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Periodontal DiseaseRisk Factors and Treatment

by Richard Champagne DMD, FAGD

LEARNING OBJECTIVES

The overall objective of this course is to provide an overview on periodontal disease, risk actors and treatment. After completing this article, the reader will be able to:• Describe the etiology, onset and progression of periodontal

disease• List and describe risk factors for periodontal disease• Review periodontal treatment options.

SPONSOR/PROVIDER: This is a Dental Learning, LLC continuing education activity. COMMERCIAL SUPPORTER: This course has been made possible through an unrestricted educational grant from ORAPHARMA. DESIGNATION STATEMENTS: Dental Learning, LLC is an ADA CERP recognized provider. ADA CERP is a service of the American Dental Association to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, nor does it imply acceptance of credit hours by boards of dentistry. Dental Learning, LLC designates this activity for 2 CE credits. Dental Learning, LLC is also designated as an Approved PACE Program Provider by the Academy of General Dentistry. The formal continuing education programs of this program provider are accepted by AGD for Fellowship, Mastership, and membership maintenance credit. Approval does not imply acceptance by a state or provincial board of dentistry or AGD endorsement. The current term of approval extends from 2/1/2016 - 1/31/2020. Provider ID: # 346890. Dental Learning, LLC is a Dental Board of California CE provider. The California Provider number is RP5062. This course meets the Dental Board of California’s requirements for 2 units of continuing education. EDUCATIONAL METHODS: This course is a self-instructional journal and web activity. Information shared in this course is based on current information and evidence. REGISTRATION: The cost of this CE course is $29.00 for 2 CE credits. PUBLICATION DATE: December 2016. EXPIRATION DATE: November 2019. REQUIREMENTS FOR SUCCESSFUL COMPLETION: To obtain 2 CE credits for this educational activity, participants must pay the required fee, review the material, complete the course evaluation and obtain a score of at least 70%. AUTHENTICITY STATEMENT: The images in this course have not been altered. SCIENTIFIC INTEGRITY STATEMENT: Information shared in this continuing education activity is developed from clinical research and represents the most current information available from evidence-based dentistry. KNOWN BENEFITS AND LIMITATIONS: Information in this continuing education activity is derived from data and information obtained from the reference section. EDUCATIONAL DISCLAIMER: Completing a single continuing education course does not provide enough information to result in the participant being an expert in the fi eld related to the course topic. It is a combination of many educational courses and clinical experience that allows the participant to develop skills and expertise. PROVIDER DISCLOSURE: Dental Learning does not have a leadership position or a commercial interest in any products that are mentioned in this article. No manufacturer or third party has had any input into the development of course content. CE PLANNER DISCLOSURE: The planner of this course, Joe Riley, does not have a leadership or commercial interest in any products or services discussed in this educational activity. He can be reached at [email protected]. TARGET AUDIENCE: This course was written for dentists, dental hygienists, and assistants, from novice to skilled. CANCELLATION/REFUND POLICY: Any participant who is not 100% satisfi ed with this course can request a full refund by contacting Dental Learning, LLC in writing or by calling 1-888-724-5230. Please direct all questions pertaining to Dental Learning, LLC or the administration of this course to [email protected]. Go Green, Go Online to www.dentallearning.net to take this course. © 2016

Periodontal disease with clinical attachment loss affects approximately 47% of American adults over the age of 30. The development and progression of chronic periodontitis depends on a number of factors including risk and the host response. Treatment options include nonsurgical therapy which may also use adjunctive therapies, and surgical therapy. Regular re-evaluation and periodontal maintenance is essential for patients who have been treated for periodontal disease.

ABSTRACT

Periodontal Disease, Risk Factors and Treatment

Introduction

The Centers for Disease Control and Prevention (CDC) conducted a survey spanning 2009-2010, and reports that approximately 47%,

or 65 million American adults over the age of 30, have periodontitis.1 Among older adults in the United States, the prevalence of periodontitis is higher. Based on the National Health and Nutrition Examination Survey (NHANES) III data from 2009-2012, the overall prevalence of periodontitis is approximately 66% in adults ≥ 65 years-of-age, with approximately 12% having severe periodontitis.1 In those over 75 years-of-age, periodontitis is more prevalent than in all other age groups and its prevalence increases with age.2 Periodontal disease is associated with periodontal pathogens in dental plaque, with initiation and progression infl uenced by risk factors and the host response.

