Chapter 6: The Composition of Bone Pamela Gehron Robey and Adele L. Boskey

From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7th Edition. www.asbmrprimer.org Table 1: Characteristics of Collagen-Related Genes and Proteins Found in Bone Matrix © 2008 American Society for Bone and Mineral Research

From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7th Edition. www.asbmrprimer.org Table 2: Gene and Protein Characteristics of Serum Proteins Found in Bone Matrix © 2008 American Society for Bone and Mineral Research

From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7th Edition. www.asbmrprimer.org Table 3: Gene and Protein Characteristics: Glycosaminoglycan-Containing Molecules in Bone © 2008 American Society for Bone and Mineral Research

From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7th Edition. www.asbmrprimer.org Table 4: Gene and Protein Characteristics of Glycoproteins in Bone Matrix © 2008 American Society for Bone and Mineral Research

Table 5: Gene and Protein Characteristics of SIBLINGs From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7th Edition. www.asbmrprimer.org Table 5: Gene and Protein Characteristics of SIBLINGs Figure 5 Cell–cell interactions in bone marrow. Hematopoietic stem cells (H), the precursors of both T cells (T) and osteoclasts (OC), reside in a stem cell niche provided by osteoblasts (OB), which, together with stromal cells (S), derive from mesenchymal stem cells (M). Bone degradation results in release of matrix-associated growth factors (thick vertical line), which stimulate mesenchymal cells and thus bone formation. This “coupling” is an essential consequence of osteoclast activity.(28) After activation, T cells secrete molecules that stimulate osteoclastogenesis and function. Cancer cells (C) release cytokines that activate bone resorption; in turn, matrix-derived factors stimulate cancer cell proliferation, the so-called “vicious cycle.” © 2008 American Society for Bone and Mineral Research

From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7th Edition. www.asbmrprimer.org Table 6: Gene and Protein Characteristics of Other RGD-Containing Glycoproteins Figure 6 Osteoclast signaling pathways. Summary of the major receptors, downstream kinases, and effector transcription factors that regulate osteoclast formation and function. Proliferation (P) of precursors is driven chiefly through ERKs and their downstream cyclin targets and E2F; maximal activation of this pathway requires combined signals from c-Fms and the integrin αvβ3. As expected, the cytoskeleton (C) is independent of nuclear control but depends on a series of kinases and their cytoskeletal-regulating targets, whereas differentiation (D) is regulated largely by controlling gene expression. The calcium/calmodulin (CaM)/calcineurin (CN) axis enhances nuclear translocation of NFAT1c, the most distal transcription factor characterized to date. © 2008 American Society for Bone and Mineral Research

From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7th Edition. www.asbmrprimer.org Table 7: Gene and Protein Characteristics of Gamma-Carboxy Glutamic Acid–Containing Proteins in Bone Matrix © 2008 American Society for Bone and Mineral Research

Table 8: Effects of Bone Matrix Molecules on Mineralization In Vitro From the Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 7th Edition. www.asbmrprimer.org Table 8: Effects of Bone Matrix Molecules on Mineralization In Vitro © 2008 American Society for Bone and Mineral Research