eMedicine Specialties > Dermatology > Papulosquamous Diseases

Psoriatic Arthritis

Author: Abby S Van Voorhees, MD, Assistant Professor, Director of Psoriasis Services and Phototherapy Units, Department of Dermatology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania
Coauthor(s): Michael J Dans, MD, PhD, Clinical Instructor, Department of Dermatology, University of California at San Francisco; Darice Williams Fadeyi, MD, Associate Physician, Lexington Avenue Dermatology
Contributor Information and Disclosures

Updated: Jan 26, 2007

Introduction

Background

Psoriatic arthritis is a chronic inflammatory arthritis that is commonly associated with psoriasis. At least 5% of patients with psoriasis develop psoriatic arthritis. The association between psoriasis and arthritis was first made in the mid 19th century, but psoriatic arthritis was not clinically distinguished from rheumatoid arthritis (RA) until the 1960s. Precisely defining psoriatic arthritis is still difficult because of a lack of specific biologic tests. It is most commonly a seronegative oligoarthritis found in patients with psoriasis with less common but characteristic differentiating features of distal joint involvement and arthritis mutilans. Because 50% of patients with psoriatic arthritis have evidence of spondyloarthropathy, often HLA-B27 associated, psoriatic arthritis has also been classified among the seronegative spondyloarthropathies.

Pathophysiology

Psoriatic arthritis is an autoimmune inflammatory condition affecting the skin and the joints as well as the insertion sites of tendons, ligaments, and fascia. Overexpression of tumor necrosis factor (TNF)-alpha is thought to play a key role. Multiple HLA associations are known. Although psoriatic arthritis is sometimes seen in the absence of detectable skin lesions, it is thought to be more frequent in patients with severe cutaneous disease. However, the exact etiology is unknown and is probably multifactorial, including immune-mediated, genetic, and environmental causes. Environmental factors may include trauma, infection, and stress.

Frequency

United States

In the United States, psoriatic arthritis affects at least 5% of patients with psoriasis. It is thought to occur in up to 1% of the general population. Prevalence rates vary widely between studies; however, a recent random telephone survey of 27,220 US residents found a prevalence rate of psoriatic arthritis to be 0.25% in the general public and 11% among patients with psoriasis.

International

Internationally, the incidence of psoriatic arthritis is 1-40%, depending on the population studied.

Mortality/Morbidity

Psoriatic arthritis usually follows an undulating course, with flares and remissions. Significant morbidity may occur, with long-standing or mutilating disease resulting in joint destruction. Although psoriatic arthritis was originally thought to be relatively mild, as many as 40% of patients may develop erosive and deforming arthritis.

Race

The effect of race on the prevalence of psoriatic arthritis is not well studied. However, whites are known to be more commonly affected than other racial groups.

Sex

Overall, men and women are affected equally. However, a male predominance occurs in the spondylitic form, and a female predominance occurs in the rheumatoid form.

Age

Psoriatic arthritis usually develops in the fourth to sixth decades of life, but it can occur at almost any age.

Clinical

History

Psoriatic arthritis may appear in a variety of clinical patterns (see Physical).

  • Psoriasis appears to precede the onset of psoriatic arthritis in 60-80% of patients. Occasionally, arthritis and psoriasis appear simultaneously. In addition, cutaneous eruptions may be preceded by the arthropathy.
  • Joint stiffness, while not specific for psoriatic arthritis, can be a prominent symptom.
  • In a patient who presents with musculoskeletal symptoms without a history of psoriasis, the diagnosis can be suspected based on a family history of psoriasis; the pattern of arthritis; and the presence of psoriasis in frequently overlooked areas, such as the umbilicus, the gluteal cleft, and the ears. Although the association between severe psoriasis and the development of psoriatic arthritis is clear, the severity of psoriasis does not appear to be related to the pattern of joint involvement.
  • Factors that do increase the risk of a patient with psoriasis developing arthritis in their lifetime include the presence of nail lesions as well as more extensive skin involvement. A family history of psoriatic arthritis also increases the risk of developing arthritis.

Physical

Diagnosis of psoriatic arthritis can be problematic in the absence of overt skin lesions. Joint findings may include dactylitis (sausage digits), enthesopathy (reflecting inflammation of the insertion points of tendon into bone), tendonitis, and spondylitis. A careful physical examination, including evaluation of the scalp, the gluteal crease, the umbilicus, the axillae, and the nails, may aid in making the diagnosis of psoriatic arthritis.

