Gingival Inflammation Modulates NLRP3 Inflammasome Signalling in Peripheral Blood Mononuclear Cells of PCOS Patients: A Case-Control Study

Polycystic ovary syndrome (PCOS) is a complex condition associated with chronic inflammation and oxidative stress and is often linked to periodontal diseases. This study aimed to determine whether gingivitis modulates the NLRP3 inflammasome in peripheral blood mononuclear cells (PBMCs) from women with PCOS. Following a case-control design, 104 women were divided into three groups: controls (n = 36), PCOS without gingivitis (PCOS, n = 44) and PCOS with gingivitis (PCOS+, n = 24). Periodontal parameters, proinflammatory regulators (NFκB p65, JNK), NLRP3 components (NLRP3, ASC, procaspase-1, caspase-1) and oxidative stress markers (superoxide, <i>NRF2</i>, <i>GCLC</i> and <i>GSR</i>) were determined. The PCOS+ group presented elevated values for bleeding on probing (BOP) and plaque and calculus indices, both of which were associated with increased protein levels of NFκB p65 and JNK, thus indicating NLRP3 inflammasome priming. Higher protein levels of NLRP3, ASC, procaspase-1 and caspase-1 in the PCOS+ group confirmed that priming had occurred, suggesting an engagement in assembly. When potential assembly signals of inflammasome were evaluated, the patients with PCOS generally presented enhanced total superoxide and an impaired antioxidant response (<i>NRF2, GCLC</i> and <i>GSR</i>). Moreover, BOP was independently associated with JNK, ASC and procaspase-1. These findings suggest that gingival inflammation modulates the innate immune response in leukocytes of women with PCOS via the NLRP3 inflammasome pathway, which is regulated by proinflammatory factors and oxidative damage.