| A predominant clinical feature of multiple myeloma (MM) patients is bone destruction, which significantly contributes to poor prognosis and accounts for much of the morbidity and mortality associated with MM. Osteoclasts(OCs) are essential mediators in the pathogenesis of myeloma bone disease. A cosnsistent histogogic finding indicates that osteoclastic bone resorption is enhanced adjacent to areas of MM cell infiltrates. Enhanced bone resorption releases various cytokines and factors from the extracellular matrix that further promote myeloma cell growth. Thus maintaining a vicious circle between the bone destructive process and tumor progression. Therefore, elucidation of the molecular mechanism of bone destruction and tumor progression is essential for development of effective therapies to improve survival as well as quality of life of MM patients.Recently, the receptor activator of NF-κB ligand (RANKL) has been characterized and described as the major effector for the osteoclast formation and activation. However, an interesting and controversial question has arisen recently about the direct expression or production of RANKL by human myeloma cells.Bone marrow mesenchymal stem cells(MSCs) are multifunctional stem cells. MSCs from patients with myeloma abnormally expressed adhesion molecules and cytokines, suggesting that these changes are required to promote myeloma. Recently, SCID-hu mice implanted with bilateral human fetal bone grafts has been used as in vivo model in the study of pathogenesis, treatment and complication for MM. However, the character of human fetal BM mesenchymal stem cells has rarely been demonstrated.Objective: Our studies aimed to effects of osteolasts on pathogenesis of multiple myeloma, including the effects of myeloma cells on the differentiation of osteoclast... |
