Włodarski K H
Clin Orthop Relat Res. 1985 Nov(200):248-65.
In mice, tumors of various origins have been found to stimulate cambium layer cells of periosteum/ perichondrium of adjacent orthotopic bone or cartilage to proliferate and/or differentiate into osteoblasts or chondroblasts. Tumors may induce new bone and/or cartilage formation. In progressively growing tumors the osteogenic/chondrogenic activity is gradually surpassed by the resorptive processes mediated either by osteoclasts, directly by tumor cells, or by tumor stroma. In regressing tumors, however, the deposits of new bone remained unresorbed, resulting in a permanent gain of bone mass. In human subjects, similar changes were observed in bone adjacent to carcinoma development. Stimulation of periosteal bone formation was observed at earlier stages of the disease, while bone resorption mainly by tumor cells and their stroma was observed in later stages of tumor development. The unresponsiveness of the heterotopically-induced bone to the Moloney sarcoma virus, in contrast to the response of orthotopic bone clearly indicates that ectopic bones do not develop a true periosteum.
在小鼠中,已发现各种起源的肿瘤会刺激相邻原位骨或软骨的骨膜/软骨膜的形成层细胞增殖和/或分化为成骨细胞或成软骨细胞。肿瘤可诱导新骨和/或软骨形成。在逐渐生长的肿瘤中,破骨细胞、肿瘤细胞直接或肿瘤基质介导的吸收过程会逐渐超过成骨/成软骨活性。然而,在消退的肿瘤中,新骨沉积未被吸收,导致骨量永久性增加。在人类受试者中,在癌旁骨中观察到了类似变化。在疾病早期观察到骨膜骨形成受到刺激,而在肿瘤发展后期主要观察到肿瘤细胞及其基质引起的骨吸收。与原位骨的反应相反,异位诱导骨对莫洛尼肉瘤病毒无反应,这清楚地表明异位骨不会形成真正的骨膜。