tingling sensation, edema and ulcerations. In chronic cases, widespread erythema on the mucosa with erosions, dry, cracking and fissuring lips is seen.
Conclusion
As dental practitioners, we use many dental materials and drugs that may cause allergic reactions that can do harm in our patients. Thus, it is necessary to act with caution during the use of these dental materials and drugs. A detailed medical and dental history and material knowledge are crucial in preventing sensitization of individual material components and side effects. The diagnosis of oral complaints suspected to be connected to oral allergies remains a challenge. A better understanding of history and clinical manifestations play a pivotal role in diagnosing and managing the conditions effectively. In dentistry, Type I and Type IV reactions are the most commonly encountered allergic phenomena. As such, dentists should not only know the most frequent elicitors but also their safest alternatives whenever removing an allergen is indicated. n RE FE RE N CE S 1. Mosby’s Dictionary of Medicine, Nursing and Health Professions. 8th ed. St. Louis: Mosby/Elsevier; 2009. 2. Von Pirquet C. Allergie. MMW Munch Med Wochenschr 1906;53:1457. 3. Tanno LK, Bierrenbach AL, Simons FER, Cardona V, Thong BY, Molinari N, et al. On behalf of the Joint Allergy Academies. Critical view of anaphylaxis epidemiology: Open questions
and new perspectives. Allergy Asthma Clin Immunol 2018 Apr 4;14:12. doi: 10.1186/s13223-018-0234-0. Accessed eCollection 2018. 4. Allaerts W, Chang TW. Skewed Exposure to Environmental Antigens Complements Hygiene Hypothesis in Explaining the Rise of Allergy. Acta Biotheor 2017 Jun;65(2):117–134. doi: 10.1007/s10441-017-9306-7. Epub 2017 Mar 24. 5. Mohan H. Textbook of Pathology. 6th ed. New Delhi: Jaypee Brothers Medical; 2010. 6. Tomasiak-Lozowska MM, Klimek M, Lis A, Moniuszko M, Bodzenta-Lukaszyk A. Markers of anaphylaxis — a systematic review. Adv Med Sci 2018 Sep;63(2):265– 277. doi: 10.1016/j.advms.2017.12.003. Epub 2018 Mar 20. 7. Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: Summary report—second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. J Allergy Clin Immunol 2006 Feb;117(2):391–7. doi: 10.1016/j. jaci.2005.12.1303. 8. Wang KY, Friedman DF, DaVeiga SP. Immediate hypersensitivity reaction to human serum albumin in a child undergoing plasmapheresis. Transfusion 2019 Jun;59(6):1921–1923. doi: 10.1111/trf.15194. Epub 2019 Feb 13. 9. Justiz Vaillant AA, Vashisht R, Zito PM. Immediate Hypersensitivity Reactions. StatPearls. StatPearls Publishing; Treasure Island, Florida: 2021. 10. Berry DC, Britton L, Joseph LM, Jessup A. Alpha-gal: A delayed onset of anaphylaxis and uncovering the cause. J Emerg Nurs 2019 Sep;45(5):567–569. doi: 10.1016/j.jen.2019.03.001. Epub 2019 May 27. 11. Brown SGA. Clinical features and severity grading of anaphylaxis. J Allergy Clin Immunol 2004 Aug;114(2):371–6. doi: 10.1016/j.jaci.2004.04.029. 12. Simons FE, Gu X, Simons KJ. Epinephrine absorption in adults: Intramuscular versus subcutaneous injection. J Allergy Clin Immunol 2001 Nov;108(5):871–3. doi: 10.1067/mai.2001.119409. 13. Simons FE, Roberts JR, Gu X, Simons KJ. Epinephrine absorption in children with a history anaphylaxis. J Allergy Clin Immunol 1998 Jan;101(1 Pt 1):33–7. doi: 10.1016/S0091-6749(98)70190-3. 14. Lieberman P, Nicklas RA, Randolph C, Oppenheimer J, Bernstein D, Bernstein J, et al. Anaphylaxis — a practice parameter update 2015. Ann Allergy Asthma Immunol 2015 Nov;115(5):341–84. doi: 10.1016/j. anai.2015.07.019. 15. Dou J, Zeng J, Wu K, Tan W, Gao L, Lu J. Microbiosis in pathogenesis and intervention of atopic dermatitis. Int Immunopharmacol 2019 Apr;69:263–269. doi: 10.1016/j.intimp.2019.01.030. Epub 2019 Feb 8. 16. Gershwin LJ. Adverse reactions to vaccination: From anaphylaxis to autoimmunity. Vet Clin North Am Small AnimPract 2018 Mar;48(2):279–290. doi: 10.1016/j. cvsm.2017.10.005. Epub 2017 Nov 29. 17. Ghazavi MK, Johnston GA. Insulin allergy. Clin Dermatol May–Jun 2011;29(3):300–5. doi: 10.1016/j. clindermatol.2010.11.009. 18. Owczarczyk-Saczonek A, Wygonowska E, Budkiewicz M, Placek W. Serum sickness disease in a patient with alopecia areata and Meniere’ disease after PRP procedure.
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Dermatol Ther 2019 Mar;32(2):e12798. doi: 10.1111/ dth.12798. Epub 2019 Jan 8. 19. TomoyasuY, Mukae K, Suda M, Hayashi T, Ishii M, Sakaguchi M. Allergic reactions to local anesthetics in dental patients: Analysis of intracutaneous and challenge tests. Open Dent J 2011;5:146–9. doi: 10.2174/1874210601105010146. Epub 2011 Aug 27. 20. McCartan BE, McCreary CE. Oral lichenoid drug eruptions. Oral Dis 1997 Jun;3(2):58–63. doi: 10.1111/ j.1601-0825.1997.tb00013.x. 21. Holmstrup P. Oral mucosa and skin reactions related to amalgam. Adv Dent Res 1992 Sep;6:120–4. doi: 10.1177/08959374920060010401. 22. Thornhill MH, Pemberton MN, Simmons RK, Theaker ED. Amalgam-contact hypersensitivity lesions and oral lichen planus. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003 Mar;95(3):291–9. doi: 10.1067/ moe.2003.115. 23. Arya S, Vengal M, Raju B, Patil N, Sathosker S, Bateja S, et al. Betel quid oral lichenoid lesions: A hospital based cross‐sectional study. J Investig Clin Dent 2017 Feb;8(1). doi: 10.1111/jicd.12180. Epub 2015 Jul 29. 24. Cekić-Arambašin A. Oralna medicina. Zagreb: Školskaknjiga; 2005. 25. Bakula A, Lugović-Mihić L, Šitum M, Turčin J andŠinković A. Contact allergy in the mouth: Common allergens relevant to dental practice. Acta Clin Croat 2011 Dec;50(4):553–561. 26. Chavan M, Jain H, Diwan N, Khedkar S, Shete A, Durkar S. Recurrent aphthous stomatitis: A review. J Oral Pathol Med 2012 Sep;41(8):577–83. doi: 10.1111/j.1600-0714.2012.01134.x. Epub 2012 Mar 13. 27. Rajendran A, Shivapathasundaram B. Shafer’s Textbook of Oral Pathology. 7th ed. India: Elsevier; 2012. 28. Sridevi P, Munisekhar MS, Harika CH, Ramakrishna A. Oral Manifestations of Autoimmune Diseases. Int J Oral Maxillofac Pathol 2012:3(4):27–33. 29. Boulinguez S, Reix S, Bedane C, Debrock C, BouyssouGauthier ML, Sparsa A, et al. Role of drug exposure in aphthous ulcers: A case-control study. Br J Dermatol 2000 Dec;143(6):1261–5. doi: 10.1046/j.13652133.2000.03898.x. 30. Wray D, Rees SR, Gibson J, Forsyth A. The role of allergy in oral mucosal diseases. QJM 2000 Aug;93(8):507–11. doi: 10.1093/qjmed/93.8.507. 31. Veien NK, Munkvad JM, Nielsen AO, Niordson AM, Stahl D, Thormann J. Topical metronidazole in the treatment of perioral dermatitis. J Am Acad Dermatol 1991 Feb;24(2 Pt 1):258–60. doi: 10.1016/0190-9622(91)70038-4. 32. Miller SR, Shalita AR. Topical metronidazole gel (0.75%) for the treatment of perioral dermatitis in children. J Am Acad Dermatol 1994 Nov;31(5 Pt 2):847–8. doi: 10.1016/s0190-9622(94)70243-8. 33. Jansen T. Azelaic acid as a new treatment for perioral dermatitis: Results from an open study. Br J Dermatol 2004 Oct;151(4):933–4. doi: 10.1111/j.1365-2133.2004.06202.x. 34. Choi YL, Lee KJ, Cho HJ, Kim WS, Lee JH, Yang JM, Lee ES, Lee DY. Case of childhood granulomatous periorificial dermatitis in a Korean boy treated by oral erythromycin. J Dermatol 2006 Nov;33(11):806–8. doi: 10.1111/j.1346-8138.2006.00183.x.
35. Ellis CN, Stawiski MA. The treatment of perioral dermatitis, acne rosacea and seborrheic dermatitis. Med Clin North Am 1982 Jul;66(4):819–30. doi: 10.1016/s0025-7125(16)31396-7. 36. Abdollahi M., Rahimi R., Radfar M. Current opinion on drug-induced oral reactions: A comprehensive review. J Contemp Dent Pract 2008 Mar 1;9 (3):001–015. 37. Abdollahi M, Radfar M. A review of drug-induced oral reactions. J Contemp Dent Pract 2003 Feb;4(1):10–31. 38. Joseph T I, Vargheese G, George D, Sathyan P. Drug induced oral erythema multiforme: A rare and less recognized variant of erythema multiforme. J Oral Maxillofac Pathol 2012 Jan;16(1):145–8. doi: 10.4103/0973-029X.92995. 39. Sokumbi O, Wetter DA. Clinical features, diagnosis and treatment of erythema multiforme: A review for the practicing dermatologist. Int J Dermatol 2012 Aug;51(8):889–902. doi: 10.1111/j.13654632.2011.05348.x. 40. Freedberg IM, Eisen AZ, Wolff K, et al. eds. Fitzpatrick’s Dermatology in General Medicine. 6th ed. New York: McGraw-Hill; 2003:585–596. 41. Sicherer SH, Sampson HA. Food allergy. J Allergy Clin Immunol 2010 Feb;125(2 Suppl 2):S116–25. doi: 10.1016/j.jaci.2009.08.028. Epub 2009 Dec 29. 42. Sicherer SH, Sampson HA. Food allergy. J Allergy Clin Immunol 2006 Feb;117(2 Suppl Mini-Primer):S470–5. doi: 10.1016/j.jaci.2005.05.048. 43. Hourihane JO, Roberts SA, Warner JO. Resolution of peanut allergy: Case control study. BMJ 1998 Apr 25;316(7140):1271–5. doi: 10.1136/ bmj.316.7140.1271. 44. Egger M, Mutschlechner S, Wopfner N, Gadermaier G, Briza P, Ferreira F. Pollen-food syndromes associated with weed pollinosis: An update from the molecular point of view. Allergy 2006 Apr;61(4):461–76. doi: 10.1111/j.1398-9995.2006.00994.x. 45. Fayez R, Obaidat N, Al-Qa’qaa A, Al-Rawashdeh B, Ma’aita M, Al-Azab N. Drugs causing fixed drug eruption: A clinical study. JRMS 2011;18(3):16–20. 46. Handisurya A, Moritz KB, Riedl E, Reinisch C, Stingl G, Wöhrl S. Fixed drug eruption caused by mefenamic acid: A case series and diagnostic algorithms. J Dtsch Dermatol Ges 2011 May;9(5):374–8. doi: 10.1111/j.16100387.2011.07621.x. Epub 2011 Mar 2. 47. Tack DA, Rogers ES. Oral drug reactions. Dermatol Therap 2002;15:236–250. doi.org/10.1046/j.1529-8019.2002.01532.x. 48. Civatte J. Drug-induced pemphigus diseases. Dermatol Monatsschr 1989;175(1):1–7. 49. Rama TA, Cernadas J. Insight into hypersensitivity reactions in dentistry. Porto Biomed J 2020 Dec;5:6:e090. doi: 10.1097/j.pbj.0000000000000090. 50. Shafers WG, Hine MK, Levy BM. A Textbook of Oral Pathology. 6th ed. Philadelphia:WB Saunders; 2009. 51. McParland H and Warnakulasuriya S. Oral lichenoid contact lesions to mercury and dental amalgam — a review. J Biomed Biotechnol 2012;2012:589569. doi: 10.1155/2012/589569. Epub 2012 Jul 24. 52. Chin SM, Ferguson JW, Bajurnow T. Latex allergy in dentistry. Review and report of case presenting as a serious reaction to latex dental dam. Aust Dent J 2004 Sep;49(3):146–8. doi: 10.1111/j.1834-7819.2004.
tb00064.x. 53. Pithon MM, Mendes JL, Da Silva CA, Lacerda Dos Santos R, Coqueiro RD. Force decay of latex and non-latex intermaxillary elastics: A clinical study. Eur J Orthod 2016 Feb;38:39–43. doi: 10.1093/ejo/cjv005. Epub 2015 Mar 3. 54. Menezes LM, Campos LC, Quintão CC, Bolognese AM. Hypersensitivity to metals in orthodontics. Am J Orthod Dentofacial Orthop 2004 Jul;126(1):58–64. doi: 10.1016/j.ajodo.2003.05.014. 55. Noble J, Ahing SI, Karaiskos NE, Wiltshire WA. Nickel allergy and orthodontics, a review and report of two cases. Br Dent J 2008 Mar 22;204(6):297–300. doi: 10.1038/ bdj.2008.198. 56. Rahilly G, Price N. Nickel allergy and orthodontics. J Orthod 2003 Jun;30:171–174. doi: 10.1093/ ortho/30.2.171. 57. Francalanci S, Sertoli A, Giorgini S, Pigatto P, Santucci B, Valsecchi R. Multicentre study of allergic cheilitis from toothpastes. Contact Dermatitis 2000 Oct;43(4):216–22. doi: 10.1034/j.1600-0536.2000.043004216.x. 58. Zirwas M J and Otto S. Toothpaste allergy diagnosis and management. J Clin Anesthet Dermatol 2010;May;3(5):42–47. PMCID: PMC2922711. T HE CORRE S P ON DIN G AU T HOR , Shilpa Padar Shastry, MDS, can be reached at shilpa.keshav@gmail.com.
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Making your transition a reality.
