Download Osteoporosis, 2nd Edition (2-Volume Set) by Robert Marcus, David Feldman, Jennifer Kelsey PDF

By Robert Marcus, David Feldman, Jennifer Kelsey

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Additional resources for Osteoporosis, 2nd Edition (2-Volume Set)

Sample text

Several of the noncollagenous bone-related proteins are implicated in initiating or regulating the mineral phase of bone from studies of the biochemical, molecular, and functional properties [275,276] (Table 1). However, ablation of the genes encoding some of the more abundant and bone restricted noncollagenous proteins (osteocalcin [277,278], osteopontin [279], biglycan [280]) have resulted in subtle changes in CHAPTER 2 Osteoblast Biology the mineral phase of bone. Future directions in which double mutants are derived may reveal severe mineralization defects.

For clinical applications of genetically engineered cells for the local reconstruction of bone tissue [155 – 159] or to treat systemic bone diseases [153,160 – 163], in vitro expansion and modification of the cells forming adherent marrow colonies are important considerations. However, mechanisms related to the retention of in vivo properties, homing, engraftment, and differentiation after transplantation must be addressed [159,164 – 166]. Many groups have shown the adherent marrow population differentiates in vivo and in vitro to several mesenchymal lineage cells: adipocytes, chondrocytes, osteoblasts, and myoblasts [reviewed in 167,116,168 – 174].

For example, ␤-catenin, which colocalizes and coprecipitates with cadherins [50], is a potential candidate. CD44, the hyaluronate receptor, is a nonintegrin adhesion receptor that is linked to the cytoskeleton. CD44 has been identified as a useful marker for osteocyte differentiation [200,201] and is also expressed in osteoclasts [327]. D. Osteocytes and Bone-Lining Cells: Gatekeepers of the Structural Integrity of Bone As the active matrix-forming osteoblast becomes encased in the mineralized matrix, the cell differentiates further into osteocytes.

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