Bone metastases of prostate cancer usually have an underlying osteoclastic component. Bone metastasis is incurable and contributes significantly to disease-specific morbidity and mortality. Management of bone metabolism in patients is a clinically significant issue. Several key factors have been found to be important in tumor-induced promotion of osteoclast activity. Receptor activator of nuclear factor-kappa B ligand (RANKL) is produced by bone metastasis of prostate cancer, enabling these metastasis to induce osteolysis through osteoclast activation. Matrix metalloproteinases (MMPs) are secreted by prostate cancer cells and promote osteolysis primarily through degradation of bone matrix. In this way, many factors derived from prostate cancer metastases can promote osteolysis, and these factors may serve as therapeutic targets. The new agents are targeted to osteoclasts (i.e.: zoledronic acid, anti-RANKL monoclonal antibody, cathepsin K inhibitor, and anti-PTHrP monoclonal antibody), are considered to be standard management in the care of bone metastasis patients in combination with chemotherapy and hormone therapy. In this review, we summarized the current understanding and therapy of bone metastasis in prostate cancer.