ABOUT THE AUTHORS

Richard Champagne DMD, FAGD Dr. Richard Champagne received his dental degree from Fairleigh Dickinson University School of Dentistry and completed his general practice residency at Robert Wood Johnson/University Hospital. He also completed a dental implant mini residency at Brookdale Hospital/New York University, and received training at the Pankey Institute for Advanced Dental Education. In addition, Dr. Champagne is a former assistant clinical instructor and guest lecturer at the University of Medicine and Dentistry of New Jersey, and the holder of 2 patents related to patient care. He has completed his Fellowship and Master with the Academy of General Dentistry, and Associate Fellowship with the American Academy of Implant Dentistry. Dr. Champagne is a member of the American Dental Association, American Academy of Implant Dentistry, Dental Organization for Conscious Sedation, American Academy of Sleep Medicine, and a founding member of the New Jersey chapter of the American Academy of Cosmetic Dentistry. Dr. is in private practice in Monmouth, New Jersey.

Integrated Media Solutions Inc./DentalLearning.net is an ADA CERP Recognized Provider. ADA CERP is a service of the American Dental Association to assist dental profession-als in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, nor does it imply acceptance of credit hours by boards of dentistry. Concerns or complaints about a CE provider may be directed to the provider or to ADA CERP at www.ada.org/cerp. Integrated Media Solutions Inc./DentalLearning.net designates this activity for 2 continuing education credits.

Approved PACE Program Provider FAGD/MAGD Credit Approval does not imply acceptance by a state or provincial board of dentistry or AGD endorsement.2/1/2016 - 1/31/2020 Provider ID: # 346890AGD Subject Codes: 490, 495

Dental Learning, LLC is a Dental Board of California CE Provider. The California Provider # is RP5062. All of the information contained on this certifi cate is truthful and accurate. Completion of this course does not constitute authorization for the attendee to perform any services that he or she is not legally authorized to perform based on his or her license or permit type. This course meets the Dental Board of California’s requirements for 2 units of continuing education. CA course code is 02-5062-16039.


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The majority of the population experiences gingivitis, an inflammatory process that does not include bone loss, the early stage of periodontal disease. Gingivitis may be acute or chronic, and require professional care. Initially, supragingi-val dental plaque formation begins with the adhesion of oral bacteria to the acquired pellicle, and if undisturbed dental plaque can accumulate. Supragingival and subgingival plaque matures over a period of several weeks.3 Subgingival dental plaque is well-developed by between three and twelve weeks of plaque maturation, and largely contains gram-negative bacteria.3 Current recommendations for preventive home care include twice-daily oral hygiene involving brushing, interdental cleaning and use of a toothpaste, to help prevent plaque build-up and oral disease.

Periodontitis and the Disease ProcessPeriodontitis is an inflammatory process, but in contrast to

gingivitis it involves clinical attachment loss.4,5 There is also a lack of evidence to support the concept that unresolved gingi-vitis always results in progression to periodontitis.5 Microbial complexes were identified in 1998, based on subgingival plaque samples from 185 adults, and categorized into six spe-cific microbial groups of bacterial species.6 The red complex compromised P. gingivalis, B. forsythus and T. denticola was considered to be the most virulent based on the research, fol-lowed by the orange complex with 12 microorganisms includ-ing P. intermedia and P. nigrescens, while A. actinomycetem-comitans was determined to belong in the blue complex.

At the current time, more than 600 species of bacteria have been identified and may be found in subgingival plaque from different patients, and up to 100 may be identifiable in one sampled site.7 Diseased periodontal pockets typically con-tain an abundance of Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola, and a significant number of other anaerobes including but not limited to A. Actino-mycetemcomitans, Fusobacterium nucleatum and Campy-lobacter spp. are also found in diseases sites.3,6,8,9 It is clear that some microorganisms involved in periodontal disease

are more virulent and more frequently found in diseased sites than others. It is the host response that influences the inflam-matory process and progression.10

Host response mechanisms in periodontal disease involve many interactions, based on the inflammatory and immune responses. Initially, bacterial antigens and irritants cause the release of antibodies, neutrophils and lymphocytes. Bacterial lipopolysaccharides stimulate the immune response, resulting in increased levels neutrophils and then of cytokines pro-duced by macrophages and neutrophils. The cytokines and chemokines then result in bone loss.11 Cytokines involved in the destruction of periodontal tissues include interleukin-1 and tumor necrosis factor alpha. This is followed by increased activation of matrix metalloproteinases (MMPs), in particular collagenase, which causes collagen breakdown within the periodontal matrix.12 Tumor necrosis factor alpha increases osteoclast activity which causes bone resorption. Other chemicals are also produced that increase the destructive inflammatory response.10

Risk factors for PeriodontitisPeriodontitis, associated with gram-negative microorgan-

isms contained in subgingival dental plaque and the host response, has both modifiable and non-modifiable risk factors.