Dr. Thomas Wagner
Dr. Russell Okihara
LIC #01418359
LIC #01886221
Dr. Ben Sapir LIC #02126473
Jim Engel LIC #01898522
(916) 812-3255 (619) 694-7077 (925) 330-2207 (310) 596-0961 47 Years in Business 40 Years in Business 13 Years in Business 48 Years in Business
Jay Harter LIC #01008086
Kerri McCullough LIC #01382259
Gina Miller LIC #02015193
Steve Caudill LIC #00411157
Jaci Hardison LIC #01927713
Christy Conway LIC #: #02143744
Kim Ta LIC #02085576
Thinh Tran LIC #01863784
(916) 812-0500 (949) 300-0312 (707) 391-7048 (714) 318-4911 (951) 314-5542 (408) 687-5001 (619) 889-6492 (949) 675-5578 39 Years in Business 37 Years in Business 32 Years in Business 32 Years in Business 28 Years in Business 19 Years in Business 18 Years in Business 13 Years in Business
PRACTICE SALES • VALUATIONS/APPRAISALS • TRANSITION PLANNING • PARTNERSHIPS • MERGERS • ASSOCIATESHIPS PLEASANTON: New Listing! Great neighborhood practice, paperless, digital, 6 ALAMO: 3 Ops, Digital, 13 Yrs Goodwill, Ops, 5 equipped. Don’t miss opportunity in Desirable Area, Not in Delta Network. 2019 this great community. #CA3023 GR $642K. #CA2968 ROCKLIN/GRANITE BAY: Hi-end 4 Ops AUBURN: 4 Ops+RE, 60 Yrs. Goodwill, GP/Cosmetic practice in affluent area. Dentrix, Digital, Laser, CEREC, Room to Paperless, digital, iTero scanner, 8+ hyg days/ Grow w/ specialties. 2019 GR wk. 2019 GR $1.6M+, 2021 Prod projected at $632K. #CA2809 $2M+. RE for sale with practice. #CA2793 BRENTWOOD: New Listing! 4 Ops, ROSEVILLE/CITRUS HTS: 4 Ops with 18 professionally designed, Dentrix, Paperless, Yrs Goodwill, Digital, Laser, Strong Hyg., Laser, great location. 2019 GR $520K on 2.5 Specialties Referred, 2021 est GR $775K. day week. #CA3008 #CA2897 CONCORD/WALNUT CREEK: New ROSEVILLE/CITRUS HTS: 6 Ops, high Listing! 5 Ops in affluent/established area traffic area, 13 yrs goodwill, Digital, lasers, 26 with RE available. Digital, CEREC, Digital NP/mo, 5 days Hygiene, specialties referred. Pano, Soft tissue Laser and so much more. Seller will work back. #CA2749 2021 GR projected to be $630K. #CA2808 ROSEVILLE/ROCKLIN: 7 Ops, hi-end FAIR OAKS/CITRUS HEIGHTS: Price practice in desirable area. Digital, CAD/CAM, Reduced! 4 Ops in desirable area, digital, lasers, Pano. 10+ hyg. days/wk, 2019 GR strong hygiene program. Seller highly $2.3M, 2021 projected motivated to retire! 2019 GR $970K on 4 $2.5M. Lease with purchase option. #CA2770 days/wk with plenty of vacation. #CA656 SACRAMENTO METRO ORTHO: EAST BAY AREA PEDO: Well-established Established practice in growing area with 5 with 8 Ops, Digital, plumbed for Nitrous, and chairs, digital Pan/Ceph and sensors, high NP count. Associate-driven with Delta paperless. Seller will assist in transition. 2021 PPO. 2019 GR $832K on 3-4 days/wk., 2020 GR $451K. #CA2986 Production $560K. #CA2523 SAN FRANCISCO PEDO: 7 Chairs, Digital, FAIRFIELD AREA: 4 Ops w/1 add’l +RE, Nitrous, Digital Pan, Beautiful Office w/ <10 Digital, Paperless, Strong Hyg. Program, Not y/o equipment. 2019 GR $953K. #CA2953 in Delta Network. 2019 GR $714K. #CA2955 SAN FRANCISCO: 4 Ops, Financial FAIRFIELD AREA: High traffic area, 7 District, SoftDent, Digital sensors and Pan. Ops Digital, Pano/CB, 23+ NP/mo. with 8+ FFS/PPO, GR $1.6M+. Delta PPO Practice Hyg. days/wk. Room to grow with with over 70 NP/mo. #CA2934 specialties. 2019 GR $1.7M and 2021 on SAN JOSE: Est for 35 yrs, 2019 GR of track to exceed 2019. #CA1824 $1.3M with Adj. Net of 38%. 6 Ops, Digital FREMONT ORAL SURGERY: 34 yr X-rays and Pan, CAD/CAM, Laser. Upscale history, diverse high-tech community. 4 Ops building near shopping. Seller can stay on P/T. Digital, 7-10 y/o equipment, Pano. 2019 GR #CA1140 $548K on 3.5 days/wk. #CA2754 SAN MATEO: New Listing! 3 Ops, digital xGREATER SONORA AREA: Rural ray, great opportunity in this highly desirable lifestyle GP/Real Estate, 5 Ops, Dentrix, area/busy retail strip center location. 2021 GR Strong hyg prog in stable community. 2019 $381K with no advertising. #CA3044 GR $698K. #CA1713 SAN MATEO: Price Reduced! 5 Ops, LAKE TAHOE AREA: 4 Ops, 37+ yrs Digital, iTero Scan, CEREC, Laser, Paperless, Goodwill. Rural lifestyle GP in growing Microscope. Seller-owned stand-alone resort community. 2019 GR $760K. building to lease. $1.4M GR on 4 days/wk. #CA1715 #CA2596 MILLBRAE: Great practice in the heart of SONOMA COUNTY: Price Adjustment! the peninsula with 60 yrs goodwill. 5 Ops. Large GP, 2019 GR $2.3M+. Stand-alone 2019 GR $1M+ on 4 days/wk. and 6 Hygiene 3,000 sf prime Real Estate, 72 NP/mo. & 10 days. Owner will work back for a short time Hyg Days. 6 Ops, Pano, Dexis, Cameras, for transition. Digital, Pano, Waterlase & Laser, Dentrix. Both Business & RE for sale Periolase. #CA1139 or Lease. Doctor Retiring. #CA544 NAPA COUNTY: Price Reduced! Beautiful SONOMA COUNTY: Price Reduced! 4 Ops wine country location, 7 Ops, stand-alone with room to expand into suite next door. GR building. GR $1M+ with 7 Days of Hygiene. over $1M for last 3 yrs. Est. 30+ years. Strong Computerized and Digital. Established in the hygiene, digital, space available to lease or community for over 37 years. #CA2912 buy. #CA2790 NORTHERN SACRAMENTO: Busy SONORA AREA: 5 Ops, Producing $825K location, Paperless, 3 Ops+4th shared, in a renovated suite. RE for sale w/practice. CEREC, Digital Pano. 2019 GR $671K on Strong Hyg program. Digital, Laser, and 24-32 hrs/wk. #CA1745 Digital Pano. #CA2850 PALO ALTO: New Listing! 9 Ops, Central S. SACRAMENTO-GREENHAVEN: location in free-standing bldg. Paperless, Associate in place. 4 Ops, Digital, Cone Digital, Laser, Digital Scanner, 2021 GR Beam, Digital Pano, Specialties referred. Not $1.8M+ on 4 days/wk. #CA3037 a Delta Premier Provider. 2021 projected $800K+. #CA2741 PLEASANTON: 7 Ops, 5 Equipped, Dentrix, Digital, Laser, Digital Pan, no need VACAVILLE AREA: 4 Ops, 3 equipped, 45 to add $, this practice has everything. GR years goodwill, Digital, paperless, most $1.3M. Won’t last. #CA2891 specialties referred. 2019 GR $723K on 30 hour week. #CA2748
NORTHERN CALIFORNIA
Northern California Office
800.519.3458
Henry Schein Corporate Broker #01230466
CENTRAL CALIFORNIA FRESNO AREA: 6 Op Valley gem, great staff in desirable area. Paperless, Trios Scanner, Digital Pan/Ceph, Lasers and 12 days of hyg/wk. 2019 GR $1.4M, 2021 projected at $1.4M again. Seller may consider option to purchase RE. #CA2004 GREATER MODESTO: 7 Ops, Desirable area, Dentrix, Digital, Laser, Digital Pano. RE for sale w/practice. Not a Delta Premier provider. 2020 GR $615K and 2021 should exceed it. #CA2795 SANTA CRUZ: New Listing! 4 Ops, Minutes to beach! Digital, CEREC, Pano, CBCT. Bread and butter practice-room to grow with specialties. FFS and Delta PPO only. #CA2938 SANTA CRUZ COUNTY: 4 Ops, near beach, in strip center. Digital Pano, X-rays, CEREC, 40 years goodwill. 2019 GR $392K on 3.5 days. #CA2822 SANTA CRUZ/APTOS PERIO: 4 Ops +RE, Paperless, Digital, CBCT, 27 years goodwill. Seller will help with smooth transition of strong referral base. #CA2725
SOUTHERN CALIFORNIA BAKERSFIELD: 7 modern Ops, FFS/PPO. Eaglesoft, Digital, M11 and Digital Pano. RE potentially for sale. Doctor selling due to emergency - highly motivated. #CA2945 COASTAL ORANGE COUNTY: New Listing! 5 Ops, 4 equipped, digital sensors & pano. Room to grow, in a well-established area. GR $735K. #CA2787 HUNTINGTON BEACH: 5 Ops, established 30 yrs. RE ownership available. PPO with specialties referred - room to grow. High net income in sought-after area. #CA2937 MONTEBELLO: 3 Ops in busy strip center location with 2 Associates, Digital X-rays, and all specialty work referred out. #CA2786 NORTHEAST ORANGE COUNTY: New Listing! 7 Ops, 4 equipped, with room to grow and bring in specialists.Well-educated patient base looking for continued quality care. RE also for sale. #CA3013 ORANGE COUNTY: 8 Ops, 6 equipped, room to bring in specialists! Digital, BioLase, iTero, Digital Pan, beautiful office, modern and clean. Premium strip center location. GR $590K. #CA2926 ORANGE COUNTY: 4 Ops in sought-after area. 34 yrs Goodwill, many hi-end procedures done in-house but room to grow other specialties. Digital. FFS/Cash. #CA2704 PALMDALE/LANCASTER: 7 Op office in fast-growing community. Paperless with Dentrix, digital X-rays, 8 days of hyg./week and dedicated staff. Room to grow with specialties! #CA2612 SAN BERNARDINO: 6 Ops, established 33 years, cash, HMO, Denti-Cal in a busy area with parking. Estimated GR for 2021 at $960K+. Seller offering RE for sale with 2 lease tenants adjacent to practice. Room to expand with spec. #CA2843 SANTA CLARITA VALLEY: New Listing! 6 Ops, great cash flow, seller will work back. 3D CT, Itero, Digital with 8 hyg days/wk. PPO/FFS and 2021 GR over $2.3M. #CA2992
www.HenryScheinDPT.com
SOUTH ORANGE COUNTY: Beautiful coastal location with 3 Ops and digital x-rays. Retiring seller has been in area for 32 years with most specialties referred. GR $500K. #CA2948 TORRANCE: 3 Ops, room for a 4th. Dentrix, digital, refers most specialties with low overhead and high net. GR $600K. #CA2815 TORRANCE:3 Ops, retiring seller with 34 yrs goodwill. Ready to take to the next level with technology of your choosing. Amazing location in desired area. 2019 GR of $300K with low expenses, a wonderful opportunity to grow. #CA2807 WHITTIER: New Listing! 4 Ops, 3 equipped, 30 yrs goodwill. Digital x-rays and pano, laser. 2021 GR $683K on 3 Dr. days/wk. Great visibility and signage in this wonderful community. #CA2788
SAN DIEGO CARDIFF-BY-THE-SEA: New Listing! Amazing location, legacy practice open 60+ years, 4 Ops, add technology of your choosing and grow income stream by keeping specialties in-house. GR $686K. #CA2988 CARLSBAD: 5 Ops, modern design, suburban growing area. Digital Pan, Digital sensor, Laser, Paperless. 30 NP/mo. Room to grow with marketing and specialties. #CA2933 EL CAJON: East County highly productive practice w/modern facility. Digital, seller refers specialties, primed for future growth. 2021 GR $1M+. #CA2975 ENCINITAS: 5 bright Ops, Strip mall loc. Digital Pan, Laser, Digital X-rays, Paperless. 25 NP/mo. Grow with specialties. #CA2935 ESCONDIDO DENTAL REAL ESTATE: New Listing! Stand-alone building with 5 fully equipped Ops, 2 with brand-new equipment. On corner lot with private parking and spacious floor plan. #CA3031 ESCONDIDO: 6 Ops, hi-prod, CBCT, Scanner, Scope, Laser. Off main road, refers out most specialties. #CA2946 N. SAN DIEGO COUNTY: 6 Ops, Dentrix, Dexis, CBCT, laser, solid foundation. Main road location with free parking. #CA2932 N. SAN DIEGO COUNTY: 4 Ops highly desirable location in busy strip mall. Digital, clean, and modern, with an excellent layout. Consistent year to year collections. #CA2961 SAN DIEGO: 4 Ops, desirable/affluent community. CEREC, CBCT, Digital, Dentrix, Paperless. Room to grow with specialties. #CA2896 SAN DIEGO: Rare opportunity, seller retiring, 4 Ops in desirable location with good cash flow. High quality work. Digital, Dentrix. #CA2851 SAN DIEGO: New Listing! 6 Ops, 4 equipped, recently updated, Digital Pan, Microscopes, and Laser. Specialties referred, room for additional hours and dentistry. #CA3005 SCRIPPS RANCH: New Listing! 5 Ops, 3 equipped, strip mall location, bright, spacious office. CEREC, CBCT, Dexis, Soft tissue Laser, Implant Motor, I/O Camera. Specialties referred. #CA3054
Southern California Office
888.685.8100
informed consent C D A J O U R N A L , V O L 5 0 , Nº 5
C.E. Credit
Informed Consent in the Older Adult Population: A MixedMethods Study Katherine Lambert, BS; Grace Yasewicz, BS; Garrett Finney, BS; Thomas Meuser, PhD; Regula Robnett, PhD; and Yang Kang, DDM, PhD
abstract Background: The purpose of this pilot study is to investigate how to adequately inform older patients about dental treatment, how to secure their informed consent for the treatment and how to learn about their perceptions of dentistry. The geriatric population will probably double in the next 30 years, yet there is limited research on improving dental informed consent. Due to the COVID-19 pandemic, dental visits have become more disorienting than ever for the older adult population, therefore it is important to implement effective informed consent procedures. Methods: Geriatric subjects were randomly assigned to read a pamphlet or watch an informational video describing implant placement. Participants then took a postcondition survey. A paired t-test and an independent t-test were used with a 95% confidence interval to determine the significance of the data. In addition, a focus group was conducted to discuss the participants’ experiences with informed consent. Results: The results reveal a statistically significant increase (p < 0.05) in the participants’ confidence of understanding dental implants after each intervention. The focus group discussion yielded three major themes in regard to the informed consent process: The critique of a pamphlet or video, the pitfalls of assumption and the importance of building trust. Conclusion: This study illustrates that both a video and pamphlet can improve patients’ understanding of the informed consent process. Practical implications: These adjunct materials are not a substitution for having a conversation with one’s dental professional. Understanding older patients as individuals with unique past dental needs is pivotal to success in this process. Keywords: Dentistry, geriatric, aging, informed consent M AY 2 0 2 2
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AUTHORS Katherine Lambert, BS, is a 2022 DMD candidate and a student research assistant at the University of New England in Portland, Maine. Conflict of Interest Disclosure: None reported. Grace Yasewicz, BS, is a 2022 DMD candidate at the University of New England in Portland, Maine. Conflict of Interest Disclosure: None reported. Garrett Finney, BS, is a 2022 DMD candidate at the University of New England in Portland, Maine. Conflict of Interest Disclosure: None reported.
Thomas Meuser, PhD, is a clinical psychologist at the University of New England. He has specialized training and experience in narrative gerontology, the neuropsychology of dementing disorders, and psychosocial intervention approaches to enhance wellbeing in older adults. Conflict of Interest Disclosure: None reported. Regula Robnett, PhD, is a professor emeritus at the University of New England. She is an occupational therapist and gerontologist. Conflict of Interest Disclosure: None reported. Yang Kang, DDM, PhD, is an associate clinical professor and the chair of the department of restorative and clinical sciences at the University of New England. Conflict of Interest Disclosure: None reported.
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n essential practice is to obtain informed consent from the patient during clinical care. In the most basic sense, informed consent should only be confirmed when a patient feels fully comfortable in their understanding of the treatment, risks and benefits of treatment and alternatives to the proposed treatment, including refusal of treatment. However, in many instances, the informed consent process is approached only from a performative legal standpoint, leaving the patient to sign the consent paperwork without feeling fully informed about the proposed treatment.1 Studies suggest patients often do not fully appreciate the importance of informed consent, including its purpose to protect patients through discussion and education about their dental health needs.2 Obtaining informed consent from older patients requires special attention. According to the U.S. Census Bureau, the population of individuals aged 65 years and older in the U.S. will double in number from 48 to 88 million by 2050.3,4 Older adults require more health care services due to an increased number of chronic diseases including those that affect both physical and cognitive abilities (such as Alzheimer’s disease).5 Persons with Alzheimer’s disease may neglect oral hygiene, and when they do present for care, may struggle to understand their treatment options. Another common condition among older adults, diabetes mellitus (DM), is known to affect both general and oral health, which demonstrates the bidirectional relationship between oral and systemic health.6–9 Poorly controlled DM may lead to periodontal disease and tooth loss, whereas treatment of periodontal disease in individuals with DM has been shown to improve the glycemic index in these same individuals.10,11
Timely treatment is important for systemic health, and informed consent is a key step to achieving this. As awareness of the importance of maintaining oral health care has evolved, older adults have retained their natural teeth much later in life and thus have required more dental care for a longer period of time.12 Older adults have seen dental practice evolve from the days of the solo practitioner, and dentistry is changing yet again during the COVID-19 pandemic. New terminologies and treatment options can challenge the health literacy of some individuals, especially those with cognitive impairment.13 Despite the importance of studying geriatric informed consent, systemic reviews by Mukherjee and colleagues1 and Jones and Holden14 note that current research on this topic is limited. One thing is clear in the dental literature, namely that obtaining truly informed consent requires more than a lecture or listing of options.15 A systematic review published by the American Dental Association concluded that providing adjunct written materials and having a conversation about the proposed procedure(s) improved informed consent outcomes.13 However, no studies have investigated the use of adjunct materials alone, without a verbal conversation with the provider. Our study is a pilot study designed to test the effectiveness of video versus pamphlet without a patient/provider conversation. The first aim of this mixed-methods study was to explore the effectiveness of two different modalities for supporting older adults to make informed oral health choices: an informative pamphlet and an explanatory video. The research team developed a list of treatments with significant implications for informed consent (e.g., cost, invasiveness) and discussed which would be best suited for the study. Implant placement was
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BOX 1
Informed Consent in Geriatric Patients Questionnaire 1. Please rate your previous knowledge about dental implants on a scale from 1-10 (1 being no previous knowledge and 10 being significant previous knowledge) 1 2 3 4 5 6 7 8 9 10 2. After watching the video/reading the pamphlet, how confident are you in your understanding of dental implant placement surgery? 1 2 3 4 5 6 7 8 9 10
BOX 2
Guiding Questions for Focus Group 1. How has your experience at the dentist been in the past? a. What procedures have you had previously? 2. How well has your dentist explained various dental procedures to you? a. Do you feel you have the opportunity to ask questions if you have them? b. Does your dentist address risks, benefits, and alternatives with you during this explanation?
3. After watching the video/reading the pamphlet, how confident are you in accepting a doctor’s treatment plan of dental implant placement surgery? 1 2 3 4 5 6 7 8 9 10
3. What area do you think we didn’t cover well throughout this process?
4. Please rate the helpfulness of this video in explaining the procedure: a. The video/pamphlet made me more confused b. The video/pamphlet was not helpful c. The video/pamphlet was somewhat helpful d. The video/pamphlet was significantly helpful
5. Are there reasons why you visit the dentist often? What about not at all?
5. On a scale from 1-10, how confident are you in your ability to understand the risks of dental implant placement surgery after watching the video/reading the pamphlet? 1 2 3 4 5 6 7 8 9 10
7. Do you appreciate your dental care provider? a. What traits make you feel this way? b. What traits do you look for in your provider?
6. On a scale from 1-10, how confident are you in your ability to understand the benefits of dental implant placement surgery after watching the video/reading the pamphlet? 1 2 3 4 5 6 7 8 9 10 7. After watching the video, how do you feel you are able to make a more informed decision about if this treatment is right for you? 1 2 3 4 5 6 7 8 9 10
chosen due to it being a common, yet complex and relatively expensive procedure. We hypothesized that the video condition would be viewed by older adults as more informative and supportive of informed consent than the pamphlet-only condition. The second aim was to document experiences and perceptions of older adults with respect to dental care and informed consent in a focus-group setting.
4. How have your experiences changed at the dentist over the years?
6. Are there any specific barriers that dissuade you from going to the dentist? a. Pain? b. Anxiety? c. Finances?
8. Does your dentist use or offer any additional materials to improve the informed consent process? a. If so, what are they? Pamphlet, video, audio/visual tool? b. Was it helpful to you to have this additional resource? 9. What do you suggest could be done to change the way society views dentists and dentistry? What about the informed consent process? 10. How has this discussion been for you? Does anyone have any final comments about what we have talked about?
The study was reviewed and approved by the University of New England Institutional Review Board.
Methods Design
To address the first aim, participants were randomly assigned to read the pamphlet or watch the video. The implant pamphlet from the American Dental Association (ADA) was chosen based on accuracy of information, concise yet comprehensive information and endorsement by the ADA.16 An eightminute “Dental Implant Consent Video,” produced by Blue Sky Bio Dental Implant Systems Inc., was selected as the video condition due to various criteria including production quality, accuracy of information and duration of the video was realistic to be shown in a dental office.17 Participants for each intervention were engaged separately as a group. Participants were then provided 15 minutes to review the pamphlet or the video information. After this exposure, each group received the same follow-up survey ( BOX 1) consisting of demographic questions and others pertaining to the participants’ comprehension of the procedure and confidence for giving informed consent prior to and after the exposure. Opinions were indicated on a 1-10 Likert scale (10 = highest agreement or rating level). To address the second aim, a focus group was conducted with all participants together to further discuss their experiences with informed consent in the dental practice setting and their general views on dentistry ( BOX 2 ) .
