Abstract
There is a worldwide epidemic of skeletal diseases causing not only a public health issue but also accounting for a sizable portion of healthcare expenditures. The vertebrate skeleton is known to be formed by mesenchymal cells condensing into tissue elements (patterning phase) followed by their differentiation into cartilage (chondrocytes) or bone (osteoblasts) cells within the condensations. During the growth and remodeling phase, bone is formed directly via intramembranous ossification or through a cartilage to bone conversion via endochondral ossification routes. The canonical pathway of the endochondral bone formation process involves apoptosis of hypertrophic chondrocytes followed by vascular invasion that brings in osteoclast precursors to remove cartilage and osteoblast precursors to form bone. However, there is now an emerging role for chondrocyte-to-osteoblast transdifferentiation in the endochondral ossification process. Although the concept of “transdifferentiation” per se is not recent, new data using a variety of techniques to follow the fate of chondrocytes in different bones during embryonic and post-natal growth as well as during fracture repair in adults have identified three different models for chondrocyte-to-osteoblast transdifferentiation (direct transdifferentiation, dedifferentiation to redifferentiation, and chondrocyte to osteogenic precursor). This review focuses on the emerging models of chondrocyte-to-osteoblast transdifferentiation and their implications for the treatment of skeletal diseases as well as the possible signaling pathways that contribute to chondrocyte-to-osteoblast transdifferentiation processes.
Highlights
The process of cell differentiation is a widely studied phenomenon which is the basis for all developmental processes
A possible and colabeled with markers typically found in osteogenic indicator of this is embodied by the expression of OSX, a marker cells (COL1, OSX) during mandibular growth, further solidifying for early osteoblasts that often manifests in late stage hyperevidence that osteoblasts are able to arise from hypertrophic trophic chondrocytes
We have shown Implications for clinical practice that thyroid hormone-deficient animals could form prehyper- The clinical relevance of understanding the potential contribution trophic chondrocytes, but bone formation was halted during of the chondrocyte-to-osteoblast differentiation route to endonormal ossification windows, and in later stages was chondral ossification and the molecular mechanisms that
Summary
The art of building bone: emerging role of chondrocyte-toosteoblast transdifferentiation in endochondral ossification. The vertebrate skeleton is known to be formed by mesenchymal cells condensing into tissue elements (patterning phase) followed by their differentiation into cartilage (chondrocytes) or bone (osteoblasts) cells within the condensations. During the growth and remodeling phase, bone is formed directly via intramembranous ossification or through a cartilage to bone conversion via endochondral ossification routes. The canonical pathway of the endochondral bone formation process involves apoptosis of hypertrophic chondrocytes followed by vascular invasion that brings in osteoclast precursors to remove cartilage and osteoblast precursors to form bone. There is an emerging role for chondrocyte-to-osteoblast transdifferentiation in the endochondral ossification process. This review focuses on the emerging models of chondrocyte-to-osteoblast transdifferentiation and their implications for the treatment of skeletal diseases as well as the possible signaling pathways that contribute to chondrocyte-to-osteoblast transdifferentiation processes
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