Modifiable risk factors Modifiable risk factors include poor oral hygiene, tobacco

smoking, stress, obesity, and the use of certain types of medica-tions are also modifiable risk factors (Table 1).

Poor oral hygiene includes those individuals who are un-able or unwilling to practice proper oral hygiene and regular professional care visits. Local factors can increase plaque accumulation and make it difficult to perform proper oral hygiene, such as the presence of cervical caries, overhangs and other defective restorations, and interdental areas where food impaction occurs.

Tobacco smoking is a significant modifiable risk for periodontal disease. Based on a number of studies, the risk for

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periodontal disease is greater, periodontitis is more severe in smokers, and progression is more rapid.13 One study assessing NHANES III data found a four-fold risk of periodontitis in tobacco smokers compared to nonsmokers.14 Tobacco smok-ing also results in vasoconstriction within gingival tissues, resulting in less propensity for bleeding even in the presence of gingival inflammation compared to nonsmokers.15 Substance abuse also increases risk for periodontal disease.16

Increased stress levels have been found to be associated with periodontal disease, and can promote poor oral hygiene habits.17 An inability or poor ability to cope with stressors leads to clinically evident responses. Increased production of cortisol, a glucocorticoid, can occur. This diminishes immuno-globulin production, negatively affecting the immune system.17 Poor coping of stress has also been found to be an indicator for more severe periodontal disease.18 It is hypothesized that this may be associated with pro-inflammatory cytokines.19

Diabetes mellitus, if uncontrolled or poorly controlled, places patients at increased risk for periodontitis.20 Patients with diabetes and untreated periodontal disease experience difficulty controlling their blood sugar levels.21 An association between obesity and increased risk for periodontitis in females has been demonstrated,22 and high body mass indexes was as-sociated with periodontal disease in NHANES III data.20

Specific medications also affect the periodontium both from a disease and treatment perspective.23 Therefore, this must also be considered in assessing a patient’s risk level. If the medication is essential this is a nonmodifiable risk.

Non-modifiable risk factors Periodontal disease risk factors that are nonmodifiable

include gender, race24 and genetics (Table 2). Males are at

greater risk for periodontal disease than females. Data also supports a strong genetic component for risk and progression of periodontal disease.25

In addition to diabetes mellitus, autoimmune diseases and acquired immunodeficiency place patients at risk for periodontitis. It is evident from studies that patients with rheumatoid arthritis are at increased risk for periodontitis.26 Patients with established rheumatoid arthritis are at risk for more severe periodontal disease than those in the early stages of rheumatoid arthritis.27 Another factor is that methotrexate and glucocorticosteroids that are used to manage rheumatoid arthritis promote periodontal disease.28

Other risk factors for periodontal disease include socioeconomic status1, hematological disorders, osteoporosis and fluctuations in hormone levels.25 The effect of osteoporosis and osteopenia on periodontal health, induced by post-menopausal hormonal changes, may be related to the effect that both of these conditions have on bone mass density. One theory is that the resultant systemic reduction in bone mass density caused by osteoporosis may make alveolar bone more susceptible to the periodontal disease process than bone that has a greater bone mass density.29 Pregnancy gingivitis occurs in up to 75% of women,30 related to increased levels of estrogen and progesterone which amplifies the body’s response to oral bacteria. This usually reverses after delivery of the baby, not progressing to clinical attachment loss. Some studies support an association between periodontal disease and premature birth and low birth weight babies, while a number do not.31

Once periodontal disease is present, periodontal treatment is aimed at eliminating bacteria, preventing its progression and gaining clinical attachment.

TABLE 1. Modifiable risk factors

Poor oral hygiene Plaque traps such as overhangs

Tobacco smoking Substance abuse

StressDiabetes mellitus – poorly controlled/ uncontrolled

Obesity Specific medications

TABLE 2. Nonmodifiable risk factors

Socioeconomic status Genetics

Rheumatoid arthritisCompromised immunity

Hematological disordersHormonal changes; osteoporosis


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Periodontal TherapiesPeriodontal therapies can be separated into two categories,

nonsurgical and surgical. Typically, behavioral changes that will improve modifiable risk factors are required in conjunc-tion with active treatment. The goal of treatment is to halt periodontal disease progression and reduce pocket depths.

