{"title":"Matrix vesicles and calcification of rachitic rat osteoid.","authors":"T F Johnson, D C Morris, H C Anderson","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Tibiae from rachitic weanling rats were studied during healing to examine the mechanism of bone mineralization. Rickets was induced by feeding the animals a low phosphate, low vitamin D diet for five weeks. Calcification was reinstituted in three ways; group I animals received 1.0 ml of NaH2PO4 i.p. and the rachitogenic diet in a darkened room; group II animals were placed in a lighted room and given standard laboratory chow; group III animals were placed in lighted room, given standard laboratory chow and received 1.0 ml of 0.1M NaH2PO4 i.p. Group I healed slowly while II and III were found to heal rapidly and at nearly identical rates. Groups II and III revealed a significantly elevated serum alkaline phosphatase activity and became hyperphosphatemic as the rickets healed suggesting a more vigorous recovery. Ultrastructurally, numerous matrix vesicles were noted in unhealed rachitic bone matrix and these structures acquired mineral upon initiation of healing. Vesicle-associated mineral aggregates increased in size penetrating through and beyond the vesicle membrane and were incorporated into the advancing mineralization front. By 48 hrs. post-healing initiation, the osteoid borders were almost completely mineralized in groups II and III. These observations suggest that in addition to pre-existing mineral, matrix vesicles can also serve as nucleating sites in the osteoid of post-fetal bone.</p>","PeriodicalId":73745,"journal":{"name":"Journal of Experimental Pathology","volume":"4 3","pages":"123-32"},"PeriodicalIF":0.0000,"publicationDate":"1989-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Experimental Pathology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Tibiae from rachitic weanling rats were studied during healing to examine the mechanism of bone mineralization. Rickets was induced by feeding the animals a low phosphate, low vitamin D diet for five weeks. Calcification was reinstituted in three ways; group I animals received 1.0 ml of NaH2PO4 i.p. and the rachitogenic diet in a darkened room; group II animals were placed in a lighted room and given standard laboratory chow; group III animals were placed in lighted room, given standard laboratory chow and received 1.0 ml of 0.1M NaH2PO4 i.p. Group I healed slowly while II and III were found to heal rapidly and at nearly identical rates. Groups II and III revealed a significantly elevated serum alkaline phosphatase activity and became hyperphosphatemic as the rickets healed suggesting a more vigorous recovery. Ultrastructurally, numerous matrix vesicles were noted in unhealed rachitic bone matrix and these structures acquired mineral upon initiation of healing. Vesicle-associated mineral aggregates increased in size penetrating through and beyond the vesicle membrane and were incorporated into the advancing mineralization front. By 48 hrs. post-healing initiation, the osteoid borders were almost completely mineralized in groups II and III. These observations suggest that in addition to pre-existing mineral, matrix vesicles can also serve as nucleating sites in the osteoid of post-fetal bone.
本研究以断颈断奶大鼠胫骨为研究对象,探讨骨矿化的机制。佝偻病是通过给这些动物喂食低磷酸盐、低维生素D的食物5周而诱发的。钙化以三种方式重新开始;ⅰ组动物在暗室中给予1.0 ml NaH2PO4灌胃和致鼠性饲料;第二组动物置于有灯光的房间,给予标准实验室食物;III组置于光照充足的室内,给予标准实验室饲料,并给予1.0 ml 0.1M NaH2PO4 i.p.。I组愈合缓慢,II组和III组愈合迅速,愈合速度几乎相同。II组和III组显示血清碱性磷酸酶活性显著升高,并随着佝偻病愈合而变得高磷血症,这表明恢复更加有力。超微结构上,未愈合的棘骨基质中可见大量基质囊泡,这些结构在愈合开始时获得矿物质。与囊泡相关的矿物聚集体的大小增加,穿透和超越囊泡膜,并被纳入推进的矿化前沿。48小时前。愈合开始后,II组和III组骨样边界几乎完全矿化。这些观察结果表明,除了先前存在的矿物质外,基质囊泡也可以作为胎后骨类骨的成核位点。