Tumor Necrosis Factor-αand Interleukin-6: Potential Interorgan Inflammatory Mediators Contributing to Destructive Periodontal Disease in Obesity or Metabolic Syndrome

Abstract

Obesity has become a worldwide health burden in the last two decades. Obesity has been associated with increased comorbidities, such as coronary artery disease, diabetes, and destructive periodontal disease. Obesity is also part of a group of risk factors occurring together in an individual, which is referred to as metabolic syndrome. Clinical studies have shown higher risk for destructive periodontal disease in obesity and metabolic syndrome. However, the role of obesity and metabolic syndrome in the onset and development of destructive periodontal disease has not yet been fully understood. In this review, we discuss a working model, which focuses on interorgan inflammation as a common etiological factor for destructive periodontal disease associated with obesity and metabolic syndrome. Specifically, we suggest that elevated levels of tumor necrosis factor-α (TNF-α) or interleukin 6 (IL-6)—both adipokines and known risk factors for destructive periodontal disease—in obesity and metabolic syndrome contribute to the onset and development of destructive periodontal disease. The connections between destructive periodontal disease and systemic conditions, such as obesity or metabolic syndrome, are complex and potentially multidirectional. This review largely focuses on TNF-α and IL-6, inflammatory mediators, as potential common risk factors and does not exclude other biological mechanisms.

Association between abdominal obesity and periodontal disease. Cross-sectional study.

“…26,27 . Among these cytokines is Tumor Necrosis Factor-α(TNF-α) that increases insulin-resistance, contributing to a generalized hyperinflammatory state that affects periodontal tissues, especially in the presence of oral pathogens 21,24 .…”

“…It also highlights leptin hormone secretion, which has a fundamental role in the regulation of the feeling of satiety, but also acts as an anti-inflammatory hormone and promotes bone formation 24 . Normally, circulating leptin levels have a direct correlation with the amount of adipose tissue, but this relationship is usually altered in obesity 24 .…”

“…Normally, circulating leptin levels have a direct correlation with the amount of adipose tissue, but this relationship is usually altered in obesity 24 .…”

Relationship between Periodontal Disease (Periodontitis) and Acute Vascular Events a Case-Control Study Enperiva Study

“…Besides the typical risk factors (RF) for POD (smoking, diabetes, obesity), a complex mechanism involving these factors along with genetic factors and infection have been found to play a role [2]. The result of chronic inflammation can be determined through clinical and radiographic parameters as well as plasma and gingival fluid analysis [3][4][5][6]. On the other hand, vascular disease and the events associated with it are one of the leading causes of morbidity and mortality in adults [7,8].…”

“…The inflammatory state is triggered and sustained by the vascular disease risk factors first described in the Framingham Study [11]. However, not all vascular events were related to those RF; during the last 15 years, POD has started to be regarded as a risk factor strongly associated with atheromatous disease [1][2][3][4][5][6][7][8][9][10][11][12]. Periodontal disease and atheromatous disease share not only risk factors such as smoking and diabetes, but also a complex multifactorial process of chronic inflammation stimulating mediators that accelerate endothelial dysfunction and/or mechanisms of cross-reacting antibodies against the periodontal flora and endothelial cell proteins; this may explain the relation between these pathologies [13][14][15].…”