Weinstein R S, Underwood J L, Hutson M S, DeLuca H F
Am J Physiol. 1984 Jun;246(6 Pt 1):E499-505. doi: 10.1152/ajpendo.1984.246.6.E499.
Defective mineralization of bone and cartilage is the classical histological finding in vitamin D deficiency. Whether this represents a direct effect on mineral deposition or is a consequence of the decreased calcium and phosphorus levels that result from impaired intestinal absorption is not clear. A method has been developed in which vitamin D-deficient rats have plasma calcium and phosphorus levels maintained in the normal range by continuous infusion. Histomorphometric analysis of undecalcified tibiae from these animals was compared with that of rats given vitamin D. Epiphyseal growth plate thickness, trabecular osteoid volume, and mean osteoid seam width were not increased. Moreover, the administration of two time-spaced courses of tetracycline revealed that the mineralization rate and the time interval between apposition and subsequent mineralization of osteoid (mineralization lag time) were identical to those in rats treated with vitamin D. Trabecular bone volume was increased (osteosclerosis) in the vitamin D-deficient rats. In vitamin D-deficient controls without infusions, the osteosclerosis was mostly osteoid, whereas the excess bone was well mineralized in the vitamin D-deficient rats infused with calcium and phosphorus. Osteosclerosis in vitamin D-deficient animals may result from both decreased bone resorption and increased osteoid apposition. This study provides firm evidence that vitamin D is not essential for mineralization in young growing rats. Decreased availability of calcium and phosphorus thus may be the sole basis of the mineralization defect seen in vitamin D deficiency.
骨和软骨矿化缺陷是维生素D缺乏的典型组织学表现。这是对矿物质沉积的直接影响,还是肠道吸收受损导致钙和磷水平降低的结果尚不清楚。已开发出一种方法,通过持续输注使维生素D缺乏的大鼠血浆钙和磷水平维持在正常范围内。对这些动物未脱钙胫骨的组织形态计量学分析与给予维生素D的大鼠进行了比较。骨骺生长板厚度、小梁类骨质体积和平均类骨质缝宽度均未增加。此外,给予两个间隔时间的四环素疗程显示,矿化速率以及类骨质沉积与随后矿化之间的时间间隔(矿化延迟时间)与给予维生素D治疗的大鼠相同。维生素D缺乏的大鼠小梁骨体积增加(骨硬化)。在未输注的维生素D缺乏对照组中,骨硬化主要是类骨质,而在输注钙和磷的维生素D缺乏大鼠中,多余的骨矿化良好。维生素D缺乏动物的骨硬化可能是由于骨吸收减少和类骨质沉积增加所致。这项研究提供了确凿的证据,表明维生素D对幼年生长大鼠的矿化并非必不可少。因此,钙和磷可用性的降低可能是维生素D缺乏时所见矿化缺陷的唯一基础。