SRS183 - Calcium channel blockers and bone aealth: a systematic review of preclinical and clinical evidence

Abstract Background Calcium channel blockers (CCBs) are widely prescribed for older adults at risk of osteoporotic fractures. Despite preclinical data suggesting CCB-mediated effects on bone remodelling, clinical findings on bone mineral density (BMD) & fractures are inconsistent. We systematically evaluated the relationship between CCB use, bone metabolism, & fracture outcomes. Methods PubMed, MEDLINE, & Embase were searched from inception to July 2025 for preclinical & clinical studies reporting fracture risk &/or parameters of bone metabolism. The primary outcome was fracture risk, with secondary outcomes including BMD, bone weight, biochemical markers of bone turnover (calcium, PTH, ALP, CTX, BMP-2, PINP), & biomechanical properties. Screening & data extraction followed PRISMA principles; risk of bias was assessed with appropriate tools (SYRCLE, RoB 2, ROBINS-I). A narrative synthesis was performed. Results 34 studies were included (17 preclinical; 17 clinical). Among clinical studies, 4/17 reported reduced BMD with CCBs; fracture risk increased in 4, decreased in 4, & was unchanged in 4; 1 study additionally reported a protective association with osteoporosis. Preclinical findings across 655 animals were mixed for BMD, calcium, PTH, ALP, & BMP-2. Notably, 5 studies reported lower CTX, 2 reported lower PINP, & 4 reported increased or unchanged bone strength with CCB exposure. Conclusions Evidence indicates CCBs may modulate bone physiology, yet clinical associations with BMD & fractures are heterogeneous. Discrepancies may reflect confounding factors like comorbidities & non-skeletal pathways affecting falls risk (for example CCB-induced orthostatic hypotension or sarcopenia); these mechanisms remain hypothesis-generating. Standardised preclinical endpoints & large, well-adjusted prospective cohorts stratified by dihydropyridine versus non-dihydropyridine agents, dose, & duration are needed to clarify skeletal effects.