Psoriasis of the joints: symptoms, diagnosis and treatment

Psoriatic arthritis is a chronic inflammatory disease of the joints and entheses in people with psoriasis or a family history of it. It is a heterogeneous condition: some patients present with predominantly peripheral arthritis and dactylitis, others with spinal and sacroiliac joint involvement, and still others with severe nail involvement and enthesitis. Early recognition is critical: structural damage with functional loss is possible already in the first few years, and timely treatment using a "treat-to-target" strategy reduces inflammatory activity and the risk of irreversible changes.

The diagnosis is established based on a combination of clinical findings, imaging data, and CASPAR classification criteria. A domain-specific approach to assessing disease activity and considering comorbid conditions that influence management are important for practice: heart disease, metabolic syndrome, inflammatory bowel disease, and uveitis. This applies not only to joints, but to systemic inflammation, which requires multidisciplinary management. [1]

Modern pharmacotherapy encompasses not only tumor necrosis factor inhibitors but also drugs that interfere with the interleukin-17 and interleukin-23 axis, as well as Janus kinase inhibitors. The choice is based on the lesion domain, risk factors, and patient preferences, with validated scales used. [2]

ICD-10 and ICD-11 codes

In the International Classification of Diseases, Tenth Revision, psoriatic arthritis is coded in block L40 as "psoriatic arthropathy," with additional subcategories for the variant of overshoot. Clinical documents most often use L40.5 and its additional subcategories.

In ICD-11, psoriatic arthritis is classified as a disease of the musculoskeletal system and connective tissue: the basic code is FA21, with additional code details to clarify the variant and domains. When creating the entry, it is important to accurately indicate the presence of cutaneous psoriasis, enthesitis, dactylitis, and axial lesions.

Table 1. Codes for medical documentation

System	Code	Name
ICD-10	L40.5	Psoriatic arthropathy
ICD-10	L40.50-L40.59	Clarifying variants of psoriatic arthropathy
ICD-11	FA21	Psoriatic arthritis
ICD-11	FA21.Y	Other specified variants of psoriatic arthritis
ICD-11	FA21.Z	Psoriatic arthritis, unspecified

Epidemiology

Prevalence in the general population is estimated to be between 0.05-0.25%. Among people with psoriasis, the proportion with clinically confirmed arthritis in meta-analyses varies from approximately 6% to 41%, with median estimates often in the range of 20-30%. Rates are influenced by screening methodology and inclusion criteria. [3]

The average age of onset is 30-50 years. The gender distribution is nearly equal, although males are more common with the axial phenotype. In some patients, arthritis precedes skin manifestations or develops when they are minimally expressed, complicating early diagnosis. [4]

A delay in diagnosis of 1–2 years is associated with higher activity and worse functional outcomes, highlighting the value of proactive screening in patients with psoriasis, particularly those complaining of back pain, dactylitis, morning stiffness, or nail changes.[5]

Reasons

Psoriatic arthritis is an immune-inflammatory disease, influenced by genetic predispositions and environmental triggers. Key immune pathways are associated with the interleukin-23 and interleukin-17 axis, as well as tumor necrosis factor (TNF) and T-cell responses.

Genetic markers include variants of the major histocompatibility complex and non-HLA associations. HLA-B27 is often considered for the axial phenotype, although its prevalence is lower than in ankylosing spondylitis. Individual HLA clusters are associated with specific phenotypes, such as polyarthritis or enthesitis. [6]

Risk factors

The risk of developing arthritis is higher in cases of severe skin lesions, nail lesions, and scalp lesions. Nail changes are considered a predictor of arthritis development due to their anatomical proximity to the extensor enthesis of the distal phalanx. [7]

Risk factors include obesity and metabolic syndrome, which are associated with higher inflammatory activity and a lower likelihood of achieving remission. A family history of psoriasis or arthritis and the presence of chronic inflammation are also important. [8]

Pathogenesis

Innate and adaptive immunity play a leading role in entheses, with mechanical stress acting as an initiating factor. Interleukin-23 activates T cells that produce interleukin-17, which sustains inflammation in the entheses, synovium, and skin. This explains the effectiveness of targeted drugs targeting the interleukin-23 and interleukin-17 axis.

Neuroimmune and microbiome signals modify inflammation, and systemic elevation of proinflammatory cytokines contributes to cardiometabolic complications. Structural changes are determined by the simultaneous coexistence of erosions and new bone proliferation. [9]

Symptoms

Typical symptoms include chronic joint pain and swelling, morning stiffness lasting more than 30 minutes, tenderness upon palpation of the entheses, diffuse "sausage-shaped" thickening of the finger, and lower back pain with morning stiffness in the axial variant. Fatigue and decreased performance are often noted. [10]

Nail lesions in the form of pitting, onycholysis, or subungual hyperkeratosis are not only a marker of the disease but also a risk factor for its development. The combination of skin plaques with dactylitis or enthesitis should raise concern, even with normal laboratory results. [11]

Classification, forms and stages

The classical clinical classification, dating back to Moll and Wright, identifies five phenotypes: distal interphalangeal predominant, asymmetric oligoarthritis, symmetric polyarthritis, spondylitic variant, and arthritis mutilans. Within a single patient, the phenotype may change over time. [12]

Modern practice relies on a "domain" approach: peripheral arthritis, enthesitis, dactylitis, skin and nail psoriasis, and axial skeleton. This facilitates treatment selection and goal setting. Severity is assessed based on the overall activity index and the achievement of minimal disease activity.

