Teriparatide Acetata(Sawai Pharmaceutical)

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.

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.

Early identification and intervention are critical to reduce fracture risk, emphasizing the need for better diagnostic tools and individualized treatment strategies.

To synthesize evidence on the efficacy of osteoanabolic therapies (teriparatide, abaloparatide, romosozumab) in adults with type 2 diabetes mellitus (T2D), focusing on changes in bone mineral density (BMD) and fractures, and to explore whether responses differ between people with and without diabetes.

Following PRISMA guidelines, we searched PubMed/MEDLINE, Embase and Scopus databases till April 30, 2025 (PROSPERO: CRD420251044760). Five studies met criteria (n = 1,469 with T2D; n = 12,052 without diabetes): two post hoc analyses of randomized controlled trials (RCTs) (ACTIVE and ARCH trials) and three observational studies. Using random-effects model, osteoanabolic therapy in T2D increased lumbar spine BMD by a mean difference (MD) of 5.06% (95% CI: 1.62, 8.50; I²=93.3%). Sensitivity analysis restricted to RCTs demonstrated a larger, highly consistent effect at lumbar spine (MD 7.49%, 95% CI: 6.56, 8.41; I²=0%). Femoral neck BMD increased by 2.61% (95% CI: 1.84, 3.38; I²=0%). Evidence for fracture outcomes in T2D was limited to a single RCT (ACTIVE), in which non-vertebral fractures were reduced with abaloparatide versus placebo (p = 0.04), whereas new vertebral fractures were not different between groups. Two observational studies showed that in people with T2D, osteoanabolic agents improved BMD as much as, or more than, in non-diabetic individuals, while fracture rates were mostly similar between the groups. Osteoanabolic agents yield meaningful BMD gains in T2D, particularly at lumbar spine, with modest improvements at femoral neck. Limited fracture data suggest possible benefit but remain underpowered, underscoring the need for diabetes-specific RCTs with fracture endpoints.