The main component of pathogenesis is degradation of cartilage. Osteoarthritis is characterized by disturbed balance between the production of a new building material to restore cartilage and the cartilage destruction.
The influence of pathologies accounts for earlier and more rapid aging of the articular cartilage. Its metabolism is disrupted, above all, the decline in the basic substance and partial loss of chondrocytes occur. In the cases of osteoarthritis the chondrocytes phenotype changes, proteoglycans and collagens which are uncharacteristic of a normal cartilage are synthesized.
In the early stage of osteoarthritis, usually in the areas of maximum load, local zones of cartilage softening emerge, in the later stages fragmentation occurs, vertical cracks are formed in it. The cartilage loses its elasticity initially in the centre, becomes rough, disintegrates into fibrils, there appear cracks, the underlying bone is exposed, eventually the cartilage can fully disappear.
When the cartilage covering is thinned the pressure experienced by articular surfaces is distributed unevenly. The impaired architecture and metabolism of the articular cartilage leads to an emergence of an overload zone. This leads to local overloads, increased friction between the articular surfaces.
In the absence of shock-absorption by the cartilaginous tissue, bone articular surfaces experience a greater and more uneven mechanical loading. Zones of dynamic overload emerge in the subchondral bone causing local microcirculation disorders, which contributes to the emergence of subchondral osteosclerosis, changes in the curvature of articular surfaces and emergence of bone and cartilage growths, osteophytes. While these compensatory changes provide an increased area of contact, reduce the pressure on the articular cartilage, they limit the range of motion in the joint.
In the articular cavity the necrotic (dead) cartilaginous and bony fragments undergo phagocytosis by leukocytes with release of the products of inflammation, which is clinically manifested by cartilage synovitis and development of immune response to degradation products.
Immune pathologic process in the articular cartilage and the synovial sheath is developing in parallel with degenerative and dystrophic processes. Inflammation leads to fibro-sclerotic changes in the cartilage soft tissues. Diffuse growth of fibrous tissue occurs, leading to a considerable thickening of the capsule.
Simultaneously there develops an atrophy of the neighbouring muscles associated with inactivity due to pains in the affected joints during movement.
Attention! The changes due to osteoarthritis are irreversible.