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Journal Article
Review
The Link Between Periodontal Inflammation and Obesity.
PURPOSE OF REVIEW: Obesity is a trigger for multiple diseases such as diabetes mellitus, hypertension, and cardiovascular diseases. Epidemiological studies have shown that obesity may be a risk factor for periodontal disease. Recently, there have been reports of presumed mechanisms of the associations between periodontitis and lipid metabolism or thermogenesis. This review aims to discuss the link between periodontal disease and energy regulatory function based on recent findings.
RECENT FINDINGS: It has been demonstrated that activation of the C-C motif chemokine ligand/C-C chemokine receptor 7 pathway in adipose tissue induces inflammation and impairment of lipid metabolism and energy regulation in mice. Porphyromonas gingivalis administration has been shown to induce further weight gain and increased adipose tissue in diet-induced obese mice. Additionally, it has been reported that Porphyromonas gingivalis -induced endotoxemia potentially affect obesity by altering endocrine functions in brown adipose tissue in mice. Several cohort studies have shown that obesity is associated with tooth loss 5 years later, and periodontal conditions of obese individuals are significantly worse 2 and 6 months after the treatment compared with those of non-obese individuals. It has also been reported that body mass index is positively associated with the periodontal inflamed surface area index, a measure of periodontal inflammation. These results suggest that not only the enhancement of inflammation due to obesity but also the activation of inflammatory signaling may affect energy regulation.
SUMMARY: Loss of adipose tissue homeostasis induces increase and activation of immune cells in adipose tissue, leading to impaired immune function in obesity. Various cytokines and chemokines are secreted from obese adipose tissue and promote inflammatory signaling. Some of these signaling pathways have been suggested to affect energy regulation. The combination of obesity and periodontitis amplifies inflammation to levels that affect the whole body through the adipose tissue. Obesity, in turn, accelerates the exacerbation of periodontitis.
RECENT FINDINGS: It has been demonstrated that activation of the C-C motif chemokine ligand/C-C chemokine receptor 7 pathway in adipose tissue induces inflammation and impairment of lipid metabolism and energy regulation in mice. Porphyromonas gingivalis administration has been shown to induce further weight gain and increased adipose tissue in diet-induced obese mice. Additionally, it has been reported that Porphyromonas gingivalis -induced endotoxemia potentially affect obesity by altering endocrine functions in brown adipose tissue in mice. Several cohort studies have shown that obesity is associated with tooth loss 5 years later, and periodontal conditions of obese individuals are significantly worse 2 and 6 months after the treatment compared with those of non-obese individuals. It has also been reported that body mass index is positively associated with the periodontal inflamed surface area index, a measure of periodontal inflammation. These results suggest that not only the enhancement of inflammation due to obesity but also the activation of inflammatory signaling may affect energy regulation.
SUMMARY: Loss of adipose tissue homeostasis induces increase and activation of immune cells in adipose tissue, leading to impaired immune function in obesity. Various cytokines and chemokines are secreted from obese adipose tissue and promote inflammatory signaling. Some of these signaling pathways have been suggested to affect energy regulation. The combination of obesity and periodontitis amplifies inflammation to levels that affect the whole body through the adipose tissue. Obesity, in turn, accelerates the exacerbation of periodontitis.
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