Mechanistic insights into polycystic ovary syndrome and periodontal disease: a systematic scoping review of inflammatory, oxidative stress, hormonal–metabolic, and microbial pathways

Abstract To identify critical evidence gaps, this scoping review mapped the extent and nature of published research exploring the biological links between polycystic ovary syndrome (PCOS) and periodontal disease. Following PRISMA-ScR guidelines and a pre-registered protocol (OSF: https://doi.org/10.17605/OSF.IO/WE3XU) a systematic search of PubMed, Scopus, EBSCO, and Google Scholar identified original human studies assessing clinical periodontal parameters and mechanistic biomarkers in PCOS patients. Screening and data extraction were conducted independently by two reviewers. Thirty-three studies met the inclusion criteria. Mapping identified a synergistic pathophysiological network across four domains. The evidence reveals an elevated systemic inflammatory baseline marked by hyper-activated endothelial markers (Endocan) alongside elevated levels of Tumor Necrosis Factor-alpha (TNF-alpha) and Interleukin-6 (IL-6), which appears to lower the threshold for local tissue destruction. This is coupled with a compromised antioxidant defense—notably nuclear factor erythroid 2-related factor 2 (NRF2) downregulation—and a "microbial dysbiosis" toward pathogenic microbial complexes. However, current data primarily identify mechanistic intersections rather than definitive causality, with the "PCOS-specific" impact often confounded by shared metabolic risk factors like insulin resistance and adiposity. Mapping this evidence reveals a profound overlap between PCOS and periodontitis through shared pathophysiological networks. Advancing this field requires a Core Outcome Set (COS) and well-designed randomized controlled trials. Clinically, recognizing periodontal disease as a potential contributor to the systemic inflammatory burden suggests that integrating routine.