Abstract

Osteoclast inhibition has become a pivotal strategy in managing conditions related to excessive bone resorption, such as osteoporosis and bone metastases. Osteoclasts are specialized cells responsible for bone breakdown, and their overactivity can lead to weakened bones, increased fracture risk, and complications in cancer patients. Targeted therapies, including bisphosphonates and denosumab, have been developed to inhibit osteoclast activity, offering significant benefits in maintaining bone density, reducing pain, and improving quality of life. This article explores the mechanisms of osteoclast inhibition, its impact on bone remodeling, and its implications for cancer therapy. By addressing excessive bone resorption, these therapies play a crucial role in both preserving bone health and managing metastatic bone disease.