Premenopausal Osteoporosis: An Under-recognized Window for Early Skeletal Intervention

BACKGROUND: Premenopausal osteoporosis is an uncommon but clinically important cause of skeletal fragility in younger women. Unlike postmenopausal osteoporosis, reduced bone mineral density (BMD) in premenopausal women may reflect low peak bone mass rather than active bone loss, and BMD alone does not reliably predict short-term fracture risk. Fragility fractures in this population should therefore prompt evaluation for potentially reversible secondary causes. AIMS AND OBJECTIVES: To summarize the current evidence regarding the epidemiology, etiological factors, clinical presentation, diagnosis, and management of premenopausal osteoporosis, with particular emphasis on its recognition and relevance to orthopedic practice. MATERIALS AND METHODS: A narrative literature review was conducted using PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar. Literature published between January 2000 and December 2025 was searched using combinations of terms including "premenopausal osteoporosis," "osteoporosis in young women," "low bone mineral density," "fragility fractures," "secondary osteoporosis," "pregnancy-associated osteoporosis," and "glucocorticoid-induced osteoporosis." Original studies, systematic reviews, meta-analyses, clinical practice guidelines, and expert consensus statements addressing bone health in premenopausal women or young adults were considered. Reference lists of relevant publications were also manually screened. Findings were qualitatively synthesized according to epidemiology, determinants of bone mass, secondary causes, diagnostic evaluation, and management. RESULTS: Premenopausal osteoporosis is rare in the general population and is predominantly associated with secondary causes rather than age-related skeletal loss. Important contributors include functional hypothalamic amenorrhea, pregnancy- and lactation-associated osteoporosis, glucocorticoid exposure, endocrine and inflammatory disorders, malabsorption, nutritional deficiencies, eating disorders, and genetic factors. Fragility fractures, particularly vertebral and major appendicular fractures, carry greater diagnostic significance than isolated low BMD. In most premenopausal women, Z-scores rather than T-scores should be used for BMD interpretation, with a Z-score ≤-2.0 described as "below the expected range for age." Management should primarily focus on identifying and correcting reversible secondary causes, optimizing nutrition and lifestyle, and addressing hormonal or systemic disease. Pharmacological treatment should be considered selectively in women with substantial fracture risk or ongoing bone loss, with particular attention to reproductive considerations and long-term drug safety. CONCLUSION: Premenopausal osteoporosis represents an important but under-recognized opportunity for early skeletal intervention. In young women, a fragility fracture should be regarded as a clinical warning sign rather than relying on BMD alone. A systematic evaluation for secondary causes, appropriate interpretation of DXA using age-adjusted Z-scores, and individualized, etiology-driven management are essential to prevent recurrent fractures and improve long-term skeletal health. Early recognition by orthopedic surgeons may provide an important opportunity for multidisciplinary metabolic bone evaluation and secondary fracture prevention.