• Diagnosing and understanding psoriatic arthritis

    ARTICLE SUMMARY: Psoriatic arthritis is a form of arthritis often seen in psoriasis patients. It causes pain, swelling, and stiffness of one or more joints. Left untreated, it can cause permanent damage. So seeking diagnosis and treatment of psoriatic arthritis is very important.

    Psoriatic arthritis, as its name suggests, is a form of arthritis that occurs in people with psoriasis. Like other forms of arthritis, psoriatic arthritis (PsA) causes pain, swelling, and stiffness of the joints. The fingers, toes, and spine are common trouble spots. Over time, PsA can damage and deform affected joints, interfering with joint function. Most people who develop PsA have been living with the skin symptoms of psoriasis for years; however, in some cases psoriasis manifests itself in the joints at the same time as, or even before, it appears on the skin. Efforts to determine what percentage of psoriasis patients will also develop psoriatic arthritis have produced widely varying results – from 6% to 39%, depending on the population being studied and the study methods used. For those who are affected, PsA is a serious matter. Approximately 75% of PsA patients report that arthritis significantly disrupts their everyday lives; between 11% and 19% are severely disabled by the disease.

    Diagnosing psoriatic arthritis

    Not everyone who has psoriasis and arthritis has PsA. People with psoriasis can develop other types of arthritis, such as rheumatoid arthritis (RA) and osteoarthritis (OA), just like anyone else in the general population. Therefore, doctors must delve into the details of arthritic symptoms in psoriasis patients in order to correctly diagnose PsA and recommend optimal treatment.

    Characteristics of psoriatic arthritis

    PsA is an inflammatory, immune-based arthritis, meaning that the joint pain and swelling is caused by an inappropriate immune system response. Other psoriasis symptoms, such as skin plaques and nail disease, probably have the same underlying immunological cause. Nearly all patients with PsA currently have, or have a history of, skin psoriasis, although in a few cases arthritis develops first followed later by other psoriasis symptoms. Nail psoriasis is particularly common in patients with PsA. Scientists have identified more than two dozen genes (so far) that play a role in making people susceptible to psoriasis; several of these are also closely associated with psoriatic arthritis. So it appears psoriatic arthritis has a genetic, hereditary component.

    Some other common features of PsA include: arthritis of the joints nearest the tips of the fingers and toes, arthritis of the spine, inflammation of tendons and ligaments at the sites of attachment to the bones (enthesitis), and inflammation/swelling of one or more fingers or toes (dactylitis or “sausage digits”). When a joint on one side of the body is involved, the corresponding joint on the other side is not necessarily involved, a so-called asymmetric distribution of disease.

    X-ray or other imaging studies of PsA-affected joints can reveal erosion of bone, narrowing of the space inside the joint, and fusion of adjacent bones. Like psoriasis itself, psoriatic arthritis can be mild, moderate or severe; however, PsA can cause significant structural damage to the joints even in cases when pain and other external symptoms are relatively mild. This is one reason that treatment is so important, as modern treatments can slow or stop the progression of damage.

    PsA affects men and women in equal numbers. Finally, rheumatoid factor, a molecule found in the blood of most people with RA, is only rarely present in those with PsA.

    Differences between psoriatic arthritis and other types of arthritis

    Rheumatoid arthritis is also an inflammatory, immune-based arthritis and shares many similarities with PsA. In fact, both diseases respond to many of the same medications, especially the new biologic therapies that target the immune system. Two or three percent of patients with RA have psoriasis (about the same as the frequency of psoriasis in the general population), so there is potential for confusion of the two conditions. Unlike PsA, however, RA is nearly always associated with rheumatoid factor in the blood. Also, patients with RA are less likely to have back pain, enthesitis, and dactylitis, and are more likely to have a symmetrical distribution of arthritic joints.

