Articular cartilage is a specialized connective tissue covering joint surfaces. Macroscopically, it has a glistening, white appearance. Microscopically, it is composed of water, collagen, proteoglycans, chondrocytes and other matrix proteins and lipids. It is avascular and alymphatic and is sheltered from the immune system . It also has no nerve supply and is therefore not sensitive to early injuries. It also has poor repair properties, because there are relatively few cells in the tissue, the metabolic rate is low, and the capacity of chondrocytes to divide and migrate in the articular cartilage is restricted by the matrix fibres. As a consequence, it is generally agreed that articular cartilage does not repair significantly after injury to the collagen mesh. Articular cartilage has been subdivided into five zones depending on the alignment of collagen fibers, which give each zone particular biomechanical advantages:
Applied Anatomy
Structure & importance of tide-mark
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- Superficial zone - resistant to shear due to tangential arrangement. Low metabolic activity and hence low healing potential.
- Transitional (middle) zone - resistant to compression, high concentration of collagen obliquely arranged at right angles to each other.
- Radial (deep) zone - resistant to compression, This zone contains the largest-diameter collagen fibrils, the highest concentration of proteoglycans, and the lowest concentration of water. Cells are arranged in columns.
- Tidemark - resistant to shear. Changes of the tidemark were found to be multiform and metabolically active in the osteoarthritic process. Endochondral ossification depletes the calcified cartilage at the cartilage/bone interface and the tidemark has been thought of as a calcification front advancing in the direction of non-calcified cartilage. Duplication of the tidemark is cited as evidence of this advancement.
Reestablishment of the tide mark is inconsistent in most cartilage repair techniques. In the adult, there is heavy deposition of apatites in the calcified zone, which prevents diffusion of nutrients across the tide-mark.The calcified zone also functions as an efficient barrier to cellular invasion. This may explain the apparent immunity of cartilage transplants to the allograft rejection process. - Calcified zone - acts as an anchor between articular cartilage and subchondral bone
Chondrocytes are highly specialized mesenchymal cells that are responsible for the production of the structural components of articular cartilage including collagen, proteoglycans and other matrix proteins and lipids. They are located in lacunae, usually scattered individually throughout articular cartilage. During growth of the articular cartilage, chondrocytes have a constant, usually roundish shape, but their shape becomes more variable depending on age, pathological state and the cartilaginous layer to which they correspond. Chondrocytes are anaerobic, and receive their nutrition via diffusion of substances within synovial fluid. Water contributes up to 80% of the wet weight of articular cartilage, and the interaction of water with the matrix macromolecules significantly influences the mechanical properties of the tissue. The principal articular cartilage collagen, type II, accounts for 90% to 95% of the cartilage collagen. They are responsible for the tensile strength. Proteoglycans are responsible for compressive strength of articular cartilage and are composed of aggrecan molecules linked to hyaluronic acid to form an aggregate macromolecule. Aggrecan molecules are composed of a protein core with multiple glycosaminoglycans subunits. The glycosaminoglycans include chondroitin-4-sulphate, chondroitin-6-sulphate and keratin sulphate. In ageing, the level of chondroitin-4-sulphate decreases and that of keratin sulphate increases.Composition
Chondrocytes
Matrix
Note: Proteoglycans are long chain polysaccharides linked to hyaluronate that are negatively charged and hold water within the cartilage by osmotic pressure, thus maintaining the tension of the collagen mesh. However, if the proteoglycans are damaged by trauma or by other agents such as enzymes in inflammatory disease or infection then the proteoglycan structure disintegrates and the water holding capacity is lost, and progressive breakdown of the collagen meshwork then occurs. This leads to exposure of the bone beneath, causing severe pain and disability.
Deep lacerations of articular cartilage extending beyond the tidemark heal with fibrocartilage produced by undifferentiated mesenchymal cells. Superficial lacerations do not heal, although some proliferation of chondrocytes may occur. Immobilisation of joints leads to atrophy of the articular cartilage and therefore continuous passive motion is believed to be beneficial to healing. In arthritic cartilage, chondrocytes are recovered in clusters of up to thirty cells, which probably represents an attempt at tissue regeneration. The acute and repetitive impact and torsional joint loading that occurs during participation in sports can damage articular surfaces causing pain, joint dysfunction, and effusions. In some instances, this articular surface damage leads to progressive joint degeneration. Three classes of chondral and osteochondral injuries can be identified based on the type of tissue damage and the repair response: (1) damage to the joint surface that does not cause visible mechanical disruption of the articular surface, but does cause chondral damage and may cause subchondral bone injury; (2) mechanical disruption of the articular surface limited to articular cartilage; and (3) mechanical disruption of articular cartilage and subchondral bone. In most instances, joints can repair damage that does not disrupt the articular surface if they are protected from additional injury. Mechanical disruption of articular cartilage stimulates chondrocyte synthetic activity, but it rarely results in repair of the injury. Disruption of subchondral bone stimulates chondral and bony repair, but it rarely restores an articular surface that duplicates the biologic and mechanical properties of normal articular cartilage. In selected patients, surgeons have used operative treatments including penetrating subchondral bone, soft tissue grafts, and cell transplants and osteochondral autografts and allografts to restore articular surfaces after chondral injuries. Experimental studies indicate that use of artificial matrices and growth factors also may promote formation of a new joint surface. However, an operative treatment of an articular surface injury that will benefit patients must not just provide a new joint surface, it must produce better long-term joint function than would be expected if the injury was left untreated or treated by irrigation and debridement alone. Therefore, before selecting a treatment for a patient with an articular cartilage injury, the surgeon should define the type of injury and understand its likely natural history. In fibrocartilage the matrix component is minimal, and the fibrous one greatly predominates. The chondrocytes are less numerous and much more widely separated than in other types, but most of them are still enclosed in lacunae.
