Cartilage is a connective tissue composed of cells (chondrocytes) and fibres (collagen or yellow elastic) embedded in a firm, gel-like matrix which is rich in a mucopolysaccharide. It is much more elastic than bone. It is found in many areas in the bodies of including the joints between bones, the rib cage, the ear, the nose, the bronchial tubes and the intervertebral discs.
It is not as hard and rigid as bone but is stiffer and less flexible than muscle.
A layer of fibrous tissue, called perichondrium surrounds it like periosteum surrounds the bone. The articular cartilage has no perichondrium, so that its regeneration after injury is inadequate.
Chondrocytes are primary cells that form cartilage.
Types of Cartilage
It is bluish white and translucent due to very fine collagen fibres. It distribution is most abundant, and has a tendency to calcify after 40 years of age. All cartilage bones are preformed in hyaline.
It is the most widespread type of cartilage is found in
- Articular surface of bones
- Forms the anterior portion of the ribs
- Support for the respiratory passages (ringlike structures of the trachea).
- Provides shape as in nose
Hyaline cartilage is flexible, elastic, bluish white, and opalescent. The cells are mainly spherical and occupy the entire lacuna, although in stained sections the cell membrane retracts and the contour appears angular or stellate.
Nearer the surface, the cells appear flattened and lie in a plane parallel to the surface. The cytoplasm contains long mitochondria, vacuoles, and, particularly in more mature larger cells, fat droplets, and glycogen. The vacuoles may be large and distend the cell. The nucleus contains one or several nucleoli.
Nearer the surface, the cells occur singly or in pairs, often within the same lacuna. Multiple cells are often aggregated into compact groups irregularly placed.
The interstitial substance appears homogeneous. This is because refractive indexes of both collagen and acid mucopolysaccharide are identical.
Glycosaminoglycans, chiefly chondroitin sulphate, are contained within the interstitial substance and are responsible for the basophilic staining.
Cartilage has no blood vessels except an occasional one passing through to other tissues. Its nourishment, depending upon the location could be from synovial fluid, perchondrium.
Fibrocartilage differs from hyaline cartilage by the presence of thick, compact bundles of collagenous fibers within its interstitial substance. These bundles are arranged parallel to each other, separated by clefts in which encapsulated cells are squeezed.
Fibrocartilage appears to be a transitional tissue between hyaline cartilage and collagenous tissue and, as such, occurs in special situations.
It is white and opaque due to abundance of dense collagen fibres. Wherever fibrous tissue is subjected to great pressure, it is replaced by fibrocartilage which is tough, strong and resilient. Examples are intervertebral disc, intra-articular discs, menisci and labra. It lines certain bony grooves in which the tendons play.
- Shock Absorbers: Fibrous cartilage acts to absorb the shocks between the vertebrae in spine.
- Support: Provides sturdiness without impeding movement.
- Movement: The white fibrocartilage forms a firm joint between bones but still allows for a reasonable degree of movement.
- Deepens Sockets: In articular cavities such as the ball-and-socket joints in the hip and shoulder regions white fibrocartilage deepens the sockets to make dislocation less possible.
It is made up of numerous cells and a rich network of yellow elastic fibers pervading the matrix, so that is more pliable. Example: cartilages in the external ear, auditory tube, and small cartilages at the inlet of larynx. It performs following functions.
- Maintain Shape: In the ear, for example, it helps to maintain the shape and flexibility of the organ.
- Support: It also strengthens and supports these structures.
Formation of Cartilage Tissue
Mesenchyme the cells becomes rounded, and the collagenous fibrils in the intercellular substance becomes enclosed by a basophilic material. The cells accumulate vacuoles, frequent mitoses occur, and daughter cells in a group are separated only by a thin partition.
A thin, shining layer, the capsule, appears about the cell cavity and represents the recently formed intercellular substance. The mesenchyme surrounding the cartilage forms a connective tissue layer covering, the perichondrium. A constant transformation of these layers and their cells into cartilage occurs during embryonic life.
The collagenous fibers are acidophilic flat bundles. They are surrounded by basophilic intercellular substance (acid mucopolysaccharides).
