Mealey. Grand Rounds with Dr. Brian L. Mealey

In medicine, there has been widespread dissemination made me pause to consider the potential clinical impli-of research demonstrating the inflammatory nature of cations of the interrelationship between periodontal in-obesity and its link to insulin resistance and type 2 dia- flammation and systemic health. This longitudinal trial betes. Medical professionals know that adipocytes are a of over 600 subjects with type 2 diabetes examined the highly metabolically active source of pro-inflammatory effect of periodontal disease on mortality.¹⁰ After adjust-cytokines like TNF-α and IL- 6, and that obesity leads ing for other known risk factors, the death rate from to elevated serum levels of these cytokines, which then ischemic heart disease was over 2 times higher in sub-can directly induce insulin resistance. ^{1, 2} They know that jects with severe periodontitis than in subjects without elevated acute phase reactants such as C-reactive pro- periodontitis or with only mild periodontitis. The death tein and fibrinogen are found in people with inflamma- rate from diabetic nephropathy was 8. 5 times higher in tory disease. ³ They also know that elevated C-reactive those with severe periodontitis, and the overall cardio-protein levels are a major risk marker for acute cardiac renal mortality rate was 3.5-fold higher, suggesting that events. ⁴ But are medical professionals also aware that the presence of periodontal disease poses a risk for car-periodontitis can induce elevated production of pro-in- diovascular and renal mortality in people with diabetes. flammatory cytokines? ⁵ Do they know that people with This is important information for all of us to know. periodontitis often have elevated serum levels of TNF-α,

IL- 6, and C-reactive protein compared to periodontally I do not have periodontal disease, but I do have diabetes. healthy people? 6, 7 Do they realize that periodontal treat- I plan to control the disease that I have to the best of ment aimed at reducing the microbial bioburden present my ability, and to prevent the disease that I don’t have. I in the oral cavity and decreasing inflammation locally plan to do the same for my patients. within the periodontium also results in reduced serum markers and mediators of systemic inflammation? ^{8 References}

11. Mohamed-Ali V, Goodrick S, Rawesh A, Katz DR, Miles JM, Yudkin JS, Klein S, Coppack SW. Subcutaneous adipose tissue

The periodontium is unique in an important sense. In no releases interleukin- 6 but not tumor necrosis factor-α, in vivo. other region of the body is an intact mucosal lining, simi- ^{J Clin Endocrinol Metab 1997;82:4196-4200.} _{lar in many respects to the lining of the genitourinary} 2. Festa A, D’Agostino Jr R, Howard G, Mykkanen L, Tracy

RP, Haffner SM. Chronic subclinical inflammation as part

^{tract and gastrointestinal tract, interrupted by the pres-} of the insulin resistance syndrome: the Insulin Resistance ence of calcified structures that penetrate the mucosal Atherosclerosis Study (IRAS). Circulation 2000;102: 42-47. _{lining. The presence of teeth protruding through the oral} 3. Malik S, Wong ND, Franklin S, Pio J, Fairchild C, Chen R.

Cardiovascular disease in U.S. patients with metabolic
^{mucosal surface establishes a dynamic wound healing} syndrome, diabetes, and elevated C-reactive protein. Diabetes
state that is unlike other regions in the body, and is anal- Care 2005;28:690-693.
_{ogous to inserting a cannula or ostomy through an intact} 4. Biasucci LM. CDC/AHA workshop on markers of inflammation
and cardiovascular disease. Application to clinical and public

^{skin surface. The presence of teeth results in establish-} health practice. Clinical use of inflammatory markers in patients ment of a sulcus or pocket in the mucosa adjacent to the with cardiovascular diseases. Circulation 2004;110:e560-e567. teeth, which becomes colonized by microorganisms that 5. Loos BG. Systemic markers of inflammation in periodontitis. J induce an inflammatory response. If not cared for prop- ^{Periodontol 2005;76:2106-2115.}

6. Wu T, Trevisan M, Genco RJ, Falkner KL, Dorn JP, Sempos ^{erly, inflammation can increase in intensity and result} CT. Examination of the relation between periodontal health in production of massive quantities of pro-inflammatory status and cardiovascular risk factors: Serum total and High _{cytokines, local destruction of the adjacent tissues, and} Density Lipoprotein cholesterol, C-reactive protein, and plasma fibrinogen. Am J Epidemiol 2000;5:273-282.

^{penetration of bacterial products through the ulcerated} 7. Noack B, Genco RJ, Trevisan M, Grossi SG, Zambon JJ, De pocket epithelium into the systemic circulation. Nardin E. Periodontal infections contribute to elevated systemic

C-reactive protein level. J Periodontol 2001;72:1231-1236.

88. D’Aiuto F, Parker M, Andreou G, Suvan J, Brett PM, Ready D,

^{The potential impact of this inflammatory response is} Tonetti MS. Periodontitis and systemic inflammation: control now being recognized. As the articles in this issue dis- of the local infection is associated with a reduction in serum cuss, periodontal inflammation can result in elevated se- ^{inflammatory markers. J Dent Res 2004;83:156-160.}

9. Genco RJ, Grossi SG, Ho A, Nishimura F, Murayama Y. A proposed
^{rum levels of inflammatory mediators that may increase} model linking inflammation to obesity, diabetes, and periodontal
insulin resistance similar to obesity, and may worsen infections. J Periodontol 2005;76:2075-2084.
glycemic control in people with diabetes. 9 Likewise, peri- 10. Saremi A, Nelson RG, Tulloch-Reid M, Hanson RL, Sievers ML,
^{odontal treatment that reduces inflammation may also Taylor GW, Shlossman M, Bennett PH, Genco R, Knowler WC.} Periodontal disease and mortality in type 2 diabetes. Diabetes
result in improved glycemic control. One study recently Care _{2005;28: 27-32.}