Hormonal Shifts and Structural Strain: A Literature Review of Menopause and Perimenopause in Relation to Overuse Injuries and Stress Fractures.

Abstract

Musculoskeletal injury risk in midlife women has traditionally been attributed to estrogen decline, but this narrow focus overlooks the broader biomechanical, neuromuscular, and structural changes associated with menopause. Estrogen plays a multisystem role in maintaining trabecular bone integrity, collagen turnover, and neuromuscular coordination. Its abrupt loss causes bone demineralization (2%-5% annually in early menopause), impairs tendon repair, and contributes to sarcopenia. Fluctuating estradiol levels during perimenopause may transiently increase ligament laxity, further destabilizing joints. Common injuries such as Achilles and rotator cuff tendinopathies, plantar fasciitis, and stress fractures are amplified by low bone mineral density, prior fracture history, aromatase inhibitor use, and rapid increases in physical activity. Although early initiation of hormone replacement therapy reduces fracture risk by 20%-40%, it is not appropriate for all patients due to contraindications and individualized risk-benefit profiles. Non-hormonal strategies-including resistance training, nutritional optimization, and early screening with dual-energy X-ray absorptiometry and peripheral quantitative computed tomography-remain underutilized, particularly among marginalized populations. This structured narrative review synthesizes evidence from endocrinology, biomechanics, and musculoskeletal epidemiology to evaluate limitations in current research, including reliance on observational data, homogeneous cohorts, and technocentric approaches with limited generalizability. Future efforts should prioritize personalized, hormone-informed exercise prescriptions, biomarker-guided monitoring, and community-based prevention strategies. The prevailing estrogen-centric paradigm may benefit from a broader multidisciplinary framework integrating biological, mechanical, and social determinants of injury risk. We propose a hormone-tissue-load mismatch model that reframes menopause as a modifiable biomechanical window for injury prevention.