Chondrification (also known as chondrogenesis) is the process by which cartilage Figure 1 is formed from condensed mesenchyme tissue, which differentiates into chondroblasts and begins secreting the molecules that form the extracellular matrix. Mesenchymal stem cells (MSCs) are undifferentiated meaning they can give rise to different cell types. Under the appropriate conditions, at sites of cartilage formation, they are referred to as chondrogenic cells. During cartilage formation undifferentiated MSCs are highly proliferative and form dense aggregates of chondrogenic cells at the center of chondrification. These condrogenic cells will then differentiate to chondroblasts which will then synthesize the cartilage extracellular matrix (ECM) which consists of ground substance (proteoglycans and glycosaminoglycans) and associated fibers such as collagen. The chondroblasts then trap themselves in a small space that is no longer in contact with the newly created matrix called lacunae which contain extracellular fluid. The chondroblast is now a chondrocyte Figure 2, which is usually inactive but can still secrete and degrade the matrix depending on the conditions.
The majority of body cartilage has been synthesized from the chondroblasts which are largely inactive at later developmental stages compared to early years (pre-pubescence). The division of cells within cartilage occurs very slowly. Therefore, growth in cartilage is usually not based on an increase in size or mass of the cartilage itself. Remodeling of cartilage is predominantly affected by changes and rearrangements of the collagen matrix, which responds to tensile and compressive forces experienced by the cartilage. Cartilage growth thus mainly refers to matrix deposition, but can include both growth and remodeling of the extracellular matrix. Early in fetal development, the greater part of the skeleton is cartilaginous. This temporary cartilage is gradually replaced by bone (Endochondral ossification), a process that ends at puberty. In contrast, the cartilage in the joints remains unossified during the whole of life and is, therefore, permanent.
Once damaged, cartilage has limited repair capabilities. Because chondrocytes are bound in lacunae, they cannot migrate to damaged areas. Also, because cartilage does not have a blood supply, the deposition of new matrix is slow. Damaged hyaline cartilage is usually replaced by fibrocartilage scar tissue. Over the last few years, surgeons and scientists have elaborated a series of cartilage repair procedures that help to postpone the need for joint replacement. These include Marrow Stimulation techniques including surgeries and stem cell injections and grafting of cartilage into damaged areas. However, due to the extremely slow growth of cartilage and its avascular properties, regeneration and growth of cartilage post-injury is very slow.