The aetiology of degenerative joint diseases is multifactorial, but on
e main cause is overloading (mechanical stress). While until recently
it was well accepted that this represented primarily a disorder of car
tilage with reactive subchondral changes, there is now some evidence t
hat it might be primarily a subchondral problem with secondary changes
in the articular cartilage. Early subchondral changes include redistr
ibution of blood supply with marrow hypertension, oedema and probably
micro-necrosis. These findings are very similar to those in avascular
necrosis of bone and raise the question of a vascular aetiology. While
these first reports need further proof, it seems clear that the artic
ular cartilage and subchondral regions are one functional unit, in whi
ch the subchondral region is more stress sensitive. Recently described
channels connecting these two regions strengthen this opinion. These
new concepts are exciting and may make a major impact in the near futu
re on the management of and research into degenerative joint disease.