We review key differences in clinical, serological, radiographic and pathogenic features of RA and PsA, and provide practical guidance for achieving a correct diagnosis. Accurate diagnosis of RA and PsA is important because differences in underlying pathogenesis and response to therapy translate into substantially different clinical outcomes. Rheumatoid arthritis RA and psoriatic arthritis PsA are common chronic inflammatory diseases; both are characterised by pain and swelling in the joints and have significant systemic manifestations.
For this reason, early diagnosis is important to determine therapeutic strategies that will optimise clinical and radiographic outcomes. Both also have similarities with other inflammatory diseases 5 and association with coprevalent forms of arthritis, such as gout and secondary osteoarthritis. In the last 20 years, biologic disease-modifying antirheumatic drugs, many with differing mechanisms of action, have become available.
These medications target the disease processes that drive inflammation and joint damage in RA and PsA. However, depending on the molecule, therapeutic selection is complicated by variable efficacy between patients with RA and the manifestations of psoriatic disease eg, enthesitis or skin psoriasis. To help practitioners determine an accurate diagnosis, key differences in clinical, serological, radiographic and pathogenic features of RA and PsA are reviewed.
The different therapeutic classes that can be of benefit in each disease are discussed in depth. RA is an autoimmune systemic inflammatory disease characterised by synovitis, bony erosions and cartilage damage.
Key clinical, serological and radiographic differences between RA and PsA are summarised in table 1. The dash — indicates the characteristic is not common. In many populations, RA prevalence is estimated to be 0. A combination of genetic factors and environmental triggers is thought to elicit autoimmune inflammatory responses in both RA and PsA. The pathogenesis of RA and PsA is not completely understood. In addition to the known association with human leucocyte antigen HLA -DR4 in RA, one theory is the development of lung inflammation, typically prior to joint symptoms, with production of antibodies to citrullinated protein antigens that mediate pathogenesis.
In both PsA and RA, inflammatory responses are characterised by the increased production of proinflammatory molecules that act in synergy to propagate chronic inflammation figure 1. Pathogenesisof PsA and RA. Reprinted from Coates et al 29 and Perera et al.
Smoking, infections or air pollution exposure may trigger local inflammation in the lungs, promoting protein citrullination and stimulating CCP production. The criteria include the number of joints involved, duration of symptoms, and the demonstration of serological markers and an elevated acute-phase reactant. For PsA, the Classification Criteria for Psoriatic Arthritis help categorise patients with inflammatory articular disease for clinical trials.
Neither classification criteria should be confused as diagnostic criteria. Joint involvement is predominantly symmetric in RA and often, but not always, asymmetric in PsA. Typically, RA affects the shoulder, elbow, wrist, metacarpophalangeal, proximal interphalangeal, hip, knee, ankle and metatarsophalangeal joints. In PsA, the distal interphalangeal joints of the hands and feet, large joints of the lower extremities, the axial spine and sacroiliac joints are commonly affected; the metacarpophalangeal and metatarsophalangeal joints and wrist can be involved as well.
PsA, rather than RA, is included in the spectrum of spondyloarthritis as PsA can affect the axial skeleton eg, sacroiliac joints and spine. Both RA and PsA exhibit proliferation of endothelial cells, but topological differences in endothelial cells suggest differing pathological features. The most common locations of enthesitis in patients with PsA are the insertion sites of the plantar fascia, the Achilles tendon and ligamentous attachments of the knee.
Signs and symptoms of enthesitis can be non-specific and difficult to distinguish from other inflammatory conditions, particularly fibromyalgia, in the absence of other manifestations common to PsA. Nail dystrophy, which is characterised by onycholysis, pitting and hyperkeratosis, is an important clinical manifestation of PsA.
Ocular disorders are common extra-articular manifestations of RA and PsA. Cutaneous manifestations are common in both RA and PsA. The most common cutaneous features of RA include rheumatoid nodules, vasculitic skin lesions and granulomatous dermatoses. Furthermore, inverse psoriasis is traditionally under-recognised, and recent findings indicate a greater prevalence of inverse psoriasis than commonly appreciated.
In contrast, PsA is a seronegative inflammatory arthropathy. Use of imaging can provide important information to help practitioners identify and differentiate between types of inflammatory arthritis. Conventional radiography can be used to identify juxta-articular bony proliferations, which can be used to help discern PsA from other types of inflammatory arthritis, and to visualise osteodestructive lesions characteristic of RA.