Nonsurgical periodontal therapy includes scaling and root planing followed by regular periodontal maintenance, typi-cally at 3-month intervals. The interval between periodontal maintenance appointments is determined for patients based on severity of disease, risk factors, complexity of medical conditions with individual considerations. Scaling and root planning may be performed by hand instruments, ultrasonic scalers, lasers or combinations of these. It involves debride-ment for the removal of supra-and sub-gingival plaque and calculus, debris, subgingival bacteria and toxins. Calculus harbors bacteria and toxin, and provides a rough area where new plaque accumulation is fostered. Periodontal bacteria can recolonize areas and accumulate to the pre-treatment level within days or weeks.32 Improved oral hygiene is needed following therapy to control plaque and control bacteria, and regular periodontal maintenance is critical.33

Depending on the host, response to treatment and associated factors such as smoking status34 or systemic disease, a decision may be made to use locally-applied or systemic agents to aid in the treatment of chronic periodontitis. Medications, both localized and systemic, may be used as an adjunct to scaling and root planing. Locally-applied therapeutic antimicrobials can be used in situations where patients respond poorly and/or may have conditions suggesting their use. Since they are applied locally, unlike systemic treatments they are used where they are needed and are designed to maintain a higher concentration at the site over a prolonged period of time that is sufficient to inhibit periodontal bacteria. Options used include minocycline applied as microspheres (Arestin, Orapharma Inc.) and doxycycline gel (Atridox, Tolmar Inc.). Determining whether to use a locally-applied antimicrobial in addition to scaling and root planning should consider the patient, host response, risk factors such as smoking, severity, and what additional benefit might be achieved.

Systemically, and as an adjunct to scaling and root plan-ning, twice-daily 20 mg capsules of doxycycline (Periostat) are subantimicrobial and have been taken orally to inhibit collage-nase activity and help protect against degradation of collagen in periodontal tissues. The changes in pocket depth vary by patient, site and initial pocket depth, and it is used for long-term control of periodontal disease in high risk patients, such as smokers.35 It is not a substitute for thorough home care or nonsurgical periodontal therapy.36

Surgical periodontal therapy may be required under some circumstances, including when access is needed to treat areas such as furcations and deep periodontal pockets. This type of pocket reduction surgery involves making a full thickness flap to facilitate the complete removal of all deposits, and remodel-ing bone if indicated. Grafting procedures using an autograft, allograft, xenograft, or alloplast may also be performed to augment hard tissue, soft tissue, or both. Guided tissue regen-eration can improve bony defects using bone graft material and a resorbable or non-resorbable barrier membrane to facilitate hard tissue growth. Some non-resorbable membranes have titanium reinforcement which can prove beneficial in situations that require that the graft be tented.

The case below discusses a patient where non-surgical scaling and root planing was performed along with adjunctive locally-applied antimicrobial therapy.

Case study The patient in this study is a 48-year-old female. She is

a nonsmoker with rheumatoid arthritis for which she takes methotrexate. Other than this, she has no relevant medical history and is healthy. The patient has attended our office regularly sinc e 2013 for check-ups and has regularly received a periodontal evaluation and routine dental care, including thorough scaling and prophylaxis. She has good oral hygiene, and also uses a prescription-strength fluoride toothpaste as well as an antimicrobial essential oils mouthrinse on a daily basis that helps reduce plaque and gingivitis.

The patient presented for her check-up and periodontal evaluation on 3/22/2016. Periodontal charting revealed multiple periodontal pockets with a depth of 4 mm to 5 mm


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in all four quadrants of the mouth. Prior to this visit, no pocket depth had exceeded 3 mm. No local factors, dietary changes, or home care changes were reported by the patient or identified as potential explanations for the increase in pocket

depths, and her level of oral hygiene was unchanged. However, the association between rheumatoid arthritis and periodontal disease was flagged as a possible contributing factor to the change in her oral health. After reviewing the periodontal

Figure 1. Bleeding on probing prior to adjunctive use of minocycline microspheres.

Figure 3. Application of minocycline microspheres.

Figure 2. Pre-treatment periodontal chart. Figure 4. Periodontal chart post-treatment.


