Periodontal inflammation may amplify genitourinary susceptibility in perimenopausal and postmenopausal womenPeriodontal Inflammation May Increase Risk of Genitourinary Infections

During perimenopause and postmenopause, changes in estrogen exposure may alter mucosal barriers, microbial ecosystems, and inflammatory responsiveness across the oral and genitourinary tracts. These stages differ in their hormonal patterns, and much of the available evidence comes from postmenopausal women or experimental models of estrogen deficiency. In the oral cavity, altered salivary function, gingival immunity, epithelial integrity, and alveolar bone metabolism may increase the inflammatory potential of established biofilms without generating a uniform menopause-associated microbial signature. When periodontitis develops, disruption of the gingival barrier can promote repeated exposure to microbial products, cytokine spillover, hepatic acute-phase responses, endothelial activation, and myeloid activation, thereby adding to systemic inflammatory burden. In parallel, hypoestrogenism can weaken vaginal, urethral, and bladder epithelial resilience, reduce Lactobacillus-associated colonization resistance, and impair tissue repair. The association between hypoestrogenism and recurrent urinary tract infection is better supported than corresponding associations with bacterial vaginosis or vulvovaginal candidiasis. Genitourinary syndrome of menopause may cause overlapping symptoms and coexist with infection. In this narrative review, we propose an estrogen-sensitive oral-systemic-genitourinary axis in which periodontal inflammation may amplify genitourinary susceptibility through systemic inflammatory signals and possibly through changes in intestinal and vaginal ecosystems. Hypoestrogenism may provide a permissive background, while local microbial or inflammatory challenges contribute to clinical disease. This proposed interaction does not require direct bacterial dissemination to the genitourinary tract. Evidence supporting the individual components is stronger than direct human evidence for the complete pathway, and a contribution from persistent myeloid reprogramming remains unproven. Longitudinal multisite studies integrating hormonal trajectories, periodontal status, systemic immune markers, and microbiologically confirmed genitourinary outcomes, together with combined periodontal and local estrogen interventions, are required to test this hypothesis in perimenopausal and postmenopausal women.