Huffer W E
Department of Pathology, University of Colorado Health Sciences Center, Denver.
Lab Invest. 1988 Oct;59(4):418-42.
The effects of PTH and vitamin D on bone are the result of their direct and indirect effects on the functional cells of bone remodeling units and their precursors. These effects are probably modified or controlled by growth factors, cytokines, and PGs generated locally by the process of bone remodeling. Bone remodeling includes resorptive and bone forming phases, each with a longitudinal and a radial component of progression in time and space. Longitudinal resorption is rapid, prolonged and is probably carried out by osteoclasts utilizing hydrogen ions and lysosomal enzymes to remove mineral and organic components of bone in a highly localized and directed fashion. Individual osteoclasts are probably long-lived cells with a nuclear and perhaps a cytoplasmic turnover rate of 8%/day, with replenishment coming from preosteoclasts in the reversal zone. Radial resorption is slower and shorter than longitudinal resorption. It is carried out by reversal phase monocytes whose exact relationship to osteoclasts is not clear. Activated collagenase diffusing from osteogenic cells in the reversal zone could also play a role. The longitudinal rate of bone formation is probably a measure of the rate of proliferation and differentiation of osteogenic cells at the site at which they were activated. The radial rate of bone formation is a measure of how rapidly osteoblasts synthesize and mineralize bone matrix once they reach the resorption surface. PTH and vitamin D have no direct effects on mature osteoclasts. They may have direct stimulatory effects on proliferation and differentiation of osteoclast precursors and their fusion with osteoclasts but this is not clear because the ontogeny of osteoclasts vis a vis monocytes and other phagocytic cells is still not clear. It is likely that their effects to increase osteoclast precursors involve interactions among lymphocytes, monocytes, and hematopoietic stem cells at a distance from bone remodeling units and are mediated by 1,25(OH)2 vitamin D3 induced synthesis of cytokines and colony-stimulating factors. Stimulatory effects of PTH, vitamin D, PGs, and cytokines on osteoclasts are mediated by as yet undefined factors produced by osteoblasts. Osteoblasts stimulated by PTH could also inhibit osteoclasts by synthesizing and releasing PGs. PTH and vitamin D have diverse and often contradictory effects on the functional activity of osteoblast-like cells in vitro that are difficult to interpret because the relationship of these cells to osteoblasts in vivo is not clear.(ABSTRACT TRUNCATED AT 400 WORDS)
甲状旁腺激素（PTH）和维生素D对骨骼的作用，是它们对骨重塑单位及其前体细胞直接和间接作用的结果。这些作用可能受到骨重塑过程中局部产生的生长因子、细胞因子和前列腺素（PGs）的修饰或调控。骨重塑包括吸收期和骨形成期，每个阶段在时间和空间上都有纵向和径向的进展成分。纵向吸收迅速、持续时间长，可能是由破骨细胞利用氢离子和溶酶体酶以高度局部化和定向的方式去除骨的矿物质和有机成分来完成的。单个破骨细胞可能是长寿细胞，其细胞核和可能的细胞质更新率为每天8%，补充来自反转区的前破骨细胞。径向吸收比纵向吸收更慢、更短。它由反转期单核细胞完成，其与破骨细胞的确切关系尚不清楚。从反转区的成骨细胞扩散而来的活化胶原酶也可能起作用。骨形成的纵向速率可能是成骨细胞在其被激活部位的增殖和分化速率的一种度量。骨形成的径向速率是成骨细胞一旦到达吸收表面后合成和矿化骨基质速度的一种度量。PTH和维生素D对成熟破骨细胞没有直接作用。它们可能对破骨细胞前体的增殖和分化以及它们与破骨细胞的融合有直接刺激作用，但这并不明确，因为破骨细胞相对于单核细胞和其他吞噬细胞的个体发生仍不清楚。它们增加破骨细胞前体的作用可能涉及淋巴细胞、单核细胞和造血干细胞在远离骨重塑单位处的相互作用，并由1,25(OH)2维生素D3诱导的细胞因子和集落刺激因子的合成介导。PTH、维生素D、PGs和细胞因子对破骨细胞的刺激作用由成骨细胞产生的尚未明确的因子介导。PTH刺激的成骨细胞也可能通过合成和释放PGs来抑制破骨细胞。PTH和维生素D在体外对成骨样细胞的功能活性有多种且常常相互矛盾的作用，难以解释，因为这些细胞与体内成骨细胞的关系尚不清楚。（摘要截断于400字）
