Aetiology
The aetiology of psoriatic arthritis (PsA) is largely unknown. PsA is a spondyloarthritis.
Hereditary/genetic factors
People who have a first-degree relative with PsA are 40 times more likely to develop the disease.[10] PsA is polygenic, with more than 40 risk genes encompassing functional elements in the innate and adaptive immune systems as well as tissue repair genes.[11]
Psoriatic disease genetics are far more complicated than simply a relationship to the human leukocyte antigen (HLA)-B27 gene. Genetic links to the major histocompatibility complex (MHC) class 1 alleles at the HLA-B and HLA-C loci have been identified for both psoriasis and PsA.[10] HLA-B genes generally contribute to musculoskeletal manifestations, while HLA-C genes are associated with skin manifestations.[10]
The associations are complex, with certain HLA alleles found to be associated with specific symptom combinations, such as HLA-B*27:05 with enthesitis, dactylitis, and symmetrical sacroiliitis and HLA-B*08:01-HLA-C*07:01 with joint fusion, deformities, asymmetrical sacroiliitis, and dactylitis.[12] Key non-HLA genes associated with PsA include those involved in the nuclear factor kappa B pathway (e.g., tumour necrosis factor [TNF]-alpha induced protein 3) and the T helper 17 cell pathway (e.g., interleukin [IL]-13 and IL-23R).[10][12] Epigenetic mechanisms such as DNA methylation can also contribute to the development of PsA.[10]
Joint or tendon trauma
Trauma to joints or tendons has been implicated in triggering PsA.[13][14]
Infection
Infections (particularly HIV infection and streptococcal infection) possibly trigger PsA by exposing antigens to the innate immune system and leading to expression of the psoriatic phenotype.[12][15]
Smoking
Smoking increases the risk of developing psoriasis in the general population, whereas the relationship is unclear in PsA.[12][16]
Immune system dysfunction
Patients with PsA have been shown to have an altered gut microbiome compared with controls, and it is thought that these changes could potentially be linked with immune system dysfunction.[12]
Pathophysiology
Psoriatic disease (i.e., psoriasis and PsA) is a multifactorial chronic inflammatory disease, the cause of which is still unknown. Genetic factors, environmental factors, and an aberrant immune response may contribute to its pathogenesis.[17][18]
Evidence suggests that psoriatic disease may be maintained by the adaptive immune system; both CD4+ and CD8+ T cells play a contributing role in both the skin and the synovium.[19][20][21][22]
Angiogenesis and endothelial cell dysfunction are early changes that result in the infiltration of immune cells to synovial tissues.[12]
Dendritic cells are thought to play a key role in antigen presentation and activating the adaptive immune response, with activated immune cells releasing a range of pro-inflammatory cytokines, such as tumour necrosis factor (TNF), interferon gamma, and interleukins 23, 17, and 22.[12]
These cytokines activate local cells, such as fibroblasts, chondrocytes, osteoblasts, and osteoclasts, which release matrix-degrading enzymes and the receptor activator of nuclear factor kappa B ligand (RANKL).[12]
Local cells also release further pro-inflammatory substances, creating a continuous cycle of inflammation, which causes the synovitis, enthesitis, cartilage damage, and bone erosions observed in PsA.[12]
Classification
Moll and Wright classification[1]
Five patterns of psoriatic arthritis:
Distal interphalangeal joint (DIP) arthritis
Asymmetrical oligoarthritis
Symmetrical polyarthritis
Arthritis mutilans
Psoriatic spondylitis with sacroiliac and spinal involvement.
CASPAR (classification criteria for psoriatic arthritis)[2]
Inflammatory articular disease (joint, spine, or entheseal) with ≥3 points from the following 5 categories (current psoriasis score 2 points; all others 1 point):
Evidence of current psoriasis, a personal history of psoriasis, or a family history of psoriasis in a first- or second-degree relative
Typical psoriatic nail dystrophy
A negative test for rheumatoid factor (not the latex test)
Either current or historical dactylitis
Radiographical evidence of juxta-articular new-bone formation appearing as ill-defined ossification near joint margins (periostitis) on plain films of the hand or foot.
These classification criteria are used for epidemiological and research studies.
Use of this content is subject to our disclaimer