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Both psoriatic arthritis (PsA) and rheumatoid arthritis (RA) are inflammatory joint conditions with a wide variability of clinical features, and both may involve multiple systems of the body. Both may affect the eyes, the skin, the joints, and the cardiovascular system. However, their differences go deeper and they require different treatments with a clear divergence in the expected response to various specific modes of therapy and prognosis.
The diseases are similar in that patients with both conditions complain of joint pain, swelling and tenderness over the proximal interphalangeal joints of the fingers and the metacarpophalangeal joints (in 70% and 80% of PsA and RA respectively). The microscopy often shows symmetrical involvement of the synovial membrane in both cases, though asymmetrical joint involvement is also common in PsA.
PsA and RA show deep underlying differences, such as:
PsA is an inflammatory disease affecting a few joints of the spine, the sacroiliac joints, and the peripheral skeleton; RA characteristically shows peripheral joint involvement.
PsA typically has a less severe clinical picture than RA, but axial skeletal involvement including sacroiliac arthritis with a strong resemblance to ankylosing spondylitis is typical. Thus it is a spondyloarthropathy. DIP arthritis is characteristic in PsA, seen in 20-60% of patients.
The type of bone lesion in PsA is a cortical erosion of significant size with indistinct margins, often just outside the joint surface of the bone with evidence of new bone formation, whereas the RA lesion is well-defined and located at the joint margin.
PsA is characterized by enthesitis leading to entheseal osteogenesis with synovitis, compared to synovitis alone in RA as seen with MRI and micro-CT scanning.
The pathogenesis of the conditions is distinct, with PsA being part of the seronegative spondyloarthropathies, while RA shows the presence of rheumatoid factor (RF) or anti-citrullinated protein antibodies (ACPA) in circulation.
Systemic inflammatory response measured by the ESR or CRP rate is much less in PsA compared to RA. PsA is thus considered to be possibly an autoinflammatory disease due to inflammasome disturbance, while RA is an autoimmune disease.
The synovial tissue obtained by biopsy in PsA shows villous structures infiltrated by mononuclear cells and heavy angiogenesis, with increased expression of vascular endothelial growth factor (VEGF), angiopoietin 2 and basic fibroblast growth factor (BFGF). The blood vessels are thickened and the endothelial cells are swollen. The network is formed of elongated and tortuous vessels indicating that cells from existing vessels have proliferated, while in RA actual neovascularization occurs to form a branching network.
New vessels are actively formed within the synovial membrane of affected joints early in the course of the disease in PsA but later in the disease in RA.
T-lymphocyte infiltration is more common in PsA while RA shows a more prominent cellular infiltrate composed of both T and B cells with more marked synovial lining cell hyperplasia.
Genetic testing shows an increased propensity to PsA in patients with the HLA Cw6 and HLA B27 with the IL23 receptor, but to RA in patients with HLA DRB1.
Both PsA and RA respond to conventional DMARDs but TNF inhibitors induce remission in 60% of patients with PsA compared to 44% in RA. These drugs inhibit bone damage and relieve spinal symptoms as well as nail disease and dactylitis, which are seen in 25% and 20% of PsA patients, respectively. The spinal effect indicates that TNF inhibitors are best used early in PsA rather than DMARDs.
Other monoclonal antibodies directed against other molecules such as CD20 are effective in RA but not PsA because of the lack of autoimmune phenomena in the latter.
A fusion molecule targeting CTLA-4 (cytotoxic T-lymphocyte-associated protein 4) is equally effective in both conditions, indicating that the downregulation of activated T cells is important in relieving both these diseases.
The prognosis is usually better with PsA.
While PsA and RA appear to have many similarities, these are more superficial than their differences, which embrace the clinical picture, the immunological changes, and cellular and molecular phenomena. These are particularly obvious in relation to the autoimmune phenomena, vascular changes in the synovium and pattern of joint inflammation and new bone formation. The final differences are with respect to the specific therapy of each of these conditions.