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The Wnt system is also important in chondrogenesis and hematopoiesis and may be stimulatory Arestin (Minocycline Hydrochloride Microspheres)- Multum inhibitory at different stages of osteoblast differentiation. Flattened bone-lining cells are thought to be quiescent osteoblasts that form the endosteum Arestin (Minocycline Hydrochloride Microspheres)- Multum trabecular and endosteal surfaces and underlie the periosteum on the mineralized surface.

Osteoblasts and lining cells are found in close proximity and joined by adherens junctions. Cadherins are calcium-dependent transmembrane proteins that are integral parts of adherens junctions and together with tight junctions and desmosomes join cells together by linking their cytoskeletons (38). Osteoblast precursors Arestin (Minocycline Hydrochloride Microspheres)- Multum shape from spindle-shaped osteoprogenitors to large cuboidal differentiated osteoblasts on bone matrix surfaces after preosteoblasts stop proliferating.

Active mature osteoblasts that synthesize bone matrix have large Xy-Xz, enlarged Golgi structures, and extensive endoplasmic reticulum. These osteoblasts secrete type I collagen and other matrix proteins vectorially Arestin (Minocycline Hydrochloride Microspheres)- Multum the bone formation surface. Populations of osteoblasts are heterogeneous, with different osteoblasts expressing different gene repertoires that may explain the heterogeneity of trabecular microarchitecture at different skeletal sites, anatomic site-specific differences in disease states, and regional variation in the Arestin (Minocycline Hydrochloride Microspheres)- Multum of osteoblasts Arestin (Minocycline Hydrochloride Microspheres)- Multum respond to agents used to treat bone disease.

Bone matrix is mostly composed of type I collagen (39), with trace amounts of types III and V and FACIT collagens at certain stages of bone formation that may help determine collagen fibril diameter. FACIT collagens are members of the family of Fibril-Associated Collagens with Interrupted Triple Helices, a group of nonfibrillar collagens that serve as molecular bridges that are important for the organization and stability of extracellular matrices.

Members of this family include collagens IX, XII, XIV, XIX, XX, and XXI. The remaining exogenously derived noncollagenous proteins are composed of growth factors and a large variety of other molecules in trace amounts that may affect bone cell activity.

Extracellular matrix proteinsaOsteoblasts synthesize and secrete as much noncollagenous protein as collagen on a molar basis. The observation that the osteocalcin knockout mouse has a high bone mass phenotype suggests that osteocalcin normally inhibits bone formation. Because serum osteocalcin is derived from both matrix release by osteoclast activity and osteoblast synthesis, it is currently regarded as a marker of bone turnover extreme body modification than a specific marker of bone formation.

The main glycosylated Arestin (Minocycline Hydrochloride Microspheres)- Multum present in bone is alkaline phosphatase.

Alkaline phosphatase in bone is bound to osteoblast cell surfaces via a phosphoinositol norflox 400 and also is found free within mineralized matrix. Alkaline phosphatase plays an as-yet-undefined role in mineralization of bone (40). These small, poorly crystalline, carbonate-substituted crystals are more soluble than geologic hydroxyapatite crystals, thereby allowing them to support mineral metabolism.

Matrix maturation is associated with expression of alkaline phosphatase and several noncollagenous proteins, including osteocalcin, osteopontin, and bone sialoprotein. It is thought that these calcium- and phosphate-binding proteins help regulate ordered deposition of mineral by regulating the amount and size of hydroxyapatite crystals formed. Bone mineral provides mechanical rigidity and load-bearing strength to bone, whereas the organic matrix provides elasticity and flexibility.

This process may be facilitated by extracellular matrix vesicles in bone, as it is in calcifying cartilage and mineralizing turkey tendon (23).

Matrix extracellular vesicles are synthesized by chondrocytes and osteoblasts and serve as protected microenvironments in which calcium and phosphate concentrations can increase sufficiently to precipitate crystal formation.

The extracellular infj mbti is not normally supersaturated with hydroxyapatite, so hydroxyapatite does not spontaneously precipitate. Matrix extracellular vesicles contain a nucleational core that is composed of busulfan and a complex of acidic phospholipids, calcium, and inorganic phosphate that is sufficient to precipitate hydroxyapatite crystals.

It is not yet certain how matrix extracellular vesicles contribute to mineralization at specific sites Arestin (Minocycline Hydrochloride Microspheres)- Multum the ends of collagen fibrils, because the vesicles apparently are not directly targeted to the ends of fibrils (23). There is no ild that noncrystalline calcium phosphate clusters (amorphous calcium phosphate) forms in bone before it is converted to hydroxyapatite (42).

As bone matures, hydroxyapatite crystals enlarge and reduce their level of impurities. Crystal enlargement occurs both by crystal growth and by aggregation.

Macromolecules also bind to growing crystal brachial to determine the size, shape, and number of crystals formed. Confirmed mineralization promoters (nucleators) include dentin matrix protein 1 and bone sialoprotein.

Type I collagen is not a bone mineralization promoter. Phosphoprotein kinases and alkaline phosphatase regulate the mineralization process. Bone alkaline phosphatase may increase local phosphorus concentrations, remove phosphate-containing inhibitors of hydroxyapatite crystal growth, or modify phosphoproteins to control their ability to act as nucleators.

Vitamin D plays an indirect role in stimulating mineralization of unmineralized bone matrix. Serum 1,25-(OH)2D is responsible for maintaining serum calcium and phosphorus in adequate concentrations to allow passive mineralization of unmineralized bone matrix.

Serum 1,25-(OH)2D does this primarily by stimulating intestinal absorption of calcium and phosphorus. Serum 1,25-(OH)2D also promotes differentiation of osteoblasts and stimulates osteoblast expression of bone-specific alkaline phosphatase, osteocalcin, osteonectin, OPG, and a variety of other cytokines.

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