Ultrasound imaging can be used to identify characteristic features of inflammatory arthritis, including enthesitis, cortical bone erosions, cartilage lesions, synovitis and tenosynovitis. Interestingly, while clinical signs of enthesitis are a hallmark of PsA, the presence of enthesitis on ultrasound cannot always help clinicians distinguish PsA from RA. Ultrasound imaging can be used to identify characteristic joint involvement that distinguishes PsA from RA.
For example, distal interphalangeal joint changes are found almost exclusively in patients with PsA compared with those with RA, 81 and dactylitis due to flexor tenosynovitis is characteristic of PsA.
MRI can be used to identify joint synovitis, bone and joint erosions, bone marrow oedema, spondylitis, periarticular inflammation, active enthesitis, nail disease and periostitis. Tenosynovitis is another common MRI observation in inflammatory arthritis; in RA, tenosynovitis is most common in the hands and wrists, whereas in PsA soft-tissue inflammation around the tendon sheath is characteristic of dactylitis.
Differences in patient comorbidities may help clinicians differentiate between RA and PsA table 2. Overall, comorbidity burden may be higher in RA than in PsA, but both diseases are similarly associated with increased risk for comorbidities linked to systemic inflammation eg, cardiovascular disease.
However, registry data suggest that the rates of obesity, diabetes mellitus and metabolic syndrome are significantly higher in patients with PsA compared with those with RA. Summary of differences in common comorbidities associated with PsA and RA 29 88 90 — Because of the differences in disease pathogenesis, clinical manifestations and response to therapy between RA and PsA, treatment strategies may differ.
Methotrexate is the most frequently used conventional synthetic disease-modifying antirheumatic drug csDMARD for the treatment of RA, and its efficacy is well-established in this patient population. In clinical studies, treatment with secukinumab and ixekizumab improved signs and symptoms of disease, inhibited radiographic progression of joint damage, and improved physical functioning and quality of life in patients with active PsA. Consistent with this finding, clinical studies of ILA inhibitors in RA have shown that these agents have limited therapeutic efficacy.
IL stimulates Th1 cells and is produced by monocytes and macrophages in response to inflammation, and IL is an upstream cytokine produced predominantly by myeloid dendritic cells to regulate Th17 cell function. In phase III clinical trials, ustekinumab significantly reduced radiographic progression of joint damage and improved signs and symptoms of disease in patients with active PsA. IL-6 is a proinflammatory cytokine produced by macrophages and T cells during acute-phase inflammatory responses.
The IL-6 inhibitors tocilizumab and sarilumab are FDA-approved for the treatment of RA and reduce disease activity and radiographic joint damage. IL-1 cytokines induce synovial inflammation and mediate bone resorption and cartilage destruction through interactions with prostaglandin E 2 and proteases, such as matrix metalloproteinases.
In patients with both psoriasis and PsA, no benefit was observed in skin symptoms compared with placebo. In clinical studies of patients with RA, rituximab plus methotrexate was effective in reducing progression of joint damage. Janus kinases JAKs are cytoplasmic tyrosine kinases that regulate cytokine signalling pathways involved in inflammatory responses.
Tofacitinib is FDA-approved for the treatment of adults with active RA and an inadequate response or intolerance to methotrexate. In clinical studies in patients with RA, treatment with tofacitinib was associated with reductions in signs and symptoms of active disease, improvements in physical function and health-related quality of life, and slowing of radiographic progression.
Tofacitinib also has demonstrated efficacy in patients with PsA. Accurate diagnosis of PsA and RA is important because, although these diseases have a number of overlapping clinical, serological and radiographic features, differences in underlying pathogenesis and response to therapy translate into substantially different clinical outcomes.
An understanding of the various clinical characteristics, triggering factors, comorbidities and extra-articular manifestations of PsA and RA can aid in the determination of the correct diagnosis.
Use of laboratory and imaging techniques can be particularly helpful in distinguishing between these two diseases. Once an accurate diagnosis has been made, clinicians can decide which therapy should be used to provide maximal improvements in the signs and symptoms of RA or PsA based on patient and disease characteristics. Contributors: All authors contributed equally to the content of the paper.
