How Psoriatic Arthritis and Rheumatoid Arthritis Differ

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Psoriatic arthritis (PsA) and rheumatoid arthritis (RA) are both autoimmune diseases that affect the joints. Both are inflammatory and progressive—causing joint stiffness, pain, and swelling, as well as persistent fatigue. In addition, both occur in flares and can be treated with medications that suppress the immune system.

However, PsA and RA are different diseases that are diagnosed with different methods, and they also require different therapeutic approaches.

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With PsA, the joint symptoms are tightly linked to inflammation of the skin from psoriasis (an autoimmune disorder targeting skin cells). With RA, the immune system primarily targets joint tissue.


Both diseases can cause destruction of the small joints in the hands and feet, as well as the larger joints of the knees, hips, shoulders, and spine. One of the main differences between PsA and RA is the distribution of affected joints.

Pattern of Joint Involvement

PsA often causes enthesitis, which is inflammation where tendons insert onto bones (such as the Achilles' tendon). This is not seen with RA.

The symmetry of joint involvement differs between these conditions:

  • With PsA, the pattern of joint involvement is often asymmetrical—the joints affected on one side of the body will not necessarily be affected on the other. Only 15% of people with PsA will have symmetrical arthritis, a condition considered more advanced and severe than asymmetrical arthritis.
  • The pattern with RA is characteristically symmetrical—the same joints on both sides of the body are affected.

Spine Involvement

Another notable difference between PsA and RA is the involvement of the spine.

  • RA will usually be limited to the cervical spine (the neck bones).
  • PsA will often manifest with arthritis in the axial spine (the backbones).
  • PsA will also affect the sacroiliac joints in the low back, where RA does not.

It is for this reason that PsA is included in the body of disorders called spondyloarthropathies and RA is not.

Bone Damage

Of the two diseases, RA has the potential to be more severe.

  • Bone erosion is a central feature of RA, which causes localized and irreversible bone loss (osteolysis), as well as joint disfigurement and the loss of joint function.
  • With PsA, the effect on the bones tends to be far less profound. Much of the bone loss in PsA is limited to the distal phalanges (the finger and toe bones nearest the fingernails or toenails).

It is only with an uncommon form of PsA (called arthritis mutilans) that joint disfigurement can develop rapidly and severely.

Fingers, Toes, and Skin

Another telling clue is the presentation of the disease on the fingers and toes.

  • With PsA, the distal joints (those nearest the nails) will be the focus of pain, swelling, and stiffness.
  • RA primarily involves the proximal joints (those situated just above the knuckles).

With severe PsA, the fingers can also take on a sausage-like appearance (called dactylitis), making it difficult to ball your fist. While this can occur with RA, it is not the hallmark that it is with PsA.

Around 85% of people with PsA also have plaque psoriasis, characterized by dry, flaky skin plaques. Half will have nail psoriasis at the time of their diagnosis.


Autoimmune diseases are conditions in which the immune system attacks normal cells and tissues. When immune cells and antibodies target a person's own body, they are referred to as autoantibodies.

Although PsA and RA both affect the joints, the targets of the autoimmune reaction differ.

Rheumatoid Arthritis

With RA, the primary target of the autoimmune assault is the joints, most specifically the synoviocytes, which are cells in the lining of the joint. The ensuing inflammation causes synoviocytes to proliferate excessively.

A cascade of events includes;

  • Thickening of the joint lining (synovial hyperplasia)
  • Infiltration of cytokines (a type of inflammatory proteins) into the joints
  • Progressive destruction of joint cartilage, bone, and tendons

Psoriatic Arthritis

With PsA, the immune system targets keratinocytes, which are a type of skin cell. When this occurs, the cells proliferate at an accelerated rate, leading to the development of psoriasis in most (but not all) cases.

Over time, inflammation can strike other parts of the body, such as the nails, eyes, and the gut. When the joints and surrounding tissues are affected, it’s called PsA.

Although synovial hyperplasia is also characteristic of PsA, it tends to be less severe than with RA. 

Researchers have not determined whether psoriasis and PsA are two distinct diseases with different genetic or environmental causes or whether PsA and psoriasis are one disease better classified under the unified title psoriatic disease.


Healthcare providers have tests, tools, and diagnostic criteria needed to make a definitive diagnosis of RA, but this is not the case for PsA.

It is possible to have psoriasis and RA, without a diagnosis of PsA. The distinction would be diagnosed based on a physical examination, laboratory tests, and diagnostic imaging.

Rheumatoid Arthritis

If you have signs and symptoms of RA, your healthcare provider will order tests to see if the results meet the diagnostic criteria established by the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR):

  • Autoantibody blood tests: Rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) autoantibodies are found in the majority of people with RA.
  • Inflammatory blood markers: C-reactive protein (CRP) and erythrocyte sedimentation (ESR), which measure inflammation, are often elevated in RA.
  • Imaging tests: An X-ray or magnetic resonance imaging (MRI) may identify bone erosion and narrowing of the joint space.

The results of the tests—as well as the duration, location, and severity of symptoms—are scored on the ACR classification system. A cumulative score of 6 or greater (of a possible 10) offers a high degree of confidence that RA is the cause of your symptoms.

Psoriatic Arthritis

Unlike RA, PsA is mainly diagnosed with a physical exam and a review of your medical history. There are no blood tests or imaging studies that can definitively diagnose the disease.

