Psoriatic arthritis – classification, diagnostic and clinical aspects

Epidemiology

Psoriatic arthritis (PsA) is a seronegative arthritis. It occurs in 5–40% of patients suffering from psoriasis vulgaris. In 2015 PsA incidence was estimated to be at the level of 3.2/10,000 individuals [1]. Present epidemiological studies have not revealed differences in the incidence of PsA in men and women [2]. However, psoriasis involving spinal joints is more common in men, whereas the form resembling rheumatoid arthritis is more common in women [3].
Skin lesions in psoriasis usually precede joint lesions, however, in about 10-15% of cases joint lesions may precede skin lesions [4]. A connection between the extent and severity of skin lesions and the advancement level of joint lesions has not been confirmed [5]. Psoriatic arthritis may develop even during the first years of life. There are two clinical forms in children: 1) a form involving from 1 to 4 joints and developing mostly in girls aged 1–2; it is characterized by chronic uveitis and so-called “sausage digits”; and 2) a form involving a random number of joints that affects children of both sexes, who are usually aged 6–12; it is characterized by the presence of HLA-B27 antigen. A development of one type of paediatric PsA does not eliminate the possibility of developing the other one [6]. In accordance with PsA classification presented by International League of Association for Rheumatology (ILAR), PsA is different from other forms of juvenile idiopathic arthritis (JIA) and is defined by co-occurrence of arthritis and psoriasis with no other signs of JIA. A child suffering from arthritis and without a diagnosed psoriasis that has two or more of the following PsA symptoms meets the criteria for PsA: dactylitis, nail lesions, onycholysis, and history of psoriasis in the first-degree relatives [6]. A multi-joint form and high values of inflammatory parameters are considered to be predictive factors of joint damage [7].

Etiopathogenesis

The bottom and causes of inflammatory lesions within joints and entheses have not been fully discovered. It comes to bone marrow oedema in the area of entheses within the joints involved in the inflammation; whereas within the subchondral bone layers, macrophage and CD8 cytotoxic lymphocyte migration is increased and infiltrates appear [8]. PsA etiopathogenesis takes into account genetic, immunological, environmental, and constitutional factors [9, 10]. Genetic studies allowed for separating two main types of psoriasis. Type 1 is strongly coupled with histocompatibility antigens such as HLA-Cw6 that is present in psoriasis in 60–65% of cases, HLA-B57, DR7, HLA-Cw7, HLA-B13, and HLA-B39. Individuals with HLA-Cw6 gene found on PSORS1, a psoriasis susceptibility locus localized on chromosome 6, are especially susceptible to develop psoriatic arthritis [11, 12]. This type of psoriasis usually affects individuals younger than 40 y/o, usually within one family, and extensive psoriatic lesions characterize it. Type 2 usually involves joints and nails; the first symptoms develop in individuals older than 40 y/o. This type is less genetically conditioned; environmental factors are most frequently listed as the cause. Psoriatic arthritis is often concomitant with HLA-B27 antigen [11, 13–15].
Environmental factors, especially infections, are also important in PsA pathogenesis. Significantly higher levels of antibodies against Yersinia enterocolitica, Yersinia pseudotuberculosis, Campylobacter jejuni, and Campylobacter fetus as well as Chlamydia trachomatis antigens were observed [16]. HIV-infections in PsA-patients induce the development of treatment-resistance severe erosive forms of the disease [17]. PsA development may be stimulated by hepatitis C virus [18].
Furthermore, it was observed that high body mass index (BMI) is associated with an increased risk of developing PsA, and obesity in young adults is an independent risk factor for the risk of developing the disease [19]. Adipose tissue produces resistin, a polypeptide that plays an important role in insulin-resistance. It was proved that intensity of joint lesions in PsA correlated with an increased resistin concentration in blood serum and synovial fluid [20]. Obesity is associated with an overproduction of proinflammatory cytokines such as interleukin 1 (IL-1), IL-6, IL-8, and tumour necrosis factor (TNF) that exert an influence on PsA exacerbation [21]. Usage of NSAIDs may have an influence on exacerbation of PsA [22].
Psoriatic arthritis is more common in individuals with psoriatic lesions found on the gluteal furrow, scalp, and nail plates. Also, a connection between PsA and extent of skin lesions is possible. Researchers suggest that it may be associated with abundant bacterial flora at those sites that triggers an immunological reaction leading to the development of psoriatic arthritis [15, 23]. It was proved that inflammation in the psoriatic skin, bone marrow, and the intestine is connected with the inflammation of the enthesis, synovitis, and changed skin phenotype. Within skin lesions, DNA is released by keratinocytes. After the binding of the released DNA with a bactericidal LL-37 peptide, interferon a a (INF-a) is secreted by plasmacytoid dendritic cells. Then, dermal dendritic cells are activated and migrate to lymph nodes draining the changed area. Th1 and Th17 lymphocytes, which activate release of proinflammatory factors in the dermis: IL-12, IL-17, and IL-22 (IL-12, IL-17, lymphoid cell and CD8+ T-lymphocytes cause an additional IL-17 secretion in the dermis), are then differentiated. Secretion of cytokines in the skin promotes proliferation of keratinocytes that in return secrete cytokines paracrinally and affect cells in the dermis. Within the bone marrow, there is a similar expansion of Th1 and Th17 cells, and other type 17 cells, as well as octacalcium (OCP) precursors. Then, IL-23 secretion and stimulation of type 17 cells are triggered.
In case of enthesis, IL-23 secretion happens due to biomechanical stress-inducing factors or a tendon injury at the enthesis. Type 17 cells are activated, and cytokines such as IL-22 and TNF start to be secreted, what results in an inflammation that exerts an influence on differentiation of mesenchymal cells into osteoblasts [6].
Enthesophytes – bony projections – form in peripheral attachments, whereas syndesmophytes – bony bridges – form in the spine. Then, type 17 cells, OCP, and dendritic cells from adjacent entheses or bloodstream end up in the joint. An increased expression of receptor activator of nuclear factor-kB ligand (RANKL) caused by synoviocytes in the lining and an increased level of TNF, IL-17, and RANKL due to an increased expression caused by infiltrating cells, accelerated differentiation of OCP into osteoblasts. Consequently, synovitis and bone resorption develop [6]. Moreover, proinflammatory cytokines such as IL-1, IL-6 and molecules belonging to TNF family play a significant role in bone destruction [6, 24]. They stimulate osteoblastogenesis, are inhibitors of proteoglycan synthesis, induce collagen and cartilage degradation by activating metalloproteinases and prostaglandin E2 [6, 24].

