Abstract

Bones are mainly composed of calcified collagenous matrix and cartilage with enclosed hematopoietic marrow and fat. Most bones are preformed in cartilage molds formed by chondroblasts during skeletal development. These molds are quickly remodeled and replaced by bone matrix formed by osteoblasts. Bone health is maintained postnatally by bone remodeling, a process in which sections of old bone are degraded by osteoclasts and later replaced by new bone. Osteoclast formation is regulated predominantly by osteoblastic cells through the osteoclastogenic cytokines, macrophage-colony stimulating factor, and receptor activator of NF-κB ligand. However, interactions between cells in both lineages positively and negatively regulate each other’s formation and functions through the effects of cytokines, chemokines, and transcription factors. Mutations in the genes that regulate the formation and functions of osteoblastic, osteoclastic, and chondroblastic cells result in a variety of bone phenotypes, including missing or supernumerary bones and increased or decreased bone mass, which can weaken bones and increase the risk of fracture. Here we review current understanding of the molecular mechanisms that regulate the formation and function of osteoclasts, osteoblasts, and chondrocytes.

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