We often think of OA as a homogenous degenerative disease entity, involving the wearing down of articular cartilage, and devoid of inflammation.
This is now seen to be untrue, in light of new discoveries. Of the 3 main tissue types involved (cartilage, bone, synovium), synovial inflammation is seen to be a major source of pain and a driver of disease progression.
Perhaps more refined clinical subtype characterisation can lead to more effective individualised treatment of OA.
Meniscal Surgery: Risk of Radiographic Joint Space Narrowing Progression and Subsequent Knee Replacement-Data from the Osteoarthritis Initiative
Controversy surrounds whether meniscal surgery may inadvertently lead to faster knee OA deterioration, resulting in joint replacement surgery eventually.
It appears from this study that if meniscal surgery is done for traumatic meniscal injury, the answer is no. In contrast, meniscal surgery for degenerative tears may be ill-advised: joint cartilage subsequently deteriorated faster, with more requiring earlier knee replacement surgery.
It appears that, like bone marrow oedema, OA progression in pre-existing cartilage damage is restricted to the same joint compartment and the immediate adjacent cartilage. There is no "spreading".
The greater the volume of synovitis, the higher the risk of OA knee. Is the relationship causal? If so, which caused which?
OA synovial fluid white blood cell count level, while not in the realm of outright inflammatory arthritides like RA or Gout, correlates with synovial volume (inflammatory burden), as well as with the degree of pain relief with intra-articular steroid injection.
Joint inflammation is associated with pain sensitization in knee osteoarthritis: The Multicenter Osteoarthritis Study
Synovitis (evidenced by increased synovial volume and/or effusion), but not bone marrow oedema, correlates with increased pain sensitization, both locally (the knee) and elsewhere (generalised).