the growth and development of the cartilage skeleton is influenced by biomechanical forces. These forces not only regulate the shape, regeneration, and aging of cartilage but also modify cell–to–extracellular matrix interactions within the cartilage.
Cartilage is capable of two kinds of growth, appositional and interstitial.
With the onset of matrix secretion, cartilage growth continues via a combination of two processes:  Appositional growth, the process that forms new carti lage at the surface of an existing cartilage; and  interstitial growth, the process that forms new cartilage
New cartilage cells produced during appositional growth are derived from the inner portion of the surrounding perichondrium. The cells resemble fibroblasts in form and function, producing the collagen component of the perichondrium (type I collagen). When cartilage growth is initiated, however, the cells undergo a differentiation process guided by an expression of the transcription factor SOX-9. The cytoplasmic processes disappear, the nucleus becomes rounded, and the cytoplasm increases in amount and prominence. These changes result in the cell becoming a chondro blast. Chondroblasts function in cartilage matrix production, including secretion of type II collagen. The new matrix  increases the cartilage mass, while new fibroblasts are produced simultaneously to maintain the cell population of the perichondrium.
New cartilage cells produced during interstitial growth arise from the division of chondrocytes within their lacunae (see Fig. 7.4). This is possible only because the chondrocytes retain the ability to divide and the surrounding matrix is distensible, thus permitting further secretory activity. Initially, the daughter cells of the dividing chondrocytes occupy the same lacuna. As new matrix is secreted, a partition is formed between the daughter cells; at this point each cell occupies its own lacuna. With continued secretion of matrix, the cells move even farther apart from each other. The overall growth of cartilage thus results from the interstitial secretion of new matrix material by chondrocytes and by the appositional secretion of matrix material by newly differentiated chondro blasts (Folder 7.2).
Cartilage has limited ability for repair.
Cartilage can tolerate considerable intense and repetitive stress. However, when damaged, cartilage manifests a striking inability to heal, even in the most minor injuries. This lack of response to injury is attributable to the avascularity of cartilage, the immobility of the chondrocytes, and the limited ability of mature chondrocytes to proliferate. Some repair can occur but only if the defect involves the perichondrium. In these injuries, repair results from activity of the pluripotential progenitor cells located in the perichondrium. Even then, however, few cartilage cells, if any, are produced. Repair mostly involves the production of dense connective tissue.
At the molecular level, cartilage repair is a tentative balance between deposition of type I collagen in the form of scar tissue and repair by expression of the cartilagespecific collagens. However, in adults, new blood vessels commonly develop at the site of the healing wound that stimulate the growth of bone rather than actual cartilage repair. The limited ability of cartilage to repair itself can cause significant problems in cardiothoracic surgery, such as coronary artery bypass graft surgery, when costal cartilage must be cut to enter the chest cavity. A variety of treatments may improve the healing of articular cartilage, including perichondral grafts, cell transplantation, insertion of artificial matrices, and application of growth factors.
When hyaline cartilage calcifies, it is replaced by bone.