Funding: Technical assistance with editing, figure preparation, and styling of the manuscript for submission was provided by Oxford PharmaGenesis Inc. Funding: Technical assistance with editing, figure preparation and styling of the manuscript for submission was provided by Oxford PharmaGenesis, Inc.
Disclaimer: The authors were fully responsible for all content and editorial decisions and received no financial support or other form of compensation related to the development of this manuscript.
LRE has no competing interests to disclose. Patient consent: Not required. Provenance and peer review: Not commissioned; externally peer reviewed. Data sharing statement: No additional data are available.
National Center for Biotechnology Information , U. RMD Open. Published online Aug Author information Article notes Copyright and License information Disclaimer.
Corresponding author. Correspondence to Dr Joseph F Merola; ude. All rights reserved. No commercial use is permitted unless otherwise expressly granted. This article has been cited by other articles in PMC.
Abstract Rheumatoid arthritis RA and psoriatic arthritis PsA have key differences in clinical presentation, radiographic findings, comorbidities and pathogenesis to distinguish between these common forms of chronic inflammatory arthritis. Keywords: psoriatic arthritis, rheumatoid arthritis, inflammatory disease. Key messages.
What is already known about this subject? What does this study add? How might this impact on clinical practice? Introduction Rheumatoid arthritis RA and psoriatic arthritis PsA are common chronic inflammatory diseases; both are characterised by pain and swelling in the joints and have significant systemic manifestations. Differences of RA and PsA RA is an autoimmune systemic inflammatory disease characterised by synovitis, bony erosions and cartilage damage. Open in a separate window. Radiographic features of RA and PsA Use of imaging can provide important information to help practitioners identify and differentiate between types of inflammatory arthritis.
Treatment options for RA and PsA Because of the differences in disease pathogenesis, clinical manifestations and response to therapy between RA and PsA, treatment strategies may differ. Conventional synthetic disease-modifying antirheumatic drugs Methotrexate is the most frequently used conventional synthetic disease-modifying antirheumatic drug csDMARD for the treatment of RA, and its efficacy is well-established in this patient population.
IL-6 inhibitors IL-6 is a proinflammatory cytokine produced by macrophages and T cells during acute-phase inflammatory responses. IL-1 receptor antagonists IL-1 cytokines induce synovial inflammation and mediate bone resorption and cartilage destruction through interactions with prostaglandin E 2 and proteases, such as matrix metalloproteinases.
Janus kinase inhibitors Janus kinases JAKs are cytoplasmic tyrosine kinases that regulate cytokine signalling pathways involved in inflammatory responses.
Conclusions Accurate diagnosis of PsA and RA is important because, although these diseases have a number of overlapping clinical, serological and radiographic features, differences in underlying pathogenesis and response to therapy translate into substantially different clinical outcomes.
Footnotes Contributors: All authors contributed equally to the content of the paper. References 1. Differentiation between early rheumatoid and early psoriatic arthritis by the ultrasonographic study of the synovio-entheseal complex of the small joints of the hands. Clin Exp Rheumatol ; 34 — Biomarkers for rheumatoid and psoriatic arthritis. Clinical Immunology ; :2— Elsevier; Gladman DD, et al. Clinical manifestations and diagnosis of psoriatic arthritis.
Accessed June 27, Treatment of psoriatic arthritis. Psoriatic arthritis adult. Mayo Clinic; Singh JA, et al. Psoriatic arthritis: Diagnosis and treatment. American Academy of Dermatology. Arthritis Foundation. Newer drug treatments for psoriatic arthritis. Accessed July 3, National Psoriasis Foundation. Accessed July 6, This distinct pattern of new blood vessel formation in PsA and the seronegative spondyloarthropathies has been confirmed in subsequent studies.
Furthermore, at a microscopic level, the increased vessels previously noted on immunohistology in PsA synovium may be due to the elongation and increased tortuosity of existing vessels, rather than an increase in the actual number of new vessels. These observations are supported by the findings on a molecular level of different vascular growth factor expression patterns, especially VEGF and Ang2, found at high levels in synovial tissue of the early stage of PsA. While the systemic response in both conditions suggests an active inflammatory immune reaction, evidence for this is more often found in RA, presumed to match the autoimmune nature of RA characterised by production of autoantibodies as outlined above.