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charting findings, treatment options and recommendations were discussed with the patient. These included scaling and root planing, locally applied antimicrobial therapy where required, a re-evaluation at 7-10 days, and three-monthly periodontal maintenance. These recommendations were all declined by the patient.

On 10/6/16, periodontal charting was again performed. The number of 4 mm to 5 mm pockets had increased, as well as bleeding on probing (Figure 1, 2). The findings of the periodontal evaluation were again discussed with the patient, including the deterioration which had occurred since her previous evaluation.

The treatment now recommended included scaling and root planing in all four quadrants, including the upper right (teeth #2-#4), upper left (#11-#14), and the entire lower left quadrant. The use of a locally applied antimicrobial agent (Arestin, Orapharma) was also recommended at specific sites: teeth #2 distal lingual (5 mm; Figure 3), #13 distal facial (5 mm), #15 distal facial (5 mm) and #20 distal facial (5 mm). These treatment recommendations were accepted by the patient, and the treatment was completed over two visits, on 10/11/16 & 10/27/16.

At the patient’s eight-week follow up hygiene appoint-ment on 12/6/16, significant improvement was noted and all periodontal tissues had returned to excellent health. It is important to note that all 5 mm pockets had reduced to 2-3 mm (Figure 4).

The patient indicated that she would keep three-month periodontal evaluation and maintenance visits. At each of these visits full periodontal charting will be performed so that any pocket depth increase will be caught at a very early stage of disease progression and treated conservatively.

ConclusionsPeriodontal disease with clinical attachment loss contin-

ues to be a significant oral health issue. Risk factors exist that are modifiable and nonmodifiable. Among modifiable risk factors, tobacco use and poor oral hygiene are signifi-cant factors for the onset and progression of periodontal disease. Nonmodifiable risk factors include diseases such as diabetes mellitus, autoimmune disorders and hormonal

changes. Once periodontal disease exists, treatment is required to halt progression and preferably obtain clinical attachment gains. Treatment options include nonsurgical periodontal therapy with or without adjunctive treatment, and in more advanced cases surgical periodontal therapy is indicated. Following periodontal therapy, regular peri-odontal maintenance therapy and good home care are essential to help prevent disease recurrence. The treatment recommended and provided for the individual patient is based on a full periodontal evaluation, the patient’s medical and dental history and risk factors. In determin-ing treatment, patient needs and preferences and clinical judgement are required.

References1. Eke PI, Dye B, Wei L, Thornton-Evans G, Genco R. Prevalence of Periodontitis in Adults in the United States: 2009 and 2010. J Dent Res. 2012;91(10):914-20. Available at: http://www.cdc.gov/oralhealth/conditions/periodontal-disease.html.

2. Eke PI, Wei L, Borgnakke WS, Thornton-Evans G, et al. Periodon-titis prevalence in adults ≥ 65 years of age, in the USA. Periodontol 2000. 2016;72(1):76-95.

3. Lovegrove JM. Dental plaque revisited: bacteria associated with periodontal disease. J NZ Soc Periodontol. 2004;87:7-21.

4. Cochran DL. Inflammation and bone loss in periodontal disease. J Periodontol. 2008;79(8 Suppl):1569-76.

5. American Academy of Periodontology. The pathogenesis of periodontal diseases. J Periodontol. 1999;70:457-470.

6. Socransky SS, Haffajee AD, Cugini MA, et al. Microbial complexes in subgingival plaque. J Clin Periodontol. 1998;25:134-144.

7. Hasan A, Palmer RM. A clinical guide to periodontology: Pathol-ogy of periodontal disease. Br Dent J. 2014;8:457-61.

8. Mariotti A, Hefti AF. Defining periodontal health BMC Oral Health. 2015;15(Suppl 1):S6.

9. Genco RJ. Current view of risk factors for periodontal diseases. J Periodontol. 1996; 67:1041-9.

10. Taubman MA, Valverde P, Han X, Kawai T. Immune response: the key to bone resorption in periodontal disease. J Periodontol. 2005;76(11 Suppl):2033-41.

11. Bascone A, Noronha S, Gómez M, et al. Tissue destruction in periodontitis: bacteria or cytokines fault? Quintessence Int.


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2005;36(4):299-306.

12. Graves DT, Cochran D. The contribution of interleukin-1 and tu-mor necrosis factor to periodontal tissue destruction. J Periodontol. 2003;74(3):391-401.

