Osteoblast-Osteoclast Communication and Bone Homeostasis
Key mediators of osteoblast-osteoclast interaction. Osteoblast-osteoclast communications are essential for fine-tuning of bone remodeling during bone homeostasis. (1) Osteoblasts and osteoclasts have direct contacts through the interactions between EFNB2-EPHB4, FAS-FASL and NRP1-SEMA3A to regulate cell proliferation, differentiation, and survival. (2) Osteoclast-mediated bone resorption releases TGF-β and IGF-1 from bone matrix to induce osteoblast-mediated bone formation. (3) Osteoblasts secrete M-CSF, RANKL, WNT5A that promote osteoclast formation and development and OPG and WNT16 that inhibit osteoclast activity. Conversely, osteoclasts secrete S1P, CTHRC1 and C3 that promote osteoblast differentiation and SEMA4D that suppresses osteoblasts differentiation.
FIGURE 1. Representation of bone structure. Two types of osseous tissue can be identified: compact bone and trabecular bone. Bone tissue is subjected to bone remodeling, a life-dominant process that plays an important role in bone mass balance and mineral homeostasis. During bone remodeling osteoclasts, derived from hematopoietic stem cells, resorb old, or damaged bone. Subsequently, osteoblasts, derived from mesenchymal stem cells, are recruited to the damaged area in order to replace bone removed by osteoclasts. Instead, osteocytes derived from osteoblasts suspend their activity when buried in the bone matrix.
Osteogenesis and aging: lessons from mesenchymal stem cells
Age-related alterations of a number of cell-intrinsic factors can shift MSC differentiation to adipogenesis. Cell-extrinsic factors such as young paracrine factors and ECM, rapamycin, and resveratrol have been proven to restore osteogenic potential of aged MSCs through modulation of these impaired cell-intrinsic factors
The Role of Zinc in Bone Mesenchymal Stem Cell Differentiation