Bone remodeling is a continuous and dynamic process of skeletal destruction and renewal. A complex regulatory mechanism with the participation of several cytokines precisely defines the role of osteoclasts in the chain of events leading to bone resorption. There are multiple mechanisms underlying the regulation of bone resorption, which can involve increased calcium excretion and decreased bone density in patients with idiopathic hypercalciuria (IH). However, the pathogenesis of bone mass reduction in IH remains uncertain. The purpose of this review is to summarize the recent published evidence on the possible mechanisms by which cytokines could be associated with the pathogenesis of IH.