Psoriatic arthritis

01Definition and overview

Psoriatic arthritis is a chronic inflammatory disease of the joints and entheses that occurs with psoriasis. It belongs to the spondyloarthritides, with ankylosing spondylitis and reactive arthritis: it is usually negative for rheumatoid factor, and it shares their enthesitis, sacroiliitis, uveitis and link to HLA-B27.

It is one disease with many faces. Clinicians now think of it as a set of domains, each assessed and treated in its own right: peripheral arthritis, axial disease, enthesitis, dactylitis, skin psoriasis and nail disease, with uveitis and inflammatory bowel disease as related conditions.

The Moll and Wright patterns

In 1973 Moll and Wright described five clinical patterns, still taught and still useful:

02Etiology and pathophysiology

Who gets it

Psoriatic arthritis runs strongly in families: a first-degree relative's risk is many times that of the general population. The genes differ in part from those of psoriasis alone:

• HLA-C*06:02, the main psoriasis gene, goes with early, extensive skin disease and, if anything, a longer delay before arthritis;
• HLA-B27 goes with axial disease, dactylitis and a shorter delay, and HLA-B*08, B*38 and B*39 with other joint patterns;
• variants in the IL-23 receptor and other genes of the IL-23 and IL-17 pathway, shared with ankylosing spondylitis and Crohn's disease.

Among people with psoriasis, the risk of arthritis is higher with severe psoriasis, nail disease, scalp and natal cleft or perianal psoriasis, obesity, and possibly after joint injury.

How it happens

1. 1

   The enthesis

   The disease probably begins where tendons and ligaments insert into bone, in the synovio-entheseal complex. Mechanical stress there, the so-called deep Koebner phenomenon, triggers local immune cells in a genetically primed host.
2. 2

   IL-23 and IL-17

   Myeloid cells release IL-23, which drives Th17 cells, gamma-delta T cells and innate lymphoid cells to make IL-17A, IL-17F and IL-22. With TNF, these inflame the synovium and the enthesis, and the same loop drives keratinocytes in the skin.
3. 3

   Bone lost

   TNF and IL-17 increase RANKL, and osteoclasts erode the bone at the joint margins and, in mutilans, resorb whole tufts and shafts.
4. 4

   Bone gained

   At the same time, osteoblasts are stimulated at the entheses and periosteum, laying down new bone: periostitis, spurs, syndesmophytes and ankylosis.

The nail is anchored to the extensor tendon enthesis of the distal joint, which is why nail disease and distal joint arthritis go together. Dactylitis is inflammation of the whole digit at once: tenosynovitis of the flexor tendon, synovitis of the small joints and soft tissue oedema.

03Clinical features

The joints, entheses and digits

• Peripheral arthritis: swollen, tender joints with morning stiffness, often less tender than they look and with a purplish skin over them; asymmetric and in a ray (all the joints of one digit) more often than in rheumatoid arthritis.
• Dactylitis, in up to half of patients at some time: a whole finger or, more often, toe swollen like a sausage. When tender it is active, and it predicts erosions in that digit.
• Enthesitis, in about a third or more: pain and tenderness at the Achilles insertion, the plantar fascia, the lateral epicondyles of the elbows and around the knee. It is hard to tell from the widespread tenderness of fibromyalgia, which often coexists.
• Axial disease, in a quarter to a half depending on how it is defined: inflammatory back or neck pain. Compared with ankylosing spondylitis it is often asymmetric, involves the cervical spine more, skips segments, is less painful and is less often HLA-B27 positive.

The skin and nails

Most patients have plaque psoriasis, often mild, and the skin must be looked for in hidden places: the scalp and hairline, behind the ears, the umbilicus, the natal cleft and perianal skin. Psoriatic nail disease affects about 80 per cent of patients with psoriatic arthritis, against fewer than half of those with psoriasis alone:

• pitting, small punched-out depressions of the nail plate;
• onycholysis, separation of the nail from its bed;
• subungual hyperkeratosis, scale piling up under the nail;
• oil-drop or salmon patches, and splinter haemorrhages.

Beyond the joints and skin

• The eye: uveitis, less common than in ankylosing spondylitis and, unlike it, more often insidious, bilateral and further back in the eye; conjunctivitis.
• The gut: Crohn's disease and ulcerative colitis are commoner, and subclinical gut inflammation is common.
• The cardiometabolic burden: obesity, the metabolic syndrome, type 2 diabetes, hypertension, gout and fatty liver disease, with a higher risk of myocardial infarction and stroke than in the general population.
• The mind: depression and anxiety are common and worsen pain and the patient's view of disease activity.

04Diagnosis and management

Finding it

People with psoriasis are asked about their joints at each review. In the UK, dermatologists and general practitioners use the Psoriasis Epidemiology Screening Tool (PEST), five yes-or-no questions, and refer to a rheumatologist when 3 or more are answered yes. The diagnosis is clinical, made by a rheumatologist, and supported by tests:

• CRP and ESR, raised in only about half, so a normal CRP does not exclude active disease;
• rheumatoid factor and anti-CCP, usually negative, though up to about 1 in 10 patients has one or the other;
• urate, often raised with psoriasis and obesity, because gout can mimic psoriatic arthritis or coexist with it;
• HLA-B27 when axial disease is suspected;
• aspiration of a single hot joint to exclude sepsis and crystals.

