Synovial fluid nourishes the chondrocytes and lubricates
the joint. Hyaline cartilage has no blood supply,
significantly limiting its reparative, restorative
capacity. OA affects the degradation–synthesis cycle of
the chondrocytes, as well as of the extracellular matrix
and the subchondral bone, which in turn leads to softening,
fibrillation, ulceration, and loss of cartilage.
OA bony changes include fractures of subchondral
trabecular (spongy) bone, marginal osteophytes (bone
spurs), and subchondral cysts. Hyaline cartilage has no
nerves, and the pain that accompanies OA arises from
the subchondral trabecular bone, the joint capsule, and
the periarticular tissues. Synovial inflammation may be
present, in part because of cartilage debris, which may
result in joint effusion (swelling). Periarticular structures,
especially the muscles, are also affected.