Scaly, erythematous plaques; guttate lesions; lakes of pus; and erythroderma are all types of psoriatic skin lesions that may be seen in the context of psoriatic arthritis. Nail pitting, Beau lines, leukonychia, onycholysis, oil spots, subungual hyperkeratosis, splinter hemorrhages, spotted lunulae, and cracking of the free edge of the nail all support the diagnosis of psoriatic arthritis, especially of the distal interphalangeal (DIP) joint type. In fact, psoriatic nail changes may be a solitary finding in patients with psoriatic arthritis.

Systemic symptoms are usually limited to ocular involvement, which affects 30% of patients with psoriatic arthritis. Ocular findings may include conjunctivitis, iritis, episcleritis, and keratoconjunctivitis sicca. Aortic insufficiency has also been reported.

Diagnosis is also suggested by the following: asymmetric joint involvement, DIP involvement in the absence of osteoarthritis, dactylitis, and absence of rheumatoid factor (RF) and subcutaneous nodules.

  • Clinical patterns of arthritis
    • Asymmetric oligoarthritis occurs in as many as 70% of patients with psoriatic arthritis. As many as 4 large joints are affected, often with acute scattered involvement of the metatarsophalangeal, proximal interphalangeal, and DIP joints. Sausage digits due to inflammation of the flexor tendons and synovium and pitting edema of the distal extremities may be observed.
    • DIP joint involvement occurs in approximately 5-10% of patients with psoriatic arthritis. One or several DIP joints may be involved. Periarticular swelling and acute inflammation with warmth and rubor may occur. DIP joint involvement and concomitant nail involvement with acute paronychia is a characteristic picture.
    • Symmetric psoriatic arthritis of the small joints of the hands and the feet, the knees, and the elbows usually follows a mild course and is difficult to distinguish from RA. RF seronegativity, a history of psoriasis, the presence of DIP involvement, and characteristic radiographic findings all support a diagnosis of symmetric polyarthritis. This form affects as many as 25% of patients.
    • Arthritis mutilans is a rare form of psoriatic arthritis occurring in 5% of patients with psoriatic arthritis. Osteolysis of the phalanges and the metacarpals causes a telescoping motion of the digits, noted as opera-glass deformity or pencil-in-cup radiographic findings. Fever may accompany arthritis mutilans.
    • Spondylitis occurs in about 5% of patients with psoriatic arthritis and is often asymptomatic. Radiographic evidence of sacroiliitis may be present in as many as 20% of patients. The axial spine may be involved alone or in conjunction with peripheral joints. The vertebrae are asymmetrically affected. Atlantoaxial joint involvement may lead to subluxation. Male patients are more frequently affected than female patients.
  • Psoriatic nail lesions, soft tissue thickening above the terminal phalanx, and radiologic involvement of the phalanx with periosteal reaction and bone have recently been described under the term psoriatic-onycho-pachydermo-periostitis (POPP). POPP must be differentiated from other forms of psoriatic arthritis, especially the DIP joint type. A periosteal reaction of the terminal phalanx in the absence of DIP joint involvement is characteristic of POPP. In addition, pain and soft tissue thickening is more common in POPP. Nail disease is common to both POPP and DIP psoriatic arthritis. The nails of the great toes are involved in most reported cases of POPP.
  • Juvenile psoriatic arthritis is usually mild and often monoarticular. Tenosynovitis and nail involvement are common. Sacroiliitis is associated with HLA-B27 positivity. When unfused epiphyses are inflamed, disordered bone growth and foreshortening can result. Children have a higher frequency of simultaneous onset of psoriasis and psoriatic arthritis.
  • Other associations
    • First described by Chamot et al in 1987, synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome is characterized by variable bone changes (hyperostosis, arthritis, aseptic osteomyelitis) of the chest wall, sacroiliac joints, and long bones. Dermatologic manifestations include palmoplantar pustulosis, hidradenitis suppurativa, pustular psoriasis, dissecting cellulitis of the scalp, Sweet syndrome, and Sneddon-Wilkinson disease. Skin and osseous involvement may occur simultaneously or be separated by as long as 20 years.
    • The number of diagnosed cases of psoriasis and psoriatic arthritis has risen dramatically in sub-Saharan Africa in association with the escalating epidemic of HIV infection. Although HIV infection is not known to affect the incidence of psoriasis, it may significantly exacerbate otherwise limited disease. The evolution of mild psoriasis to erythroderma in the setting of a flare-up of psoriatic arthritis may be a sign of HIV infection.

