The Role of Visfatin Levels in Gingival Crevicular Fluid as Potential Biomarker in The Relationship Between Obesity and Periodontal Disease

Overweightness and obesity are defined as the accumulation of fat in body tissues that might impair overall health. Adults are considered overweight if their body mass index (BMI, calculated as weight in kg/[height in meters]2) is ≥ 25 and obese if BMI ≥ 30 kg/m2. The prevalence of overweightness and obesity has increased worldwide during recent decades.

Obesity is usually related to a chronic low-grade systemic inflammation resulting in significant changes in the concentrations of cytokines and hormones, which subsequently leads to the development of obesity-linked disorders, including insulin resistance, type II diabetes, cardiovascular diseases, dyslipidemia, and metabolic syndrome. Since the host response is among the most crucial factors affecting the pathogenesis of periodontal disease, multiple studies have addressed the possible associations between BMI, overweightness, obesity, diabetes, the serum level of lipids, cholesterol, and periodontal breakdown, with mixed results. Many studies have demonstrated a positive association between obesity and periodontitis and suggested that obesity-related inflammation might promote periodontitis by secretion of inflammatory markers by the adipose tissue, which might subsequently increase gingival inflammation. The association between obesity and periodontal disease is based on the amassing of white adipose tissue (WAT) and increased secretion levels of adipokines from WAT.

WAT is an energy storage organ with some metabolic activities, participating in the endocrine and secretory systems. WAT secretes several immune-modulatory adipokine molecules, such as adiponectin, leptin, visfatin, resistin, chemerin, tumor necrosis factor-alpha (TNF-alpha), interleukin-1β (IL-1β), and interleukin-6 (IL-6). It has been found that these molecules are involved in a wide range of physiologic and pathologic processes, including immunity and inflammation. Thus, cytokines and hormones released from adipose tissue might play a role in the destruction of periodontal tissue by inducing hyperinflammatory responses.

Visfatin is a multi-potential mediator that functions as a growth factor, cytokine, an enzyme with a role in energy metabolism, and as a proinflammatory mediator. It is mainly released from adipose tissue, especially from macrophages, and can also be released from lymphocytes, dendritic, muscle, and bone marrow cells. Visfatin has an important role in the regulation of the immune response. Visfatin inhibits neutrophil apoptosis during inflammation and increases TNF-alpha, IL-1β, and IL-6 levels. The expression of visfatin is increased under inflammatory conditions, such as rheumatoid arthritis, cardiovascular diseases, type-II diabetes mellitus, and periodontal disease.

Although several studies have demonstrated the relationship between periodontitis and obesity, no study has evaluated the levels of visfatin in gingival crevicular fluid (GCF) in obese individuals with periodontitis. Increased adipocytes levels, such as visfatin, cause secretion of cytokines, which are known to play an important role in periodontitis, and might trigger periodontitis formation and development.