Rossi J F, Chappard D, Marcelli C, Laplante J, Commes T, Baldet P, Janbon C, Jourdan J, Alexandre C, Bataille R
Departement d'Oncologie Médicale et d'Immunothérapie, Institut du Cancer (Val d'Aurelle II), Montpellier, France.
Br J Haematol. 1990 Dec;76(4):469-75. doi: 10.1111/j.1365-2141.1990.tb07902.x.
Multiple myeloma (MM) is characterized by the presence of lytic bone lesion and frequent hypercalcaemia. These are due to an excessive osteoclastic resorption in association with a low bone formation, as demonstrated by bone histomorphometry. Conversely, B-cell malignancies other than MM are rarely associated with lytic bone lesion and/or hypercalcaemia. In this study we have analysed quantitative bone histology in 65 patients with B-cell malignancies other than MM at diagnosis: chronic lymphocytic leukaemia (CLL, n = 20), non-Hodgkin's lymphoma (NHL, n = 25), Waldenström's disease (WD, n = 14), hairy cell leukaemia (HCL, n = 6). Fifty patients presented no clinical evidence of increased bone resorption, including no lytic bone lesions radiologically detectable and/or no hypercalcaemia. 80% of these patients (40/50) had increased bone resorption parameter using quantitative bone histology, including 19/29 (65.5%) patients with CLL or WD and 21/21 (100%) patients with NHL or HCL (P less than 0.01). As a control group, seven patients lacking bone marrow involvement on bone sample presented no excessive bone resorption. However, eight patients presented lytic bone lesions and/or hypercalcaemia. All of these patients had increased resorption parameters with high numbers of osteoclasts per surface trabecular bone (mean = 35.3), as opposed to the patients lacking lytic bone lesions and/or hypercalcaemia (mean = 6.6, n = 28) and to normal individuals (mean +/- SD = 3.8 +/- 1.7 and 6.3 +/- 2.6, respectively before and after 60 years). In all the cases, excessive histologic bone resorption was mediated by mononuclear small osteoclasts (mean osteoclast length +/- SD = 27.3 +/- 4.1 as compared to normal range = 35.0 +/- 1.0, P less than 0.001). In different in vitro models, these small mononuclear osteoclasts are considered as progenitors. These data suggest an abnormal osteoclast differentiation in B-cell malignancies other than MM, probably due to differences in the production of local factors acting on bone remodelling.
多发性骨髓瘤（MM）的特征是存在溶骨性骨病变和频繁的高钙血症。这些是由于破骨细胞过度吸收并伴有低骨形成，骨组织形态计量学已证实这一点。相反，除MM外的B细胞恶性肿瘤很少与溶骨性骨病变和/或高钙血症相关。在本研究中，我们分析了65例诊断为除MM外的B细胞恶性肿瘤患者的定量骨组织学情况：慢性淋巴细胞白血病（CLL，n = 20）、非霍奇金淋巴瘤（NHL，n = 25）、华氏巨球蛋白血症（WD，n = 14）、毛细胞白血病（HCL，n = 6）。50例患者没有骨吸收增加的临床证据，包括放射学上未检测到溶骨性骨病变和/或无高钙血症。这些患者中有80%（40/50）使用定量骨组织学检测显示骨吸收参数增加，其中CLL或WD患者中有19/29（65.5%），NHL或HCL患者中有21/21（100%）（P小于0.01）。作为对照组，7例骨样本未累及骨髓的患者未出现过度骨吸收。然而，有8例患者出现溶骨性骨病变和/或高钙血症。所有这些患者的吸收参数均增加，每表面小梁骨的破骨细胞数量较多（平均 = 35.3），这与无溶骨性骨病变和/或高钙血症的患者（平均 = 6.6，n = 28）以及正常个体（60岁前后平均±标准差分别为3.8±1.7和6.3±2.6）不同。在所有病例中，过度的组织学骨吸收由单核小破骨细胞介导（平均破骨细胞长度±标准差 = 27.3±4.1，与正常范围 = 35.0±1.0相比，P小于0.001）。在不同的体外模型中，这些单核小破骨细胞被视为祖细胞。这些数据表明，除MM外的B细胞恶性肿瘤中破骨细胞分化异常，可能是由于作用于骨重塑的局部因子产生存在差异。
