Because of the complex, zonally anisotropic internal structure of the cartilage resulting in a short T2 relaxation time and because of its low thickness (1 to at best 6 mm).
In the early stages of cartilage degeneration and in the immediate neighborhood of cartilage defects proteoglycan depletion is observed. Local softening of cartilage at arthroscopic probing usually is ascribed to a local disruption of the collagenous fiber architecture, with subsequently altered water and proteoglycan content. Mechanically induced degeneration usually starts from a focal superficial lesion, leading to continuous erosion of cartilage tissue.
Diagnostic criteria of the various classification schemes for cartilage lesions are related to arthroscopic grading schemes. They comprise intracartilaginous signal intensity alterations, eventually a focal blistering of cartilage with intact cartilage surface, fissuring, and reduction of cartilage thickness (focal as a defect or more widespread, diffuse).
In addition to cartilage alterations in degenerative or inflammatory joint disease, subchondral cysts or synovial proliferations are apparent. In case of hemosiderin depositions with hemophilic arthropathy or cases of pigmented villonodular synovitis, characteristic susceptibility induced synovial proliferations are apparent.
In case of hemosiderin depositions with hemophilic arthropathy or cases of pigmented villonodular synovitis, characteristic susceptibility induced signal voids can be visualized using T2*weighted GRE sequences.