Clinical presentation

Psoriatic arthritis clinical symptoms include pain felt in the spine and involved joints, chronic enthesopathy, peripheral joint inflammation in the upper and lower limbs, and lesions in the nail plate [6, 24, 25]. The Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) isolated several types of PsA with regard to the level of disease severity and clinical presentation associated with that. The classification facilitates making therapeutic decisions [26–28].
The GRAPPA classification is based on the knowledge of joint structure and an ability to find lesions in them (fig. 1) [25].

Diagnostic criteria

Diagnosing PsA is based on Classification Criteria for Psoriatic Arthritis (CASPAR) criteria from 2006 (table 1) [29]. According to them, PsA is diagnosed when a patient suffers from peripheral joint inflammation, spondyloarthritis or sacroiliitis, enthesopathy, and he/she achieved ≥ 3 points according to CASPAR classification [5, 29, 30]. CASPAR classification allows for diagnosing PsA in patients without skin lesions.

Disease forms

In 2009 Assessment of Spondyloarthritis International Society (ASAS) isolated axial and peripheral forms of PsA [31]. Axial PsA is diagnosed on the basis of radiologic criteria in case of unilateral sacroiliitis, whereas peripheral PsA involves peripheral joints, tendon attachments, capsular ligaments, and fasciae.
Duration and symptom intensification in PsA are very variable what makes correct clinical classification difficult. Forms of PsA may be concurrent or develop one after another during different periods of the disease [32]. PsA forms classified with regard to lesion exacerbation are presented in table 2 [33].