    Osteoarthritis occurs when the protective cartilage inside joints is damaged or worn away by years of use. OA is extremely common in older people – 60% of people aged 65 or older have symptoms of OA – so statistically speaking, an older person with psoriasis and arthritis is more likely to have OA than PsA. Some features of OA and PsA overlap. The affected joints are usually asymmetrically distributed, and the finger and toe joints are often involved. However, patients with OA do not normally have spinal arthritis, enthesitis, or dactylitis, and many of the abnormalities seen in X-rays of PsA-affected joints, such as fusion of bones within the joint, are uncommon in OA. Because treatments available for the two conditions differ, it is important to accurately distinguish between them. For example, the biologic therapies that can produce dramatic improvements in PsA are not used to treat to OA.

    Psoriatic arthritis and the immune system

    A lot is still unknown about the biological processes responsible for psoriasis and PsA, but most researchers now agree that a class of immune cells called T cells is responsible for psoriasis symptoms in both skin and joints. T cells are essential for fighting off infection. Normally, T cells spring into action upon exposure to infectious agents such as bacteria and viruses. Some T cells stem the spread of viruses by killing virally infected cells. T cells also produce inflammatory cytokines, substances that support the immune response in a variety of ways including recruiting immune cells to sites of infection, promoting wound healing, and inducing fever. Once the infection is cleared, T cells are deactivated and inflammation subsides.

    For reasons that are not clear, T cells are chronically active in psoriasis patients. When activated T cells congregate in the skin, they give rise to skin plaques; when they lodge in the joints, they cause PsA. The initial trigger for T cell activation might be a bacteria or a virus, or it might be a component of the patient’s own skin cells (a so-called autoimmune reaction). Injury to the skin or joints may play a role. Genetic factors are also important. The molecules on the surface of T cells differ slightly from person to person, and particular subtypes of these molecules have been linked to a higher risk of developing psoriasis and PsA.

    In PsA, activated T cells take up residence inside the joints and cause persistent, painful inflammation. One of the cytokines released by T cells during this process, tumor necrosis factor alpha (TNF-alpha), appears to be particularly detrimental to the joints. TNF-alpha promotes breakdown of cartilage and bone and inhibits production of new bone. In addition, it helps newly activated T cells migrate to the joint, perpetuating the abnormal immune response. For these reasons, perhaps, therapies directed against TNF-alpha have proved to be very effective at relieving symptoms of PsA and slowing progressive joint damage.

    Treatment of psoriatic arthritis

    Treatment of PsA reflects the fact that the disease has elements in common with both skin psoriasis and RA. Optimal PsA treatment benefits from cooperation between dermatologists (experts in skin disease) and rheumatologists (experts in arthritis).

    [We are updating our information on treating psoriatic arthritis and will re-publish it shortly.]


    Selected References

    Furfaro, N. “Diagnostic Signs and Symptoms of Psoriatic Arthritis.” Dermatology Nursing. 2006 Oct;Suppl:7-9, 22.

    Gladman, DD. “Clinical, radiological, and functional assessment in psoriatic arthritis: is it different from other inflammatory joint diseases?” Annals of the Rheumatic Diseases. 2006 Nov;65 Suppl 3:iii22-4.

    Lee, MR and Cooper, AJ. “Immunopathogenesis of psoriasis.” Australasian Journal of Dermatology. 2006 Aug;47(3):151-9.

    Mease, P. “Current Treatment for Psoriatic Arthritis and Other Spondyloarthritides.” Rheumatic Disease Clinics of North America. 2006 Dec;32 Suppl 1:11-20.

    Soriano, ER and McHugh, NJ. “Therapies for Peripheral Joint Disease in Psoriatic Arthritis. A Systematic Review.” The Journal of Rheumatology. 2006 Jul;33(7):1422-30.

    Turkiewicz, AM and Moreland, LW. “Psoriatic Arthritis: Current Concepts on Pathogenesis-Oriented Therapeutic Options.” Arthritis & Rheumatism. 2007 Apr;56(4):1051-66.