Psoriatic Arthritis

Notes

Inflammatory Arthritis | Rheumatology | Seronegative Spondyloarthropathies

Overview

Psoriatic arthritis (PsA) is a chronic, immune-mediated inflammatory arthritis associated with psoriasis, affecting up to 30% of patients with skin psoriasis. It commonly presents in adults aged 30–50 years, with equal gender distribution. The disease is highly variable, involving peripheral joints, axial skeleton, entheses, and skin/nails. Delay in diagnosis is common and can result in irreversible joint damage.

Definition

Psoriatic Arthritis (PsA): Seronegative spondyloarthropathy associated with psoriasis, affecting joints, entheses, and axial skeleton.
Psoriasis Well-demarcated, erythematous plaques with silvery scale (often scalp, elbows, knees).
Enthesitis: Inflammation at tendon or ligament insertion sites into bone.
Dactylitis: Diffuse swelling of entire digits due to synovitis and tenosynovitis.
Pencil-in-cup deformity: Classic radiographic change due to erosive and proliferative joint damage in PsA.

Anatomy and Physiology

Aetiology and Risk Factors

Genetics: HLA-B27 (axial), HLA-Cw6 (psoriasis)
Family history of psoriasis or PsA
Psoriasis: particularly widespread, involving scalp, groin or nail involvement
Environmental triggers: trauma (Koebner phenomenon), infections
Obesity and smoking increase severity and risk

Nail psoriasis is a strong predictor of future PsA development.

Pathophysiology

Genetic predisposition → dysregulated immune response
Trigger (trauma/infection) leads to activation of dendritic cells, Th17 cells, and production of cytokines (IL-17, IL-23, TNF-α)
Leads to synovitis, enthesitis, osteitis, and bone proliferation and erosion
- Skin: Psoriasis involves the epidermis and dermis—keratinocyte hyperproliferation and inflammation
- Joints: PsA affects synovial joints (peripheral and axial)
- Entheses: Common sites include Achilles tendon, plantar fascia, patellar tendon
- Nail unit: Nail matrix and bed involvement results in pitting, onycholysis

PsA shows both destructive and proliferative bone changes—unique among inflammatory arthritides.

Clinical Manifestations

Peripheral arthritis:
Axial disease: Sacroiliitis, spondylitis (more asymmetric than AS). Can involve cervical or thoracic spine initially (unlike the classic SIJ in ankylosing spondylitis)
Enthesitis: Achilles, plantar fascia, costochondral junctions
Dactylitis
Psoriasis
Nails: Pitting, onycholysis, subungual hyperkeratosis
Anterior uveitis (less common)

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Nail involvement is often a marker of underlying DIP and enthesitis.

Diagnosis

CASPAR Criteria (ClASsification criteria for Psoriatic ARthritis):

Inflammatory articular disease (joint, spine, or entheseal) plus ≥3 points:

Psoriasis (current = 2 pts; personal/family history = 1 pt)
Nail dystrophy (1 pt)
Negative RF (1 pt)
Dactylitis (current or history, 1 pt)
Juxta-articular new bone formation on imaging (1 pt)

Investigations:

RF and anti-CCP: typically negative (seronegative)
CRP/ESR: may be elevated
Imaging:
- X-ray: joint space narrowing, erosions, new bone formation, pencil-in-cup deformity
- MRI: enthesitis, synovitis, sacroiliitis
Ultrasound: detects enthesitis and synovitis

Differential Diagnoses

Condition	Differentiating Feature
Rheumatoid arthritis	Symmetric, RF/anti-CCP positive, no nail/skin psoriasis
Osteoarthritis	DIP involvement but no dactylitis, no erosions
Gout	Monoarticular, crystals on aspiration
Ankylosing spondylitis	Younger males, bilateral sacroiliitis, no skin psoriasis

In patients with psoriasis and new joint symptoms, actively screen for PsA.

Treatment

Mild Disease

NSAIDs
Intra-articular corticosteroids

Moderate to Severe Disease (or with poor prognostic markers)

csDMARDs
- Traditional: Methotrexate, sulfasalazine, leflunomide (esp. for peripheral arthritis)
- Newer: Ampremilast (more so for skin) or Deucravacitinib
bDMARDs:
- TNF inhibitors: adalimumab, etanercept
- IL-17 inhibitors: secukinumab, ixekizumab
- IL-17 A/F inhibitor: Bimezikumab
- IL-12/23 inhibitor: ustekinumab
- IL-23 inhibitors: guselkumab
tsDMARDs: JAK inhibitors (e.g. upadacitinib, tofacitinib)

Lifestyle & Supportive

Weight loss, smoking cessation
Physical therapy, patient education

Biologics selection may depend on dominant phenotype (e.g. axial vs peripheral vs skin).

TNFaI can cause a paradoxical worsening of psoriasis.

Complications and Prognosis

Complications

Joint damage and deformity (may occur within 2 years of onset)
Reduced function and quality of life
Chronic pain and disability
Increased cardiovascular risk (due to systemic inflammation)

Poor prognostic factors:

High CRP
Polyarticular disease
Dactylitis
Nail disease
Early erosive changes

References

Mease PJ, Gladman DD, Papp KA, et al. Prevalence of rheumatologist-diagnosed psoriatic arthritis in patients with psoriasis in European/North American dermatology clinics. J Am Acad Dermatol. 2013;69(5):729–735.
Gossec L, Baraliakos X, Kerschbaumer A, et al. EULAR recommendations for the management of psoriatic arthritis with pharmacological therapies: 2019 update. Ann Rheum Dis. 2020;79(6):700–712.
Taylor W, Gladman D, Helliwell P, et al. Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arthritis Rheum. 2006;54(8):2665–2673.
Ogdie A, Weiss P. The epidemiology of psoriatic arthritis. Rheum Dis Clin North Am. 2015;41(4):545–568.