内軟骨性骨化における破(軟)骨細胞機能障害の影響

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Endochondral ossification is preceded by the vascular invasion into hypertrophic chondrocyte lacunae. Although it has been described that the osteoclasts or chondroclasts are primarily responsible for the breakdown of the transverse septa facing the front of vascular invasion, there are some questions to be clarified in this theory. To address this question, we conducted morphological approach using in vivo model of selectively suppressed osteoclast function by treatment with maximal inhibitory dose of the bisphosphonate incadronate. Five or 10-day-old mice were given a subcutaneous injection of incadronate at a dose of 1.0mg/kg for 5 or 10 consecutive days, and then the femur and tibia were excised. Histologically, the femoral or tibial epiphysis of the incadronete treated mice appeared to be almost the same as untreated control mice, although their metaphysis exhibited a significant increase in thickness. At the epiphyseal end, the vascular invasion into the chondrocyte lacunae was evident. Although TRAP-positive osteoclasts appeared to increase in number and size throughout the metaphysis, only a few mononuclear TRAP-positive cells were found near the epiphyseal-metaphyseal junction, none of which existed at the front of vascular invasion. Immunohistochemistry demonstrated an intense expression of MMP-9 protein in both cellular component and extracellular matrix at the front of vascular invasion. The expression of VEGF protein was found intensely in the metaphysis and weakly in the hypertrophic chondrocytes in the epiphyseal growth plate. From the present study, we suggest that the vascular invasion led by MMP-9 and VEGF is primarily responsible for the breakdown of the transverse septa of hypertrophic chondrocytes lacunae and osteoclastic cells are not involved in this phenomenon.
奥羽大学の論文
2006-03-31

内軟骨性骨化における破(軟)骨細胞機能障害の影響

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