Assessment of severity

PsA severity assessment includes [5, 34–39]: 1. Number of painful (68 possible) and oedematous (66 possible) joints.
2. Pain intensity assessed by a patient on VAS: 0–10 points, where 0 means no pain, and 10 means the highest imaginable pain.
3.Quality of life: Health Assessment Questionnaire Score (HAQ-SK), Psoriatic Arthritis Quality of Life (PsAQoL), Dermatology Life Quality Index (DLQI), and EuroQol 5-domain (EQ-5D).
4. Patient’s general self-assessment (psychical, physical, and social aspects): Short Form-36 (SF-36), and Beck Depression Inventory – Short Form (BDI).
5. Level of inflammation severity assessed by means of inflammatory parameters present in peripheral blood: e.g. acute phase protein, ESR.
6. Level of intensity, activity of the disease, and pain assessed with the use of Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) or Likert scale.
Questionnaires allowing for identification of early PsA forms have been devised. Four such tools are available: Psoriatic Arthritis Screening and Evaluation (PASE) [38] that is used for screening tests for PsA; Psoriasis Epidemiology Screening Tool (PEST) [40] used to identify individuals with PsA within a group of psoriatic patients; Toronto Psoriatic Arthritis Screen (ToPAS II) [41] that is a promising instrument for early diagnosis of PsA in both psoriatic patients and general population; and Early Psoriasic Arthritis Screening Questionnaire (EARP) that not only does allow for early identification of PsA in psoriatic patients, but also enables the assessment of the severity level of this disease [42].

Diagnostic imaging

Classic radiography is useful in assessing the severity of joint lesions, because a radiological picture characteristic for PsA, including joint space narrowing, erosions within synovial joints (e.g. knee joints) as well as cartilaginous and fibrous joints (e.g. sacroiliac joints), and inflammatory lesions of tendon attachments and ligaments, are confirmed only in advanced stages of the disease [32].
Differentiation between bone erosions present in PsA and bone erosions present in rheumatoid arthritis is possible only with the use of high-resolution computed tomography, magnetic resonance imaging, or ultrasound exam [43, 44]. If the disease progresses, the erosions deepen, and proliferative reactions with formation of enthesophytes and osteophytes develop; also, joint destruction occurs. Furthermore, generalized osteoporosis may develop. A characteristic feature of peripheral psoriatic arthritis is asymmetry of lesions and simultaneous concomitance of ankylosis and osteolysis within joints found in the same area, e.g. foot or hand [32].
A feature that differentiated PsA from other joint inflammations within the spine is a large extent of radiological lesions, their significant size, and asymmetrical placement with omission of some vertebrae [14]. Radiological lesions in psoriasis of the spine that take the form of “flocky” ossifications parallel to lateral surfaces of vertebral bodies are called parasyndesmophytes. They appear already in early stages of PsA. Advanced psoriasis of the spine may take the form of a “bamboo spine”, similarly to ankylosing spondylitis (AS), or manifest itself as vertebral squaring, ankylosis of facet joints, and ossification of joint ligaments [37].
Within the course of psoriatic arthritis the most characteristic is an early involvement of iliac side of the sacroiliac joint, asymmetry of the lesions or their unilateral location. At early stages, the following appear: shallow erosions, subchondral sclerotization, and segmental widening of the joint space. At later stages, proliferative lesions lead to developments of bone bridges, narrowing of the joint space, and ankylosis [37]. Dynamic contrast-enhanced magnetic resonance (DCE-MRI) allows for determining the level of vascularization in the bone marrow, what is an indirect indicator of inflammation activity. A characteristic symptom for PsA visible in DCE-MRI is inflammation of periarticular soft tissues at early stages of the disease, which may occur without a visible synovitis.
A full-body MRI may be useful. The application of this exam along with ultrasound allows for identifying active inflammatory lesions within joints in about 80% of PsA-patients when there are no clinical signs [14, 32, 34, 43–45]. Epidemiological observations showed that erosive form of the disease develops in about half of untreated patients with early PsA 2 years after the diagnosis [7].

