铝对大鼠骨基质明胶诱导性异位骨形成及矿化影响的研究

 采用不脱钙骨切片技术,配合四环素双标记和骨组织形态计量学及铝染色,研究了不同的铝浓度在肾功能正常与肾功能不全时对诱导性异位骨形成及矿化的影响.实验大鼠分为5组:对照组(C);低剂量铝组(LDA);高剂量铝组(HDA);慢性肾功能不全组(CRF);慢性肾功能不全加高剂量铝组(CRF-HDA);实验结果表明:LDA、CRF组与C组之间无明显差异(P>0.05).HDA及CRF-HDA组骨组织内四环素荧光双记线短、少,多为单标线,且粗细不一,增宽融合,表面有较多的类骨质沉积,尤以CRF-HDA组为甚.提示高剂量铝可影响大鼠骨基质明胶诱导性异位骨形成,阻碍其矿化作用,引起骨软化.尤其在慢性肾功能不全时,可加重此变化.

Effects of aluminium on bone matrix gelatin-induced ectopic bone formation and mineralization

The effects of aluminium in different concentrations on induced ectopic bone formation and mineralization in rats with normal and abnormal renal function were studied by non-decalcified section technique, tetracycline double labelling ,bone tissue morphmetry and aluminium staining. The experimental rats were divided into five groups:control group(C),low dose aluminium group (LDA) ,high dose aluminium group(HDA),chronic renal failure group(CRF),and chronic renal failure plus high dose alumimium group(CRF HDA). The results show that there is no statistically significant difference between the groups LDA ,CRF and C(P>0. 05). In HDA group and especially in CRI HDA group ,the bone tissues show fewer short tetracycline fluorescent double labelling lines but more single labelling lines in varying size ,broadened fusion and copious osteoid deposition. It is suggested that high dose aluminium can affect in rats bone matrix gelatin-induced ectopic bone formation and hinder its mineralization,giving rise to osteomalacia. This change is aggravated especially in case of chronic renal failure.