13. Collins FM. Tobacco Cessation. Health benefits and interven-tions. September 2015. Available at: www.dentallearning.net.

14. Tomar SL, Asma S. Smoking-attributable periodontitis in the United States: findings from NHANES III. National Health and Nutri-tion Examination Survey. J Periodontol. 2000;71(5):743-751.

15. Scott DA, Singer DL. Suppression of overt gingival inflammation in tobacco smokers - clinical and mechanistic considerations. Int J Dent Hyg. 2004;2(3):104-10.

16. Khocht A, Schleifer SJ, Janal MN, Keller S. Dental care and oral disease in alcohol dependent persons. J Subst Abuse Treat. 2009;37(2):214-8.

17. Reners M, Brecx M. Stress and periodontal disease. Int J Dent Hyg. 2007;5:199-204.

18. Genco RJ, Ho AW, Grossi SG, et al. Relationship of stress, distress and inadequate coping behaviors to periodontal disease. J Periodontol. 1999;70(7):711-23.

19. Genco RJ, Grossi SG, Ho A, et al. A proposed model linking inflammation to obesity, diabetes, and periodontal infections. J Peri-odontol. 2005;76(11 Suppl):2075-84.

20. Löe H. Periodontal disease: the sixth complication of diabetes mellitus. Diabetes Care. 1993;16(1):329-34.

21. Preshaw PM, Alba AL, Herrera D, et al. Periodontitis and diabe-tes: a two-way relationship. Diabetologia. 2012;55:21-31.

22. Gaio EJ, Haas AN, Rösing CK, et al. Effect of obesity on peri-odontal attachment loss progression: a 5-year population-based prospective study. J Clin Periodontol. 2016;43(7):557-65.

23. Ciancio SG. Medications: a risk factor for periodontal disease diagnosis and treatment. J Periodontol. 2005;76(11 Suppl):2061-5.

24. Delgado-Angulo EK, Bernabé E, Marcenes W. Ethnic inequali-ties in periodontal disease among British adults. J Clin Periodontol. 2016;43(11):926-33.

25. Yousef A. AlJehani. Risk Factors of Periodontal Disease: Review of the Literature. Int J Dent. 2014; Article ID 182513.

26. Dissick A, Redman RS, Jones M, et al. Association of periodontitis with rheumatoid arthritis: a pilot study. J Periodontol. 2010;81:223-0.

27. Scher JU, Ubeda C, Equinda M, et al. Periodontal disease and the oral microbiota in new-onset rheumatoid arthritis. Arthritis Rheum. 2012; 64:3083-94.

28. Deeming GMJ, Collingwood J, Pemberton MN. Methotrexate and oral ulceration. Br Dent J. 2005;198(2):83-5.

29. Tezal M, Wactawski-Wende J, Grossi SG, et al. The relationship between bone mineral density andperiodontitis in postmenopausal women. J Periodontol. 2000;71:1492-8.

30. Steinberg B. Women’s oral health issues. J Calif Dent Assoc. 2000;28:663-7.

31. George A, Shamim S, Johnson M, et al. Periodontal treatment during pregnancy and birth outcomes: a meta-analysis of ran-domised trials. Int J Evid Based Healthc. 2011;9(2):122-47.

32. van Winkelhoff AJ, van der Velden U, de Graaff J. Microbial succession in recolonizing deep periodontal pockets after a single course of supra- and subgingival debridement. J Clin Periodontol. 1988;15:116-22.

33. Tan AES. Periodontal maintenance. Austr Dent J. 2009;54(s1):S110-S7.

34. Darby IB, Hodge PJ, Riggio MP, Kinane DF. Clinical and micro-biological effect of scaling and root planing in smoker and non-smoker chronic and aggressive periodontitis patients. J Clin Periodontol. 2005;32(2):200-6.

35. Machion L, Andia DC, Lecio G, et al. Locally delivered doxycy-cline as an adjunctive therapy to scaling and root planing in the treatment of smokers: a two-year follow-up. J Periodontol. 2006;77(4):606-13.

36. AAP. Statement on Periostat® as an adjunct to scaling and root planing (2000).

Webliography American Academy of Periodontology. The pathogenesis of peri-odontal diseases. J Periodontol. 1999;70:457-470. Available at: http://www.joponline.org/doi/pdf/10.1902/jop.1999.70.4.457.Armitage GC. Development of a Classification System for Periodon-tal Diseases and Conditions. Annal Periodontol. 1999; 4(1):1-6. Avail-able at: http://www.joponline.org/doi/pdf/10.1902/annals.1999.4.1.1.

