Obesity and excessive accumulation of adipose tissue are increasingly recognized as chronic inflammatory conditions that negatively affect multiple physiological systems, including the skeletal system. Adipose tissue is now understood to function as an active endocrine organ that secretes a wide range of bioactive molecules known as adipokines. These adipokines play critical roles in regulating metabolic processes, immune responses, and bone remodeling. Growing evidence suggests that dysregulated adipokine secretion associated with obesity contributes to impaired bone homeostasis and altered osteoimmune interactions. Adipokines derived from both white adipose tissue (WAT) and bone marrow adipose tissue (BMAT) exert endocrine, paracrine, and autocrine effects on bone cells, including osteoblasts, osteoclasts, and osteocytes. Through these mechanisms, adipokines influence bone formation, resorption, and overall skeletal integrity. Several adipokines, such as leptin, adiponectin, resistin, and visfatin, have been shown to modulate osteoblast differentiation and activity, osteoclastogenesis, and immune cell signaling pathways that intersect with bone metabolism. The inflammatory milieu created by altered adipokine profiles further disrupts the balance between bone formation and resorption, linking metabolic disorders with bone fragility and increased fracture risk. In addition, adipokines serve as key mediators at the interface of bone and immune systems, highlighting their importance in the field of osteoimmunology. Understanding the complex interactions between adipose tissue, immune cells, and skeletal cells is essential for elucidating the mechanisms underlying obesity-related bone disorders. This review summarizes advances in comprehending the function of adipokines in the context of bone health and osteoimmunology.