Periodontal disease and endocrine imbalance: a molecular pathways perspective
Abstract
Periodontitis is a chronic multifactorial inflammatory disease whose pathological consequences extend well beyond the oral cavity to affect systemic health through the dissemination of pro-inflammatory mediators, bacteremic episodes, and the amplification of low-grade systemic inflammation. Concurrently, the endocrine system functions as a central regulator of periodontal tissue homeostasis, with hormone receptors for estrogens, androgens, glucocorticoids, insulin, thyroid hormones, and vitamin D expressed across the principal cell populations of the periodontium, including gingival fibroblasts, PDL cells, osteoblasts, osteoclasts, and epithelial cells. This narrative review synthesizes current evidence on the molecular pathways mediating the bidirectional relationship between periodontal disease and endocrine imbalance, integrating experimental, clinical, and systems-level bioinformatics data to provide a comprehensive mechanistic framework for this interaction. We examine how estrogen deficiency, progesterone excess, androgen dysregulation, insulin resistance, adipokine imbalance, thyroid dysfunction, glucocorticoid excess or deficiency, and perturbations of the parathyroid hormone and vitamin D axes each contribute to periodontal susceptibility through distinct but convergent molecular mechanisms involving NF- κ B activation, NLRP3 inflammasome-driven IL-1 β and IL-18 maturation, cytokine network dysregulation, oxidative stress amplification, and disruption of the…
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