Peura S R, Marks S C
Department of Cell Biology, University of Massachusetts Medical School, Worcester 01655, USA.
Bone. 1995 Apr;16(4 Suppl):335S-340S. doi: 10.1016/8756-3282(94)00047-4.
Toothless (tl-osteopetrotic) rats have little or no endogenous bone resorption, no marrow spaces, and very few osteoclasts and macrophages, and their live metatarsal rudiments cannot support the development of normal osteoclasts in vitro. The recent demonstration that exogenous colony-stimulating factor 1 (CSF-1) improves skeletal sclerosis and increases osteoclasts in tl rats in vivo, prompted us to explore conditions that enable osteoclasts to be formed in tl metatarsals in vitro. Coculture of neonatal tl metatarsals with CSF-1 alone produced no osteoclasts, but the addition of normal spleen and bone marrow cells and parathyroid hormone or 1,25-dihydroxyvitamin D produced osteoclasts in most cultures. Identical cultures of metatarsals from the CSF-1 deficient op/op mouse produced similar results. Within the contexts of the role of CSF-1 in osteoclastogenesis and the different biologic manifestations of osteopetrosis in these two mutations, we interpret these results to mean that other factors are required to restore osteoclast function completely in tl rats and op mice. Thus, experimental studies of these mutations are likely to provide new insights on both osteopetrosis and osteoclast biology.
无牙（tl-骨质石化）大鼠几乎没有或完全没有内源性骨吸收，没有骨髓腔，破骨细胞和巨噬细胞极少，并且其活的跖骨原基在体外无法支持正常破骨细胞的发育。最近有研究表明，外源性集落刺激因子1（CSF-1）可改善tl大鼠体内的骨骼硬化并增加破骨细胞数量，这促使我们探索能使tl大鼠跖骨在体外形成破骨细胞的条件。单独将新生tl大鼠跖骨与CSF-1共培养未产生破骨细胞，但添加正常脾细胞、骨髓细胞以及甲状旁腺激素或1,25-二羟维生素D后，大多数培养物中都产生了破骨细胞。对CSF-1缺陷型op/op小鼠的跖骨进行相同培养也得到了类似结果。鉴于CSF-1在破骨细胞生成中的作用以及这两种突变中骨质石化的不同生物学表现，我们将这些结果解释为，在tl大鼠和op小鼠中，需要其他因子来完全恢复破骨细胞功能。因此，对这些突变的实验研究可能会为骨质石化和破骨细胞生物学提供新的见解。