Table 2. Clinical domains influencing therapy choice

Domain	Examples of manifestations	What changes in tactics
Peripheral joints	Oligoarthritis, polyarthritis	Choice of basic therapy and targeted agents
Enthesitis	Achilles tendon, plantar fascia	Consideration of interleukin-17 inhibitors
Dactylitis	Sausage finger	Marker of activity and poor prognosis
Axial skeleton	Inflammatory back pain	Priority of tumor necrosis factor and interleukin-17 inhibitors
Skin and nails	Plaques, onycholysis	Efficacy against skin manifestations

Complications and consequences

Without treatment, erosions, deformations, joint fixation, and disability are possible. In the axial variant, mobility is limited, syndesmophytes form, pain, and sleep disturbances occur. Some patients develop arthritis mutilans with "telescopic" fingers. [13]

Systemic inflammation increases cardiometabolic risks: arterial hypertension, dyslipidemia, obesity, type 2 diabetes, and premature cardiovascular events. This necessitates active screening for risk factors and their correction. [14]

When to see a doctor

Reasons for an urgent consultation with a rheumatologist include joint pain and swelling with morning stiffness lasting more than 30 minutes in a person with psoriasis or a family history, dactylitis, tenderness of the entheses, inflammatory back pain, or a rapid decline in hand or foot function. The shorter the interval from onset to the start of therapy, the higher the chance of controlling the disease. [15]

Immediate referral is required in cases of severe pain with fever and monoarthritis to rule out septic arthritis, acute eye symptoms to rule out uveitis, and severe back pain with neurological deficit.

Diagnostics

The initial evaluation includes a medical history, skin and nail examination, counting tender and swollen joints, entheseal and dactylitis assessment, pain scales, and functional questionnaires. Laboratory markers of inflammation assist in monitoring but may be normal. Rheumatoid factor and anti-cyclic citrullinated peptide antibodies are usually negative. [16]

Imaging is aimed at identifying synovitis, enthesitis, and sacroiliitis. X-rays help document erosions and juxta-articular bone proliferation. Ultrasound improves accuracy in enthesitis and dactylitis. Magnetic resonance imaging is useful for the early detection of inflammation in the sacroiliac joints and spine. [17]

The CASPAR classification criteria are used to standardize the diagnosis: inflammatory lesions of the joints, spine, or entheses plus 3 points from a set of features. In the early stages, sensitivity is somewhat lower than in established disease, but remains clinically acceptable. [18]

Table 3. CASPAR criteria, quick reference

Category	Points
Current psoriasis	2
History of psoriasis or family history of psoriasis	1
Nail dystrophy	1
Negative rheumatoid factor	1
Dactylitis, past or present	1
X-ray evidence of new bone at the joint edges of the hands or feet	1

Table 4. Visualization: what and when to prescribe

Problem	Method	What are we looking for?
Suspected enthesitis	Doppler ultrasound	Hypoechogenicity, thickening, blood flow at the enthesis
Dactylitis	Ultrasound	Tenosynovitis, synovitis of the finger joints
Early sacroiliitis	Magnetic resonance imaging	Bone marrow edema, synovitis, erosions
Structural changes in the hands and feet	X-ray	Erosions and juxta-articular new bone, "pencil in a glass"

Differential diagnosis

It is necessary to differentiate from rheumatoid arthritis, especially in cases of symmetrical polyarthritis of the hands. The absence of pronounced periarticular osteoporosis, the combination of erosions with periosteal proliferation and enthesitis, as well as a distal interphalangeal pattern and "radial" lesions of one finger in its entirety, all support the diagnosis of psoriatic arthritis. [19]

Gout and crystal arthropathies, reactive arthritis, osteoarthritis with an erosive component, ankylosing spondylitis, and septic arthritis should be excluded. Crystalloscopy data, cultures, and the nature of the lesion on imaging are taken into account. [20]

Table 5. How psoriatic arthritis differs from rheumatoid arthritis

Sign	Psoriatic arthritis	Rheumatoid arthritis
Serology	Often seronegative	Often seropositive
Visualization	Erosions plus bone proliferation	Erosions without proliferation
Pattern	Distal interphalangeal joints, "ray" of the finger, dactylitis	Mainly metacarpophalangeal and proximal interphalangeal
Nails, skin	Often involved	Not typical

Treatment

Basic measures include education, weight management, smoking cessation, and physical activity under the guidance of a specialist. Nonsteroidal anti-inflammatory drugs help relieve pain and stiffness but do not prevent structural progression. Intra-articular glucocorticosteroids are administered locally, avoiding long-term systemic courses.

