Targeted Therapy in Osteoporosis: The Promise of Monoclonal Antibodies and Small Molecules
نویسندگان
1 Traumatology Department, The 964th Hospital of PLA Joint Logistic Support Force, Changchun 130062, China
2 Traumatology Department, The 964th Hospital of PLA Joint Logistic Support Force, Changchun 130062, China
3 Traumatology Department, The 964th Hospital of PLA Joint Logistic Support Force, Changchun 130062, China
4 Pharmacy Department, The 964th Hospital of PLA Joint Logistic Support Force, Changchun 130062, China
5 Medical Service Training Centre, 964 Hospital, Joint Logistics Support ForceChang-chun 130062, China
6 Endocrinology Department, The 964th Hospital of PLA Joint Logistic Support Force, Changchun 130062, China
7 Traumatology Department, The 964th Hospital of PLA Joint Logistic Support Force, Changchun 130062, China
8 Traumatology Department, The 964th Hospital of PLA Joint Logistic Support Force, Changchun 130062, China
doi
10.22034/ircmj.2025.480818.1507چکیده
Background and Objectives: Osteoporosis is a widespread disease affecting over 500 million people worldwide, with one in three women and one in five men over the age of 50 sustaining an osteoporotic fracture. Conventional treatment methods, such as bisphosphonates and SERMs, address the inhibition of bone resorption but are restricted by side effects and differences in efficacy. Targeted therapies provide novel options, such as monoclonal antibodies and small molecules that interfere with specific molecular pathways. Methods: A systematic review of PubMed/MEDLINE and Google Scholar literature until September 2024 was performed. The search keywords were “osteoporosis,” “monoclonal antibodies,” “small molecules,” and “bone resorption.” We included clinical and preclinical studies that assessed efficacy, mechanisms, and safety and minimized bias through independent screening by two reviewers. Results: Several monoclonal antibodies (e.g., denosumab, romosozumab) act by inhibiting important pathways (e.g., RANKL, sclerostin) regulating bone resorption and formation. These agents include small molecules, such as teriparatide and abaloparatide, that mimic the parathyroid hormone that stimulates bone formation. Although these therapies increase bone density and decrease fractures, concerns regarding long-term safety, including cardiovascular risks and rebound effects following cessation, persist. Combination therapies and personalized approaches may overcome these problems. Conclusion: Targeted therapies for the management of osteoporosis and fracture prevention have come a long way in dealing with bone resorption and formation. Integrating genetic biomarkers and machine learning will enable personalized treatment strategies for safer and more effective solutions for patients, which is an exciting avenue for future research.