Abstract. Background/Aim: Androgen deprivation therapy (ADT) is a mainstay therapy for prostate cancer (PCa). ADT induces bone loss and increases the risk of osteoporosis and fractures. Recently, loss of bone quality has received attention as a factor that causes loss of bone strength independent of bone mineral density (BMDProstate cancer (PCa) is the most common cancer in males in Western countries and its incidence has increased in Japan (1). Androgen deprivation therapy (ADT) with gonadotropinreleasing hormone (GnRH) agonists, GnRH antagonists or bilateral orchiectomy is a well-established treatment for advanced PCa (2). ADT is also used to manage cases of localized PCa when radical treatment cannot be administered (3). The administration of ADT improves disease-free survival and overall survival in men with locally advanced PCa treated with radiation therapy (4). ADT functions by decreasing testosterone to castrate levels. ADT also markedly decreases serum estradiol levels because estradiol is derived from the peripheral conversion of testosterone by aromatase, also called estrogen synthase. Therefore, side-effects associated with estrogen deficiency are also observed. Estradiol plays a role in bone formation and bone resorption in men (5). Therefore, ADT decreases bone mineral density (BMD) and increases the incidence of clinical fractures (6, 7). The risk of fracture increases with an increasing duration of ADT (6, 7). Patients with prostate carcinoma bone metastases are faced with the risk of skeletal complications, including pathologic fractures, which are collectively termed skeletal-related events (SREs) (8). SREs are associated with mortality, increased pain, decreased quality of life and increased treatment costs (9).Although several drugs, including bisphosphonates and selective estrogen-receptor modulators, can prevent a decreased BMD, clinical trials of those drugs have revealed that the effects on fracture prevention are insufficient (10, 11). In contrast, denosumab was found to increase BMD at all sites and decrease the incidence of new vertebral fractures among men receiving ADT for non-metastatic PCa (12). Furthermore, denosumab decreased the risk of skeletal complications compared to zoledronic acid in castrationresistant prostate cancer (CRPC) patients with bone metastases (13). The administration of denosumab decreased the serum levels of bone turnover markers (BTMs), including type-1 C-teropeptide (sCTX) and tartrate-resistant alkaline phosphatase 5b (TRAP-5b) compared to placebo (14). Therefore, BTMs are often used to predict the effects of denosumab during CRPC patient care.