Osteoclast formation from peripheral blood of patients with bone-lytic diseases

Recent literature indicates that osteoclast formation in vitro from peripheral blood of patients with diseases associated with bone loss such as rheumatoid arthritis, osteoporosis, periodontitis and bone metastatic cancer may occur spontaneously being independent of addition of osteoclast formation stimulating factors such as macrophage colony forming factor (M-CSF) and receptor activator of NFκB ligand (RANKL). This could provide important clues to our understanding on how osteoclast precursors are primed within the circulation whilst commuting to the site of ultimate osteoclast differentiation. When comparing the various bone-lytic diseases, the common view emerges that accessory cells, such as T- and B-lymphocytes provide osteoclastogenesis stimulating factors. The roles of B- and T-cells in providing osteoclastogenesis-positive signals such RANKL, TNF-α and IL-7 are discussed. Immune cells present in the circulation may play an important role in preparing the osteoclast precursor for its ultimate destiny, contributing to the bone resorbing multinucleated cell at the required bone site