Giuliani Nicola, Rizzoli Vittorio
Cattedra di Ematologia e CTMO, Universita Degli Studi di Parma, Parma, Italy.
Leuk Lymphoma. 2007 Dec;48(12):2323-9. doi: 10.1080/10428190701648281.
Bone destruction is the hallmark of multiple myeloma (MM) due to the high capacity of malignant plasma cells to induce a severe imbalance of bone remodeling. Growing evidences suggest that MM cell interactions with bone marrow (BM) osteoblast have a critical role in the pathophysiology of osteolytic lesions. Indeed histomorphometric studies have demonstrated that MM patients with osteolytic bone lesions have lower numbers of osteoblasts and decreased bone formation together with osteoclast activation. Recently, the biological mechanisms involved in the osteoblast inhibition induced by MM cells have begun to be elucidated, underlying the main role of the block of osteoblast differentiation in the development of bone lesions. In this article, we summarize the main mechanisms regulating MM cell and osteoblast interactions.
骨破坏是多发性骨髓瘤（MM）的标志，因为恶性浆细胞具有很高的能力，可导致骨重塑严重失衡。越来越多的证据表明，MM细胞与骨髓（BM）成骨细胞的相互作用在溶骨性病变的病理生理学中起关键作用。事实上，组织形态计量学研究表明，患有溶骨性骨病变的MM患者成骨细胞数量较少，骨形成减少，同时破骨细胞活化。最近，MM细胞诱导成骨细胞抑制所涉及的生物学机制已开始得到阐明，这突出了成骨细胞分化受阻在骨病变发展中的主要作用。在本文中，我们总结了调节MM细胞与成骨细胞相互作用的主要机制。
