Joint instability causes cartilage irritation and lesions as well as degeneration of the joint components.

Cartilage lesions are developed as a secondary phenomenom due to excessive biomechanical tension.

•  The cartilage loses its transparency, is bleached, and is eliminated in microscopic fragments.
•  The cartilage shows notches and wrinkles.
•  The subchondral surface is exposed and bone eburnation becomes evident.
•  Osseous proliferation begins.

Inflammatory mediators and fragments of cartilage are liberated inside the joint perpetuating thereby the cycle of the degenerative joint disease.

The fragments of liberated cartilage are microscopic, however, some can reach a few millimeters. They are in charge of self-maintaining and perpetuating the joint disease.

Deterioration of the matrix occurs in the most superficial area of the cartilage. Vertical fissures can be easily seen, which progress in depth., subchondral sclerosis of defense, osteofites, geodas or pseudocysts and sinovitis.

Subchondral bone

At this stage of the disease osseous proliferation starts.

Acute inflammatory arthropathy begins when the subchondral bone is exposed to sinovial liquid.




In the anatomic cut of the head of the femur can be observed:

•  Weakness of the cartilage surface, osteopenic spongy subchondral, exostosis and necrosis.

•  Joint enlarging due to an increase or deformation of the osseous components.

•  Thickening of the joint capsule.

•  Swelling of the periarticular tissues.

Anatomic cut
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