Data Analysis
Descriptive statistics and mean difference analyses (t-test) were employed to characterize the data using SPSS version 24. The focus group was recorded, transcribed and subject to grounded thematic analysis and consensus coding. All members of the research team independently reviewed the transcript, noting themes and representative quotations, and then met in small groups to M AY 2 0 2 2
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TABLE 1
Age Distribution of Pamphlet Group and Video Group Age
Pamphlet group
Video group
55–64
2
0
65–74
3
5
75–s84
1
2
> 85
1
0
TABLE 2
Gender Distribution of Pamphlet Group and Video Group Gender
Pamphlet group
Video group
Male
1
4
Female
6
3
TABLE 3
Education Level of Pamphlet Group and Video Group Education level
Pamphlet group
Video group
High school
2
0
Associates
2
0
Bachelors
1
0
Graduate
2
7
determine codes that adequately described the conversations in segments.18,19 The various agreed-upon codes were compiled into four broad themes, which were determined by the entire research team.
Results Participants
Volunteer participants (n = 14) were recruited through a community research registry, the UNE Legacy Scholars Program, and randomly assigned to one of the two conditions. All were white residents of greater Portland, Maine, who ranged in age from 55 to 85, and nine of 14 (64%) were female. The UNE Legacy Scholars Program is open to anyone aged 55 and older and all UNE scholar enrollees were eligible to volunteer for this study. Education levels ranged from high school graduate to graduate school (TA BLE 1 ). Twelve participants were volunteers for 260
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the subsequent focus group.
Survey Results
Likert scale survey responses were averaged for each question. A paired samples t-test was performed in SPSS to compare the participants’ knowledge of dental implants within each group before and after the intervention. The mean confidence level of understanding dental implant placement surgery before and after reading the pamphlet/watching the video was significantly different in both groups; both reading and viewing enhanced confidence and understanding (TA BLE 2 ). In addition, an independent t-test was performed to compare the participants’ confidence level in understanding the risks and benefits of dental implant placement surgery as well as in giving informed consent. The pamphlet group and the video group were not significantly different (TA BLE 3 ).
Focus Group Results Critique of Pamphlet or Video
Participants in both conditions reported enhanced understanding of dental implant surgery following exposure, but with a preference for the video. One major complaint about the pamphlet was the lack of a timeline provided for the implant process. One participant said, “It’s far too basic; it doesn’t go into any depth about what you should be expecting to experience, how long it’s going to take for this whole process to work, etc.” Overall, the participants did not perceive the pamphlet as sufficient. While many of the participants agreed that the pamphlet was quite basic, participants noted shortcomings in the video as well. Most agreed that the video (if watched on their own time or with the dental professional) was preferred, but neither of the educational materials adequately
addressed the cost and complexity of the procedure (including the time factor). Additional information would be needed to make an informed choice. Participants suggested that providing one or both educational materials prior to a scheduled appointment to prime subsequent questioning and discussion would result in, “(Having) a better idea before walking into the dentist’s office, so that I don’t feel totally ignorant and hesitant to even ask a question, because oftentimes, they act like it is obvious what the problem is.” Throughout the focus group, participants commented on the importance of the dental team’s ability to relay information clearly and with sufficient depth to promote comprehension and an informed choice. Another option offered was that of providing the pamphlet and/or video in the dental office and allowing the patient to ask questions while reading or watching. One participant suggested, “I think … to view either the pamphlet or the video with somebody in the dental office — that way it’ll be clearer for me. If you’re home and watching it, you can’t ask a question about what’s going to happen.” Participants also noted a lack of internet access (at home) as a barrier for some elders to benefit from digital materials. Paper still has a place in the informed consent process. The group noted that the video or pamphlet should supplement, not replace an interactive discussion with the provider.
The Pitfalls of Assumptions
When discussing the experiences individuals had with informed consent, many brought up the tendency of the dentist to assume patient comprehension. Dental terminology is not easy for the layperson to understand. Many of the participants noted that both the pamphlet and the video used words that were
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TABLE 4
Survey Participants’ Knowledge on Dental Implant Before and After Reading the Pamphlet or Watching the Video Pamphlet group (n = 7)
Video group (n = 7)
Mean (std. deviation)
Mean (std. deviation)
Previous
After reading the pamphlet
Previous
After watching the video
3 (2.38)
9 (0.816)
5.43 (2.76)
8.86 (1.07)
Confidence level of understanding dental implant placement surgery
Sig. (2-tailed)
p < 0.001
p = 0.039
Participants had a higher level of understanding dental implant surgery after reading the pamphlet (p < 0.001) or watching the video (p = 0.039).
unfamiliar and neither explained them effectively. One participant stated, “There are some terms in there, some appropriate medical (or) dental terms that you all understand and make the assumption that we understand what edentulous or periodontal is, and so remember the audience.”
Building Trust Is Essential
Participants emphasized the importance of mutual trust between the patient and the provider as a crucial aspect of giving true informed consent. Encouraging mutual discussion about dental treatment is seen as key. One participant noted his previous experience, “This individual who was doing the implant informed consent had zero chairside ability at all. They were rude, didn’t want to answer questions, nothing, and I just was so turned off by it, so consequently … never followed through with it.” All the participants agreed that the process should be collaborative; one stated, “It goes to the doctor’s relationship with the patient and making the patient feel comfortable to show that they’re not stupid, you know, that they can say ‘I
don’t get it,’ ‘What’s it mean?’ ‘What are you doing and why?’” Another participant requested for the professional to “talk to me about what’s going on in my mouth in a way I can understand … that makes all the difference in the world to me,” while another participant stated, “I would start asking questions and kind of get half answers, and … it was like ‘why are you bothering me with these questions?’” These concerns all relate to the development of mutual trust or lack thereof. Participants noted the importance of involvement of the entire dental team (dental assistants and dental hygienists) in the informed consent process, not just the dentist. Some group members expressed that they have a positive relationship with their dentist and hold a high degree of mutual trust. Others felt the opposite. One participant stated, “I think there’s an awful lot of the trust that used to happen between the dentist and the patient (that) is disintegrating, unfortunately, so that the informed consent process is a lot more important now.” One participant stated, “Dentists should not get too comfortable with the fact that … the patient signed the informed consent. Don’t assume that ‘I may
have forgotten to tell so-and-so something, but I have this informed consent paper, so I don’t have to worry.’ That’s not a good way to go into this. You want to ensure that people really do understand … and have a calm way to ask questions. Trust is paramount in any profession. It is crucial.”
Discussion
This mixed methods study explored the relative effectiveness of learning about dental implant treatment through a written pamphlet versus a training video. Broader perceptions of dental care, particularly those related to informed consent, were examined through a subsequent focus group with the same participants. Our results indicate that educational materials are helpful in an informed consent process, but they cannot substitute for interactive questioning and dialogue with a provider. This study demonstrated that both the pamphlet group and the video group reported enhanced confidence in their ability to give informed consent. Both modalities served to improve the level of understanding of the implant procedure, and interestingly, although several participants had undergone the procedure, they felt they did not have adequate knowledge coming into the study. After the intervention, they had a better understanding of the risks and benefits. This finding indicates that both the pamphlet and the video are effective supplemental resources that can be used in the dental setting to increase a patient’s knowledge base and confidence in giving informed consent. However, note the word supplemental. Neither the pamphlet nor the video are recommended as substitutes for frank discussions between practitioner and patient. Participants overall felt that they needed to be given the time to read or watch the adjunct resource materials M AY 2 0 2 2
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TABLE 5
Survey Participants’ Understanding Level of the Risks and Benefits of Dental Implant Before and After Reading the Pamphlet or Watching the Video Confidence level
Pamphlet group (n = 7)
Video group (n = 7)
Mean (Std. Deviation)
Mean (Std. Deviation)
P-value (2-tailed)
Participants’ confidence in understanding risks of dental implant placement surgery
6.86 (2.73)
8.71 (0.95)
0.131
Participants’ confidence in understanding benefits of dental implant placement surgery
8.86 (0.90)
9.14 (1.22)
0.626
Participants’ confidence in ability to give informed consent
8.29 (1.80)
8.57 (1.27)
0.738
There was no significant difference in understanding of risks or benefits of dental implant surgery after watching the video or reading the pamphlet.
independently. Yet the timeline for this process did not reach consensus. One suggested that this should take place prior to the office visit, while others preferred viewing the video during the visit with time set aside for the provider to answer questions. Participants all felt that having the time to read the informed consent document and ask questions prior to the procedure would improve their confidence in giving informed consent for a treatment plan. When discussing experiences individuals had with informed consent, participants brought up the tendency for the dentist (or dental professional) to assume patient comprehension. Examples ranged from assumptions of understanding dental terminology, the dental procedure itself, treatment options, risks and benefits of each option and the cost of dental procedures. The discussion about assumptions led to further concerns about the omission of important information about time involved and high monetary cost. One example given was the need for both implant placement and restoration of the implant with an 262
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implant-supported crown. Assuming the patient knows both steps are necessary without explanation or discussion can negatively affect patient satisfaction. Providers automatically may speak in dental jargon, not realizing the patient may not be fully comprehending. This was noted by participants both when discussing treatment with the provider and also in the adjunct materials. For example, both included the term “osseointegration.” Although the provider may use these materials to aid the informed consent process, it is still ultimately the responsibility of the provider or the provider’s staff to use appropriate “plain language” that can be easily understood by the patient. Offering the patient the opportunity to pose questions by asking, “What questions do you have?” versus “Do you have any questions?” invites follow-up inquiries.20 Avoiding assumptions of comprehension benefits both the provider and the patient by setting clear expectations on actual procedures, healing times, number of appointments and cost. Some dentists may not feel they have the time to sit and
answer questions posed by patients. Yet to promote best practice, making time for mutual discussion is a necessity. If the dentist cannot provide the time, training other office staff members, such as implant coordinators and assistants, to answer questions within their scope of practice may provide an alternative solution. Participants emphasized the importance of mutual trust between the patient and the provider as a necessary prerequisite component of giving true informed consent. Only a few participants expressed that they had a strong mutually trusting relationship with their dentist. The focus group discussion included the importance of younger providers especially building trusting relationships with older patients, as many of the older patients had gone to the same dentist for decades prior to their dentist retiring. One participant went as far as to say trusting relationships between patients and providers were “disintegrating” and pointing out informed consent is more important now than ever. Participants felt that to build trust the provider must take the time needed to discuss the treatment, seek trust and gain understanding from the patient prior to signing the informed consent. The focus group concluded that the signing of the consent form should not be the goal of providers; the goal should be to ensure a high degree of understanding of the dental procedures. Providing a high-quality pamphlet or video prior to the appointment would be a way to allow the patient to come to their appointment prepared with questions for the dentist. The consensus seemed to be that the adjunct materials were helpful, but only in addition to discussion with a dentist. These materials cannot, and should not, replace a valuable discussion with the dentist about a treatment. This discussion needs to take as long as necessary for each patient to achieve an
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adequate level of understanding. The “teach-back” method can be helpful to ensure adequate comprehension.21
Limitations
This clinical research project aimed to begin the conversation about informed consent in dentistry. The first limitation was our small sample size largely because this was a pilot study. Furthermore, although the participants were randomly assigned to the pamphlet group or video group, the groups’ education level may have been significantly different: The groups were too small to establish this for sure. While the focus group yielded important information for dental professionals, the results were from a small number of somewhat like-minded participants and may not be transferable to a larger more diverse older population, although this study does offer a place to start. Another limitation was being limited to the use of one pamphlet and one video, which were chosen as the most appropriate by the research team. Participants may have reacted differently had alternate videos or pamphlets been chosen. Many other videos and pamphlets outlining the dental implant process are available. We chose to focus on the informed consent process of dental implant placement due to the growing popularity of the treatment, but there are many other treatments in the dental office where informed consent would need to be obtained. The results from our study can only be applied to patients being more confident to provide informed consent for implant placement. We could have analyzed pre- and postsurvey scores for more of the questions (rather than just confidence level), but the results would not have been conclusive anyway due to the fact that these educational materials, while likely to improve knowledge base, would not be recommended as the primary
procedure for garnering informed consent.
Conclusion
Obtaining informed consent is a required process for many dental procedures. The process can be completed in a quick, careless manner just to meet the regulations or mindfully to ensure that the patient truly understands prior to signing. Adjunct materials such as videos or pamphlets may enhance levels of understanding but can never replace the vital discussion between the dental professional and patient. When working with older adults, perhaps even more care must be taken to ensure trust and facilitate the desired level of comprehension. Older adults may have conditions such as decreased sensory awareness and cognitive decline that necessitate additional attention. Dental professionals can use this information about the informed consent process to create positive changes in their practices that will enhance the experience for both patients and professionals. n AC KN OW L E DGM E N T This project was supported by Dr. Yang Kang’s grant from the Center for Excellence in Aging & Health at the University of New England. Student Research Scholarship was provided by the University of New England College of Dental Medicine. The authors thank Jane Page, Kelly Abrams, Brenna McNally and Lori Rand of the Student Academic Success Center for their help. In addition, they extend their appreciation to Mohamed ElSalhy, BDM, PhD, research coordinator at the University of New England Research Department.
RE FE RE N C E S 1. Mukherjee A, Livinski AA, Millum J, et al. Informed consent in dental care and research for the older adult population: A systematic review. J Am Dent Assoc 2017 Apr;148(4):211– 220. doi: 10.1016/j.adaj.2016.11.019. Epub 2017 Jan 5. 2. Hajivassiliou EC, Hajivassiliou CA. Informed consent in primary dental care: Patients’ understanding and satisfaction with the consent process. Br Dent J 2015 Sep 11;219(5):221– 4. doi: 10.1038/sj.bdj.2015.687. 3. Ortman JM, Velkoff VA, Hogan H. An aging nation: The older population in the United States. Updated 2014. 4. He W, Goodkind D, Kowal P. An Aging World: 2015. Updated 2016. 5. Grady C. Enduring and emerging challenges of informed consent. N Engl J Med 2015 May 28;372(22):2172. doi: 10.1056/NEJMc1503813.
6. Kramarow EA. Dental care among adults aged 65 and over, 2017. NCHS Data Brief 2019 May;(337):1–8. 7. Taylor GW. Bidirectional interrelationships between diabetes and periodontal diseases: An epidemiologic perspective. Ann Periodontol 2001 Dec;6(1):99–112. doi: 10.1902/annals.2001.6.1.99. 8. Mealey BL. Periodontal disease and diabetes: A two-way street. J Am Dent Assoc 2006 Oct;137 Suppl:26S–31S. doi: 10.14219/jada.archive.2006.0404. 9. Kudiyirickal MG, Pappachan JM. Diabetes mellitus and oral health. Endocrine 2015 May;49(1):27–34. doi: 10.1007/ s12020-014-0496-3. Epub 2014 Dec 9. 10. Luo H, Pan W, Sloan F, Feinglos M, Wu B. Forty-year trends in tooth loss among American adults with and without diabetes mellitus: An age-period-cohort analysis. Preventing Chronic Disease. 2015;12:E211. doi: 10.5888/pcd12.150309. 11. Wu C, Yuan Y, Liu H, et al. Epidemiologic relationship between periodontitis and type 2 diabetes mellitus. BMC Oral Health 2020;20(1):1–15. doi:10.1186/s12903020-01180-w. 12. Shuman SK, Owen MK. Ethical issues in oral healthcare for older adults. Generations 2016;40(3):70–78. 13. Moreira NCF, Pachêco-Pereira C, Keenan L, Cummings G, Flores-Mir C. Informed consent comprehension and recollection in adult dental patients: A systematic review. J Am Dent Assoc 2016 Aug;147(8):605–619.e7. doi: 10.1016/j.adaj.2016.03.004. Epub 2016 May 10. 14. Jones JA, Holden ACL. Consent in geriatric dental care and research is important but seldom discussed. J Evid Based Dent Pract 2019 Mar;19(1):95–97. doi: 10.1016/j.jebdp.2019.01.002. Epub 2019 Jan 11. 15. Reid KI. Informed consent in dentistry. J Law Med Ethics 2017 Mar;45(1):77–94. doi:10.1177/1073110517703102. 16. American Dental Association. Dental implants: Are they an option for you? 2020. 17. Blue Sky Bio Dental Implant Systems. Dental Implant Consent Video. May 7, 2015. 18. King MD, Meuser TM, et al. Decoding the Miss Daisy syndrome: An examination of subjective responses to mobility change. J Gerontol Soc Work 2011 Jan;54(1):29–52. doi: 10.1080/01634372.2010.522231. 19. Agnew J, Jorgensen D. Informed consent: A study of the OR consenting process in New Zealand. AORN J 2012 Jun;95(6):763–70. doi: 10.1016/j. aorn.2010.11.039. PMID: 22633383. 20. Riffenburgh A, Stableford S. Health literacy and clear communication: Keys to engaging older adults and their families. In: Robnett R Brossoie N, Chop W eds. 4th ed. Burlington, Mass.: Jones & Bartlett Learning; 2020:109–128. 21. Dinh HTT, Bonner A, Clark R, Ramsbotham J, Hines, S. The effectiveness of the teach-back method on adherence and self-management in health education for people with chronic disease: A systematic review. JBI Database System Rev Implement Rep 2016 Jan;14(1):210–47. doi: 10.11124/ jbisrir-2016-2296. T HE CORRE S P ON DIN G AU T HOR , Yang Kang, DDM, PhD, can be reached at ykang@une.edu.
