Oligoarthritis refers to the simultaneous inflammation of several, but not more than four joints. It is a general term that describes a condition to be encountered in patients suffering from distinct autoimmune, infectious or idiopathic diseases, e.g., oligoarticular juvenile idiopathic arthritis, reactive arthritis, and psoriatic arthritis.
Patients suffering from oligoarthritis typically present with symptoms associated with joint inflammation and functional impairment of joints. Affected joints are usually tender, and patients claim arthralgia. Closer inspection may reveal joint swelling or joint effusion, and chronic disease may result in joint deformities. Generally, motion ranges are reduced, and patients describe stiffness. Movements may induce crepitation.
Anamnestic data, symptom onset, distribution patterns as well as disease progression largely depend on the underlying disease. The following examples shall illustrate the diversity of clinical pictures presented by oligoarthritis patients as well as the importance of thorough anamnesis and physical examination.
Of note, joint inflammation may not induce clinical symptoms at all .
Oligoarthritis may be diagnosed in patients presenting with arthralgia and symptoms indicating an ongoing inflammation in up to four joints, but additional measures may be necessary to identify subclinical joint disease. Laboratory analyses of blood samples, sonography and possibly invasive techniques may be very helpful to that end. Oligoarthritis is typically associated with elevated concentrations of serum inflammatory markers like C-reactive protein, and the erythrocyte sedimentation rate is usually enhanced. Leukocytosis is characteristic of acute inflammatory disorders. Sonography has been successfully used to diagnose subclinical joint inflammation. Eventually, joint biopsies may be carried out to support a tentative diagnosis and to rule out more severe differential diagnoses. Malignancies don't usually provoke oligoarthritis, but neoplasms have occasionally been related with this disorder .
In order to identify the underlying disease, target-oriented measures should be chosen based on a list of likely differential diagnoses. In this regards, workup may comprise the following:
It is of utmost important to make a precise diagnosis and to chose an adequate therapeutic regimen to avoid further damage to cartilage, underlying bone and other anatomical structures compromised by joint inflammation. Although symptomatic therapy may help to relieve arthralgia and to restore motion ranges, cure of the primary disease is the best way to avoid recurrence. Although the latter may occur spontaneously - e.g., in case of RA - analgesic and anti-inflammatory medication may mask the underlying disease and cause detrimental diagnostic delays .
Symptomatic treatment generally consists in the administration of non-steroidal antiinflammatory drugs that reduce pain and inflammation. In case of persistent or exacerbating arthritis, corticosteroid therapy may be considered. Corticosteroids may be applied per os, parenterally or intraarticularly. Furthermore, disease-modifying antirheumatic drugs like azathioprine, methotrexate, etanercept and infliximab may be administered to control immune-mediated oligoarthritis. However, long-term administration of such drugs may be associated with safety risks, and evidence regarding their effectivity is often scarce. With regards to OJIA, only methotrexate has been shown to be superior to conventional treatment as described before . For treatment of PA, tumor necrosis factor-α inhibitors like etanercept; ustekinumab, a monoclonal antibody targeting interleukin-12 and -23; and secukinumab, an antibody directed against interleukin-17A, may be used . Antibiotics may be indicated in case of RA, although evidence of beneficial effects has only been provided for determined forms of the disease. In this context, antimicrobial treatment is generally recommended for post-streptococcal RA. If arthritis has already developed after genitourinary or gastrointestinal infections, antibiotics are of little use .
Surgical interventions are rarely required.
Patients diagnosed with oligoarthritis due to primary disorders potentially associated with ocular and renal damage should undergo regular ophthalmological examinations and urine analyses.
Entities causing oligoarthritis are associated with distinct prognoses:
Oligoarthritis may be developed by patients suffering from a wide variety of diseases. Few entities are primarily related to an inflammation of more than one but less than five joints. OJIA, RA and PA as well as undifferentiated arthritis are classic examples of such pathologies. As implied by its designation, the etiology of OJIA remains largely unknown. Genetic predisposition and possibly environmental factors may trigger the onset of an autoimmune response, possibly accompanied by the production of autoantibodies like rheumatoid factor and anti-cyclic citrullinated peptide antibodies . Autoantibodies may also be detected in sera obtained from PA patients, although the assessment of antibody titers is not a sensitive diagnostic tool . PA is considered an autoimmune disease developed by about a fourth of psoriasis patients, but little is known about the triggers of joint inflammation in individuals suffering from scaling cutaneous lesions. Psoriasis-associated skin lesions have been assumed to be provoked by dysregulation of immune cell function and cytokine release following trauma or infection. Cytokines may reach the skeleton and modify the function of cartilage- and bone-forming cells . RA is a type of sterile arthritis commonly triggered by previous genitourinary or gastrointestinal infection with Chlamydia trachomatis or enteric pathogens (e.g., Salmonella spp., Yersinia spp.), respectively . Streptococcus spp. and a wide variety of other bacterial pathogens may also provoke RA, particularly in genetically predisposed individuals. The preceding infection may or may not provoke clinical symptoms. In case it doesn't, the patient is generally diagnosed with undifferentiated arthritis, a clinically similar entity of unknown etiology. Of note, undifferentiated arthritis may also turn into polyarthritis. Indeed, oligoarthritis is characteristic of evolving polyarthritis. In this context, autoimmune disorders like rheumatoid arthritis, seronegative arthritis, and systemic lupus erythematosus as well as infectious diseases like Lyme disease and Whipple disease should be considered  . For detailed information on polyarthritis, the interested reader is referred to the respective article.