Therapeutic procedures

Newest guidelines of European League Against Rheumatism (EULAR), published in 2017 and regarding treatment of both early and advanced forms of PsA, include the following [28, 46]:
1. A patient that has symptoms of arthritis should be examined by a rheumatologist not later than 6 weeks from the appearance of the symptoms.
2. A physical examination is a method of choice in early PsA diagnostics. The diagnosis may be confirmed by ultrasound, computed tomography or magnetic resonance imaging.
3. If the final diagnosis cannot be made on the basis of physical examination and imagining, and the patient has early symptoms of arthritis and is at risk of recurrent or chronic erosive arthritis expressed by the number of involved joints, presence of rheumatoid factor, acute-phase proteins as well as anti-citrullinated peptide (anti-CPP) autoantibodies, and diagnostic imagining test results, a treatment involving conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), e.g. methotrexate, leflunomide, or sulfasalazine, should be introduced.
4. Conventional treatment should be introduced not later than within 3 months from the appearance of symptoms, even if not all PsA criteria are met. In patients with recurrent or chronic arthritis, conventional therapy should be based on methotrexate given there are no contraindications (in such cases leflunomide, sulfasalazine, or apremilast are alternatives).
5. In patients with mild axial PsA that manifests itself clinically with back pain, but without limiting the function of spinal joints, it is recommended to use nonsteroidal anti-inflammatory drugs (NSAIDs), e.g. naproxen, indomethacin, and celecoxib. Nonsteroidal anti-inflammatory drugs should be used in minimal effective doses for the shortest time possible, and prior gastrological, nephrological, and cardiological assessment.
6. In patients with axial form that do not react to NSAISs and suffer from back pain and morning stiffness, it is recommended to use IL-17 or IL-23 inhibitors (secukinumab and ustekinumab respectively). Treatment efficacy in axial PsA is assessed by mean of BASDAI. The disease is considered active if BASDAI ≥ 4. BASDAI < 3 or reduction with at least 2 points means that the applied treatment is effective.
7. Systemic glucocorticosteroids reduce joint pain and slower the process of their destruction, but due to the possibility of dose accumulation and potential side effects, the glucocorticosteroids should be use for a possibly short period of time (6 months maximum) in minimal doses. Intra-articular steroid injections in peripheral PsA should be used only in cases of significant exacerbation of general and local inflammation When introducing systemic glucocoticosteroids in patients with psoriasis or psoriatic arthritis it has to be considered that it may be associated with increased risk of developing generalised pustular psoriasis.
8. In peripheral PsA, an initial assessment of active inflammation is performed on the basis of guidelines presented at the 8th Congress of OMERACT (Outcome Measures in Rheumatoid Arthritis Clinical Trials) prior to the treatment. The activity of inflammation should be assessed every 1, 2 or 3 months by means of laboratory and imaging tests as well as physical examination of the joints. If there is no significant improvement after 3 months of conventional therapy or the disease still involves more than 3 joints, it is recommended to apply biological treatment with first-line TNF inhibitors. If there is still no sufficient response to treatment, it is recommended to start a therapy with monoclonal antibodies (infliximab, adalimumab, golimumab, certolizumab, etanercept).
9. In patients with severe erosive PsA and signification limitations of joint functions, it is recommended to use TNF inhibitors as the first-line treatment, and in case they are not effective enough, to introduce biological drugs from other groups (secukinumab, ustekinumab).
Biological and bio-like drugs registered for use in PsA include TNF inhibitors (adalimumab, certolizumab, etanercept, golimumab, and infliximab), interleukin inhibitors (secukinumab, ustekinumab, ixekizumab), and tofacitinib that is a Janus kinase 1 and Janus kinase 3 inhibitor. Criteria for assessment of response to treatment in axial and peripheral PsA include the following protocols: DAS28 (Disease Activity Score 28 Joints), ACR criteria [47], DAPSA (Disease Activity in Psoriatic Arthritis) [48], PASDAS (Psoriatic Arthritis Disease Activity Score) [49], mCPDAI (modified Composite Psoriatic Disease Activity Score) [50], and PsARC (Psoriatic Arthritis Response Criteria) [51]. In addition, it should be emphasized that apart from phonological treatment, early rehabilitation of locomotor system, quitting smoking, normalization of the body mass, oral cavity sanitization, and stabilization of possible concomitant diseases are necessary.

Conclusions

Early detection and treatment of PsA gives an opportunity for disease remission and prevention of joint destruction. Therapeutic and prophylactic decisions should consider the influence of the disease on patients’ quality of life. Special attention should be paid to new biological drugs.

Conflict of interest

The authors declare no conflict of interest.

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