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C .E. CREDIT QUESTIONS
May 2022 Continuing Education Worksheet This worksheet provides readers an opportunity to review C.E. questions for the article “Informed Consent in the Older Adult Population: A Mixed-Methods Study” before taking the C.E. test online. You must first be registered at cdapresents360.com. To take the test online, please click here. This activity counts as 0.5 of Core C.E. 1. Which of the following statements about informed consent is incorrect: a. It is primarily a legal process that requires the patient to read and sign a consent-to-treatment document. b. It must discuss the risks and benefits of treatment. c. It must include alternatives to treatment including treatment refusal. d. Its main purpose is to protect patients through discussion and education about their dental health needs. 2. True or False: A systematic review published by the American Dental Association concluded that providing adjunct written materials and having a conversation about the proposed procedure(s) improved informed consent outcomes. 3. In this study, which compared providing the information for informed consent in a pamphlet with providing that information in a video, the primary feedback on the pamphlet was which of the following: a. The information it contained was thorough and easy to understand. b. It was simpler and less time consuming than watching a video. c. The diagrams were instructive. d. It was considered too basic and insufficient to make an informed decision. 4. Feedback on the video included which of the following: a. It failed to address the cost and complexity of the procedure. b. It did not discuss the treatment timeline. c. Participants felt additional information was necessary to make an informed decision. d. All of the above 5. Which of the following statements was not part of the focus group discussions on informed consent: a. Dental terminology is often difficult for the layperson to understand, though it is frequently used by dentists and the educational materials they provide. b. The process should be collaborative. c. To reduce confusion, the dentist should be the only one involved in informed consent discussions and to answer patient questions. d. Trust is paramount to the informed consent process. 6. True or False: This study demonstrated that both the pamphlet and
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the video served to improve the level of understanding of the implant procedure group, and both groups reported enhanced confidence in their ability to give informed consent. 7. Which of the following suggestions did focus group members make to improve the informed consent process: a. Use plain language; avoid dental jargon. b. Ask “What questions do you have?” versus “Do you have any questions?” c. Include healing times, number of appointments and cost in the discussion. d. All of the above 8. Which of the following was not a conclusion of the focus group: a. Providing a high-quality pamphlet or video prior to the appointment might be a way to allow the patient to come to their appointment prepared with questions for the dentist. b. The informed consent discussion needs to take as long as necessary for each individual patient to achieve an adequate level of understanding. c. The “teach-back” method can be helpful to ensure adequate comprehension. d. The ultimate goal of informed consent is the patient’s signature on the consent form. 9. This study’s limitations included all but which of the following: a. Small sample size. b. Homogeneity of the groups’ education level. c. Results may not be transferable to a larger, more diverse older population. d. Use of just one pamphlet and one video. 10. True or False: The study results indicated that educational materials are helpful in an informed consent process but cannot substitute for interactive questioning and dialogue with a provider.
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Management of the Glycemic Index Through Periodontal Management With Pharmacological Agents Christian Pretto, DDS; Joshua Tordjman, DDS; and Aviv Ouanounou, BSc, MSc, DDS
abstract Background: Periodontitis and its negative effects on systemic health can affect patients with Type 2 diabetes mellitus (T2DM) and glycemic management in particular. The chronic inflammatory response elicited in response to the bacterial biofilm present in individuals with periodontitis may propagate the chronic inflammation seen in patients with T2DM. Types of studies: This review focuses on current literature exploring the management of periodontitis through pharmacological agents and nonsurgical treatment to regulate the glycemic index in T2DM patients. Results: Chronic periodontitis can affect glycemic control and influence the development and severity of diabetic complications. A cyclical relationship can be formed where uncontrolled hyperglycemia propagates a chronic inflammatory response leading to both increased insulin resistance and increased damage to periodontal tissues. Practical implications: Current evidence suggests that scaling and root planing significantly reduce HbA1c levels in T2DM patients with chronic periodontitis, however, the use of antibiotics to treat periodontitis as adjuncts is equivocal in this matter. Doxycycline and minocycline may have an effect if administered locally, however, more research is needed. Similarly, there is limited research examining the effect of azithromycin on glycemic control. Keywords: Periodontitis, diabetes, SRP, HbA1c, antibiotics
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AUTHORS Christian Pretto, DDS, completed his Doctor of Dental Surgery at the University of Toronto in 2021. He currently works as a general dentist in Thunder Bay, Ontario. Conflict of Interest Disclosure: None reported.
Joshua Tordjman, DDS, graduated from the University of Toronto Faculty of Dentistry in 2021. He is completing his hospital dental residency at Mount Sinai Hospital in Toronto, Ontario. Conflict of Interest Disclosure: None reported. Aviv Ouanounou, BSc, MSc, DDS, is an associate professor in the department of clinical sciences (pharmacology and preventive dentistry), Faculty of Dentistry at the University of Toronto. He is a fellow of the International College of Dentistry, the International Congress of Oral Implantologists, the American College of Dentistry and the Pierre Fauchard Academy. Conflict of Interest Disclosure: None reported.
P
eriodontitis and its consequences on the oral cavity have been researched extensively. The shift in the oral microbiome toward anaerobic gram negative bacteria and an enhanced chronic inflammatory response can result in permanent alterations to the periodontium characterized by collagen degradation, alveolar bone loss and eventual tooth loss.1 More recently, however, the link between periodontitis and its negative effects on systemic health has been a popular research topic, in particular its relationship with diabetes and glycemic management. A hallmark of Type 2 diabetes mellitus (T2DM), both in the initiation and propagation of the disease, is a cytokineinduced chronic low-grade inflammatory response resulting in insulin resistance.2 It is believed that the chronic inflammatory response elicited in response to the bacterial biofilm present in individuals with periodontitis may propagate the chronic inflammation seen in individuals with Type 2 diabetes. This process may be driven through the production of similar proinflammatory cytokines and activation of pathways linked to insulin resistance.3 Therefore, it has been hypothesized that chronic periodontitis can affect glycemic control and influence the development and severity of diabetic complications. This review focuses on the findings of current literature exploring the management of periodontitis through pharmacological agents and nonsurgical treatment to regulate the glycemic index in individuals Type 2 diabetes.
Periodontitis
Periodontitis is a chronic multifactorial inflammatory disease of the periodontium. It is characterized by the gradual irreversible loss of the alveolar bone leading to compromised masticatory function, tooth mobility and eventual 266
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tooth loss.4 Despite the multifactorial nature of the disease, the progression from a healthy periodontium to periodontitis is dependent largely on the shift of the oral microbiome from a symbiotic state to a dysbiotic one.5 FIGURE 1 depicts the categorization of bacterial groups into their six respective complexes based on their properties and pathogenicity, with red complex bacteria having a strong association with the development of periodontitis. Tannerella forsythia, Porphyromonas gingivalis and Treponema denticola are pathogens that are associated with the development of multiple clinical parameters of periodontitis, including increased pocket depth and bleeding on probing.6–8 These red complex bacteria are rarely found in isolation and are often associated with the presence of bacteria of the orange complex, highlighting the dynamic relationship that exists in periodontal pockets.8 Additionally, Aggregatibacter actinomycetemcomitans, part of the blue complex, has also been associated with certain forms of periodontitis.9 The ecological plaque hypothesis was built on previous theories and proposed that changes in the environment could disrupt the dynamic equilibrium that exists between the host and the resident microflora, favoring the overgrowth of periodontal pathogens, including those in the red complex.10 These changes arise from a multitude of factors including diet, salivary composition and pH as well as inflammation.11 It is understood that chronic inflammation drives the progression from gingivitis to periodontitis. Initial, nonspecific plaque accumulation leads to an inflammatory response and subsequent gingivitis. The increased gingival crevicular fluid and blood present create an ideal environment for pathogens associated with periodontitis to thrive, creating a shift to a pathogenic microflora. Despite
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TABLE 1
Glycated Hemoglobin (HbA1c) Levels14 HbA1c (glycosylated hemoglobin) Red Tannerella forsythia
Blue
Porphyromonas gingivalis
Aggregatibacter actinomycetemcomitans
Treponema denticola
Yellow Streptococcus gordonii Streptococcus intermedius
Green
Streptococcus mitans
Capnocytophaga sp.
Streptococcus oralis
Campylobacter concisus
Streptococcus sanguis
Eikenella corrodens
Orange Campylobacter gracilis Campylobacter rectus Campylobacter showae Eubacterium nodatum
Actinobacillus actinomycetemcomitans
Fusobacterium nucleatum Prevotella intermedia
Purple Veillonella parvula
Prevotella nigrescens
Actinomyces odontolyticus
Streptococcus constellatus
FIGURE 1. Complexes of bacteria that colonize the periodontium. Red C = complex bacteria are the highest risk for periodontitis development, while orange and blue complex bacteria are closely related to periodontal disease.4,5,7
the fact that chronic inflammation is the primary driver in this ecological shift, the increase in prominence of pathogens such as P. gingivalis can further propagate the inflammatory response.11 Given the role of inflammation in periodontitis, systemic manifestations of inflammation have also been noted, including prolonged states of hyperglycemia.12
Type 2 Diabetes Mellitus
T2DM is an endocrine disorder characterized by a diminished physiological response to insulin, resulting in a persistent state of hyperglycemia.13 Despite the advancement in prevention and management of T2DM, both personal and financial burdens imposed by the disorder remain prominent. In 2017, the direct medical costs of diagnosed diabetes was approximately $237 billion in the U.S. alone, in addition to $90 billion due to reduced productivity associated
with diabetes.14 Complications associated with unmanaged blood glucose levels in individuals with T2DM are well documented. Complications include, but are not limited to, diabetic neuropathy, nephropathy, macro- and microvascular complications, retinopathy, impaired wound healing and an increased risk for infection.15,16 Given the negative implications of poorly managed blood glucose levels, accurate monitoring is essential in order to minimize the impact of the disease on one’s quality of life. Glycated hemoglobin (HbA1c) remains the gold standard marker for assessing glycemic control in individuals with T2DM.17 HbA1c measurements provide insight into the average blood glucose levels over the past 60 to 90 days, as plasma levels of glucose directly relate to levels of glycated hemoglobin.18 While blood glucose tests represent a snapshot
Normal
< 5.7%
Prediabetic
5.7% to 6.4%
Diabetic
6.5% +
at the time at which a test was performed, tests for Hb1Ac accurately depict trends over a longer period and directly relate to the risk of development of long-term complications associated with diabetes.18 TABLE 1 depicts the established ranges of Hb1AC, dividing individuals into nondiabetic (4.0%-5.6%), prediabetic (5.7%-6.4%) and diabetic (> 6.5%). To minimize complications associated with the disorder, lifestyle modifications such as diet and exercise as well as maintaining an HbA1c below 7% are recommended.18 Any improvement in glycemic control in diabetic patients will reduce complications as a direct and indirect result of diabetes.19
Relationship Between Periodontitis and Type 2 Diabetes
The impact of uncontrolled hyperglycemia and diabetes on the development and progression of periodontitis is well documented.20–22 In recent years, the idea of a bidirectional relationship between the two diseases has emerged. The deleterious effects of prolonged hyperglycemic states on the periodontium are well known. Impaired neutrophil function, including decreased response to chemotaxis and phagocytosis as well as increased inflammatory response, has been observed.23 In addition, impaired bone matrix production, altered collagen synthesis and increased collagen degradation was found in gingival fibroblasts of diabetic patients. Administration of insulin has been shown to prevent these destructive impacts to the periodontium.23 The recent link examining periodontitis and its effects on diabetes, however, is routed in the chronic activation of the innate immune system. Increased production of proinflammatory cytokines and chronic activation of the M AY 2 0 2 2
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innate immune system can shift the microflora to a pathogenic variation with an increase in prominence of periodontal pathogens.24 Ultimately, this can result in periodontal breakdown and the eventual progression from gingivitis to periodontitis. Furthermore, as stated previously, the accumulation of periodontal pathogens can further propagate the inflammatory response through the release of inflammatory mediators such as IL-1B, TNF-a and PGE2 from monocytes, among other cells.25 While several risk factors including obesity, lack of exercise and smoking have been identified in the development of T2DM, chronic lowgrade inflammation is being increasingly explored as the underlying mediator in the progression of the disease.26 Therefore, it has been suggested that an overgrowth of gram-negative periodontal pathogens may be related to elevated insulin resistance and impaired glycemic control.3 The result would be a positive feedback loop in which poorly controlled diabetes can lead to periodontitis, and the accumulation of periodontal pathogens can further propagate a chronic immune response leading to increased insulin resistance.
Nonsurgical Treatment of Periodontitis and Type 2 Diabetes Mellitus
Currently, there are several means by which dentists aim to improve periodontal conditions. Scaling and root planing (SRP), brushing and flossing, pharmacotherapy and surgical intervention or a combination of those previously mentioned are options considered to manage periodontitis. The treatment of the disease presents inherent problems due to the nature of biofilms and the resistance they have to host defenses and antimicrobials. The gold standard for the nonsurgical management of periodontitis is SRP.27 It is well acknowledged that SRP reduces microbial load in addition to improving 268
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clinical parameters of periodontitis including probing depth (PD) and bleeding on probing (BOP). Despite the significant reduction in microbial load, several studies have demonstrated that within eight weeks recolonization occurs gradually, eventually reaching pretreatment levels.27–29 This is largely due to the inability for SRP to completely eradicate periodontal pathogens as a result of both operator and instrument limitations. Additionally, routine oral hygiene practices by the patients themselves may be ineffective, as bacteria
Antibiotics are less effective due to the complexity of biofilms as well as possessing antimicrobial resistance determinants.
associated with the red complex are often found adjacent to the gingival epithelium deeper in periodontal pockets.8 The use of antimicrobials to manage periodontal disease as an adjunct to mechanical therapy has become increasingly explored in recent years. Given the influence of pathogenic bacteria in the progression of periodontitis, antimicrobials would appear to have a strong position in the management of the disease. However, antibiotics are less effective due to the complexity of biofilms as well as possessing antimicrobial resistance determinants.30 Studies have shown that both pathogenic and commensal bacteria can act as reservoirs for antibiotic resistance genes, with horizontal transfer of these genes occurring in the biofilm.30 Therefore, while not recommended to
be used alone, studies have examined the use of SRP with adjunctive antimicrobial administration to improve clinical outcomes of periodontal therapy compared to SRP alone. Antimicrobials are not, however, the only adjunct being examined with SRP in periodontal patients. Melatonin, a hormone which has been found in the oral cavity, has been shown to be significantly lowered in periodontitis patients.31 A recent double-blind, placebo-controlled, single-center study of 50 diabetic periodontitis patients demonstrated that combined nonsurgical treatment with systemic melatonin treatment provided simultaneous improvements in both periodontal condition and glycemic control after eight weeks when compared with nonsurgical treatment alone.32 A Cochrane Systematic Review reported that SRP alone was effective at improving glycemic control, but the effect seen was only significant for four months posttherapy. It was shown that HbA1c levels were significantly reduced (0.29%) at three to four months posttherapy, but only 0.02% after six months posttherapy.33 The review also compared multiple studies that examined SRP alone versus SRP with antimicrobial therapy and found no significant difference in HbA1c levels at three to four months posttherapy when antimicrobials were added.33 In a 12-month single-center, investigator-blinded, randomized study of surgical periodontal treatment and subgingival SRP of 264 moderate to severe periodontitis patients with Type 2 diabetes, HbA1c levels were reported to drop significantly (0.6%) versus the control group (supragingival scaling and polishing).34 In a clinical trial of 100 patients with T2DM, nonsurgical therapy significantly reduced HbA1c levels when compared with a no-treatment control group. Importantly, when patients
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TABLE 2
Antibiotics, Dosages and Durations for Treatment of Periodontitis39 Antibiotic
Dosage
Duration
Amoxicillin
500 mg
Three times per day × 8 days
Azithromycin
500 mg
Once daily × 4–7 days
Ciprofloxacin
500 mg
Twice daily × 8 days
Clindamycin
300 mg
Three times daily × 10 days
Doxycycline or minocycline
100 mg to 200 mg
Once daily × 21 days
Metronidazole
500 mg
Three times daily × 8 days
Metronidazole + amoxicillin
250 mg of each
Three times daily × 8 days
Metronidazole + ciprofloxacin
500 mg of each
Twice daily × 8 days
Combination therapy
were stratified on the basis of HbA1c levels, poor glycemic control patients revealed 11.8% and 14.9% decreases in HbA1c levels at three and six months posttreatment, respectively.35 The authors reported after multiple linear regression analysis, the higher the HbA1c level at baseline, the greater the decrease in value, and this was independent of the diabetic treatment that the patient was taking.35 It should be noted however that in a six-month single-masked, randomized clinical trial of 514 patients with moderate to severe chronic periodontitis and physician diagnosed diabetes mellitus, no statistically significant difference in HbA1c levels were noted between the treatment group that received SRP and a chlorhexidine mouthwash and the control group.36 Enrollment criteria required that participants had an HbA1c ≥ 7% and < 9% and therefore could not dismiss that individuals outside of this range may experience a decrease in HbA1c following nonsurgical periodontal treatment. Additionally, the study did not examine the use of systemic or topical antibiotics as an adjunct to nonsurgical periodontal therapy as well as surgical periodontal treatment.36 Overall, additional research into the use of nonsurgical treatment for periodontitis should be conducted, further examining its use as a means of improving glycemic control in poorly controlled T2DM patients.
Antimicrobials in the Treatment of Periodontitis
A wide selection of antimicrobials have been proposed as adjuncts to SRP with an aim to improve periodontal conditions in cases of chronic periodontitis that do not respond to SRP alone (TA BLE 2 ). Antimicrobial agents used in the treatment of periodontitis should be specific for pathogens responsible for the development and progression of the disease.37 Unfortunately, no single antibiotic is completely effective at targeting all pathogenic bacteria found in periodontal pockets. To address this issue, pairing antibiotics or adding an adjunct, such as amoxicillin and metronidazole or amoxicillin and clavulin, respectively, offers a broader coverage and has been explored to better manage periodontitis and, subsequently, HbA1c levels.38 Minocycline, doxycycline and macrolides have also been examined for their potential to improve glycemic control through their use in periodontal therapy.39,40
Doxycycline
Doxycycline is a member of the tetracycline family of antibiotics, inhibiting bacterial protein synthesis through interruption of translation. Doxycycline has a bacteriostatic effect with a wide spectrum of activity, demonstrating effectiveness against both aerobic and anaerobic gram-positive and
gram-negative bacteria.41 Additionally, doxycycline has been shown to down regulate the expression of inflammatory cytokines including IL-1, IL-6, TNFɑ and PGE2.42 Given the role of doxycycline in the modulation of inflammatory pathways in addition to its antimicrobial effects, its use in management of periodontitis and the glycemic index would appear justified. The recommended dose of systemic doxycycline in conjunction with SRP in the management of periodontitis is 100 mg BID the first day, followed by 100 mg QD.41 One of the first attempts to manage HbA1c through systemic antimicrobial therapy was with doxycycline. Grossi et al. studied 113 Native Americans with periodontal disease and T2DM who received SRP with topical water and systemic doxycycline (100 mg) for two weeks, topical 0.12% CHX and systemic doxycycline (100 mg) for two weeks, topical povidone-iodine and systemic doxycycline (100 mg) for two weeks, topical 0.12% CHX and placebo or topical water and placebo (control).43 After three months, the doxycyclinetreated groups displayed significantly reduced HbA1c levels (approximately 10% reduction from the pretreatment values), the greatest reduction among all treatment groups.43 Since then, the use of doxycycline to manage periodontitis and subsequently HbA1c levels has had mixed results. Singh et al. explored the use of oral doxycycline (100 mg QD on the first day followed by BID for the subsequent 14 days) with SRP relative to SRP alone to treat periodontitis and manage blood glucose levels. It was demonstrated that SRP with doxycycline has a significant reduction in HbA1c levels at three months posttherapy relative to SRP alone (mean difference of 0.78% relative to 0.6% respectively).44 A randomized clinical trial examined 50 prediabetic (fasting blood glucose levels between M AY 2 0 2 2
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100 mg/dL to 125 mg/dL) patients with periodontal disease who were treated with SRP with or without oral doxycycline (100 mg). They reported that both groups had a significant reduction in fasting blood glucose levels compared with baseline after six months. However, there were no significant differences between groups with and without doxycycline.45 In a longitudinal randomized case-control study examining the effects of SRP with and without oral doxycycline (100 mg) on glycemic control of 66 prediabetic and periodontitis patients, HbA1c levels were significantly reduced in both groups (SRP with and without oral doxycycline) relative to baseline. However, there was no significant difference between both groups with regard to HbA1c levels.46 A meta-analysis of 143 patients with chronic periodontitis and T2DM who received SRP and doxycycline compared with SRP alone showed no significant difference with doxycycline and HbA1c levels compared to the control group, however, all groups had lower overall HbA1c levels. The dosages used for periodontal therapy varied from low dose (20 mg BID for three months) to normal dosage (100 mg/day for 15 days) to preloading dosages (200 mg initial dose, 100 mg for two weeks).47 Therefore, there is evidence to suggest that doxycycline may have an effect on improving glycemic control; however, there are studies suggesting the opposite.
