Ectopic mineralization

Sakamoto, A., Chen, M., Kobayashi, T., Kronenberg, H. M., and Weinstein, L. S. (2005) Chondrocyte-specific knockout of the G protein G(s)alpha leads to epiphyseal and growth plate abnormalities and ectopic chondrocyte formation. J. Bone Miner. Res. 20, 663-671. 

Calcium Multiple physiologic actions through regulation of multiple enzymatic pathways Strontium suppresses bone resorption and increases bone formation, calcium and phosphate required for bone mineralization Osteoporosis, osteomalacia, deficiencies in calcium or phosphate Ectopic calcification... 

One of the most sensitive bioassays for osteoblast and osteoclast activities in vivo is the use of ectopic models of bone formation and bone matrix resorption (38,39). Devitalized, demineralized bone powders (DBP) are subcutaneously implanted in young rats. There is a phenotypic conversion of connective cell tissue mesenchyme into cartilage. Subsequently this cartilage becomes calcified, vascularized and bone is deposited in two weeks. If mineral-containing bone particles (BP) are implanted, a different phenomenon is observed. Large multinucleated osteoclast-like cells are recruited to the site of implantation. There is a complete resorption of the BP four weeks after implantation. In collaboration with Dr. Julie Glowacki of the Harvard University School of Medicine, we took advantage of these procedures and used implants of normal DBP and BP into rats that had been maintained on the three experimental diets C, L, and D (40). 

Mineralization therefore occurs in bone because of the exclusive co-expression in osteoblasts of type I collagen and tissue-nonspecific alkaline phosphatase (TNAP). The abnormal appearance of TNAP in any cell that also produces fibrillar collagen (ectopic TNAP expression) gives rise to pathological (nonbacterial) mineralization, which is outside the scope of this text. 

Giachelli, C.M. (1999) Ectopic calcification gathering hard facts about soft tissue mineralization. 

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