>WHO SHOULD READ THIS?
All PAs who provide primary care.
>WHY IS THIS IMPORTANT?
Type 2 diabetes mellitus (DM) is a markedly complex metabolic disorder without a clear etiology. The initial cause of insulin resistance and subsequent hyperglycemia, hypertriglyceridemia, obesity, and the myriad other associated disorders remains elusive and is likely multifactorial. What is clear is that the number of persons with DM continues to grow and that the most vulnerable, particularly older and economically disadvantaged persons, are disproportionately affected.
DM is the seventh leading cause of death in the United States and is related to a 2‐ to 4‐fold higher risk of death from cardiovascular and cerebrovascular disease. In 2011, the CDC reported that among Americans with DM, 67% had hypertension, 28.5% of those aged 40 years or older had diabetic retinopathy, and greater than 60% had mild to severe neuropathic disease. Moreover, 44% of all new cases of kidney failure and 60% of nontraumatic lower limb amputations occurred in this population. DM was also associated with a 2.9‐fold increased risk for severe periodontitis among adults aged 45 years or older with a glycosylated hemoglobin (A1C) of greater than 9%. Risk of severe periodontitis was even greater (4.6 times) among smokers with poorly controlled diabetes.1
The CDC reported that in 2010, DM affected 8.3% of the US population (25.8 million total cases: 18.8 million diagnosed and 7 million undiagnosed) and that 26.9% of US residents aged 65 years and older (10.9 million) had DM. Based on 2005‐2008 data on fasting glucose or A1C levels, an estimated 35% of US adults aged 20 years or older had prediabetes, and fully 50% of adults aged 65 years or older suffered from the same condition. The number of persons with prediabetes was estimated to be as high as 79 million, or 25.4% of the US population, in 2010.1
Disparities in DM risk occur between population groups. For example, national estimates of DM prevalence in 2009 showed that in comparison to 7.1% of non‐Hispanic whites, 14.2% of American Indians and Alaskan natives aged 20 years or older who received care from the Indian Health Service had diagnosed DM. Moreover, in a similar comparison, 8.4% of Asian Americans (18% higher than non‐Hispanic whites), 11.8% of Hispanics (66% higher), and 12.6% of non‐Hispanic blacks (77% higher) had diagnosed DM. Compared with non‐Hispanic white adults, the risk of diagnosed DM among Hispanics was highest for Mexican Americans and Puerto Ricans (87% and 94% higher than non‐Hispanic white adults, respectively).1
* Primary care PAs should incorporate a thorough oral examination as a regular part of their care of a patient with diabetes.
* Reinforce the importance of regular dental checkups for all patients.
* Educate patients about and reinforce good home dental hygiene practices, including daily flossing and at least twice‐daily brushing.
* Educate patients about the connection between glycemic control and oral health.
>A PERIODONTAL CONNECTION
Periodontitis is more prevalent among persons with DM, the poor, and the elderly. In fact, periodontal disease has been called the sixth complication of DM, after the classic pentad of retinopathy, neuropathy, nephropathy, macrovascular disease, and delayed wound healing.2 Other oral manifestations of diabetes include burning mouth syndrome, candidiasis, dental caries, gingivitis, glossodynia, lichen planus, neurosensory dysesthesias, salivary dysfunction, taste dysfunction, and xerostomia.3,4
Patients with DM whose blood glucose levels are well‐controlled have reduced rates of periodontal disease compared with patients whose blood glucose is poorly controlled.5 Moreover, elimination of periodontal infection by full‐mouth extraction,6 treatment with topical antibiotics,7–9 or scaling and root planing7,9 results in significant improvement in glycemic control. Thus, the literature strongly supports not only the increase in risk for periodontitis in patients with DM but also suggests an improvement in glycemic control in patients whose oral infection is effectively controlled.
>WHAT IS THE PATHOPHYSIOLOGY OF PERIODONTAL DISEASE?
Periodontal disease occurs when bacterial infection of the structures surrounding teeth results in their gradual detachment from alveolar bone. The mechanism involves disruption of root cementum and perialveolar ligaments, which secure the tooth in its bony socket. Gingivitis is the early, reversible phase of this process, whereas periodontal disease is difficult to treat or not reversible. Manifestations of periodontitis include gingival inflammation; increased depth of “pockets” between the gum and tooth; and bleeding with minimal disruption, eg, brushing. Periodontal disease is classified using the following system: gingival disease, chronic periodontitis, aggressive periodontitis, periodontitis as manifestation of systemic disease, necrotizing periodontal disease, or periodontal abscess.10 Periodontal disease is an inflammatory process that has systemic effects and is characterized by the presence of cytokines, eg, tumor necrosis factor‐alpha (TNF‐α) and interleukin‐6 (IL‐6), and acute phase proteins, such as C‐reactive protein (CRP).11
>WHAT ARE THE CURRENT RECOMMENDATIONS?
