chondrogenesis

Additional studies emphasized the role of Sulfs in chondrogenesis.

Also, the zone of proliferating chondrocytes was reduced by 90%, indicating defects in chondrogenesis.

Moreover, the results suggest that elevated TGF-β1 levels result in chondrogenesis within the synovial tissue.

They could show, that the combination provided high biofunctionality with improved chondrogenesis and long term local supply of TGF-β1.

Because Sulfs were important in normal chondrogenesis, they were investigated in cartilage diseases.

In skeletally immature individuals, the blood supply to the epiphyseal bone is good, supporting both osteogenesis and chondrogenesis.

Notch1 is expressed in the mesenchymal condensation area and subsequently in the hypertrophic chondrocytes during chondrogenesis.

The micromass culture system [ 10 ] provides the three-dimensional environment needed for chondrogenesis, cartilage maturation and hypertrophy.

Similar to the previous report, we have observed evidence for intra-synovial chondrogenesis as well as osteometroplasia following TGF-β1 gene transfer.

Sulf1 was expressed highly in condensing mesenchyme and, in cell culture, caused prechondrocytes to differentiate into chondrocytes, indicating QSulf1 is needed for early chondrogenesis.

In addition, TGF-β1 expression in the adenovirally infected synovial lining also resulted in induction of chondrogenesis in the synovium.

This technique is known as AMIC (Autologous Matrix-Induced Chondrogenesis) and was first published in 2003.

Additionally it was intended to provide a simple technique for securely retaining the fragile blood clot in larger defects and to possibly enhance the chondrogenesis of MSCs.

Autologous Matrix-Induced Chondrogenesis (AMIC) is a biological treatment option which repairs articular cartilage damage.

The authors propose that the microdrilling surgery creates a blood clot scaffold on which injected PBPC's can be recruited and enhance chondrogenesis at the site of the contained lesion.

Autologous matrix-induced chondrogenesis, which is also known as AMIC, is a biological treatment option for articular cartilage damage bone marrow stimulating technique in combination with a collagen membrane.

Chondrification (also known as chondrogenesis) is the process by which cartilage is formed from condensed mesenchyme tissue, which differentiates into chondrocytes and begins secreting the molecules that form the extracellular matrix.

The fibrodysplasia ossificans progressiva R206H ACVR1 mutation activates BMP-independent chondrogenesis and zebrafish embryo ventralization (PDF)

These effects are seen because isotretinoin like all retinoids (including excessive vitamin a intake) negatively impairs chondrogenesis (formation of new cartilage), with diminishing cartilage in the epiphyseal plate to ossify, growth slows down and subsequently stops when all remaining cartilage has been ossified.

GDF11 is also a negative regulator of neurogenesis , the production of islet progenitor cells , the regulation of kidney organogenesis , pancreatic development , the rostro-caudal patterning in the development of spinal cords , and is a negative regulator of chondrogenesis.