Periodontal diseases are caused by oral bacteria that start the local inﬂammatory responses that initiate the clinical signs of bleeding on probing (BOP), loss of attachment, bone and tooth loss. (1) Periodontal infection have been linked to systemic conditions and diseases, such as heart disease, diabetes, obesity, and metabolic syndrome.(2, 3, 4, 5) The association between periodontal diseases and these systemic diseases is hypothesized to be caused by a low-grade, chronic inﬂammatory burden. It has been postulated that locally secreted cytokines and periodontal pathogens may enter the bloodstream and contribute to damage elsewhere in the body.
A recently published study explored relationships among serum adipokines, vitamin D, and clinical and microbial parameters of chronic periodontitis before and after treatment. (6) Weight, height, and smoking status were recorded for 56 patients with chronic periodontitis. Plaque, gingivitis, bleeding on probing, suppuration, probing depth, and clinical attachment level were measured at all teeth present. Subgingival bioﬁlm samples from each tooth were analyzed for levels of 40 bacterial species using checkerboard DNA–DNA hybridization. Serum levels of interleukin-6 (IL-6), tumor necrosis factor-a, adiponectin, leptin, resistin, and vitamin D were measured at baseline. Sample collection was then performed in a subset of the population 6 months after therapy.
The results showed positive correlations between adiponectin/vitamin and between IL-6/leptin, negative correlations between IL-6/vitamin D and leptin/vitamin D, but no associations between serum analytes and clinical or microbial parameters. Sex and body mass index were associated with levels of adipokines. Periodontal therapy improved clinical and microbiologic parameters but did not inﬂuence the levels of serum analytes. The conclusion was that adipokines and IL-6 levels were affected by sex and body mass index, and serum analytes were not inﬂuenced by periodontal therapy. The study proposes that chronic periodontitis might play a minor role, if any, in serum levels of inﬂammatory mediators in systemically healthy individuals. The inﬂuence of sex and BMI outweighed any potential role that local periodontal infection and inﬂammation may have on systemic markers of inﬂammation in the absence of generalized periodontitis or systemic modifying factors.
So do we not perform periodontal therapy? Of course we do! Although there is controversy regarding the direct impact of periodontal therapy on systemic inﬂammation, there is consensus regarding the local clinical and microbiologic beneﬁts of periodontal therapy. Any positive systemic effect that might occur as a result of periodontal treatment would be an additional benefit to the essential role of treatment in maintaining the periodontal tissues. Discussing this with patients is imperative so they understand the local and possible systemic benefits of periodontal therapy.
1. Cochran DL. Inﬂammation and bone loss in periodontal disease. J Periodontol 2008; 79(Suppl. 8):1569-1576.
2. Humphrey LL, Fu R, Buckley DI, Freeman M, Helfand M. Periodontal disease and coronary heart disease incidence: A systematic review and meta-analysis. J Gen Intern Med 2008; 23:2079-2086.
3. Novak MJ, Potter RM, Blodgett J, Ebersole JL. Periodontal disease in Hispanic Americans with type 2 diabetes. J Periodontol 2008; 79:629-636.
4. Morita I, Okamoto Y, Yoshii S, et al. Five-year incidence of periodontal disease is related to body mass index. J Dent Res 2011; 90:199-202.
5. Benguigui C, Bongard V, Ruidavets JB, et al. Metabolic syndrome, insulin resistance, and periodontitis: A cross-sectional study in a middle-aged French population. J Clin Periodontol 2010; 37:601-608.
6. Teles FR, Teles RP, Martin L, Socransky SS, and Haffajee AD. Relationships Among Interleukin-6, Tumor Necrosis Factor-a, Adipokines, Vitamin D, and Chronic Periodontitis. J Periodontol 2012;83:1183-1191.
7. http://www.nhlbisupport.com/bmi/. Accessed September 12, 2012.
Maria Perno Goldie, RDH, MS
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