Pazzaglia U E, Zatti G, Ragni P, Ceciliani L
Clinica Ortopedica e Traumatologica dell'Università, I.R.C.C.S. Policlinico San Matteo, Pavia.
Ital J Orthop Traumatol. 1988 Sep;14(3):369-75.
The role of mineralization was studied in an experimental model of osteoinduction consisting of the implant of decalcified bone matrix in the rat muscle. After vascular connective tissue invasion of the matrix, the first phenomena is the appearance of hydroxyapatite crystals in the area of chondroid metaplasia from where the deposit of calcium-phosphate is extended to the surrounding decalcified matrix. The recalcified areas act as a substratum for the neo-osteogenesis. The appearances observed reproduced those of enchondral ossification, where the first osteoblasts differentiated on the calcified cartilaginous matrix and began to supply new bone matrix. Non-decalcified bone matrix implants were surrounded by a connective tissue capsule with features identical to those of a foreign body reaction and with total absence of vascular invasion. The absence of induction in this type of implant may be related either to masking of the osteoinducing protein in the calcified matrix, or to the absence of cells with osteogenic differentiation potential due to the lack of cellular invasion of the implant.
在大鼠肌肉中植入脱钙骨基质构成的骨诱导实验模型中，研究了矿化的作用。在血管结缔组织侵入基质后，首先出现的现象是在软骨样化生区域出现羟基磷灰石晶体，磷酸钙沉积物从该区域扩展到周围的脱钙基质。再钙化区域作为新骨形成的基础。观察到的现象重现了软骨内成骨的现象，即最初的成骨细胞在钙化的软骨基质上分化并开始提供新的骨基质。未脱钙的骨基质植入物被结缔组织囊包围，其特征与异物反应相同，且完全没有血管侵入。这种类型的植入物缺乏诱导作用可能与钙化基质中骨诱导蛋白的掩盖有关，或者与由于植入物缺乏细胞侵入而导致缺乏具有成骨分化潜能的细胞有关。
