Osteochondroprogenitor cell

They have the ability to differentiate into osteoblasts or chondrocytes depending on the signalling molecules they are exposed to, giving rise to either bone or cartilage respectively.

Osteoprogenitor cells can be identified by their associations with existing bone or cartilage structures, or their placement in the embryo, as the sites for osteogenesis and chondrogenesis are now known.

[3] [5] β-catenin of the canonical Wnt signalling pathway plays a role in cell fate determination, as it is critical for osteoblastogenesis, and the differentiation of chondrocytes into osteoblasts.

Conditional inactivation of TGF-βr2 of osteochondroprogenitor cells in the cranial neural crest resulted in faster osteoprogenitor differentiation and disorganised chondrogenesis.

For example, osteoblastic condensations are closer to epithelial surfaces so they will be exposed to more biophysical and biochemical stimuli due to the proximity and increased cell-epithelial interactions.

[11] With increasing age the functionality of adult stem cells declines as DNA damages and mutations accumulate.

[12] Deletion of the Trsp gene in osteochondroprogenitor cells results in abnormal bone growth, delayed ossification, chondronecrosis and dwarfism.

Kashin-Beck is a result of combinatorial environmentally induced by factors such as: toxic mould, contaminated grains by mycotoxins, and mostly by selenium deficiency, which is necessary for selenoprotein function.

[13] Loss of the regulator, Pten, of the Phophatidylinositol3' kinase pathway results in skeletal overgrowth and growth plate dysfunction, due to overproduction of the matrix and accelerated hypertrophic differentiation.