Your healthcare provider will look for clues that are strongly indicative of PsA, including:

  • Asymmetrical joint involvement
  • Skin involvement
  • Nail involvement
  • A family history of PsA and/or psoriasis
  • Instigating factors known to trigger the disease, including strep infections, certain medications, and cold, dry weather exposure

An X-ray or MRI may identify a "pencil-in-a-cup" deformity, in which the tip of the finger looks like a sharpened pencil, and the adjacent bone is worn down to a cup-like shape. This deformity affects around 5% to 15% of people with PsA, usually in the more advanced stages of the disease.

If the skin is affected, a skin biopsy can provide strong evidence of PsA and help differentiate it from other chronic skin conditions.

Other lab and imaging tests are used mainly to exclude other possible causes rather than to confirm PsA.

Other conditions that are often in the differential diagnosis of PsA include:


Exercise, weight loss, and smoking cessation are considered standard facets of treatment for both RA and PsA. Mild to moderate symptoms are commonly treated with over-the-counter or prescription-strength nonsteroidal anti-inflammatory drugs (NSAIDs).

Other treatments are tailored to the specific condition.


Corticosteroids are a type of drug used to temper inflammation. Prednisone is the most commonly used corticosteroid, and when used for the treatment of RA or PsA, it is typically used either in pill form or injected into a joint to provide short-term relief.

  • With PsA, corticosteroids are sometimes used during acute flares when symptoms are severe. However, they are used with caution, as they can trigger a severe form of psoriasis known as Von Zumbusch pustular psoriasis or erythroderma, a complication that can be life-threatening.
  • With RA, low-dose corticosteroids are often prescribed in combination with other drugs. To avoid side effects, they are only used short-term. Corticosteroids can also be injected into a joint to treat acute pain.

Disease-Modifying Antirheumatic Drugs (DMARDs)

Disease-modifying antirheumatic drugs (DMARDs) like methotrexate and Arava (leflunomide) are effective in managing both RA and PsA. Although there is a wealth of evidence supporting their use in treating RA, their effectiveness in people with PsA is far less conclusive.

Methotrexate (considered the first-line DMARD for many autoimmune disorders) is approved for the treatment of psoriasis, but not PsA. With that being said, it is frequently used off-label for treating PsA.

TNF Inhibitors

TNF inhibitors are biologic drugs that block tumor necrosis factor (TNF), an immune protein. While TNF plays a role in both PsA and RA, its mechanism of action is more central to treating the damage caused by PsA, and TNF inhibitors tend to work better in people with PsA than RA.

According to a 2011 study from Denmark, 60% of people with PsA achieved sustained remission while on TNF inhibitors compared to only 44% of those with RA.

TNF inhibitors commonly used in the treatment of PsA and RA are Enbrel (etanercept), Humira (adalimumab), and Remicade (infliximab).

Timing of Treatment

Generally speaking, RA is treated at the time of diagnosis to prevent irreversible bone erosion and osteolysis that can develop within a span of two years. Early aggressive treatment is especially important for those who are likely to develop severe RA based on testing outcomes.

PsA, unlike RA, may only need to be treated when symptoms arise. When the symptoms subside or the disease is in remission, it may be possible to take a break from treatment. However, if PsA is accompanied by moderate to severe psoriasis, ongoing treatment (including methotrexate, biologics, or a combination of therapies) may be prescribed to benefit both conditions.

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9 Sources
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  1. Sankowski AJ, Lebkowska UM, Cwikła J, Walecka I, Walecki J. Psoriatic arthritis. Pol J Radiol. 2013;78(1):7-17. doi:10.12659/PJR.883763

  2. Schett G, Gravallese E. Bone erosion in rheumatoid arthritis: mechanisms, diagnosis and treatment. Nat Rev Rheumatol. 2012;8(11):656-664. doi:10.1038/nrrheum.2012.153

  3. Girolomoni G, Gisondi P. Psoriasis and systemic inflammation: underdiagnosed enthesopathy. J Eur Acad Dermatol Venereol. 2009;23 Suppl 1:3-8. doi:10.1111/j.1468-3083.2009.03361.x

  4. Menter A. Psoriasis and Psoriatic Arthritis Overview. Am J Manag Care. 2016;22:S216-S224.

  5. Aletaha D, Neogi T, Silman AJ, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum. 2010;62(9):2569-81. doi:10.1002/art.27584

  6. Haddad A, Johnson SR, Somaily M, et al. Psoriatic Arthritis Mutilans: Clinical and Radiographic Criteria. A Systematic Review. J Rheumatol. 2015;42(8):1432-1438. doi:10.3899/jrheum.141545

  7. Li P, Zheng Y, Chen X. Drugs for Autoimmune Inflammatory Diseases: From Small Molecule Compounds to Anti-TNF Biologics. Front Pharmacol. 2017;8:460. doi:10.3389/fphar.2017.00460

  8. Glintborg B, Østergaard M, Dreyer L, et al. Treatment response, drug survival, and predictors thereof in 764 patients with psoriatic arthritis treated with anti-tumor necrosis factor α therapy: results from the nationwide Danish DANBIO registry. Arthritis Rheum. 2011;63(2):382-90. doi:10.1002/art.30117

  9. Heidari B. Rheumatoid Arthritis: Early diagnosis and treatment outcomes. Caspian J Intern Med. 2011;2(1):161-170.

Additional Reading

By Carol Eustice
Carol Eustice is a writer covering arthritis and chronic illness, who herself has been diagnosed with both rheumatoid arthritis and osteoarthritis.