The American Dental Association advocates special consideration for patients with diabetes.12 The recommendations include (1) emphasizing soft‐tissue management, including use of antibiotics to prevent and treat oral infections; (2) considering a 3‐ to 4‐month recall cycle for checkups and cleanings to prevent and treat gingivitis; (3) educating patients regarding proper home care, including brushing twice a day and cleaning between teeth daily with floss or interdental cleaners; and (4) informing patients about such products as chlorhexidine gluconate rinses (Peridex, Periogard, generics) to prevent gingivitis.
In addition, optimizing blood glucose levels and maintaining A1C levels at less than 7.0% significantly contributes to reduced risk for development of periodontal disease. Therefore, the PA should work closely with all patients who have diabetes to maintain blood glucose in the recommended range. In addition, the oral examination should be part of the standard evaluation of all persons with diabetes. Particular attention should be paid to signs of the diseases associated with diabetes, including inflammation, bleeding, erosions, thrush, caries, plaque buildup, loose teeth, and other signs of disease. All patients with diabetes should be encouraged to follow the preventive services recommended by their dentist.
A link between inflammation, inflammatory mediators, and insulin sensitivity has come to light, and this relationship is central to the pathogenesis of DM.2 Thus, physical and psychological stress, obesity, and other inflammatory conditions may contribute to the initiation of DM. Periodontal disease is itself an inflammatory condition that contributes to a systemic inflammatory state.13 Effective treatment of periodontal disease results in reduced levels of inflammatory cytokines in patients with DM, which correlates with improvement in glycemic control.14,15
The link between inflammation and metabolic disturbances, including insulin resistance, metabolic syndrome, and type 2 DM, is under active investigation. Inflammasomes, which are proteins released in response to inflammatory stimuli, including infection and obesity, appear to trigger release of inflammatory cytokines, and these cytokines have been implicated in initiating insulin resistence.16 Thus, periodontal disease, along with other infectious processes and obesity, may eventually be found to predispose a patient to development of DM.
Finally, a new class of compounds, the resolvins, has been found to play an important role in the resolution of inflammatory processes and appears to be particularly effective in the treatment of experimental periodontal disease.17 These derivatives of the omega‐3 fatty acids have been found to reduce bone resorption in experimental periodontal disease models and may be effective treatments in the near future.
2. Bascones-Martinez A, Matesanz-Perez P, Escribano-Bermejo M, et al. Periodontal disease and diabetes-review of the literature. Med Oral Patol Oral Cir Bucal.
3. Ship JA. Diabetes and oral health: an overview. J Am Dent Assoc.
2003;134(suppl 1):4S-10S, 2003.
4. Lamster IB, Lalla E, Borgnakke WS, Taylor GW. The relationship between oral health and diabetes mellitus. J Am Dent Assoc.
5. Soskolne WA. Epidemiological and clinical aspects of periodontal diseases in diabetics. Ann Periodontol.
6. Khader YS, Al Habashneh R, Al Malalheh M, Bataineh A. The effect of full-mouth tooth extraction on glycemic control among patients with type 2 diabetes requiring extraction of all remaining teeth: a randomized clinical trial. J Periodontal Res.
7. Darré L, Vergnes JN, Gourdy P, Sixou M. Efficacy of periodontal treatment on glycaemic control in diabetic patients: a meta-analysis of interventional studies. Diabetes Metab.
8. Katagiri S, Nitta H, Nagasawa T, et al. Multi-center intervention study on glycohemoglobin (HbA1c) and serum, high-sensitivity CRP (hs-CRP) after local anti-infectious periodontal treatment in type 2 diabetic patients with periodontal disease. Diabetes Res Clin Pract.
9. Simpson TC, Needleman I, Wild SH, et al. Treatment of periodontal disease for glycaemic control in people with diabetes. Cochrane Database Syst Rev.
10. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol.
11. Hernández M, Dutzan N, García-Sesnich J, et al. Host-pathogen interactions in progressive chronic periodontitis. J Dent Res.
13. Loos BG. Systemic markers of inflammation in periodontitis. J Periodontol.
14. O'Connell PA, Taba M, Nomizo A, et al. Effects of periodontal therapy on glycemic control and inflammatory markers. J Periodontol.
15. Sun WL, Chen LL, Zhang SZ. Inflammatory cytokines, adiponectin, insulin resistance and metabolic control after periodontal intervention in patients with type 2 diabetes and chronic periodontitis. Intern Med.
16. Strowig T, Henao-Mejia J, Elinav E, Flavell R. Inflammasomes in health and disease. Nature.
17. Ji R-R, Xu ZZ, Strichartz G, Serhan CN. Emerging roles of resolvins in the resolution of inflammation and pain. Trends Neurosci.
© 2012 Lippincott Williams & Wilkins, Inc.