Although overall incidence and prevalence of oligoarthritis are unknown, the condition is presumably underdiagnosed. High prevalence of subclinical disease has been encountered in a study using sonography to examine both symptomatic and asymptomatic joints of school children in the United States . With regards to epidemiology, major difference between oligoarthritis and polyarthritis is the earlier age of onset of the former.
Additionally, epidemiological data can be provided regarding individual entities associated with this condition.
Pathophysiological events provoking oligoarthritis depend on the underlying disease. Still, dysregulation of immune cell function and cytokine release plays a crucial role in the induction and maintenance of oligoarthritis. On the one hand, immune-modulatory environmental influences may trigger the onset of OJIA in genetically predisposed individuals . Distinct populations of immune cells, e.g. T lymphocytes, plasma cells and natural killer cells, may be affected. On the other hand, psoriasis is associated with an activation of dendritic cells in the skin . These cells release interferon-α, a cytokine that promotes a determined subpopulation of dendritic cells to migrate to the lymph nodes. Here, they release interleukin-12 and -23, which affect T cell differentiation and maturation. Eventually, differentiated T cells return to circulation, reach end organs and produce tumor necrosis factor-α, interferon-γ, and interleukin-17, among others. In patients suffering from RA, the immune response triggering the onset of joint inflammation takes place in affected joints. In detail, antigens may spread via the cardiovascular system, reach joints, and induce an immune reaction associated with damage to anatomic structures composing the joint.
Further research is required to clarify the pathogenetic differences between distinct forms of juvenile idiopathic arthritis, to ascertain why psoriasis patients do or don't develop arthritis, and which conditions predispose for RA. Finally, there is a considerable overlap between these entities, since patients may develop psoriatic juvenile idiopathic arthritis and because determined forms of juvenile idiopathic arthritis predispose for RA. The central role of cytokines in all these pathologies is best illustrated by the patients' response to immunomodulatory therapy.
Specific measures can be recommended only for determined forms of oligoarthritis. RA, for instance, is triggered by an infection with Chlamydia trachomatis or enteric pathogens. Accordingly, measures to prevent sexually transmitted diseases and an appropriate general hygiene may reduce the individual risk of RA.
Oligoarthritis is a descriptive term referring to the simultaneous inflammation of two to four joints in an individual patient. In contrast, individuals suffering from an inflammation of a single joint are diagnosed with monarthritis, and those presenting with even more extensive joint diseases receive a diagnosis of polyarthritis. Distinction between monarthritis, oligoarthritis and polyarthritis may be of diagnostic value. For instance, traumatic joint injury is generally restricted to a single joint or to a determined region of the human body, e.g., the patient's feet or knees, as opposed to systemic autoimmune disease, metabolic disorder or nutrient deficiency, which rather manifest in form of multiple joint lesions. However, these are not exclusion criteria for either form of arthritis. In fact, both monarthritis and polyarthritis may turn into oligoarthritis upon an exacerbation or partial remission, respectively, and vice versa. Thus, it is strongly recommended to consider common causes of monarthritis or polyarthritis when dealing with a patient suffering from oligoarthritis. Anamnestic data, distribution patterns, and clinical symptoms not related to joint inflammation are of utmost importance at the time of establishing a list of potential differential diagnoses.
It is beyond the scope of this article to discuss every possible trigger of oligoarthritis. Thus, general information is provided wherever possible. Additionally, more detailed data are included regarding oligoarticular juvenile idiopathic arthritis (OJIA), reactive arthritis (RA), and psoriatic arthritis (PA), which are common causes of oligoarthritis.
Oligoarthritis refers to the simultaneous inflammation of two to four joints in an individual patient. Oligoarthritis may affect people of any race, both genders and all age groups, but diseases triggering multiple joint inflammation are generally more or less prevalent in determined patient groups. In pediatric patients, the most common cause of oligoarthritis is a specific form of juvenile idiopathic arthritis. However, children may also develop joint inflammation within two months after a genitourinary or gastrointestinal infection, and this form of arthritis is deemed reactive arthritis. The latter may also occur in adults. Furthermore, adult patients with a medical history of psoriasis may be diagnosed with psoriatic arthritis. In sum, a wide variety of autoimmune disorders, infectious diseases, metabolic and endocrine dysbalances as well as neoplasms may provoke oligoarthritis.
Symptoms characteristic of oligoarthritis are joint pain and tenderness of surrounding tissues, joint swelling, stiffness and reduced motion ranges. In severe cases, joint inflammation may provoke permanent deformities. Depending on the underlying disease, patients may show distinct distribution patterns and additional symptoms, and the treating physician will consider all this information when making a diagnosis and choosing an appropriate therapy.