Minocycline
Minocycline, like doxycycline, belongs to the class of antibiotics known as tetracyclines. Minocycline shares several characteristics with doxycycline, including its mechanism of action targeting bacterial protein synthesis as well as its broad spectrum of activity.41 An advantage of minocycline relative to other antibiotics is its lipid 270
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soluble properties, allowing increased penetration into secretions such as saliva and gingival crevicular fluids (GCF).37,48 Minocycline can be found in GCF at levels five times that found in blood.48 Tetracyclines, including minocycline, have found success in the treatment of aggressive forms of periodontitis, largely due to their effectiveness against A. actinomycetemcomitans.37 Minocycline is frequently administered topically to increase its availability and minimize systemic side effects. Topical administration of minocycline in the
Minocycline is frequently administered topically to increase its availability and minimize systemic side effects.
form of minocycline HCL microspheres has been shown to significantly reduce red complex bacteria relative to SRP alone.49,50 Additionally, adjunctive local administration of minocycline has been shown to improve probing depths when compared to SRP alone.50 Preparations for topical minocycline microspheres include 1 mg of minocycline hydrochloride supplied in either 1 or 12 unit-dose cartridges.51 Dosing is variable and dependent on the size, shape and number of periodontal pockets being treated. Treatment regimens are up to three treatments at three-month intervals in pockets with depths of 5 mm or greater.51 Given the effectiveness of minocycline in reducing red complex bacteria and improving periodontal conditions, several studies have examined
the efficacy of minocycline on the management of HbA1c levels when used to treat periodontitis. In a randomized clinical trial, 28 poorly controlled T2DM patients with chronic periodontitis (HbA1c >/= 8.5% for over five years) were treated with SRP with and without subgingival minocycline (2% gel) versus supragingival plaque control for six months. The results showed that HbA1c was reduced between the three-month and six-month mark, with 64.3% of patients in the SRP group and 57.1% of patients in the SRP plus minocycline group showing improvements in HbA1c levels; however, there was no significant difference between the groups.38 This trial had a very small sample size and could be expanded to increase the power of the study and better determine the nature of minocycline as an adjunct treatment for management of glycemic control. This research group had also shown previously that subgingival minocycline ointment significantly improved periodontal parameters by reduced probing depths, clinical attachment loss, gingival index and IL-1b content in the gingival crevicular fluid per site. The group attributed this to the antimicrobial nature of the drug.52 Another study examining the use of minocycline was conducted to examine the effects the antibiotic had on TNF-a levels, a product of adipose tissues known to play a role in insulin resistance as well as microbial load and HbA1c levels. The study examined 13 T2DM patients treated only with local minocycline administration (10 mg) into each periodontal pocket once per week for one month. A significant reduction in the number of microorganisms in the periodontal pockets was reported, as well as a reduction in circulating TNF-a levels. Furthermore, HbA1c levels were significantly reduced (0.8%).53 It is important to note the low sample size
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of this group and the lack of a control group in this study. Minocycline, like doxycycline, may also improve glycemic control, however, more research with a larger sample size is needed.
Azithromycin
Macrolide antibiotics, which include azithromycin, are a class of antibacterial agents that function through the disruption of translation and subsequent inhibition of protein synthesis.54 Azithromycin has garnered interest for its possible use in both treatment of periodontitis and modulation of HbA1c levels. It has a broad spectrum that is particularly effective against anaerobes and gram negative bacilli.41 Azithromycin accumulates well in GCF due to its ability to be taken up by phagocytes, acting as reservoirs for the drug.55 In addition, azithromycin has been found to remain at levels above the minimum inhibitory concentration for P. gingivalis, P. intermedia and A. actinomycetemcomitans two weeks following administration.56 The sustained activity may be linked to the high intracellular concentration of azithromycin in phagocytes, relative to other pharmacological agents. While the antimicrobial effects of azithromycin are well documented, studies have shown that it also has effects on GCF volume and inflammatory marker production.57 GCF volume has repeatedly been shown to correlate with gingival inflammation. GCF volume has been shown to be decreased in individuals on azithromycin therapy with minimal plaque for the first seven days following initiation, highlighting its possible role in suppression of inflammation.57 Additionally, a decrease in levels of pro-inflammatory cytokines including IL-1B, IL-8 and TNF-a has been observed in the GCF of individuals taking azithromycin.57 Azithromycin is typically prescribed as 500 mg QD for four
to seven days.41 A randomized clinical trial treated 105 Type 1 and Type 2 diabetic patients with moderate periodontitis with SRP with or without azithromycin (500 mg/day for three days) or azithromycin (500 mg/day for three days) with supragingival prophylaxis. There was no decrease in HbA1c levels when patients were treated with azithromycin and supragingival prophylaxis. However, there was a significant decrease of 0.8% in HbA1c within the azithromycin plus SRP group compared with the placeboSRP group (0.3% reduction) after nine
GCF volume has repeatedly been shown to correlate with gingival inflammation.
months.58 Therefore, azithromycin alone may not have an effect on glycemic control but may in fact have an adjunctive effect once the bacterial source is mechanically disrupted.
Amoxicillin and Amoxicillin/ Metronidazole
Amoxicillin is an antibiotic derivative of penicillin G, targeting cell wall synthesis to inhibit bacterial replication through bactericidal means. As a result, amoxicillin has a broad spectrum of activity against gram-positive bacteria, while also having increased coverage of gram-negative relative to penicillin.59 As discussed previously, the biofilm that exists in periodontal pockets harbor antibiotic resistance genes that can be transferred among the bacteria. In
particular, beta lactamase activity is frequently found in biofilms of individuals with periodontitis, cleaving the beta lactam ring of amoxicillin, rendering it ineffective.59 Therefore, amoxicillin is often given in combination with a beta lactamase inhibitor such as clavulanic acid or an adjunctive antibiotic such as metronidazole to increase coverage.37 Metronidazole targets bacteria through DNA synthesis inhibition, covering a spectrum consisting primarily of obligate anaerobes, both gram-positive and negative.59 The typical dose of amoxicillin and metronidazole for management of periodontal disease is 500 mg TID for 14 days and 400 mg TID for 14 days respectively.60,61 Studies have looked at the utilization of amoxicillin alone as well as in combination with metronidazole to manage HbA1c levels when used to treat chronic periodontitis. A recent clinical trial evaluated 60 prediabetic patients with chronic periodontitis who received SRP and amoxicillin (500 mg TID for five days) compared to a control group who received no periodontal treatment during the three-month period. Both fasting plasma glucose and HbA1c levels were significantly reduced in the treatment group four months after treatment began. It is important to note however that these patients were not randomly assigned according to the study.62 Due to the significant improvement in glycemic control, perhaps chronic periodontitis should be treated more aggressively in prediabetic patients in order to improve glycemic status. The DIAPERIO randomized controlled clinical trial assessed 91 diabetic (Type 1 and Type 2) patients who were given SRP and systemic amoxicillin (2 g/ day for seven days) compared with a no-treatment group (who were later given the same procedures due to ethical reasons after the trial was over). After M AY 2 0 2 2
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TABLE 3
Authors
Type
Treatment
Outcome
Sample Size
Simpson et al. (2015)
Systematic review
SRP alone
Significant improvement of HbA1c at 3-4 months, but not at six months
920 participants
D’Aiuto et al. (2018)
Randomized controlled trial
SRP alone
Significant improvement of HbA1c levels (0.6%)
264 moderate-severe periodontitis patients with T2DM
Kaur et al. (2015)
Randomized controlled trial
SRP alone
Significant improvement of HbA1c levels when compared with a notreatment control group. The higher the HbA1c level at baseline, the greater the decrease in value
100 T2DM with chronic periodontitis
Grossi et al. (1997)
Randomized controlled trial
SRP with topical water and systemic doxycycline (100 mg) for two weeks, topical 0.12% CHX and systemic doxycycline (100 mg) for two weeks, topical povidone-iodine and systemic doxycycline (100 mg) for two weeks, topical 0.12% CHX and placebo or topical water and placebo (control)
Doxycycline-treated groups displayed significantly reduced HbA1c levels (approximately 10% compared with pretreatment values) at three months
113 periodontitis patients with T2DM
Alshehri et al. (2015)
Randomized controlled trial
SRP with/without doxycycline (100 mg)
Both groups had a significant reduction in fasting blood glucose levels compared with baseline after six months
50 prediabetic patients (fasting blood glucose levels between 100-125 mg/ dL) with periodontitis
Javed et al. (2014)
Randomized case-control study
SRP with/without doxycycline (100 mg)
Significant improvement of HbA1c at three months post-nonsurgical therapy in both groups
66 prediabetic and periodontitis patients
Wang et al. (2014)
Meta-analysis
SRP with/without doxycycline (low dose (20 mg BID for three months), normal dosage (100 mg/day for 15 days), preloading dosages (200 mg initial dose, 100 mg for two weeks)
No significant difference with doxycycline and HbA1c levels compared to the control group, however all groups had lower overall HbA1c levels
143 chronic periodontitis and T2DM patients
Lin et al. (2012)
Randomized controlled trial
SRP with and without subgingival minocycline (2% gel) versus supragingival plaque control for six months
Significant improvement of HbA1c between the three-month and six-month mark compared with supragingival plaque control, however, there was no significant difference between SRP and SRP + minocycline groups
28 poorly controlled T2DM patients with chronic periodontitis
Iwamoto et al. (2001)
Longitudinal study
Local minocycline administration (10 mg) into each periodontal pocket once per week for one month
HbA1c levels were significantly reduced (0.8%)
13 T2DM patients with periodontitis
Botero et al. (2013)
Randomized controlled trial
SRP with or without azithromycin (500 mg/day for three days) or azithromycin (500 mg/day for three days) with supragingival prophylaxis
Significant improvement of HbA1c (0.8%) within the azithromycin + SRP group compared with the placeboSRP group (0.3% reduction) after nine months; no decrease in HbA1c levels when patients were treated with azithromycin + supragingival prophylaxis
105 Type 1 and Type 2 diabetic patients with moderate periodontitis
Joseph et al. (2017)
Nonrandomized case-control clinical trial
SRP and amoxicillin (500 mg TID for five days) compared to a control group who received no periodontal treatment during the three-month period.
Both fasting plasma glucose and HbA1c levels were significantly reduced in the treatment group four months after treatment began
60 prediabetic patients with chronic periodontitis
Vergnes et al. (2018)
Randomized controlled trial
SRP and systemic amoxicillin (2g/ day for seven days) for three months compared with a “no treatment” group
No statistical difference was found in HbA1c levels between both groups
91 diabetic (Type 1 and Type 2) patients with chronic periodontitis
Miranda et al. (2014)
Randomized controlled trial
SRP with placebo or the combination of No statistical difference was found in amoxicillin + metronidazole HbA1c levels between both groups
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58 T2DM patients with chronic periodontitis
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Increased damage to periodontal tissues
Exaggerated immune response to local bacteria
Release of inflammatory mediators
Increased insulin resistance
Increased systemic inflammation
AGEs and ROS worsening hyperglycemic status
FIGURE 2 . Cyclical relationship of the effects of Type 2 diabetes mellitus and chronic periodontitis. AGEs = advanced glycation end products; ROS = reactive oxygen species.64–66
three months, no statistical difference was found in HbA1c levels between both groups.63 In a one-year randomized placebo-controlled clinical trial, SRP with the combination of amoxicillin and metronidazole had no effect on HbA1c levels in 58 T2DM patients with chronic periodontitis compared to baseline measurements and SRP alone. However, the authors note that larger sample sizes might be necessary in order to examine glycemic control properly.60
Discussion
This review discusses different nonsurgical treatments of periodontitis and the concomitant effect on glycemic control (TA BLE 3 ). The relationship between T2DM and chronic periodontitis is bidirectional, where T2DM is a risk factor for periodontitis and periodontitis increases systemic inflammation markers that can worsen glycemic control.64 Due
to the two-way relationship, a cycle is created where glycemic status is poorly controlled, leading to an increase in vascular complications, impairing periodontal healing and thus increasing inflammation (FIGURE 2 ). The resulting increase in serum inflammatory mediators may worsen insulin resistance and subsequently diabetic complications.64 Further compounding the issue periodontal inflammation has on glycemic control is the fact that diabetic individuals have an exaggerated immune response to a periodontal bacterial challenge relative to healthy individuals.65 Local periodontal bacteria produce byproducts leading to an increase in serum inflammatory mediators and cytokine production by the host.66 Persistent states of hyperglycemia prime monocytes in diabetic individuals, which may be one mechanism by which diabetics elicit a more profound inflammatory response to periodontal pathogens and
develop more severe periodontitis.65,67 A key mediator in the development of insulin resistance and subsequently diabetes is the production of advanced glycation end products (AGEs).68 AGEs are proteins, amino acids or lipids that have become glycated as a result of exposure to reducing sugars. Increases in AGEs in diabetic individuals are a result of an increase in circulating glucose concentrations, AGE precursors and oxidative stress. Increases in AGEs are becoming increasingly linked to the development of insulin resistance.68 Several studies, including one by Guo et al., have demonstrated a significant increase in both ROS and AGEs in individuals with periodontal disease.5 It has also been shown that periodontitis is associated with increased expression of the transmembrane receptor protein for advanced glycation end products (RAGE) and a decrease in circulating soluble RAGE (sRAGE).69 sRAGE acts as a decoy receptor, lacking the signaling capabilities of RAGE.69 AGEs interact with RAGE on monocytes and macrophages residing in GCF and elicit a potent inflammatory response.70 The result is an increase in proinflammatory cytokines including TNF-a and IL-1b, which is commonly seen in both T2DM and periodontal disease.67,70 Therefore, management of periodontitis may decrease systemic inflammation, allow for better glycemic management and help reduce insulin resistance. It is well known that SRP in chronic periodontitis patients improves periodontal conditions, as seen by the marked improvements observed in the clinical parameters that define the disease when SRP is conducted. However, the systemic effects, such as better glycemic control through improved Hb1Ac levels, that result from improved periodontal health are M AY 2 0 2 2
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less documented. It is proposed that the mechanical disruption of underlying biofilms residing in gingival pockets can disrupt the cyclical relationship that exists between periodontitis and T2DM (FIGURE 2 ). A possible mechanism for this effect can be seen through a reduction of serum inflammatory mediators, hsCRP and TNF-a, as reported by Artese et al. Another possible mechanism can be through the reduction of IL1b, a pro-inflammatory cytokine, in the gingival crevicular fluid following SRP.71,72 This decrease in systemic inflammation may improve insulin resistance in T2DM and allow for better management of HbA1c levels.64 While SRP is the gold standard for the nonsurgical treatment of periodontitis, the limitations with regards to both operator ability and instrument design leave room for improvement. Adjunctive use of antimicrobials with SRP has been proposed as a way to further improve both clinical periodontal parameters as well as manage blood glucose levels in patients with diabetes and periodontal disease. Results from studies examining the adjunctive use of various antimicrobials with SRP compared to SRP alone to improve glycemic control yield mixed results. Doxycycline and minocycline were suggested to have a positive relationship with reducing HbA1c levels when given systemically. However, just as many papers report no significant relationship. Local delivery of antimicrobials is reported to have more effect on glycemic control; however, these studies have low sample sizes. Lack of standardization among studies represents a potential issue that makes comparing studies and making inferences on the potential applicability of the results difficult. Variation in antimicrobial regimens and doses, study populations, time between treatment and assessment as well as the reporting 274
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of means when there may be significant individual variation all represent issues making the comparison of studies difficult. Future studies should aim to maintain a standard in both treatment and evaluation, increasing the length of clinical trials and exploring other antimicrobials that have not been evaluated yet in terms of glycemic control. Azithromycin is one drug that should be researched more in depth, as there was a positive relationship when used adjunctively with SRP.73 Furthermore, systemic markers of inflammation should be examined for mechanisms of glycemic fluctuations as a result of periodontitis. The effect of surgical periodontal treatment on glycemic control in patients with Type 2 diabetes should also be investigated more thoroughly. Newer treatments of periodontitis, such as a gum diode laser, warrant further investigation as well. The diode laser, at a wavelength of 980 nanometers and a power of 2 watts, has been shown to have bactericidal effect on most bacteria, including anaerobes, as a result of elevated tissue temperatures.74 Finally, naproxen or other NSAIDs to target inflammatory mediators should be evaluated as well. In conclusion, additional research into the management of HbA1c in T2DM patients should be conducted, particularly in instances of poorly controlled diabetes. Additionally, the practice of prescribing systemic antimicrobials with the aim of improving glycemic control should be reevaluated. n RE FE RE N CE S
1. Mehrotra N, Singh S. Periodontitis. StatPearls Publishing; 2020. 2. Rehman K, Akash MSH. Mechanisms of inflammatory responses and development of insulin resistance: How are they interlinked? J Biomed Sci 2016 Dec 3;23(1):87. doi: 10.1186/s12929-016-0303-y. 3. Santos Tunes R, Foss-Freitas MC, Nogueira-Filho Gda R. Impact of periodontitis on the diabetes-related inflammatory status. J Can Dent Assoc 2010;76:a35.
