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Psoriatic arthritis (PSA), also called psoriatic spondylitis, is a type of inflammatory arthritis. PsA occurs in about one-third of people with psoriasis, causing pain and inflammation in joints throughout the body. The causes of PsA are not fully understood, but researchers have identified several genetic and environmental risk factors.
PsA is an autoimmune disease, meaning the body’s immune system mistakenly attacks healthy cells and tissues as if they were viruses or bacteria. In PsA, the immune system attacks the ligaments and joints, leading to inflammation and damage.
PsA is part of a family of related autoimmune disorders collectively called spondylitis, or spondyloarthritis.
The cause of PsA is not understood. However, rheumatologists and researchers believe that the onset of PsA can be triggered by a combination of biological and environmental factors.
Research has identified genetic factors associated with the development of PsA. Like other types of spondyloarthritis, PsA has been linked to specific variations on certain inherited genes — such as HLA-B27 — that are involved in the immune system. Researchers have identified several such genes.
An abnormal immune response is responsible for causing symptoms of all types of inflammatory arthritis. They can involve a variety of inflammatory mediators, substances in the body that promote inflammation.
T cells, a type of immune cell, are heavily involved in PsA. These cells release proteins called cytokines — chemical messengers that stimulate inflammation. This inflammation causes joint swelling, pain, and damage. Studies show that higher numbers or activity of these T cells and the cytokines they release are linked to PsA symptoms and severity.
Many treatments for PsA specifically target these immune responses. Many biologic disease-modifying antirheumatic drugs (DMARDs) work by helping control the immune response in PsA.
Drugs such as abatacept (sold as Orencia) work by controlling T cell activity, turning down the immune response mediated by T cells and cytokines. Other biologic drugs inhibit tumor necrosis factor (TNF), a potent proinflammatory cytokine. TNF inhibitors include drugs such as adalimumab (Humira), etanercept (Enbrel), and infliximab (Remicade).
Other biologics used to treat PsA, such as secukinumab (Cosentyx) and ustekinumab (Stelara), target a type of cytokines called interleukins.
A newer class of biologics, called Janus kinase (JAK) inhibitors, are also being used to treat PsA. Drugs such as upadacitinib (Rinvoq) and tofacitinib (Xeljanz) treat PsA by blocking the action of a variety of pro-inflammatory cytokines.
Research has found that certain infections may contribute to the development of PsA.
In particular, infection with Streptococcus pyogenes, which causes strep throat, seems to correlate with increased PsA risk. Other infections believed to trigger PsA include the sexually transmitted disease chlamydia and bacteria that cause infectious diarrhea, including species of Campylobacter and Yersinia.
Several viral infections may possibly be linked to PsA development, including HIV and hepatitis C. Viruses believed to cause rheumatoid arthritis may also cause PsA, including parvovirus B19, cytomegalovirus, and Epstein-Barr virus.
Other environmental factors that may potentially cause PsA include physical trauma and injuries as well as certain work-related physical activities.
People with psoriasis can experience what is known as the Koebner phenomenon. This phenomenon causes new skin lesions to appear at the site of skin injuries, including scratches, cuts, and burns. Even minor injuries can induce a mild immune response, but in susceptible individuals, this can cause new autoimmune lesions to appear.
This Koebnerization effect also appears to affect tissues such as tendons in people with PsA. This may explain how work-related PsA develops. Research has found that people who work in jobs that involve repeated heavy lifting (100 pounds per hour or more) and pushing heavy loads (more than 200 pounds per hour) are more likely to develop PsA.
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Many risk factors have been associated with PsA. Additional research is needed, however, to determine why and how they contribute to disease.
Psoriasis, a skin condition characterized by scaly lesions (plaques), is the most significant risk factor for PsA. However, people without skin psoriasis can also develop PsA. According to the National Psoriasis Foundation, PsA develops in nearly 30 percent of people with psoriasis, most commonly about 10 years after skin symptoms arise. In approximately 10 percent to 15 percent of people, PsA symptoms begin before skin psoriasis develops.
People with more severe psoriasis have a higher risk of PsA. People with psoriasis lesions or plaques on their nails (nail pitting), scalp, or genital region are also more likely to develop PsA.
PsA runs in families. Nearly 40 percent of people with PsA have a family member with psoriasis or arthritis, according to the American College of Rheumatology. Combined with the known association between PsA and certain inherited genes, this supports the assertion that genetics play a significant role in the development of PsA.
PsA is significantly more prevalent in white people, according to the Arthritis Foundation. However, studies have shown that Asian and Hispanic people tend to present with more extensive and severe PsA. Additionally, research has found that Pakistani populations have a higher risk of developing PsA based on family history, even higher than white populations.
People of any sex are equally likely to develop PsA. Some studies have suggested a link between hormones and PsA, but no definite connection has been proven.
PsA can occur at any age. PsA usually appears between the ages of 30 and 50, although children with psoriasis are also at risk.
Other environmental risk factors for PsA include:
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Ariel D. Teitel, M.D., M.B.A. is the clinical associate professor of medicine at the NYU Langone Medical Center in New York. Review provided by VeriMed Healthcare Network. Learn more about him here.
Kristopher Bunting, M.D. studied chemistry and life sciences at the U.S. Military Academy, West Point, and received his doctor of medicine degree from Tulane University. Learn more about him here.