Causes

Although the exact cause of psoriatic arthritis is unknown, genetic, environmental, immunologic, and vascular factors contribute to one's predisposition.

  • Genetic factors
    • Approximately 40% of patients with psoriasis or psoriatic arthritis have first-degree relatives who are affected. The sibling occurrence risk is about 8%. Although concordance rates of psoriatic arthritis in twins are not yet known, a 65-72% concordance rate of psoriasis exists between monozygotic twins, compared with a 15-30% concordance for dizygotic twins. A 65-72% concordance exists between monozygotic twins compared with a 15-30% concordance for dizygotic twins.
    • The following HLA associations have been elucidated:
      • Early-onset psoriasis - HLA-Cw6, HLA-B57, HLA-DR7, and HLA-B17
      • Psoriatic arthritis - HLA-B7 and HLA-B27
      • Psoriasis and psoriatic arthritis - HLA-Cw6, HLA-B13, HLA-B17, and HLA-B39
      • Ankylosing spondylitis - HLA-B27
      • Protective - HLA-B22
    • TNF-alpha promoter polymorphisms are also thought to be associated with psoriatic arthritis.
  • Environmental factors: Although trauma and infection are thought to play a role in the etiology of psoriatic arthritis, no conclusive evidence exists to support this notion. Infection-mediated molecular mimicry is theorized to play a pathogenic role through immunologic factors.
  • Immunologic factors: Much evidence suggests that a T-cell–mediated process drives the pathophysiology of psoriasis and psoriatic arthritis. Activated T cells may contribute to the enhanced production of cytokines found in synovial fluid. Th1 cytokines (eg, TNF-alpha, interleukin (IL)–1-beta, IL-10) are more prevalent in psoriatic arthritis than in RA. Monocytes also play a role in psoriatic arthritis and are responsible for the production of matrix metalloproteinases, which may mediate the destructive changes in the joints of patients with psoriatic arthritis.
  • Vascular factors: Slight differences exist in the vascular patterns of joints in psoriatic arthritis compared with those of RA, suggesting possible different pathogenic mechanisms of these diseases.

More on Psoriatic Arthritis

Overview: Psoriatic Arthritis
Differential Diagnoses & Workup: Psoriatic Arthritis
Treatment & Medication: Psoriatic Arthritis
Follow-up: Psoriatic Arthritis
Multimedia: Psoriatic Arthritis
References

References

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Further Reading

Keywords

psoriasis, seronegative spondyloarthropathy, polyarthritis, rheumatoid arthritis, oligoarthritis, chronic inflammatory arthritis, asymmetric oligoarthritis, asymmetrical oligoarthritis, symmetric oligoarthritis, symmetrical oligoarthritis, arthritis mutilans, spondylitis, DIP psoriatic arthritis, distal interphalangeal joint arthritis, juvenile psoriatic arthritis, psoriatic nail lesions

Contributor Information and Disclosures

Author

Abby S Van Voorhees, MD, Assistant Professor, Director of Psoriasis Services and Phototherapy Units, Department of Dermatology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania
Abby S Van Voorhees, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, National Psoriasis Foundation, Phi Beta Kappa, Sigma Xi, and Women's Dermatologic Society
Disclosure: Amgen Honoraria Consulting; Astellas Grant/research funds Other; Abbott Honoraria Consulting; Genentech Honoraria Consulting; Incyte Grant/research funds Other; Centocor Honoraria Consulting; Warner Chilcott  Consulting; Merck Salary Review panel membership

Coauthor(s)

Michael J Dans, MD, PhD, Clinical Instructor, Department of Dermatology, University of California at San Francisco
Michael J Dans, MD, PhD is a member of the following medical societies: American Academy of Dermatology and American Medical Association
Disclosure: Nothing to disclose.

Darice Williams Fadeyi, MD, Associate Physician, Lexington Avenue Dermatology
Darice Williams Fadeyi, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Alexa F Boer Kimball, MD, MPH, Associate Professor of Dermatology, Harvard University School of Medicine; Director of Clinical Unit for Research Trials in Skin, Associate Dermatologist, Department of Dermatology, Massachusetts General and Brigham and Women's Hospitals
Alexa F Boer Kimball, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Christen M Mowad, MD, Assistant Professor, Department of Dermatology, Geisinger Medical Center
Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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