4. Nazir MA. Prevalence of periodontal disease, its association with systemic diseases and prevention. Int J Health Sci (Qassim) Apr–Jun 2017;11(2):72–80. 5. Lasserre JF, Brecx MC, Toma S. Oral microbes, biofilms and their role in periodontal and peri-implant diseases. Materials (Basel) 2018 Sep 22;11(10):1802. doi: 10.3390/ma11101802. 6. Socransky SS, Haffajee AD. Periodontal microbial ecology. Periodontol 2000 2005;38:135–87. doi: 10.1111/j.16000757.2005.00107.x. 7. Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL Jr. Microbial complexes in subgingival plaque. J Clin Periodontol 1998 Feb;25(2):134–44. doi: 10.1111/j.1600-051x.1998. tb02419.x. 8. Mohanty R, Asopa SJ, Joseph MD, Singh B, Rajguru JP, Saidath K, et al. Red complex: Polymicrobial conglomerate in oral flora: A review. J Family Med Prim Care 2019 Nov 15;8(11):3480–3486. doi: 10.4103/jfmpc.jfmpc_759_19. eCollection 2019 Nov. 9. Gholizadeh P, Pormohammad A, Eslami H, Shokouhi B, Fakhrzadeh V, Kafil HS. Oral pathogenesis of Aggregatibacter actinomycetemcomitans. Microb Pathog 2017 Dec;113:303– 311. doi: 10.1016/j.micpath.2017.11.001. Epub 2017 Nov 5. 10. Bartold PM, Van Dyke TE. Periodontitis: A host-mediated disruption of microbial homeostasis. Unlearning learned concepts. Periodontol 2000 2013 Jun;62(1):203–17. doi: 10.1111/j.1600-0757.2012.00450.x. 11. Nyvad B, Takahashi N. Integrated hypothesis of dental caries and periodontal diseases. J Oral Microbiol 2020;12(1):1710953. doi: 10.1080/20002297.2019.1710953. eCollection 2020. PMCID: PMC6968559. 12. Preshaw PM, Alba AL, Herrera D, Jepsen S, Konstantinidis A, Makrilakis K, et al. Periodontitis and diabetes: A two-way relationship. Diabetologia 2012 Jan;55(1):21–31. doi: 10.1007/s00125-011-2342-y. Epub 2011 Nov 6. 13. Goyal R, Jialal I. Diabetes Mellitus Type 2. StatPearls. Treasure Island (Fl): StatPearls Publishing Copyright 2022, StatPearls Publishing LLC. 14. American Diabetes Association. Economic costs of diabetes in the U.S. in 2017. Diabetes Care 2018 May;41(5):917– 928. doi: 10.2337/dci18-0007. Epub 2018 Mar 22. 15. Cannon A, Handelsman Y, Heile M, Shannon M. Burden of illness in Type 2 diabetes mellitus. J Manag Care Spec Pharm 2018 Sep;24(9-a Suppl):S5–S13. doi: 10.18553/ jmcp.2018.24.9-a.s5. 16. Okonkwo UA, DiPietro LA. Diabetes and wound angiogenesis. Int J Mol Sci 2017 Jul 3;18(7):1419. doi: 10.3390/ijms18071419. 17. Carlson AL, Mullen DM, Bergenstal RM. Clinical use of continuous glucose monitoring in adults with Type 2 diabetes. Diabetes Technol Ther 2017 May;19(S2):S4–S11. doi: 10.1089/dia.2017.0024. 18. Sherwani SI, Khan HA, Ekhzaimy A, Masood A, Sakharkar MK. Significance of HbA1c test in diagnosis and prognosis of diabetic patients. Biomark Insights 2016 Jul 3;11:95–104. doi: 10.4137/BMI.S38440. eCollection 2016. 19. King P, Peacock I, Donnelly R. The UK prospective diabetes study (UKPDS): Clinical and therapeutic implications for Type 2 diabetes. Br J Clin Pharmacol 1999 Nov;48(5):643–8. doi: 10.1046/j.1365-2125.1999.00092.x. 20. Salvi GE, Carollo-Bittel B, Lang NP. Effects of diabetes
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mellitus on periodontal and peri-implant conditions: Update on associations and risks. J Clin Periodontol 2008 Sep;35(8 Suppl):398–409. doi: 10.1111/j.1600-051X.2008.01282.x. 21. Chávarry NG, Vettore MV, Sansone C, Sheiham A. The relationship between diabetes mellitus and destructive periodontal disease: A meta-analysis. Oral Health Prev Dent 2009;7(2):107–27. 22. Llambés F, Arias-Herrera S, Caffesse R. Relationship between diabetes and periodontal infection. World J Diabetes 2015 Jul 10;6(7):927–35. doi: 10.4239/wjd.v6.i7.927. 23. Daniel R, Gokulanathan S, Shanmugasundaram N, Lakshmigandhan M, Kavin T. Diabetes and periodontal disease. J Pharm Bioallied Sci 2012 Aug;4(Suppl 2):S280–2. doi: 10.4103/0975-7406.100251. 24. Hoare A, Soto C, Rojas-Celis V, Bravo D. Chronic inflammation as a link between periodontitis and carcinogenesis. Mediators Inflamm 2019 Mar 27;2019:1029857. doi: 10.1155/2019/1029857. eCollection 2019. 25. Okada H, Murakami S. Cytokine expression in periodontal health and disease. Crit Rev Oral Biol Med 1998;9(3):248– 66. doi: 10.1177/10454411980090030101. 26. Tsalamandris S, Antonopoulos AS, Oikonomou E, Papamikroulis GA, Vogiatzi G, Papaioannou S, et al. The role of inflammation in diabetes: Current concepts and future perspectives. Eur Cardiol 2019 Apr;14(1):50–59. doi: 10.15420/ecr.2018.33.1. 27. Tariq M, Iqbal Z, Ali J, Baboota S, Talegaonkar S, Ahmad Z, et al. Treatment modalities and evaluation models for periodontitis. Int J Pharm Investig 2012 Jul;2(3):106–22. doi: 10.4103/2230-973X.104394. 28. Mombelli A. Microbial colonization of the periodontal pocket and its significance for periodontal therapy. Periodontol 2000 2018 Feb;76(1):85–96. doi: 10.1111/prd.12147. Epub 2017 Nov 30. 29. Ryan ME. Nonsurgical approaches for the treatment of periodontal diseases. Dent Clin North Am 2005 Jul;49(3):611–36, vii. doi: 10.1016/j.cden.2005.03.010. 30. Kim SM, Kim HC, Lee SW. Characterization of antibiotic resistance determinants in oral biofilms. J Microbiol 2011 Aug;49(4):595–602. doi: 10.1007/s12275-011-0519-1. Epub 2011 Sep 2. 31. Cutando A, Galindo P, Gómez-Moreno G, Arana C, Bolaños J, Acuña-Castroviejo D, et al. Relationship between salivary melatonin and severity of periodontal disease. J Periodontol 2006 Sep;77(9):1533–8. doi: 10.1902/ jop.2006.050287. 32. Anton DM, Martu MA, Maris M, Maftei GA, Sufaru IG, Tatarciuc D, et al. Study on the effects of melatonin on glycemic control and periodontal parameters in patients with type II diabetes mellitus and periodontal disease. Medicina (Kaunas) 2021 Feb 5;57(2):140. doi: 10.3390/ medicina57020140. 33. Simpson TC, Weldon JC, Worthington HV, Needleman I, Wild SH, Moles DR, et al. Treatment of periodontal disease for glycaemic control in people with diabetes mellitus. Cochrane Database Syst Rev 2015 Nov 6;2015(11):CD004714. doi: 10.1002/14651858.CD004714.pub3. 34. D’Aiuto F, Gkranias N, Bhowruth D, Khan T, Orlandi M, Suvan J, et al. Systemic effects of periodontitis treatment in patients with Type 2 diabetes: A 12 month, single-centre, investigator-masked, randomised trial. Lancet Diabetes Endocrinol 2018 Dec;6(12):954–65. doi.org/10.1016/
S2213-8587(18)30038-X. Epub 2018 Oct 24. 35. Kaur PK, Narula SC, Rajput R, R KS, Tewari S. Periodontal and glycemic effects of nonsurgical periodontal therapy in patients with Type 2 diabetes stratified by baseline HbA1c. J Oral Sci 2015 Sep;57(3):201–11. doi: 10.2334/ josnusd.57.201. 36. Engebretson SP, Hyman LG, Michalowicz BS, Schoenfeld ER, Gelato MC, Hou W, et al. The effect of nonsurgical periodontal therapy on hemoglobin A1c levels in persons with Type 2 diabetes and chronic periodontitis: A randomized clinical trial. JAMA 2013 Dec 18;310(23):2523–32. doi: 10.1001/jama.2013.282431. 37. Prakasam A, Elavarasu SS, Natarajan RK. Antibiotics in the management of aggressive periodontitis. J Pharm Bioallied Sci 2012 Aug;4(Suppl 2):S252–5. doi: 10.4103/09757406.100226. 38. Lin SJ, Tu YK, Tsai SC, Lai SM, Lu HK. Non-surgical periodontal therapy with and without subgingival minocycline administration in patients with poorly controlled type II diabetes: A randomized controlled clinical trial. Clin Oral Investig 2012 Apr;16(2):599–609. doi: 10.1007/s00784011-0535-x. Epub 2011 Mar 18. 39. Krayer JW, Leite RS, Kirkwood KL. Non-surgical chemotherapeutic treatment strategies for the management of periodontal diseases. Dent Clin North Am 2010 Jan;54(1):13–33. doi: 10.1016/j.cden.2009.08.010. 40. Santos CM, Lira-Junior R, Fischer RG, Santos AP, Oliveira BH. Systemic antibiotics in periodontal treatment of diabetic patients: A systematic review. PLoS One 2015 Dec 22;10(12):e0145262. doi: 10.1371/journal.pone.0145262. eCollection 2015. 41. Kapoor A, Malhotra R, Grover V, Grover D. Systemic antibiotic therapy in periodontics. Dent Res J (Isfahan) 2012 Sep;9(5):505–15. doi: 10.4103/1735-3327.104866. 42. Newman M, Takei H, Klokkevold P, Carranza F. Newman and Carranza’s Clinical Periodontology. 13th ed. Elsevier; 2018:944. 43. Grossi SG, Skrepcinski FB, DeCaro T, Robertson DC, Ho AW, Dunford RG, et al. Treatment of periodontal disease in diabetics reduces glycated hemoglobin. J Periodontol 1997 Aug;68(8):713–9. doi: 10.1902/jop.1997.68.8.713. 44. Singh S, Kumar V, Kumar S, Subbappa A. The effect of periodontal therapy on the improvement of glycemic control in patients with Type 2 diabetes mellitus: A randomized controlled clinical trial. Int J Diabetes Dev Ctries 2008 Apr;28(2):38–44. doi: 10.4103/0973-3930.43097. 45. Alshehri FA, Javed F. Impact of scaling and root planing on clinical periodontal status and glycemic levels in prediabetic patients. Interv Med Appl Sci 2015 Mar;7(1):17–21. doi: 10.1556/IMAS.6.2014.004. Epub 2015 Mar 20. 46. Javed F, Ahmed HB, Mehmood A, Bain C, Romanos GE. Effect of nonsurgical periodontal therapy (with or without oral doxycycline delivery) on glycemic status and clinical periodontal parameters in patients with prediabetes: A shortterm longitudinal randomized case-control study. Clin Oral Investig 2014 Nov;18(8):1963–8. doi: 10.1007/ s00784-014-1185-6. Epub 2014 Jan 22. 47. Wang TF, Jen IA, Chou C, Lei YP. Effects of periodontal therapy on metabolic control in patients with Type 2 diabetes mellitus and periodontal disease: A meta-analysis. Medicine (Baltimore) 2014 Dec;93(28):e292 doi: 10.1097/ MD.0000000000000292. 48. Khatri PM, Bacha S. Systemic antimicrobial therapy
(minocycline) as an adjunct to non-surgical approach to recurrent chronic generalized gingival hyperplasia. J Indian Soc Periodontol 2014 Mar;18(2):249–53. doi: 10.4103/0972-124X.131345. 49. Goodson JM, Gunsolley JC, Grossi SG, Bland PS, OtomoCorgel J, Doherty F, et al. Minocycline HCl microspheres reduce red-complex bacteria in periodontal disease therapy. J Periodontol 2007 Aug;78(8):1568–79. doi: 10.1902/ jop.2007.060488. 50. Paquette DW, Ryan ME, Wilder RS. Locally delivered antimicrobials: Clinical evidence and relevance. J Dent Hyg 2008 Oct;82 Suppl 3:10–5. Epub 2008 Oct 1. 51. Valeant Pharmaceuticals International Inc. Arestin. 2017. 52. Lu HK, Chei CJ. Efficacy of subgingivally applied minocycline in the treatment of chronic periodontitis. J Periodontal Res 2005 Feb;40(1):20–7. doi: 10.1111/j.1600-0765.2004.00763.x. 53. Iwamoto Y, Nishimura F, Nakagawa M, Sugimoto H, Shikata K, Makino H, et al. The effect of antimicrobial periodontal treatment on circulating tumor necrosis factoralpha and glycated hemoglobin level in patients with Type 2 diabetes. J Periodontol 2001;72(6):774–8. 2001 Jun;72(6):774–8. doi: 10.1902/jop.2001.72.6.774. 54. Champney WS, Burdine R. Azithromycin and clarithromycin inhibition of 50S ribosomal subunit formation in Staphylococcus aureus cells. Curr Microbiol 1998 Feb;36(2):119–23. doi: 10.1007/s002849900290. 55. Fujise O, Miura M, Hamachi T, Aida Y, Nishimura F. Regenerative effect of azithromycin on periodontitis with different levels of gingival inflammation: Three case reports. Aust Dent J 2014 Jun;59(2):245–51. doi: 10.1111/adj.12177. 56. Jain N, Lai PC, Walters JD. Effect of gingivitis on azithromycin concentrations in gingival crevicular fluid. J Periodontol 2012 Sep;83(9):1122–8. doi: 10.1902/ jop.2012.110558. Epub 2012 Feb 14. 57. Ho W, Eubank T, Leblebicioglu B, Marsh C, Walters J. Azithromycin decreases crevicular fluid volume and mediator content. J Dent Res 2010 Aug;89(8):831–5. doi: 10.1177/0022034510368650. Epub 2010 Apr 16. 58. Botero JE, Yepes FL, Ochoa SP, Hincapie JP, Roldan N, Ospina CA, et al. Effects of periodontal non-surgical therapy plus azithromycin on glycemic control in patients with diabetes: A randomized clinical trial. J Periodontal Res 2013 Dec;48(6):706–12. doi: 10.1111/jre.12058. Epub 2013 Feb 27. 59. Akhavan BJ, Khanna NR, Vijhani P. Amoxicillin. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2022. 60. Miranda TS, Feres M, Perez-Chaparro PJ, Faveri M, Figueiredo LC, Tamashiro NS, et al. Metronidazole and amoxicillin as adjuncts to scaling and root planing for the treatment of Type 2 diabetic subjects with periodontitis: Oneyear outcomes of a randomized placebo-controlled clinical trial. J Clin Periodontol 2014 Sep;41(9):890–9. doi: 10.1111/jcpe.12282. Epub 2014 Jul 17. 61. Tamashiro NS, Duarte PM, Miranda TS, Maciel SS, Figueiredo LC, Faveri M, et al. Amoxicillin plus metronidazole therapy for patients with periodontitis and Type 2 diabetes: A 2-year randomized controlled Trial. J Dent Res 2016 Jul;95(7):829–36. doi: 10.1177/0022034516639274. Epub 2016 Mar 24. 62. Joseph R, Sasikumar M, Mammen J, Joseraj MG, M AY 2 0 2 2
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Radhakrishnan C. Nonsurgical periodontal-therapy improves glycosylated hemoglobin levels in pre-diabetic patients with chronic periodontitis. World J Diabetes 2017 May 15;8(5):213–221. doi: 10.4239/wjd.v8.i5.213. 63. Vergnes JN, Canceill T, Vinel A, Laurencin-Dalicieux S, Maupas-Schwalm F, Blasco-Baqué V, et al. The effects of periodontal treatment on diabetic patients: The DIAPERIO randomized controlled trial. J Clin Periodontol 2018 Oct;45(10):1150–1163. doi: 10.1111/jcpe.13003. Epub 2018 Sep 14. 64. Artese HP, Foz AM, Rabelo Mde S, Gomes GH, Orlandi M, Suvan J, et al. Periodontal therapy and systemic inflammation in Type 2 diabetes mellitus: A meta-analysis. PLoS One 2015;10(5):e0128344. doi: 10.1371/journal. pone.0128344. 65. Nishimura F, Iwamoto Y, Soga Y. The periodontal host response with diabetes. Periodontol 2000 2007;43:245–53. doi: 10.1111/j.1600-0757.2006.00171.x. 66. Górska R, Gregorek H, Kowalski J, Laskus-Perendyk A, Syczewska M, Madaliński K. Relationship between clinical parameters and cytokine profiles in inflamed gingival tissue and serum samples from patients with chronic periodontitis. J Clin Periodontol 2003 Dec;30(12):1046–52. doi: 10.1046/j.0303-6979.2003.00425.x. 67. Soorya KV, Suchetha A, Lakshmi P, et al. The effect of scaling and root planing on glycaemic control, periodontal status and gingival crevicular fluid TNF-α levels in an Indian population — to reveal the ambivalent link. J Clin Diagn Res 2014 Nov;8(11):ZC22–6. doi: 10.7860/JCDR/2014/9490.5115. Epub 2014 Nov 20. 68. Nowotny K, Jung T, Höhn A, Weber D, Grune T. Advanced glycation end products and oxidative stress in Type 2 diabetes mellitus. Biomolecules 2015 Mar 16;5(1):194–222. doi: 10.3390/biom5010194. 69. Detzen L, Cheng B, Chen CY, Papapanou PN, Lalla
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E. Soluble forms of the receptor for advanced glycation endproducts (RAGE) in periodontitis. Sci Rep 2019;9(1):8170. doi: 10.1038/s41598-019-44608-2. 70. Mealey BL. Periodontal disease and diabetes. A two-way street. J Am Dent Assoc 2006 Oct;137 Suppl:26S–31S. doi: 10.14219/jada.archive.2006.0404. 71. Sağlam M, Köseoğlu S, Taşdemir I, Erbak Yılmaz H, Savran L, Sütçü R. Combined application of Er:YAG and Nd:YAG lasers in treatment of chronic periodontitis. A splitmouth, single-blind, randomized controlled trial. J Periodontal Res 2017 Oct;52(5):853–862. doi: 10.1111/jre.12454. Epub 2017 Mar 23. 72. Tsang YC, Corbet EF, Jin LJ. Subgingival glycine powder airpolishing as an additional approach to nonsurgical periodontal therapy in subjects with untreated chronic periodontitis. J Periodontal Res 2018 Jun;53(3):440–445. doi: 10.1111/ jre.12532. Epub 2018 Mar 25. 73. Oates TW. Understanding the effects of periodontal therapy plus azithromycin on glycemic control in patients with diabetes remains elusive. J Evid Based Dent Pract 2014 Jun;14(2):73–5. doi.org/10.1016/j.jebdp.2014.04.023. 74. Gadzhula NG, Shinkaruk-Dykovytska MM, Cherepakha OL, Goray MA, Horlenko IM. Efficiency of using the diode laser in the treatment of periodontal inflammatory diseases. Wiad Lek 2020;73(5):841–5.