Repair tissue that fills osteochondral defects is less stiff and more permeable than normal articular cartilage, and the orientation and organization of the collagen fibrils in even the most hyaline-like chondral repair tissue do not follow the pattern seen in normal articular cartilage. The decreased stiffness and increased permeability of repair cartilage matrix may increase loading of the macromolecular framework during joint use and result in progressive structural damage, thereby exposing the repair chondrocytes to excessive loads that additionally compromise their ability to restore the matrix. depletion of matrix proteoglycans, fragmentation and fibrillation, increasing collagen content, and loss of cells with the appearance of chondrocytes within 1 year or less. The remaining cells often assume the appearance of fibroblasts as the surrounding matrix comes to consist primarily of densely packed collagen fibrils. This fibrous tissue usually fragments and often disintegrates, thus leaving areas of exposed bone. The inferior mechanical properties of chondral repair tissue may be responsible for its frequent deterioration.Functions
Response to injury
Basic science in repair
Articular cartilage injuries.
Buckwalter JA. Clin Orthop Relat Res. 2002 Sep;(402):21-37
University of Iowa Department of Orthopaedics, Iowa City 52242, USA.
Why do we need hyaine cartilage repair tissue?
The mechanisms of genetic regulation and degeneration of articular cartilage are important to our understanding the evolution of many degenerative and traumatic diseases. The available evidence indicates that normal matrix turnover depends on the ability of chondrocytes to detect alterations in the macromolecular composition and organization of the matrix, including the presence of degraded molecules, and to respond by synthesizing appropriate types and amounts of new molecules. In addition, the matrix acts as a signal transducer for the cells. Loading of the tissue due to use of the joint creates mechanical, electrical, and physicochemical signals that help to direct the synthetic and degradative activity of chondrocytes. In arthritis, proteoglycan degradation is thought to be an early and reversible process, whereas the breakdown of the collagen network is believed to be irreversible, contributing to loss of joint function. Articular cartilage is extremely sensitive to proteolysis induced by contaminant bacteria. Inflammatory cytokines and tissue-damaging proteinases play important roles in joint destruction in Rheumatoid Arthritis. The pannus is a sheet of inflammatory granulation tissue that spreads from the synovial membrane and invades the joint in rheumatoid arthritis.
Osteochondritis dissecans (OCD) is a relatively common condition causing knee pain in children and young adults. It is a condition affecting subchondral bone that manifests as a pathologic spectrum. Initially stages have intact articular surface but softening. This can progress to early articular cartilage separation, partial detachment of an articular lesion, and Cartilage in disease
Changes in OA
Infection and inflammatory arthritis
What happens in Osteochondritis Dissecans and AVN
Although the etiology of these lesions is unclear, it is believed that repetitive microtrauma may interrupt the already tenuous epiphyseal blood supply in the growing child and contribute to the development of osteochondritis dissecans lesions. differences between osteochondrotic and normal cartilage.
There is a decrease in acidic glycosaminoglycans in OCD with thinned subchondral growth plate compared to normal osteochondral samples. Borders to the healthy tissue are clearly visible micro- and macroscopically. Scanning electron microscopy revealed structural differences in the subchondral area. Immunohistochemistry found a general decrease in glycosaminoglycan content and a change in composition. Only faint staining for chondroitin and keratan sulfates was observed in osteochondritic cartilage, whereas increased staining was shown for keratan sulfate in bone. The intraosseous supply to the medial femoral condyle appeared to consist of a single nutrient vessel supplying the subchondral bone with an apparent watershed area of limited supply compared to the lateral femoral condyle.
Articular cartilage gives synovial joints the ability to provide low-friction and pain-free motion.
Articular cartilage defects are common. They are present in 60% of all knee arthroscopies. Severe lesions (Grade III or IV) are present in 5-7% of young patients at arthroscopy and most commonly over the Patella and Medial Femoral Condyle. These lesions can often be missed on MRI scans.
The natural history of progression of these lesions is still not clear but these are potential candidates for cartilage repair with prospects of improving pain, function and delaying osteoarthritis 
 
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