4. Genetic consideration –
RA higher in twins (Monozygotic -12-15%,
Dizygotic -3%)
Increased frequency in first degree relatives.
The MHC-ClassII gene,HLA-DR4,is the
major susceptible haplotype.
Other- DR1 –indians ,DW15 –japanese.
6. Pathophysiology
Genetic ,epigenetic and environmental factors are implicated
in pathogenesis of RA.
Clinical onset- infiltration of synovial membrane with-
Lymphocytes ,
Plasma cell,
dendritic cell,
macrophages.
CD4+ lymphocytes,including Th1cells and Th17 cells play a
central role by interacting with other cells in the synovium.
7.
8. Proinflammatory cytokines act on
synovial fibroblasts, to promote
swelling of the synovial membrane
and damage to soft tissue cartilage.
Activation of osteoclasts and
chondrocytes drives destruction of
bone and cartilage.
The RA joint is hypoxic and promotes
neoangiogenesis.
9. The inflammatory granulation
tissue (Pannus) formed by the
above sequence of events
spreads over and under the
articular cartilage, which is
progressive eroded and
destroyed.
Later, fibrous or bony ankylosis
may occur.
Muscle adjacent to inflamed
joints atrophy may be
infiltrated with lymphocytes.
10.
11.
12. Clinical features
Highly variable.
Typical presentation is with pain, joint
swelling and stiffness affecting the small
joints of the hands, feet and wrist.
Sometimes- very acute onset, morning
stiffness, polyarthritis and pitting oedema.
13. Most common joint involved Include MCP,
PIP, wrist,MTP,ankle, elbow,shoulder,hip
DIP,sacroiliac and vertebral joints are spared
except atlantoaxial (C1-C2).
Myelopathy
16. Z deformity of the thumb.
Dorsal subluxation of ulna at distal radioulnar joint,
May cause rupture of 4th and 5th extensor tendons.
Triggering of fingers (d/t nodules in the flexor
tendon sheaths)
17.
18. ‘Cock up’ toe deformity (Dorsal subluxation
of MTP joint)
Secondary adventitious bursae and collosities.
19. In hindfoot , calcaneovalgus
(eversion)- damage to the ankle and
subtalar joint .
Flat foot – loss of longitudinal
rupture of tibialis posterior tendon.
