Obesity and pelvic organ prolapse: Review

Obesity is a major public health challenge with substantial effects on women's health and quality of life. Pelvic organ prolapse (POP), characterized by the descent of pelvic organs into the vaginal canal, is influenced by both obesity-related mechanical forces and molecular alterations. This review aimed to evaluate the relationship between obesity and POP, with particular emphasis on etiopathogenesis, clinical consequences, and implications for prevention and treatment strategies.

This was a narrative review of the literature examining the relationship between obesity and pelvic organ prolapse. A literature search was performed using PubMed, Scopus, and Google Scholar databases. Relevant studies addressing obesity, pelvic organ prolapse, extracellular matrix remodeling, genetic susceptibility, epigenetic mechanisms, inflammation, and surgical outcomes were reviewed and synthesized. The available evidence was evaluated with respect to mechanical loading, connective tissue alterations, molecular pathways, and clinical implications.

Increased intra-abdominal pressure resulting from visceral adiposity was identified as a major mechanical factor contributing to pelvic floor weakening. In addition, obesity was found to influence extracellular matrix remodeling through altered collagen metabolism, adipokine imbalance, chronic inflammation, and epigenetic modifications. These mechanisms may contribute to the development and progression of POP, complicate surgical management, and increase the risk of recurrence. Current evidence also suggests that genetic susceptibility and connective tissue disorders may amplify the effects of obesity on pelvic floor dysfunction.

Obesity represents both an important risk factor and a therapeutic challenge in pelvic organ prolapse, adversely affecting women's quality of life. Understanding the interaction between mechanical, molecular, genetic, and epigenetic mechanisms may facilitate individualized prevention and management strategies for women with obesity. Further clinical and translational studies are needed to clarify these mechanisms and support the development of personalized approaches to POP prevention and treatment.