Mineralization osteoid matrix secretion

Mineralization is the precipitation of calcium phosphate, but biochemical mediation of this process is not fully understood. In this chapter, the chemistry underlying mineralization (Sect. 1) and the structures ofbones and teeth (Sect. 2) are described. Osteoblasts secrete osteoid matrix and matrix vesicles that transport type I collagen and calcium phosphate, respectively, to the matrix where they will mineralize. Secreted matrix vesicles take up calcium and phosphate until they burst and release the calcium phosphate, which then redissolves and remineralizes around the type I collagen (Sect. 3). Glycoproteins involved in correctly modeling bone and dentin, and the role of osteocalcin in limiting excessive bone growth is then discussed (Sect. 4). There follows a detailed description of enamel (E) mineralization and of the major proteins involved (Sect. 5) followed by two summaries the difference between enamel and bone mineralization, and the vitamins required for mineralization (Sect. 6). 

Intramembranous ossification is responsible for most of the mineralization of the skull, including the maxilla and mandible. It begins with the differentiation and activation of osteoblasts from fibroblast-related precursors within a region of connective tissue that demarcates where the bone will develop. The osteoblasts secrete a nonmineralized protein-rich (osteoid) matrix and, as they move away, the matrix mineralizes (Fig. 9.3a). The periosteum remains uncalcified and contains latent and undifferentiated osteoblasts for bone remodeling. Odontoblasts (Ob) and cementoblasts secrete an osteoid-like matrix similar to that of intramembraneous ossification. 

Skeletal tissue mineralization (bone formation) is initiated by osteoblasts, which secrete the osteoid matrix (Fig. 9.4). They express type I procollagen in secretory vesicles together with matrix vesicles that pinch off from the membrane. The matrix vesicles are pushed away from the cell surface, possibly by the flow of fluid containing calcium and phosphate ions that are also transported through the cell from the extracellular fluid on the outer surface. Collagen fibers develop further away from the cell surface than from fibroblasts. 

Figure 9.8 outlines how matrix vesicles increase and decrease the concentration of pyrophosphate. NTP-PPi hydrolase synthesizes pyrophosphate from stromal fluid nucleotides, mostly ATP (ATP —> AMP + PPi). Many cells secrete ATP into the extracellular fluid and it passes into the blood plasma where it affects a variety of cells independently of its function in intracellular energy metabolism. In mice, a nonfunctional ANK protein or a deletion of NTP-PPi hydrolase decreases the extracellular pyrophosphate concentration and the phenotype exhibits extensive mineralization. Thus, the hydrolysis of pyrophosphate appears to be a major function of alkaline phosphatase (TNAP) after the calcium phosphate precipitate has raptured the matrix vesicles. Rapid mineralization of collagen and the rest of the osteoid matrix ensue without a need to transport any more Ca2+ or Pi to the region. 

Enamel matrix is partially mineralized before its matrix is completed, whereas bone, dentin, and cementum secrete a preformed organic (osteoid) matrix to which calcium phosphate is added separately from matrix vesicles. 

Osteoblastic activity initiates the process of mineralization. Unmineralized bone is known as osteoid. Minerals are deposited in specific holes that are located between collagen fibrils produced by the osteoblast. The architecture of the fibrils is designed to withstand external stress. Mineralization begins shortly after the formation of the secreted matrix. This process occurs in osteons, also referred to as Haversian systems, and is completed in several weeks. Blood vessels penetrate bond through channels known as Haversian canals. 

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