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. 2012 Dec;36(6):404-11.
doi: 10.4093/dmj.2012.36.6.404. Epub 2012 Dec 12.

Periodontitis and insulin resistance: casual or causal relationship?

Affiliations

Periodontitis and insulin resistance: casual or causal relationship?

Abhijit N Gurav. Diabetes Metab J. 2012 Dec.

Abstract

Insulin resistance (IR) is now considered as a chronic and low level inflammatory condition. It is closely related to altered glucose tolerance, hypertriglyceridemia, abdominal obesity, and coronary heart disease. IR is accompanied by the increase in the levels of inflammatory cytokines like interleukin-1 and 6, tumor necrosis factor-α. These inflammatory cytokines also play a crucial part in pathogenesis and progression of insulin resistance. Periodontitis is the commonest of oral diseases, affecting tooth investing tissues. Pro-inflammatory cytokines are released in the disease process of periodontitis. Periodontitis can be attributed with exacerbation of IR. Data in the literature supports a "two way relationship" between diabetes and periodontitis. Periodontitis is asymptomatic in the initial stages of disease process and it often escapes diagnosis. This review presents the blurred nexus between periodontitis and IR, underlining the pathophysiology of the insidious link. The knowledge of the association between periodontitis and IR can be valuable in planning effectual treatment modalities for subjects with altered glucose homeostasis and diabetics. Presently, the studies supporting this association are miniscule. Further studies are mandatory to substantiate the role of periodontitis in the deterioration of IR.

Keywords: Diabetes mellitus, type 2; Glucose homeostasis; Glucose homeostasis model assessment; Insulin resistance; Periodontitis.

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Conflict of interest statement

No potential conflict of interest relevant to this article was reported.

Figures

Fig. 1
Fig. 1
Bidirectional relationship between diabetes mellitus and periodontitis. AGEs, advanced glycation end products; PMN, polymorphonuclear neutrophil; ROS, reactive oxygen species; IL, interleukin; TNF-α, tumor necrosis factor-α; PGE2, prostaglandin E2; LPS, lipopolysaccharide.

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