Resistin Is Increased in Periodontal Cells and Tissues: In Vitro and In Vivo Studies

Abstract

Resistin, a proinflammatory adipokine, is elevated in many inflammatory diseases. However, little is known about its performance in periodontitis. The present study is aimed at evaluating resistin expression and synthesis in periodontal cells and tissues under inflammatory/microbial stress in addition to its effects on the periodontium. In vivo, 24 male rats were randomly divided into two groups: control and ligature-induced periodontal disease. After 6 and 12 days, animals were sacrificed to analyze gene expression of adipokines, bone loss, inflammation, and resistin synthesis. In vitro, human periodontal ligament (PDL) fibroblasts were used to evaluate the expression of resistin after inflammatory stimuli. In addition, PDL fibroblasts were exposed to resistin to evaluate its role on soft and hard tissue metabolism markers. The periodontitis group demonstrated significant bone loss, an increase in the number of inflammatory cells and vascular structures, an increase in resistin expression and synthesis, and a decrease in the expression of adiponectin, leptin, and its functional receptor. PDL fibroblasts showed a significant increase in resistin expression and synthesis in response to the inflammatory stimulus by IL-1β. Resistin induced an increase in cytokine expression and a decrease in the regulation of some hard tissue and matrix formation genes in PDL fibroblasts. These data indicate that resistin is produced by periodontal cells and tissues, and this effect is enhanced by inflammatory stimuli. Moreover, resistin seems to interfere with soft and hard tissue metabolism during periodontitis by reducing markers related to matrix formation and bone tissue.

Association between lipid metabolism and periodontitis in obese patients: a cross-sectional study

“…Bacterial infection can stimulate to secretion of inflammatory mediators and proteases, and gingival epithelial cells can remove them by innate and acquired immune responses [ 38 ]. In addition, some scholars have also found that leptin and resistin have a certain impact on the pathogenesis of periodontitis [ 39 , 40 ]. What’s more, one of the biological explanations for obesity negatively affects the progression of periodontitis and the response to periodontal therapy may be also due to the unaffected leptin, resistin and adiponectin levels after the periodontal non-surgical treatment [ 41 ].…”

Obesity Modifies the Proteomic Profile of the Periodontal Ligament

“…Thus, many adipokines are produced not only in the adipose tissue by adipocytes but also by other cells and tissues during obesity. Interestingly, adipokines have also been found in periodontal ligament (PDL) cells and tissues [ 10 , 11 , 12 , 13 ].…”

Serum Resistin Levels and Related Genetic Variants Are Associated With Bone Mineral Density in Postmenopausal Women

“…Resistin has a diverse role in the human body and influence cellular structure and function of various tissues. It has proinflammatory properties and stimulates the production and secretion of pro-inflammatory cytokines (8) resulting in abnormal endothelial function (9).It generates oxidative stress and induces the proliferation of vascular smooth muscle cells (VSMCs) thus reducing the levels of nitric oxide (NO) resulting in reduced vasodilation, increased cell adhesion, thrombosis, angiogenesis and vascular permeability ultimately leading to atherosclerosis and increase incidence of cardiovascular events (10).…”