Eke PI, Dye B, Wei L, Thornton-Evans G, Genco R. Prevalence of Peri-odontitis in Adults in the United States: 2009 and 2010. J Dent Res. 2012;91(10):914-20. Available at: http://www.cdc.gov/oralhealth/conditions/periodontal-disease.html.

Scher JU, Ubeda C, Equinda M, et al. Periodontal disease and the oral microbiota in new onset rheumatoid arthritis. Arthritis Rheum. 2012; 64:3083-94. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428472/pdf/nihms-375837.pdf.


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1. The Centers for Disease Control and Prevention (CDC) reports that approximately ____________ of American adults over the age of 30 have periodontitis.a. 27%b. 35%c. 47%d. 55%

2. There is evidence to support the concept that unresolved gingivitis always results in progression to periodontitis.a. Trueb. False

3. Bacterial lipopolysaccharides stimulate the immune response, resulting in increased levels of ____________ and then of ____________. a. red blood cells; cytokinesb. cytokines; macrophagesc. neutrophils; cytokinesd. bacterial byproducts; statins

4. At the current time, more than 600 species of bacteria have been identified and may be found in subgingival plaque from different patients, and up to ____________ may be identifiable in one sampled site.a. 30b. 50c. 75d. 100

5. Tumor necrosis factor alpha increases ____________.a. the bacterial loadb. osteoclast activityc. destruction of collagend. elastin activity

6. ____________ is a modifiable risk factor. a. poor oral hygieneb. tobacco smokingc. stress d. all of the above

7. Tobacco smoking has been shown to result in a ____________ risk of periodontitis.a. three-foldb. four-foldc. six-foldd. eight-fold

8. A ____________ was associated with periodontal disease in NHANES III data.a. high body mass indexb. high triglyceride levelc. high cholesterol leveld. low cortisol level

9. Data supports a strong genetic component for risk and progression of periodontal disease.a. Trueb. False

10. Methotrexate and glucocorticosteroids are used to manage rheumatoid arthritis, and ____________.a. promote memory lossb. promote periodontal diseasec. reduce anti-inflammatory chemicalsd. reduce the level of periodontal bacteria

CEQuizTo complete this quiz online and immediately download your CE verification document, visit www.dentallearning.net/PER-ce, then log into your account (or register to create an account). Upon completion and passing of the exam, you can immediately download your CE verification document. We accept Visa, MasterCard, Discover, and American Express.


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11. Post-menopausal hormonal changes induce ____________.a. osteoporosis and osteopeniab. osteoblast activityc. lower bone mass indicesd. higher levels of anti-inflammatory agents

12. Pregnancy gingivitis occurs in up to ____________ of women.a. 55%b. 65%c. 75%d. 85%

13. Periodontal treatment is aimed at ____________.a. eliminating bacteriab. preventing periodontal disease progressionc. gaining clinical attachmentd. all of the above

14. Typically, behavioral changes that will improve ____________ risk factors are required.a. geneticb. indeterminatec. modifiabled. most significant

15. Scaling and root planing involves debridement for the removal of ____________.a. supra-and sub-gingival plaque and calculusb. debrisc. subgingival bacteria and toxinsd. all of the above

16. A decision may be made to use locally-applied or systemic agents to aid in the treatment of chronic periodontitis and help with periodontal improvements, depending on ____________.a. the patient’s ability to perform thorough oral hygiene post-treatmentb. mitigating circumstancesc. the host response and associated factors such as smoking statusd. the patient’s age

17. Locally-applied therapeutic antimicrobials are applied locally and are designed to ____________.a. maintain a low concentration at the site over a prolonged period

of timeb. maintain a high concentration at the site over a prolonged

period of timec. prevent overdosing of antimicrobialsd. provide for a tapering off effect

18. Determining whether to use a locally-applied antimicrobial in addition to scaling and root planing need only consider what additional benefit might be achieved.a. Trueb. False

19. Some non-resorbable membranes have ____________ reinforcement which can prove beneficial in situations that require that the graft be tented.a. zirconiumb. titaniumc. lithiumd. gut

20. Following periodontal therapy, ____________ are essential to help prevent disease recurrence.a. regular periodontal maintenance therapy and good home careb. antimicrobialsc. mouthrinsesd. all of the above

