Periodontal disease is a chronic, multifactorial, and infectious disease caused by bacteria. It is characterized by the formation of an inflammatory response in the supporting bone and connective tissue against microbial dental plaque, and the nature of the resulting inflammatory response determines the course of periodontal disease. Type 2 Diabetes Mellitus (T2DM), obesity, and periodontal disease are closely related, presenting a triad association. Obesity is the crucial cause of T2DM and periodontitis is the sixth complication of diabetes. Asprosin circulates in the blood at nanomolar levels and is taken to the liver, where it activates the G protein-cAMP-PKA pathway, causing rapid glucose release into the circulation. Insulin-resistant humans and mice have been reported to have pathologically elevated plasma asprosin levels. It will be investigated whether asprosin, which we know to be effective on glucose metabolism, is affected by the periodontal condition.
Asprosin, a recently discovered glucogenic adipokine, is mainly synthesized by white adipose tissue and released during fasting. Appetite, glucose metabolism, insulin resistance, cell apoptosis, etc. asprosin is associated with diseases such as diabetes, obesity, polycystic ovary syndrome, and cardiovascular diseases. Periodontal tissue may act as a source of endocrine-like inflammatory mediators (such as TNF-α, IL-6 and IL-1) that are important in periodontal inflammation and can affect glucose and lipid metabolism. Production of TNF-α and IL-6 in adipose tissues strengthens the relationship between obesity, T2DM and periodontitis.we postulated that asprosin may be candidate for explaining the triangular relationship among obesity, T2DM, and periodontal disease.