Inflammatory arthritis is characterized by inflammation of tissues surrounding the joints. Connective tissue diseases, crystal deposition diseases, infectious arthritis and spondyloarthropathies are examples of inflammatory arthritis. Osteoarthritis does not fall into the category of inflammatory arthritis because it is a degenerative disease.
Current treatment for inflammatory arthritis focuses on alleviating symptoms rather than targeting the cause of the condition. This approach primarily employs anti-inflammatory medications for first-line treatment. For severe cases, immunomodulatory drugs are used.
For decades, researchers have examined and debated the possibility of an infectious cause for inflammatory arthritis. A notable body of research has identified Mycoplasma as a possible causative organism for many cases of inflammatory arthritis. This article outlines these findings and discusses their implications for practice.
The category of inflammatory arthritis encompasses several types of arthritis, including rheumatoid and psoriatic arthritis. These forms of arthritis have an etiology that is not thoroughly understood, but each type is thought to involve autoimmune processes.1,2
Rheumatoid arthritis is characterized by variable levels of joint inflammation, usually occurring bilaterally in peripheral joints. Symptoms range from mild intermittent stiffness, swelling and discomfort to severe and debilitating joint damage.1 The cause of rheumatoid arthritis is unknown, but a proposed theory is that it involves an immune system reaction to infection in patients who are genetically predisposed to this response.1 Polyclonal immunoglobulin and autoantibody rheumatoid factor are produced within the synovial tissue, leading to local formation of immune complexes.1 Antibodies to the components of synovial tissue may also contribute to inflammation.1
In patients with rheumatoid arthritis, the synovium contains secreted products of activated lymphocytes, macrophages and fibroblasts. The local production of these cytokines and chemokines appears to account for many of the pathologic and clinical manifestations of rheumatoid arthritis.1
In comparison, psoriatic arthritis occurs only in patients with psoriasis. It is a diagnosis based on exclusion of other arthritis etiologies and the presence of psoriatic skin lesions. Erythrocyte sedimentation rate and C-reactive protein are often elevated in psoriatic arthritis, but these are nonspecific findings.2
Interestingly, the inflamed synovium evident in psoriatic arthritis resembles that seen in rheumatoid arthritis.2Many rheumatology experts believe that psoriatic arthritis is immune-mediated because the synovium in affected patients shows infiltration with T cells, B cells, macrophages and NK receptor-expressing cells. Also evident is upregulation of leukocyte homing receptors.2 These features suggest a shared etiology of autoimmune-related inflammation in psoriatic and rheumatoid arthritis.