A Follicle-Stimulating Hormone Exacerbates the Progression of Periapical Inflammation Through Modulating the Cytokine Release in Periodontal Tissue.

Menopause is directly related to a systemically low grade of inflammation, indicating that postmenopausal women might be more prone to the development of inflammation. The high levels of circulating follicle-stimulating hormone (FSH) may cause hypogonadal bone loss during postmenopausal osteoporosis independent of estrogen. Previous research revealed that FSH could aggravate alveolar bone loss during experimental periapical lesions in ovariectomized rats; however, the mechanisms for these effects remain unclear. In this study, we showed that FSH enhanced the expression and secretion of the proinflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha to a significant degree in human periodontal ligament (hPDL) cells. Furthermore, FSH upregulated Porphyromonas gingivalis lipopolysaccharide (pg LPS)-induced proinflammatory cytokine production. Furthermore, in vivo studies demonstrated that FSH increased the levels of the aforementioned cytokines in the serum and enhanced the expression of Toll-like receptor 4 at both the messenger RNA and protein levels in hPDL cells and periodontal tissues. Our research suggests that high FSH levels may regulate the immune status of periodontal tissues during the postmenopausal period and, to a certain extent, suggested that postmenopausal women might be more prone to the development of inflammation of the periapical periodontitis and more obvious bone loss.