The CASPAR criteria

The Classification Criteria for Psoriatic Arthritis (2006) were made for research but serve well in the clinic. A patient with inflammatory articular disease (of the joints, spine or entheses) is classified as having psoriatic arthritis with 3 points or more:

They are about 99 per cent specific and 91 per cent sensitive, and a patient with no psoriasis of their own can meet them.

Imaging

• Plain X-rays of the hands and feet show erosions and new bone together: marginal erosions that deepen into the pencil-in-cup deformity, fluffy periostitis along the shafts, ankylosis of the distal joints, resorption of the terminal tufts (acro-osteolysis), and the absence of the periarticular osteopenia of rheumatoid arthritis.
• The spine and pelvis show asymmetric sacroiliitis and bulky, non-marginal syndesmophytes, often in the cervical spine.
• Ultrasound with power Doppler shows synovitis, tenosynovitis and enthesitis before X-ray changes; MRI shows sacroiliitis, spinal inflammation and bone oedema at entheses.

Assessing activity

Each domain is measured: 68 tender and 66 swollen joints, enthesitis at set sites (the Leeds Enthesitis Index), dactylitic digits, the skin as the Psoriasis Area and Severity Index (PASI) or the body surface area involved, the nails, function (the Health Assessment Questionnaire) and the patient's own view. Two composite targets are used:

• minimal disease activity, met when 5 of 7 criteria are achieved: tender joints 1 or fewer, swollen joints 1 or fewer, PASI 1 or less or body surface area 3 per cent or less, pain and patient global scores low, little disability, and 1 or fewer tender entheses;
• the DAPSA score, the sum of tender and swollen joint counts, pain, patient global assessment and CRP: 4 or less is remission and 14 or less low activity.

Treatment

Rheumatologist and dermatologist decide together when the skin is significant, and the patient shares the decision. Treatment aims at remission or, failing that, low disease activity, reviewed every 1 to 3 months: activity should be at least halved by 3 months and the target reached by 6, or treatment is changed. Exercise, physiotherapy, stopping smoking and losing weight help every patient.

1. 1

   Symptoms

   An NSAID relieves pain and stiffness, alone only in mild disease and for a short time. A corticosteroid injection settles a joint, a tendon sheath or an enthesis, avoiding the Achilles tendon, which can rupture. Oral steroids are no longer part of the European recommendations and help only selected patients, as a short bridge at the lowest dose: they add to the cardiometabolic risk, and the skin can flare as they are withdrawn.
2. 2

   A conventional DMARD

   For polyarthritis, or for oligoarthritis with poor prognostic factors (erosions, raised CRP, dactylitis, nail disease), a conventional DMARD is started promptly. Methotrexate, 15 to 25 mg once a week with folic acid, is preferred when the skin is significant; sulfasalazine and leflunomide are alternatives. They do not help axial disease or enthesitis alone.
3. 3

   A biologic

   If the target is not reached with at least one conventional DMARD, a biologic DMARD is added or substituted. For the joints, European recommendations prefer no one class; the choice follows the other domains. Enthesitis and axial disease that persist despite NSAIDs go straight to a biologic.
4. 4

   A JAK inhibitor

   After at least one biologic, or when a biologic is not appropriate, a JAK inhibitor may be used, with the safety restrictions below.
5. 5

   Switching

   If a biologic or JAK inhibitor fails or is not tolerated, another is tried, including one more of the same class. In sustained remission, the dose can be cautiously tapered.

Choosing the mode of action, by European and GRAPPA recommendations:

The drugs and what to watch:

Before a biologic or JAK inhibitor, patients are screened for latent tuberculosis, hepatitis B and C and HIV, and their vaccines are brought up to date; the details are in the biologic drugs topic.

Since 2023, the European Medicines Agency has advised that JAK inhibitors be used in people aged 65 or over, current or past long-term smokers, and those at increased risk of major cardiovascular events or cancer only when no suitable alternative exists, and with caution in anyone at risk of venous thrombosis. Deucravacitinib, an oral TYK2 inhibitor used for skin psoriasis, was licensed for psoriatic arthritis in 2026 in the United States and the EU, after a DMARD has failed; it came after the 2023 European recommendations, which do not place it. Hydroxychloroquine is generally avoided, because it can worsen psoriasis. Joint replacement, or fusion of a destroyed small joint, is needed in a minority.

05Epidemiology

Psoriasis affects about 2 to 3 per cent of Europeans, and about 1 in 5 of them has psoriatic arthritis, more in hospital clinics than in the community. In the population as a whole, it affects roughly 1 to 2 people in 1000. Men and women are affected equally, although axial disease is commoner in men and polyarthritis in women. It usually starts between 30 and 50, on average about ten years after the psoriasis. Many patients attending dermatology clinics have undiagnosed arthritis, which is why screening matters.

06Prognosis

Psoriatic arthritis is not the mild disease it was once thought to be. In an early-arthritis clinic, about half of patients had erosions after two years despite the conventional DMARDs of the time, and a delay of more than six months before seeing a rheumatologist is linked to more erosions and worse function. Polyarthritis, raised inflammatory markers, dactylitis, nail disease, early erosions and many previous treatments predict progression. Arthritis mutilans, though rare, disables.

Biologics and targeted drugs have changed the outlook: many patients now reach minimal disease activity, and the drugs that block TNF, IL-17 and IL-23 slow radiographic damage. Cardiovascular risk is raised, so blood pressure, lipids, glucose, weight and smoking are managed as part of the arthritis; older clinic series found a shorter life, but a large population study found no clear excess mortality overall. Depression, fatigue and the visible skin disease weigh on quality of life, and are asked about at every review.