Elongated cells within the perichondrium lose their spindle shape and are transformed to spherical cells, the chondrocytes, surrounded by capsules. This process is termed appositional growth of cartilage.
Other form of growth is appostional wherein the cells within the cartilage multiply within their capsules and add to the surrounding matrix.
Changes in Osteoarthritic Cartilage
Osteoarthritis results from changes in joint cartilage and its matrix.
Normal Cartilage Structure
Normal cartilage is composed
- Proteoglycans which are responsible for the compressive stiffness of the tissue and its ability to withstand load.
- Collagen, which provides tensile strength and resistance to shear.
- Matrix metalloproteinases, including stromelysin, collagenase, and gelatinase
Matrix metalloproeinases can degrade all the components of the extracellular matrix at neutral pH. Each is secreted by the chondrocyte (cell that forms cartilage) as proenzyme (substance that eventually forms enzyme). Proenzyme must be activated by cleavage of the protein.
The level of matrix metalloproeinases [MMP] activity in the cartilage at any given time represents the balance between activation of the proenzyme and inhibition of the active enzyme by tissue inhibitors.
Interleukin 1 stimulates the synthesis and secretion of the latent MMPs and of tissue plasminogen activator.
Plasminogen be synthesized by the chondrocyte or may enter the cartilage from the synovial fluid.
Both plasminogen and stromelysin may play a role in activation of the latent MMPs. Interleukin 1 also suppresses prostaglandin synthesis by the chondrocyte, a substance required for matrix repair.
This in turn leads to inhibition of matrix repair.
The balance of the system lies with at least two inhibitors namely tissue inhibitor of metalloproteinase and plasminogen activator inhibitor I.
Both are synthesized by the chondrocyte and limit the degradative activity of MMPs and plasminogen activator, respectively. If tissue inhibitor of metalloproteinase or plasminogen activator inhibitor I is destroyed or is reduced to ineffective concentration, plasmin and other degrading enzymes are free to act on matrix substrates.
Stromelysin enzyme can degrade the protein core of the prostaglandins and activate latent collagenase. This Conversion of latent stromelysin to active protease enzyme by plasmin provides a second mechanism for matrix degradation.
Polypeptide mediators like insulin-like growth factor-1 and transforming growth factor, stimulate biosynthesis of prostaglandins. They regulate matrix metabolism in normal cartilage and may play a role in matrix repair in OA.
These growth factors modulate catabolic as well as anabolic pathways of chondrocyte metabolism, by down-regulating chondrocyte receptors for IL-1, they may decrease PG degradation.
In addition to its responsiveness to cytokines and a variety of other biologic mediators, chondrocyte metabolism in normal cartilage can be modulated directly by mechanical loading.
It is believed that feel that the primary changes in osteoarthritic cartilage begin in the cartilage. A change in the arrangement and size of the collagen fibers is apparent, perhaps due to disruption of the glue that binds adjacent fibers together in the matrix.
This is among the earliest matrix changes observed and appears to be irreversible.
Wear may be a factor in the loss of cartilage but there is a strong eveidence that lysosomal enzymes and matrix metalloproteinases account for much of the loss of cartilage matrix in osteoarthritic cartilage.
Matrix metalloproteinases, plasmin, and cathepsins all appear to be involved in the breakdown of articular cartilage on OA.
Tissue inhibitor of metalloprteinases may work to stabilize the system, at least temporarily, while growth factors, such as Insulin growth factor, and basic fibroblast growth factor are involved in repair processes that may heal the lesion or, at least, stabilize the process.
The chondrocytes in osteoarthritic cartilage undergo active cell division and are very active metabolically, producing increased quantities of DNA, RNA, collagen, PG, and noncollagenous proteins.
Prior to cartilage loss and PG depletion, this marked biosynthetic activity may lead to an increase in prostaglandin concentration, which may be associated with thickening of the cartilage and a stage of homeostasis referred to as “compensated” OA.
These mechanisms may maintain the joint in a reasonably functional state for years. The repair tissue, however, often does not hold up as well under mechanical stresses as normal hyaline cartilage, and eventually, at least in some cases, the rate of prostaglandin synthesis falls off and full thickness loss of cartilage occurs.
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