Periodontal Disease and Diabetes Mellitus: The Role of Tumor Necrosis Factor‐α in a 2‐Way Relationship

Abstract

It is generally accepted that obesity is associated with many other multiple-risk factor syndromes such as hypertension, hyperlipidemia, type 2 diabetes mellitus, and periodontal disease. The number of obese people is increasing rapidly in both western and eastern countries. Adipocytes in the adipose tissues of obese people produce large quantities of biologically active molecules such as leptin, an important molecule regulating energy expenditure and body weight. Therefore, adipocyte-derived active molecules, named adipocytokines, are candidate molecules accounting for the close association between obesity and other multiple-risk factor syndromes. The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) is produced by adipocytes, and its blood concentration is elevated in obese patients and declines with weight loss. Studies have demonstrated that TNF-alpha suppresses insulin action via its specific receptor; hence, it exacerbates insulin resistance. In addition to adipocytes, monocytes/macrophages produce large quantities of TNF-alpha. Thus, TNF-alpha, produced from monocytic cells due to inflammatory diseases, may have an additive influence on insulin sensitivity to adipocyte-derived TNF-alpha. Here, we hypothesized that 1) TNF-alpha produced by the adipose tissues of obese patients acts as a risk factor for periodontal inflammation, and 2) TNF-alpha produced due to periodontal inflammation may be an additional important factor influencing insulin sensitivity in both obese and type 2 diabetic patients. We believe that this interaction is a possible mechanism accounting for a 2-way relationship between type 2 diabetes and periodontal disease.

Association between periodontal condition and kidney dysfunction in Japanese adults: A cross‐sectional study

“…In older Japanese subjects, periodontitis has also been shown to become worse along with worsening eGFR category (classified as >60, 30–59, and <29 ml/min −1  1.73 m −2 ) (Iwasaki et al, 2012). Furthermore, several studies have suggested a bidirectional relationship between glycemic control and periodontal disease (Okada et al, 1996; Nagasawa et al, 2010; Nishimura et al, 2003). It is generally accepted that elevated glucose levels promote the pathophysiology of periodontitis (Preshaw & Bissett, 2013).…”

“…It is characterized by destruction of connective tissue, the periodontal ligament, and alveolar bone, leading to a significant increase of systemic exposure to bacteria (Okada et al, 1996). Many investigators have suggested a two‐way relationship between diabetes and periodontitis (Nagasawa et al, 2010; Nishimura et al, 2003; Preshaw et al, 2012). Interestingly, it has been reported that periodontal infection shows a positive correlation with endothelial dysfunction (Tonetti et al, 2007) and that infection with Porphyromonas gingivalis increases endothelial injury in obese mice (Ao et al, 2014).…”

The Effect of Scaling and Root Planing on Glycaemic Control, Periodontal Status and Gingival Crevicular f luid TN f - α Levels in an Indian Population- To Reveal the Ambivalent Link

“…Presence of this cytokine may contribute to the heightened state of inflammation that is observed in diabetic subjects [14,15].…”

Asociación de la enfermedad periodontal y diabetes mellitus tipo 2 (Association between periodontal disease and type 2 diabetes mellitus)

“…La periodontitis y los trastornos endocrinos, como la diabetes mellitus, abarcan una respuesta caracterizada por inflamación y secreción de citoquinas que destruyen el periodonto, causando alteraciones sistémicas (15,16).…”