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Please direct all questions pertaining to Dental Learning, LLC or the administration of this course to [email protected]. COURSE EVALUATION and PARTICIPANT FEEDBACK: We encourage participant feedback pertaining to all courses. Please be sure to complete the evaluation included with the course. INSTRUCTIONS: All questions have only one answer. Participants will receive confirmation of passing by receipt of a verification certificate. Verification certificates will be processed within two weeks after submitting a completed examination. EDUCATIONAL DISCLAIMER: The content in this course is derived from current information and research based evidence. Any opinions of efficacy or perceived value of any products mentioned in this course and expressed herein are those of the author(s) of the course and do not necessarily reflect those of Dental Learning. Completing a single continuing education course does not provide enough information to make the participant an expert in the field related to the course topic. It is a combination of many educational courses and clinical experience that allows the participant to develop skills and expertise. COURSE CREDITS/COST: All participants scoring at least 70% on the examination will receive a CE verification certificate. Dental Learning, LLC is an ADA CERP recognized provider. Dental Learning, LLC is also designated as an Approved PACE Program Provider by the Academy of General Dentistry. The formal continuing education programs of this program provider are accepted by AGD for Fellowship, Mastership, and membership maintenance credit. Please contact Dental Learning, LLC for current terms of acceptance. Participants are urged to contact their state dental boards for continuing education requirements. Dental Learning, LLC is a California Provider. The California Provider number is RP5062. The cost for courses ranges from $19.00 to $90.00. RECORD KEEPING: Dental Learning, LLC maintains records of your successful completion of any exam. Please contact our offices for a copy of your continuing education credits report. This report, which will list all credits earned to date, will be generated and mailed to you within five business days of request. Dental Learning, LLC maintains verification records for a minimum of seven years. CANCELLATION/REFUND POLICY: Any participant who is not 100% satisfied with this course can request a full refund by contacting Dental Learning, LLC in writing or by calling 1-888-724-5230. Go Green, Go Online to www.dentallearning.net to take this course. © 2016

PLEASE PHOTOCOPY ANSWER SHEET FOR ADDITIONAL PARTICIPANTS.

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QUIZ ANSWERSFill in the circle of the appropriate answer that corresponds to the question on previous pages.

EDUCATIONAL OBJECTIVES• Describe the etiology, onset and progression of periodontal disease;

• List and describe risk factors for periodontal disease;

• Review periodontal treatment options.

If you have any questions, please email Dental Learning at [email protected] or call 888-724-5230.

COURSE SUBMISSION: 1. Read the entire course.2. Complete this entire answer sheet in

either pen or pencil.3. Mark only one answer for each question.4. Mail or fax answer form. For immediate results:1. Read the entire course.2. Go to www.dentallearning.net/PER-ce.3. Log in to your account or register to create an

account.4. Complete course and submit for grading to

receive your CE verification certificate.

A score of 70% will earn your credits.

Dental Learning, LLC500 Craig Road, First FloorManalapan, NJ 07726

*If paying by credit card, please note:Master Card | Visa | AmEx | Discover

*Account Number

______________________________________________

*Expiration Date

______________________________________________

The charge will appear as Dental Learning, LLC.

If paying by check, make check payable to Dental Learning, LLC.

ALL FIELDS MARKED WITH AN ASTERISK (*) ARE REQUIRED

AGD Codes: 490, 495

Price: $29 CE Credits: 2Save time and the environment by taking this course online.

COURSE EVALUATIONPlease evaluate this course using a scale of 3 to 1, where 3 is excellent and 1 is poor.

1. Clarity of objectives . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 2 1

2. Usefulness of content . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 2 1

3. Benefit to your clinical practice . . . . . . . . . . . . . . . . . . . . 3 2 1

4. Usefulness of the references . . . . . . . . . . . . . . . . . . . . . . 3 2 1

5. Quality of written presentation . . . . . . . . . . . . . . . . . . . . 3 2 1

6. Quality of illustrations . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 2 1

7. Clarity of quiz questions . . . . . . . . . . . . . . . . . . . . . . . . . 3 2 1

8. Relevance of quiz questions . . . . . . . . . . . . . . . . . . . . . . 3 2 1

9. Rate your overall satisfaction with this course . . . . . . . . 3 2 1

10. Did this lesson achieve its educational objectives? Yes No

11. Are there any other topics you would like to see presented in the future? __________________________________________________________________________

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dental learning...the current term of approval extends from 2/1/2016 - 1/31/2020. provider id: #...

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