For active peripheral arthritis, synthetic disease-modifying agents are recommended: methotrexate, leflunomide, and sulfasalazine. They are effective against synovitis but less effective against enthesitis and dactylitis. If the response is insufficient or there are unfavorable prognostic signs, targeted agents are used.

Targeted biologics include tumor necrosis factor inhibitors and agents targeting the interleukin-17 and interleukin-23 axis. In recent years, their indications have expanded: bimekizumab has received approval for psoriatic arthritis in major regions. Interleukin-23 inhibitors, such as guselkumab and risankizumab, are available, including for concomitant intestinal inflammation. The choice depends on the disease domain, comorbidities, and patient preference. [21]

Targeted synthetic drugs include Janus kinase inhibitors such as upadacitinib and tofacitinib, which are effective for articular and some extra-articular manifestations. For the axial phenotype, tumor necrosis factor and interleukin-17 inhibitors are often prioritized. The strategy is regular assessment and adjustment until minimal disease activity or remission is achieved.

Table 6. Drug groups and clinical guidelines

Group	Examples	When especially appropriate	Monitoring and security
Nonsteroidal anti-inflammatory drugs	Ibuprofen, naproxen	Symptomatic control	Gastrointestinal risks, kidneys, blood pressure
Synthetic base	Methotrexate, leflunomide, sulfasalazine	Peripheral arthritis	Blood, liver, teratogenicity
Biological anti-tumor necrosis factor	Adalimumab, etanercept, infliximab, etc.	Polyarthritis, axial phenotype, uveitis	Infections, tuberculosis, vaccination
Interleukin-17 inhibitors	Secukinumab, ixekizumab, bimekizumab	Enthesitis, dactylitis, axial phenotype, skin	Infections, inflammatory bowel disease in some patients
Interleukin-23 inhibitors	Guselkumab, risankizumab	Skin and nails, peripheral arthritis	Infections
Janus kinase inhibitors	Upadacitinib, tofacitinib	Intolerance to other classes, peripheral arthritis	Infections, lipids, risk of thrombosis

Vaccination and safety of therapy

Before initiating biological and targeted synthetic therapies, screening for latent tuberculosis, assessment of chronic viral hepatitis, and scheduled vaccinations, preferably before immunosuppression, are recommended. Inactivated vaccines can usually be administered during therapy; live vaccines are planned in advance. Repeated screening for tuberculosis during treatment is performed based on individual risk. [22]

Table 7. Minimum safety screening

Direction	What to do before therapy
Tuberculosis	Anti-visit screening for latent infection
Viral hepatitis	Serology and activity assessment
Vaccination	Updating inactivated vaccines, planning live vaccines
Risk factors	Body weight, blood pressure, lipids, blood sugar

Treatment goals and monitoring

The "treat to target" approach aims to achieve minimal disease activity or remission. Assessment is based on the MDA criteria and the DAPSA disease activity index, which take into account the number of tender and swollen joints, pain, general condition, and inflammatory markers. Regular reassessment 1-3 months after changes in therapy is standard.

Table 8. Threshold targets for therapy goals

Indicator	Target
Minimal Disease Activity	Fulfillment of the MDA criteria set
DAPSA	Low activity or remission on the scale
Patient-reported outcomes	Significant improvement in pain and function

Prevention and lifestyle

Weight management and strength and flexibility training improve symptoms and reduce stress on the entheses. Sleep, stress management, smoking cessation, and alcohol limitation are important. Given the increased cardiovascular risk, a systematic approach to blood pressure, lipids, and glycemia is necessary. [23]

Forecast and observation

With early initiation of therapy and a treat-to-target strategy, many patients achieve stable symptom control and prevent progression. Delayed diagnosis and active systemic inflammation increase the risk of structural changes and cardiovascular events, warranting close collaboration between a rheumatologist, dermatologist, and internist. [24]

Appendix: Visual markers on X-ray and magnetic resonance imaging

The combination of erosions with new bone proliferation and periostitis distinguishes psoriatic arthritis from rheumatoid arthritis. Classic features include juxta-articular bone growth and a rare but recognizable "pencil-in-glass" appearance in destructive forms. On magnetic resonance imaging (MRI), bone marrow edema and signs of active sacroiliitis are important in the axial variant. [25]

Table 9. Radiological “hints” to the doctor

Method	Key findings
X-ray of the hands and feet	Erosions plus new bone, "pencil in a glass", periostitis
Magnetic resonance imaging of the sacroiliac joints	Bone marrow edema, synovitis, erosions
Ultrasound of entheses	OMERACT pattern: hypoechogenicity, thickening, Doppler signal