T H E CO RRE S P ON DIN G AU T HOR , Aviv Ouanounou, BSc, MSc, DDS, can be reached at aviv.ouanounou@dentistry.utoronto.ca.
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his month, the Journal continues its ongoing collaboration with the California State Office of Oral Health with the inclusion of the California Department of Public Health’s “Sugar Toolkit.” Reducing sugar intake is a high priority for the CDPH, CDA and dental and medical professionals everywhere. This toolkit integrates motivational interviewing techniques and adapts the effective tobacco cessation intervention known as the “5A’s” (ask, advise, assess, assist and arrange) to reduce sugar intake. It is also important to note that the Medi-Cal Dental Program reimburses providers for nutritional counseling for children ages 0 to 6 as well as tobacco cessation counseling for adults. The Journal is pleased to help disseminate this resource for immediate use. The Sugar Toolkit is also available online along with downloadable and printable Rethink Your Drink materials.
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Letters to Providers This guide was originally developed by the State of Alaska, and with permission, has been revised by the California Department of Public Health (CDPH), the Office of Oral Health (OOH) to meet California needs.
The Centers for Disease Control and Prevention Division of Oral Health supported this effort as dental providers are uniquely positioned to promote healthy behaviors to prevent chronic disease. Dental health and obesity prevention professionals are working together to help reduce sugary drink consumption and prevent serious health outcomes for California families.
“When Sugar is Not So Sweet” is a brief guide that includes simple visuals and messages dental providers can use to talk with patients about reducing and eliminating sugar-sweetened beverage (SSB) consumption to reduce dental decay and other associated chronic diseases. The guide also helps patients come up with a plan to help reduce and/or eliminate SSB consumption.
When Sugar Is Not So Sweet: A brief guide to explain how sugary drinks can harm your health Adapted for use by:
SSBs are the leading source of added sugar in American’s daily diets. Added sugars contribute about 13% of total daily calories.1 About 47% of calories from added sugars come from sugary drinks.1
The California Department of Public Health Office of Oral Health November 2020
SSB consumption has been shown to be correlated to tooth decay in children.2,3 In California, 54 percent of kindergartners and 70 percent of third graders have experienced dental caries (tooth decay), and nearly one-third of California children have untreated tooth decay.4 Two out of five California children (42%) consume one or more SSBs per day.5
Originally Developed by: Bill Walker, Governor State of Alaska Valerie Davidson, Commissioner Department of Health and Social Services
This guide integrates motivational interviewing techniques and adapts the effective tobacco cessation intervention known as the “5A’s”6 (Ask, Advise, Assess, Assist, and Arrange) to address SSBs.
Division of Public Health Section of Chronic Disease Prevention and Health Promotion Obesity Prevention and Control Program Women’s, Children’s and Family Health Oral Health Program 2017
CDPH is focused on reducing oral health risks by providing resources and education to decrease the consumption of SSBs. The Overall goal of these programs is to educate Californians about health drink options, help identify drinks with added sugars, and to make the link between consumption of SSBs and associated health risks.
For more information, please contact the California Department of Public Health, Office of Oral Health at DentalDirector@cdph.ca.gov
1. US Department of Health and Human Services and US Department of Agriculture. 2015-2020 Dietary Guidelines for Americans. 8th Edition. December 2015. 2. T.Marshall et al, Dental Caries and Beverage Consumption in Young Children. Pediatrics, 2003 3. J.Wilder et al, The association between sugar-sweetened beverages a dental caries among third-grade students in Georgia, Journal of Public Health Dentistry, 2015. 4. California Department of Public Health, Oral Disease Burden, 2017. 5. UCLA Center for Health Policy Research, California Health Interview Survey (CHIS), 2015-2017 6. Centers for Disease Control and Prevention. Best Practices for Comprehensive Tobacco Control Programs — 2014. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014.
1
How to use this guide This guide will help dental providers talk through the 5A’s of a brief office intervention to help patients reduce their sugary drink consumption: • Ask about sugary drinks • Advise to reduce consumption of sugary drinks • Assess readiness for making a change • Assist with developing a plan of action • Arrange for follow-up and support
This guide is designed as a flip book with two types of pages: 1. The patient view has mainly pictures, graphs and few words. 2. The provider view shows a thumbnail picture of the patient view and gives instructions, messages, tips and example responses that you can use during your discussion with patients.
The philosophy: This guide uses the Motivational Interviewing (MI) method, a technique that shows promising results in helping people make positive behavior changes for obesity prevention. This conversation technique is recommended by the American Academy of Pediatrics.15
On the provider view pages, you’ll find common design elements to help you talk with your patients. Patient view: A small thumbnail of the patient view allows you to remember what the patient is looking at as you guide the discussion.
Motivational Interviewing allows patients to voice their concerns and ideas for behavior change, rather than having the provider tell patients what changes to make, and why. The basic conversation techniques follow: open questions, affirmation, reflective listening and summary reflections. The goal is helping patients determine a behavior change to promote healthy lifestyles. The youth or parent determines what they want to focus on and the healthcare provider uses reflective listening to guide them toward change.
These shaded green boxes provide the purpose of the patient view and some general instruction. They are not to be read aloud.
The paper: This guide is printed using Synaps waterproof paper that can be sanitized and wiped as needed.
The example responses in the blue boxes share a potential discussion with a patient. You will vary your response based on your professional clinical judgment. Some example responses include bolded statements, such as “Did I get that right?”. These bolded statements are recommended for you to say out loud as you respond to your patient.
These are key messages to be shared out loud with your patients. They aren’t meant to be read word-for-word, but certain phrases are in bold, larger font to help you quickly scan the page for the most important, key messages. The guide lists “Other ways to say this or ask this” to give alternatives if the sample text doesn’t meet your conversation style.
These tips provide background information, frequently asked questions, or other helpful explanations. ASK
ADVISE
ASSESS
ASSIST
ARRANGE
A progress bar in the lower right-hand corner of the provider view pages identifies where you stand in the 5A’s progression. This bar helps you track progress, skip ahead or go backward as necessary in the discussion with patients.
PATIENT VIEW
REFLECT
DISCUSS Use this visual of various beverages to start a discussion about what your patient drinks.
Reflect back the patient’s response to confirm understanding. Ask about the pros and cons of the drinks they picked.
“Let’s look at these images together. Tell me which of these drinks you have on a typical day?”
“ So, your family drinks mostly water, fruitflavored drinks, and milk every day. What do you think are good things and bad things about these drinks?”
Other ways you could ask: “So, when you’re thirsty, what do you like to drink?” “How many of these drinks do you have each day?” “ Which of these are your favorite drinks?” “ Which of these drinks do you give your child when they’re thirsty?” “ What does your family drink during meals/snacks/as a treat?”
Asking the patient to start the conversation about the good things and bad things about sugary drinks helps them be in charge, rather than just passively receiving advice.
SUMMARIZE Summarize the good and bad responses they give you. Start with the good and end with the bad. Do not add your own bad examples.
Ask the child first, then confirm with the caregiver. Ask more about amounts or timing. If needed, use brand names to clarify images.
ASK
ADVISE
INSTRUCTIONS
ASSESS
ASSIST
“ Your kids really see juice pouches as a treat, and they’re easy to pack in a lunch box. These pouches can be expensive, though, and you’re concerned they have too much sugar for your children’s teeth. Did I get that right?”
ARRANGE
KEY MESSAGE
EXAMPLE RESPONSE
3
TIPS
PATIENT VIEW ASK
ADVISE
ASSESS
ASSIST
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Take this opportunity to advise your patient to cut back on sugary drinks. Use this image to help describe the process of tooth decay when teeth are exposed to sugar. “ I’m concerned about how sugary drinks are affecting your child’s teeth and overall health.” “I know you want your child’s teeth to be healthy, and one way to do that is to cut back on sugary drinks. Is it OK if I spend just a minute showing you a bit more information?” “ This image is showing us a simple way to understand how sugar and sugary drinks hurt your teeth. When you drink or eat sugar, the bacteria that are naturally in your mouth start eating that sugar. That creates acid in your mouth. That acid starts attacking the teeth and dissolves the enamel of your teeth. The enamel is really important because it covers your teeth to protect them. When you lose enamel, your teeth start decaying and painful cavities can form. Cutting back on sugary drinks can make you much healthier and prevent you from feeling the pain of cavities.”
If the patient reports drinking few sugary drinks, compliment them, but also take a minute to encourage them to continue limiting sugary drinks. “ I realize your family rarely has sugary drinks. That is great, and I encourage you to continue limiting them. Is it OK if I spend just a minute showing you a bit more information to help you protect your child’s teeth and overall health?” INSTRUCTIONS
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EXAMPLE RESPONSE
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PATIENT VIEW
Tooth Decay from sugary Drinks
Photographs from Southcentral Foundation
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Use this image to improve your patient’s knowledge and understanding of how sugary drinks can hurt their teeth, and the importance of caring for baby teeth.
“ Over time, sugary drinks can lead to tooth decay. The first stage of decay may be difficult to notice on teeth. As enamel starts to dissolve, you may notice some changes to the teeth. More advanced dental decay can appear brown or black.16 At times, untreated advanced decay cannot be fixed, and the tooth may need to be removed.”
Share more information to help the patient understand the importance of healthy baby teeth.
Taking care of teeth — even baby teeth — is important. Baby teeth hold the space in the mouth needed for permanent teeth that come in later. Cavities that develop in teeth can be painful. Cavities can cause problems with: • eating. • sleeping. • speaking. • learning. Fixing baby teeth by filling them, pulling them out, or putting crowns on them can: • be expensive. • cause pain. • change the appearance of a child’s smile as they grow up. ASK
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Use this image to improve your patient’s knowledge and understanding of how sugary drinks can hurt their health.
Health risks from sugary drinks Cavities and decayed, painful teeth
“Sugary drinks and added sugar harm more than just teeth. These drinks can lead to a number of serious health problems that can last throughout your child’s lifetime.”
Type 2 diabetes that can last throughout your child’s lifetime
Increased risk of heart disease • High blood pressure • High cholesterol
Unhealthy weight gain
Unhealthy weight gain • “Being overweight or obese is a serious health concern.” • “ That’s in part because excess weight is linked to other serious health problems, like type 2 diabetes.” Type 2 diabetes4 • “ Type 2 diabetes used to be considered a health problem that only adults could get. That’s not the case anymore.” • “ Type 2 diabetes happens when too much sugar builds up in your blood, and that puts stress on your body.” • “For some children, type 2 diabetes can be a health struggle for the rest of their lives and require medication and other changes to diet and physical activity.” Heart disease 5,6 • “Some people are surprised to learn that sugary drinks can lead to heart disease over time.“ • “Sugary drinks can increase your child’s risk of high blood pressure and high cholesterol.“ • “If those health problems aren’t treated and managed, they can lead to serious heart problems as your children get older.” 1,2,3
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PATIENT VIEW
The statements below can help you respond to additional questions from patients. You DO NOT have to read each one out loud. Obesity during childhood can harm the body in a variety of ways. Children who have obesity are more likely to have:17-27 • high blood pressure and high cholesterol, which are risk factors for heart disease. • increased risk of type 2 diabetes. • sleep problems, such as sleep apnea. • breathing problems, such as asthma. • gastrointestinal problems, such as reflux disease or constipation. • hip and knee joint problems and pain. • fatty liver disease or gallstones. • a skin condition called acanthosis nigricans. • psychosocial disorders, such as anxiety, fatigue, depression, low self-esteem, eating disorders, as well as social problems, such as bullying and stigma.
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EXAMPLE RESPONSE
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SCORE 1-3: NOT READY FOR CHANGE Are you ready?
“I understand you aren’t ready to make a change right now and that’s OK. Is it OK if I make a note of our discussion today and we talk about it a bit more at your next appointment?”
1 NOT
End your conversation about sugary drinks and make a note in the patient record.
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VERY READY FOR CHANGE For scores 4-7 (contemplation) and 8-10 (preparation/action), ask what makes them ready to change. You gave yourself a score of [#] for being ready to change the types of drinks you serve your family. Why did you pick this score and not a 2?”
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“ Look at this scale of 1 to 10, where 1 is not ready and 10 is very ready. How ready are you to make a change about serving fewer sugary drinks to your family?”
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Use this readiness ruler to assess your patient’s interest in making a change. Match the appropriate brief intervention with their score for readiness for change.
“That is great you would like to make a change. I have a few tools that will help you decide which changes will work best for you and your family.”
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Use your clinical judgment on which actions to take. If a patient is already making plans to reduce sugary drinks, you may decide to skip one or more of the pages that “Assist” with making a plan and move to page 18, “Arrange” for follow up.
Letting the patient describe why they scored themselves a 4-10 instead of a 1-3 affirms their ability or desire to change and is more effective than trying to convince them to move into a higher score. Use their words to talk about their motivation to change.
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SCORE 4-10: SOMEWHAT OR
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EXAMPLE RESPONSE
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Which drinks are hiding the most added sugar? 20 oz
16 oz
SODA
E NE RGY DRINK
20 oz
20 oz
VITA MIN DRINK
8 oz
14 oz
16 oz
SPORTS DRINK
POWDE R E D DRINK
8 oz
SW E ETE NE D FL AVOR E D COFFE E MILK
16 oz
MILK
WATE R
PATIENT VIEW Summarize the patient’s responses and affirm what the patient says.
Use this image to improve your patient’s knowledge and understanding of how much added sugar is hiding in common drinks so they can make a plan to choose healthier drinks.
“ Yes, it is surprising that vitamin and sports drinks have so much sugar, even though they are marketed to families as healthier options.” “As you said, water and milk don’t have any added sugar so they are the healthiest choices.” “ Does any of this information bring up changes you’d like to make for your family?”
“Let’s look at these drinks. Tell me which drinks you think have the most added sugar and the least.”
Summarize their responses, and then reveal the hidden sugar by flipping the plastic cover sheet over the pictures of drinks.
“ That’s great you want to serve fewer powdered drinks. Many of my patients are surprised by how much added sugar is in powdered drinks.”
“ You can see how much sugar is hiding in each drink. What do you notice when you look at these drinks? Is there anything that surprises you?”
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“Now that we know how much sugar is hiding in these drinks, let’s review the health advice.” The U.S. Dietary Guidelines for Americans say to limit added sugar to less than 10 percent of the calories you eat and drink every day for good health.18 • For a moderately active child, that’s only about 10 teaspoons. • For a typical 2,000 calorie diet for an adult, that is no more than 12 ½ teaspoons.”
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18 14 12 10 8 6 4 2 0
VITAMIN DRINK 20 oz
SPORTS DRINK 20 oz
POWDERED DRINK 16 oz
SODA 20 oz
Just ONE sugary drink often has more sugar than your child should have in one day.
PATIENT VIEW Summarize the patient’s responses, affirming what the patient says.
Reinforce your patient’s discussion of desires, abilities or reasons to change behavior. Reinforcing statements by repeating them or summarizing them to patients can help empower them and support their success in making a change.
“ You’re right. Most of the drinks we just looked at have too much added sugar for good health.” “ You’re right. These drinks do have too much added sugar for good health. Cutting back on these drinks can make a big difference.”
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DAILY LIMIT FOR CHILDREN
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FRUIT FLAVORED DRINK 10 oz
Other ways to say this: “It might sound complicated to figure out your limit of added sugar each day. Here’s a simpler way to think about it. Added sugar — whether it’s in your foods or your drinks — should be a really small amount of what you consume each day. Cutting out these sugary drinks avoids a lot of sugar and protects your child’s teeth.” “As you can see from this image, even a 16-ounce powdered drink has more added sugar than a child should have all day. A child can go over the daily limit of added sugar with just that one drink at breakfast — without considering added sugar from sweetened cereals, snacks, or other drinks during the day.” “What do you think about this health advice? Does any of this information help you think of changes you’d like to make for your family?” ASK
DAILY LIMIT FOR ADULTS
20
Teaspoons of Sugar
Use this image to improve your patient’s knowledge and understanding of the U.S. Dietary Guidelines, so they can make a plan to choose healthier drinks.
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TIPS
Use this image to assist your patient in choosing a step in their plan to choose healthier drinks.
“Sometimes it helps to make a plan if you think through some options. Do you see anything on this page that would be a way your family could make a change? Do you want to pick a change or two that you think will work for your family?” Other ways to ask:
PATIENT VIEW
“ How well do you think this option would work for you and your family to start cutting back on sugary drinks? Why or why not?”
If a patient has gone through this tool before, refer to your patient notes and try some of these example responses.
“ What else might work best for your family?” “ Who can support you in making this change?”
“ Last time, you chose this step to cut back on sugary drinks. How has that been working for your family? Would you like to keep taking that step?” “ What about these other options? Could you add any of them to cut back even more on serving sugary drinks to your family?”
These steps are not the only options. If a patient already described a step earlier in the conversation, you can move directly to the next page.
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Choose healthy drinks for healthy teeth. Drink water and low-fat milk.
PATIENT VIEW
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AFFIRM
Provide your patient with a reminder, and make a note in their record to follow up at a future appointment. For the reminder, you can use the card that came with this guide or use your handout.
Offer support and affirm your patient’s ability to make a positive change.
“The ideas you have to make a change [list ideas back to patient] are great. They’re going to improve your child’s health and help protect their teeth from cavities.”
