Purpose of review:Premenopausal osteoporosis, characterized by low bone mass and fractures, is rare but poses long-term skeletal risks. Unlike postmenopausal osteoporosis, it often stems from inadequate peak bone mass accrual or secondary causes such as systemic diseases, medications, or lifestyle factors. This review explores contemporary approaches to defining, diagnosing, and treating low bone mass and osteoporosis in premenopausal women.
Recent findings:Prevalence varies according to ethnicity and is further influenced by the diagnostic criteria, with higher risks in Caucasian and Asian women. Key determinants of peak bone mass achieved by the late 20 s include genetics (60–80% of variability), nutrition (calcium, vitamin D, and protein), lifestyle (exercise, smoking, and alcohol), and occupational exposures (e.g., heavy metals and sedentary work). Pregnancy and lactation-associated osteoporosis also cause transient bone loss, particularly in high-risk individuals. Bone mineral density by dual-energy X-ray absorptiometry is the gold standard for diagnosis despite of certain limitations. Additionally, emerging technologies like radiofrequency echographic multi spectrometry show promise. Management focuses on optimizing bone health through adequate nutrition, weight-bearing exercises, and addressing secondary causes, when present like rheumatoid arthritis, long-term glucocorticoid use, hypogonadism, etc. Pharmacological options such as bisphosphonates and teriparatide can be considered in high-risk cases, but evidence on their safety and efficacy in premenopausal women is limited, and concerns about teratogenicity remain.
Summary:Early identification and intervention are critical to reduce fracture risk, emphasizing the need for better diagnostic tools and individualized treatment strategies.