Carter R L, Tsao S W, Burman J F, Pittam M R, Clifford P, Shaw H J
Am J Surg. 1983 Oct;146(4):451-5. doi: 10.1016/0002-9610(83)90229-5.
Patterns and mechanisms of local bone invasion by squamous carcinomas of the head and neck have been investigated. Detailed surgical pathology has shown that these tumors invade contiguous skeletal or metaplastic bone principally through an indirect process; the normal bone resorbing cells of the host (osteoclasts) are activated and erode bone in front of the advancing tumor edge. Tumor cells take over the destructive process when the osteoclast response has waned. These morphologic patterns have been reproduced in an in vitro model where calcium-45-labelled mouse calvaria, cocultured with a tumor for 3 days, are resorbed by osteoclasts. Freshly excised tumors, established tumor cell lines, and tumor xenografts release osteolysins in vitro which act as osteoclastic stimulants. They include both prostaglandins E2 and F2 alpha, and nonprostaglandin factors, and are derived from tumor cells and from the associated host stroma. Virtually all the tumors examined released osteolysins and resorbed bone in vitro independent of their site, size, degree of differentiation, and the presence or absence of clinical bone invasion.
对头颈部鳞状细胞癌局部骨侵袭的模式和机制进行了研究。详细的手术病理学表明，这些肿瘤主要通过间接过程侵犯相邻的骨骼或化生骨；宿主正常的骨吸收细胞（破骨细胞）被激活，并在肿瘤前沿侵蚀骨质。当破骨细胞反应减弱时，肿瘤细胞接管破坏过程。这些形态学模式已在体外模型中重现，其中与肿瘤共培养3天的钙-45标记的小鼠颅骨被破骨细胞吸收。新鲜切除的肿瘤、已建立的肿瘤细胞系和肿瘤异种移植物在体外释放溶骨素，其作为破骨细胞刺激物起作用。它们包括前列腺素E2和F2α以及非前列腺素因子，并且源自肿瘤细胞和相关的宿主基质。几乎所有检查的肿瘤在体外都释放溶骨素并吸收骨质，而与它们的部位、大小、分化程度以及临床骨侵袭的有无无关。
