Rheumatoid arthritis primarily involves the synovial membrane of the j
oints, together with that of the tendon sheaths and bursae. These stru
ctures are targeted in a selective and symmetrical manner. The inflamm
atory cell infiltrate is usually dominated by mononuclear phagocytes.
These are recruited into the synovial lining as type A synoviocytes. A
proportion of the mononuclear cell population has proven to be specia
lized antigen-presenting accessory cells. The T and B lymphocyte infil
trate is quite variable in intensity, but may become highly organized.
Polymorphonuclear leukocytes pass rapidly into the joint space. The c
ellular characteristics of rheumatoid nodules have some similarities w
ith those of the synovial membrane. In a minority of patients, immunog
lobulin production and circulating immune complex formation reaches le
vels which precipitate the appearance of a complement mediated vasculi
tis. This may lead to tissue damage in remote organs.