The use of the term is technically inaccurate, as mesenchymal parents can also technically differentiate into osteoblasts or fat.
Chondroblasts, or perichondrial cells, is the name given to mesenchymal progenitor cells in situ that, from endochondral ossification, will form chondrocytes in the matrix of growing cartilage. Another name for them is subchondral steroids.
They have chromatic nuclei and are stained with basic dyes. These cells are essential in chondrogenesis due to their role in forming chondrocytes and the cartilage matrix that will eventually form cartilage.
Chondroblasts are called chondrocytes when they become embedded in the cartilage matrix, which consists of proteoglycans and collagen fibers until they are found in the gaps of the matrix.
Once embedded in the cartilage matrix, they grow the cartilage matrix by increasing the extracellular matrix of the cartilage rather than dividing further.
Within developing adults, most chondroblasts are found in the perichondrium. This is a thin layer of connective tissue that protects cartilage and is where chondroblasts help expand cartilage size when prompted by hormones such as GH, TH, and glycosaminoglycans.
They are located in the perichondrium because the perichondrium, situated outside the developing bone, is not as tightly wrapped in the cartilage’s extracellular matrix as inside and because the capillaries are found here.
The type of growth maintained by chondroblasts is called appositional bone growth, and it increases the girth of the affected tissue. It is important to note that the perichondrium, and therefore the chondroblasts, are not found on the articular cartilage surfaces of the joints.
Training and composition matrix
The extracellular matrix secreted by chondroblasts comprises fibers, collagen, hyaluronic acid, proteoglycans, glycoproteins, water, and a set of macromolecules.
Collagen fibers within the finished cartilage make up 10-20% of the volume, 65-80% water, and proteoglycan-hyaluronic acid adds the remaining portion.
Due to the proliferative nature of chondroblasts, cells make up a more significant portion of the composition than is usually found within finished cartilage.
Type II collagen fibers are responsible for giving the future cartilage matrix its tensile strength. The structure of these fibers, like most collagen fibers, forms a triple helix structure.
Proteoglycans resist the compression they generally exert on cartilage and generate the swelling pressure responsible for the stress that protects the matrix from compression load.
They adhere to 100 chondroitin sulfate molecules and 50 keratan sulfate glycosaminoglycan chains.
Together with collagen fibrils, these chains are attached to a hyaluronic acid backbone that creates an interstitial intrafibrillar space in which water is retained by the negative charge of proteoglycans.
As the name suggests, mesenchymal progenitors originate from the mesoderm.
When formed from the mesoderm, these cells are formed explicitly from embryonic stem cells by induction through BMP4 and fibroblast growth factor FGF2 while the fetus is in utero.
It has been suggested that the differentiation of embryonic stem cells with these growth factors could prevent stem cells, once injected into potential patients, from forming teratomas or tumors caused by stem cells.
A significant genetic component of this process is Sox9, an HMG box transcription factor, which marks progenitor cells for chondrogenic differentiation.
Inactivation of the Sox9 gene will result in the loss of all cartilage and thus the formation of chondroblasts. This factor is also expressed together with Sox5 and Sox6.
Runx2 is another crucial genetic component of chondroblast formation. Expression of this gene has been found to result in the suppression of chondroblast differentiation.
Expression of this gene will also cause the already formed cartilage to undergo endochondral ossification, which will cause the cartilage to form bone.
Chondroblast differentiation is favored in an environment with high compressive force and low partial oxygen pressure that combine to inhibit protein 3, a protein that inhibits cartilage differentiation.
These preferences are essential as mature cartilage tissue is avascular and, therefore, would be unsuitable for a high oxygen environment.
The chondroblasts migrate into the cartilage each time the chondrocytes are destroyed by mechanical force.
The remaining chondrocytes divide to form more chondroblasts. HMGB-1 is a growth factor that promotes chondrocyte division, while receptors for advanced glycation products mediated by chemotaxis clean up cellular debris resulting from damage.
The chondroblasts then secrete a matrix of cartilage around themselves to reform the lost cartilage tissue.
However, regeneration is still too slow for patient care to effectively depend on this repair mechanism.