“ This is a card to help remind you of the change you would like to make at home. I’ll put it in your bag with your toothbrush to take with you today. ” “ I would like to check in with you again at our next appointment. Is that OK? I’m going to make a note on my chart so we can talk about it next time.”
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References 1. Daniels S, Hassink S. The Role of the Pediatrician in Primary Prevention of Obesity. Pediatrics. 2015; 136;1:e275-e292. 2. Shivakumar KM, Prasad S, and Chandu GN. International Caries Detection and Assessment System: A new paradigm in detection of dental caries. J Conservative Dentistry 2009 Jan-Mar; 12(1): 10–16. doi: 10.4103/0972-0707.53335 accessed 10/2/2017 at https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC2848805/ 3. Cote AT, Harris KC, Panagiotopoulos C, et al. Childhood obesity and cardiovascular dysfunction. J Am Coll Cardiol. 2013;62(15):1309–1319. 4. Lloyd LJ, Langley-Evans SC, McMullen S. Childhood obesity and risk of the adult metabolic syndrome: a systematic review. Int J Obes (Lond). 2012;36(1):1–11 5. Bacha F, Gidding SS. Cardiac abnormalities in youth with obesity and type 2 diabetes. Curr Diab Rep. 2016;16(7):62. doi: 10.1007/s11892-016-0750-6. 6. Mohanan S, Tapp H, McWilliams A, Dulin M. Obesity and asthma: pathophysiology and implications for diagnosis and management in primary care. Exp Biol Med (Maywood). 2014;239(11):1531–40. 7. Narang I, Mathew JL. Childhood obesity and obstructive sleep apnea. J Nutr Metab. 2012; doi: 10.1155/2012/134202. 8. Pollock NK. Childhood obesity, bone development, and cardiometabolic risk factors. Mol Cell Endocrinol. 2015;410:52-63. doi: 10.1016/j.mce.2015.03.016. 9. Africa JA, Newton KP, Schwimmer JB. Lifestyle interventions including nutrition, exercise, and supplements for nonalcoholic fatty liver disease in children. Dig Dis Sci. 2016;61(5):1375–1386. 10. Risk factors of Acanthosis nigricans, Mayo Clinic website http://www.mayoclinic.org/diseases-conditions/acanthosis-nigricans/basics/risk-factors/con-20025600 accessed September 2017 11. Morrison KM, Shin S, Tarnopolsky M, et al. Association of depression and health related quality of life with body composition in children and youth with obesity. Journal of Affective Disorders 2015;172:18–23. 12. Halfon N, Kandyce L, Slusser W. Associations between obesity and comorbid mental health, developmental, and physical health conditions in a nationally representative sample of US children aged 10 to 17. Academic Pediatrics. 2013;13.1:6–13. 13. Beck AR. Psychosocial aspects of obesity. NASN Sch Nurse. 2016;31(1):23–27. Suggested Citation: Alaska Department of Health and Social Services. When Sugar Is Not So Sweet: A brief guide to explain how sugary drinks can harm your health. Anchorage, Alaska: Section of Chronic Disease Prevention and Health Promotion, Division of Public Health. October 2017. The printing of this publication was supported by Cooperative Agreement Number DP001007 funded by the Centers for Disease Control and Prevention (CDC). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the CDC or the U.S. Department of Health and Human Services.
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Decode dental benefit plans. CDA’s smart Practice Support analysts can help you decipher provider agreement requirements, manage claims efficiently and better understand appeal rights. Get support challenging a decision or filing a claim, and navigate the dispute resolution process with our Dental Benefit Plan Handbook. Explore your CDA member resources at cda.org/DentalBenefits.
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RM Matters
C D A J O U R N A L , V O L 5 0 , Nº 5
Invest in Interviewing To Reduce Risk of Bad Hires TDIC Risk Management Staff
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or an attentive employer, the interviewing process can be a good predictor of a future employee’s potential for success — or barriers to it. When one interviewer asked a candidate how long they worked at their last place of employment, the candidate responded, “I’d say my biggest weakness is my listening skills.” Responses like this illustrate why identifying red flags is essential to the interviewing process. While recent dental staffing shortages may make it tempting to offer a position to the first person who turns in an application, a measured, thoughtful approach to hiring is recommended. The time and planning that you invest to develop your practice’s hiring process will save you money, maintain consistency and reduce the potential risks of “warm body hiring.” The interview portion of your hiring process should take place after a careful screening of potential candidates through clear job descriptions and applications. If you are fortunate enough to have many applicants, conducting brief phone interviews and screening can help to narrow the field. When meeting with candidates virtually or in person, use the opportunity to both learn more about the personality behind the resume and put your best foot forward as a potential employer. Be mindful that each candidate is essentially interviewing you as a potential boss.
Interview Best Practices
The Dentists Insurance Company’s Risk Management analysts often field questions from dental practice owners dealing with employment challenges. Here are a few of their recommendations 292
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for conducting effective interviews: ■ Prepare for each interview by reviewing the candidate’s application and resume and making notes of any specific questions that need to be addressed. ■ Create a list of questions that will be asked of all candidates to determine their experience and competencies. This will arm you with fair and adequate comparisons of those interviewed. Be mindful of the critical employment laws that
■
exist through the U.S. Department of Labor and your state labor bureaus as you do so. California Dental Association members have access to a list of appropriate sample questions in a library of employment practice resources. Keep the interview organized by explaining the process at the beginning. For example, let the candidate know you will be sharing a bit about the practice and your team dynamics and that you will have a
answers
From one-on-one risk management advice by phone to informed consent forms to expert-led seminars, we’re here to help you practice with confidence. We are The Dentists Insurance Company. Learn more at tdicinsurance.com/rm
Protecting dentists. It’s all we do.
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list of questions for them. Make sure to provide time for the candidate to answer any questions they might have about your practice and team as well. ■ Ask open-ended questions to establish rapport and to assess the candidate’s experience and qualifications. ■ After each interview, file your list of questions and other information collected during the interview and selection process in the applicant’s file to avoid allegations of discrimination. To comply with state law, employers should limit requests for information during the interview and selection process to those details essential to determining a person’s experience and qualifications to do the job (with or without reasonable accommodations). Employers are prohibited from requesting information, either verbally or through an application form, that identifies an applicant’s membership in protected groups. As one question leads to another, the conversation may veer into subjects prohibited in the employment context. It is never acceptable to ask candidates about: ■ Race/color. ■ Sexual orientation. ■ Pregnancy/breastfeeding/fertility. ■ Gender/gender identity/ gender expression. ■ Current or prior compensation (including benefits). ■ Criminal history.
Navigating Working Interviews
A unique aspect of the hiring process for dental practices is the clinical or working interview for dental associates or hygienists. These working interviews may be beneficial in the decisionmaking process by allowing candidates to demonstrate their skills in a clinical setting and observe how the practice
owner conducts their office. For practice owners, working interviews are the best way to observe a candidate’s technique and see how they interact with patients and staff. TDIC’s Risk Management analysts caution both practice owners and candidates to be mindful of the scope of liability coverage during working interviews. Sometimes owners mistakenly believe the interviewing dentists will be covered under the owner’s existing professional liability policy. This is not likely the case.
Candidates should contact their insurer to request a binder for a working interview.
Candidates should contact their insurer to request a binder for a working interview. Do not conduct a working interview without verifying the candidate’s coverage.
A Working Interview Case Study
A recent call to TDIC’s Risk Management Advice Line illustrates the importance of liability coverage in these situations. As reported by the practice owner, a candidate for an associate dentist role was invited to spend the day treating patients as part of a working interview. One of the treatment scenarios was a patient who presented for an extraction. The patient’s original treatment plan was to extract teeth Nos. 16 and 7-10. Tooth No. 11 had guarded prognosis, and the short-term plan
was to monitor this tooth. The candidate noted circumferential bone loss associated with tooth No. 11 and believed that a better option would be to extract this tooth. The candidate then proceeded to extract tooth No. 11 without first consulting with the patient or the owner-dentist. Later that day, the patient’s wife called when she noted this deviation from the original treatment plan and capitalized on this “error.” She stated that the dentist did not have her husband’s consent for the additional extraction. The patient’s wife claimed to have guidance from another dentist recommending that to address the loss of tooth No. 11, an implant would be required and would include additional restorative treatment. She ended the phone call by saying: “You and that new, young dentist will be paying for your mistake.” The analyst who took the call discussed the potential for a claim to be made against both the practice and the hiring candidate. The analyst advised that this experience was a good opportunity to review the practice’s procedures for working interviews and to set parameters for how the candidate might be observed and supervised. The analyst also suggested discussing the expectations when the candidate was performing in this role, especially if there was the potential for a change in the treatment plan. Ultimately, this situation created risk for both parties that would require placing their liability carriers on notice of a potential claim. Fortunately, the practice had secured information on the candidate’s liability insurance in advance of the interview. The claims representative for the insurance carrier agreed to reach out to the patient and his wife and attempt to amicably resolve the matter. Even after a new hire is thoughtfully onboarded and trained to join your team, it is difficult to forecast who will be the best long-term fit. However, you can M AY 2 0 2 2
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greatly improve the odds of a “good hire” with attention to details and mitigating risks during the interview process. You can always reach out to the Risk Management Advice Line for guidance in interviewing, hiring and other employment issues. Hiring decisions are among the most important ones you will make as a practice owner. Your choice of candidates will affect your staff, the well-being of your practice and the welfare of your patients. n The Dentists Insurance Company’s Risk Management Advice Line is a benefit available at no cost to CDA members and policyholders protected by TDIC. To schedule a consultation, visit tdicinsurance.com/RMconsult or call 877.269.8844.
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Every Californian deserves a healthy smile. You already know how dentistry relieves pain, restores dignity and instills hope. Join the CDA Foundation’s mission to improve the oral health of all Californians. Together with volunteers and donors, we support dentists’ efforts to give back to their communities and reduce barriers to care. • • • • •
Student Loan Repayment Grants to make careers in public health possible Dental Materials & Supplies Grant for non-profit dental care organizations Volunteer-led CDA Cares clinics that shine a light on underserved areas Support of RDA apprenticeship programs to fill dentistry’s staffing pipeline Peer-to-peer Wellness Program for dentists’ physical and mental well-being
See how you can contribute today at cdafoundation.org.
CDA PRESENTS
New learning options just for CDA members! Through membership, benefit from access to online library of free and discounted courses. Log in, learn and earn C.E. when it works for you!
Oral Cancer Awareness In this two-part on-demand webinar, hear from cancer survivors and learn how clinical teams make a difference in early detection. Better understand screening, referrals, treatment options and how to support patients.
Respiratory Protection with CDPH Earn 1.0 unit C.E. and enjoy waived fees through a self-study version of CDA’s popular live event. Learn about California regulations and how to implement a respiratory protection program in your practice.
GET STARTED TODAY! Already a CDA member? Set up your Online Learning account with the same email you use to access your cda.org account to access a members-only catalog and special pricing. Not yet a member? Set up your account and sign in to access select courses, or join CDA expanded learning options. Learn more at cda.org/online-learning.
Regulatory Compliance
C D A J O U R N A L , V O L 5 0 , Nº 4
Cal/OSHA Citations of Dental Practices CDA Practice Support
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review of Cal/OSHA dental facility inspection data from October 2016 to September 2021 provides useful information to dentists who seek to reduce compliance risk. A total of 37 dental practices were inspected during this period, 43 fewer dental practices than the previous five years.1 The assumed reason for the significant drop in the number of inspections is the COVID-19 pandemic. Twenty-two of the 37 inspected facilities were cited for a total of 44 violations. All but one of the cited facilities had between 1 and 3 citations. One dental practice was cited for five violations.2 The most common citation issued to dental facilities was for failing to have a written injury and illness prevention plan. Ten facilities did not have the required written plan. Facilities also were cited for: ■ Not having a system of communicating workplace hazards to employees. ■ Not having a procedure to investigate occupational injuries and illnesses. ■ Not maintaining records of scheduled and periodic inspections One dental practice’s citation for not having a procedure to investigate occupational injuries and illnesses was part of the agency’s COVID-19 inspections. The citation, categorized as “serious,” has an initial penalty of $3,150 and is being contested at the time of this writing. In addition to the items listed above, a written injury and illness prevention plan must: ■ Identify the person(s) with authority and responsibility for implementing the program.
Describe a system for ensuring employees comply with safe work practices, such as recognition program, disciplinary actions and training. ■ Include methods or procedures for correcting unsafe conditions or work practices. If a dental practice claims exemption to the Cal/OSHA Aerosol Transmissible Disease (ATD) regulation, the plan must include procedures for screening ■
patients for ATDs and management of patients suspected of having an ATD. A COVID-19 prevention plan must be either a standalone plan or an addendum to the injury and illness prevention plan. Sample plans are available on cda.org/practicesupport as part of the Regulatory Compliance Manual. Several citations were issued for violations of the bloodborne pathogens regulation during this period. The violations included:
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Failing to have a written exposure control plan. ■ Failing to have a sharps injury log. ■ Failing to record injury on sharps injury log within 14 working days. ■ Keeping food or drinks in refrigerators or freezers where blood or OPIM were present. ■ Failing to replace sharps container to avoid overfilling. ■ Failing to have appropriate container for regulated waste. ■ Failing to have appropriate PPE available. Dental practices also were cited for violations of these requirements: ■ Hazard communication: written plan, hazardous chemical list, labeling of containers of hazardous materials, staff training. ■ Electrical safety: adequate working space for equipment, adequate guarding of working space. ■ Sanitation: prevent uncontrolled accumulation of water that may lead to mold growth. ■ Sanitary facilities: separate toilet facilities for each gender (dependent on the number of employees). ■ First aid: adequate supplies or usability. ■ Emergency eye wash: availability. ■ Air tank: permit. ■ Fire extinguisher: provision of, inspection and testing, annual maintenance check. ■ Exit: unobstructed. Cal/OSHA categorizes its citations by factors such as whether a violation was willful and by the extent and severity of the violation. A dental practice’s noncompliance with requirements for handling sharps safely was deemed a “serious” violation, and it resulted in a proposed penalty of $4,500. This is the section of the bloodborne pathogens regulation that was cited: ■
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I5193 (d)(3)(C) Requirements for Handling Contaminated Sharps. 1. All procedures involving the use of sharps in connection with patient care, such as withdrawing body fluids, accessing a vein or artery or administering vaccines, medications or fluids, shall be performed using effective patient-handling techniques and other methods designed to minimize the risk of a sharps injury. 2. Immediately or as soon as possible after use, contaminated sharps shall be placed in containers meeting the requirements of subsection (d)(3)(D) as applicable. 3. At all times during the use of sharps, containers for contaminated sharps shall be: ■ Easily accessible to personnel and located as close as is feasible to the immediate area where sharps are used or can be reasonably anticipated to be found (e.g., laundries); ■ Maintained upright throughout use, where feasible; and ■ Replaced as necessary to avoid overfilling. A failure to report to Cal/OSHA a serious work-related injury or fatality led one dental practice to be cited. The citation and proposed penalty of $5,000 are being contested at the time of this writing. n RE FE RE N CE S
1. Cal/OSHA Citations of Dental Practices. J Calif Dent Assoc 2017 May;45(5):261–2. 2. United States Department of Labor. OSHA Inspections Within Industry database. Accessed Feb. 10, 2022.
Regulatory Compliance appears monthly and features resources about laws that impact dental practices. Visit cda.org/ practicesupport for more than 600 practice support resources, including practice management, employment practices, dental benefit plans and regulatory compliance.
Tech Trends
C D A J O U R N A L , V O L 5 0 , Nº 4
A look into the latest dental and general technology on the market
Yoink ($8.99, Matthias Gansrigler)
BoneBox Dental Lite (Free, BoneBox)
Clipboards on desktop and mobile devices are extremely useful. Every day, users copy and paste a plethora of things within an app or in between apps. This productivity tool has traditionally been limited to copying and pasting one item at a time. Yoink for iPhone and iPad provides an unlimited clipboard experience across multiple mobile devices, expanding the versatility of this commonly used tool.
Mobile apps can be effective and engaging educational tools. Because few teaching modalities can rival the mobile app’s portability, interactivity and “wow” factor, Apple’s App Store has been flooded with these applications. Topics from cooking to writing have their own sections of instructional apps, so why shouldn’t dentistry be the same? BoneBox Dental — from iSO-FORM — is a dental anatomy application designed by anatomists for the dental community.
Yoink is a “shelf” app that stores virtually anything users may need to recall later. Anything that can be dragged, shared, copied or downloaded can be kept in the app such as files, text, images, links, videos and more. Users can add items to the shelf once they enable the app through the Share Sheet button. The traditional method of copying and pasting directly to the app is also available. Users can transfer items from the shelf to any app through several means depending on the device. For iOS and iPadOS devices, users can enable the Yoink keyboard, which displays shelf items for easy drag-and-drop or copy and paste. For iPadOS devices only, the shelf is available directly from the app using Side-by-Side or Slide-Over mode. Files stored in Yoink are also accessible from the Files app once the extension is enabled. Simple tasks to add items to the shelf can also be found through Siri Shortcuts. Shelf items are synchronized and available across multiple iOS and iPadOS devices when iCloud sync is enabled. When the Clipboard Monitor feature is enabled, content in the clipboard can be automatically stored in Yoink when the app is opened. Shelf items are also available to share via Handoff on macOS devices with the Yoink app for Mac, which is sold separately. With multiple ways to interact with the shelf, this app is indispensably accessible to any productivity user workflow.
Developed on the Unity game engine, BoneBox Dental is a no-frills educational experience. Upon opening, users are greeted with a partial maxilla and mandible. There appears to be a graphics bug where flecks of black mar the model when it is rotated, but this does not distract from the image. The mouth can be opened and closed with a three-fingered pinch or spread motion. Tapping on a tooth in either arch isolates it for viewing. Users can rotate and magnify to their heart’s content before returning to the mouth. The 3D models look anatomically correct; however, it does not have any variations, limiting its breadth of information to the most common presentations of each tooth. BoneBox Dental boasts a quiz function that asks users to identify all 32 teeth in a multiple-choice game. Users are shown one tooth at random, asked to select a response from a list of four choices, then scored at the end of the quiz. Overall, BoneBox Dental is a novel way for those with a dental background to improve their basic tooth identification skills. Because of its lack of features, the public may find it of little use. — Alexander Lee, DMD
With Yoink for iPhone and iPad, users have a clipboard that can store an unlimited number of items and be easily shared across mobile devices, making this already useful tool even more productive and efficient. — Hubert Chan, DDS
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