In PsA, the systemic immune response may also be apparent, however, it is often less marked than in RA. In many clinical studies and trials, it is noted that the mean rise in circulating markers of inflammation, such as erythrocyte sedimentation rate, C reactive protein CRP , or serum amyloid A, is significantly lower in the PsA population in contrast with patients with RA.
Similarities in this respect have been drawn between PsA and other systemic conditions characterised by disturbance of the inflammasome. Macroscopic appearance of synovial membrane vascularity in A.
Rheumatoid arthritis RA compared with B. Psoriatic arthritis PsA , illustrating straight, branching blood vessels in RA compared with a tortuous vascular pattern in PsA synovium. The introduction of tumour necrosis factor inhibitors TNFi led to a major shift in the treatment of RA and PsA irrespective of the diagnosis.
PsA is not a benign disease, as progression and joint damage are observed over time. A cohort of patients with PsA attending an early arthritis clinic, and receiving treatment with synthetic DMARDs, demonstrated significant bone erosions over a 2-year period. Several new biological agents targeting novel molecules implicated in the inflammatory pathway have now been developed and are available.
The interesting observation thus far is that some of these treatments are highly effective in RA but have shown little benefit in the treatment of patients with PsA.
This may not be surprising, as noted above, there is an absence of circulating autoantibodies in PsA. One biological agent, a fusion protein against CTLA-4 abatacept results in down modulation of T-cell activation, however, does show similar activity in both patients with PsA and RA. Several Mab targeting this key regulatory pathway have now been developed and studied in the setting of PsA and psoriasis.
Ustekinumab studies in RA have been completed but not yet published, another anti-IL17 Mab, AIN secukinumab, was reported to be efficacious in psoriasis, uveitis and rheumatoid arthritis, and the effect in RA has been confirmed, with a stable adverse event profile, in a double-blind, randomised, placebo-controlled study of over patients with RA.
Finally, two anti-IL17 receptor antibodies, brodalimumab and ixekizumab, were shown in short phase II studies to be significantly beneficial in plaque psoriasis. In conclusion, this review outlines the similarities and the differences in PsA and RA. By contrast, the differences may be more than skin deep! Significant differences have been observed at the clinical, immunological, cellular and molecular levels. Specifically, the most defined differences focus around the absence of autoantibodies, RF and ACPA, the vascular morphology and angiogenic growth factor expression in the synovial tissue, and the pattern of periarticular inflammation, bone erosion and formation at the entheseal complex of peripheral and spinal joints.
Finally, while some synthetic and biological DMARDs appear to be effective in both patients with PsA and RA, again, specific differences in response to new targeted therapies are being observed which may be explained by specific differences in the molecular pathogenesis of PsA compared with RA. Provenance and peer review: Commissioned; externally peer reviewed. Data sharing statement: No additional data are available.
National Center for Biotechnology Information , U. RMD Open. Published online Apr Douglas James Veale 1, 2 and Ursula Fearon 1, 2.
Author information Article notes Copyright and License information Disclaimer. Correspondence to Professor Douglas J Veale; ei. This article has been cited by other articles in PMC. Abstract In many ways, it may be easier to highlight what rheumatoid arthritis RA and psoriatic arthritis PsA have in common. Key messages. But I thought, wow, maybe it will increase awareness and maybe, just maybe, more studies and treatment options will become available.
But I never once heard of psoriatic arthritis. So here I am now, living with psoriatic arthritis. I am now well versed in the world of biologicals, NSAIDs, steroids, physical therapy, arthritis gadgets, shoes, etc. Well, just like rheumatoid arthritis , it is an auto-immune disease. Both cause an erosive inflammatory arthritis pain, stiffness and swelling in addition to chronic fatigue. And both can have symptoms that vary greatly from person to person.
However the distribution of joint involvement differs between the two diseases and psoriatic arthritis involves the skin as well as the joints. Both diseases can cause destruction of the small joints in your hands and feet as well as larger joints such as knees, hips, shoulders and even the vertebrae in your spine.
Classic rheumatoid arthritis primarily involves the PIP joints the middle joint of your finger and toes and wrist, and is generally a symmetrical disease effecting both sides of the body equally. Also with rheumatoid arthritis, nodules specific to this disease are often present. Psoriatic arthritis is typically an asymmetric disease, involving one side of the body but it can be symmetrical too.
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