Type Of Inflammatory Arthritis Research Articles

Prevalence of joint disease in patients with psoriasis: implications for therapy.

Joint diseases are common among patients with psoriasis. Psoriatic arthritis, the most important of these, can be defined as a rheumatoid factor-negative inflammatory arthritis associated with psoriasis and has emerged as a specific disease independent from rheumatoid arthritis. Psoriatic arthritis is divided into several clinical subsets, which is helpful in differentiating it from other types of inflammatory arthritis. The prevalence of arthritis in patients with psoriasis may be far higher than the previously accepted average of 7%. In a recent study of 5,795 members of the Nordic Psoriasis Associations, the prevalence was found to be 30%. Arthritis has a significant impact on quality of life in patients with psoriasis. These factors should be recognised as they have implications for therapy, since a number of drugs can delay or stop joint damage when given in time. This also applies to the new biologic agents, although at present these therapies are generally restricted to patients non-responsive to other available drugs. Alone or in combination, the new drugs may achieve higher response rates and have better safety profiles than older therapies. However, long-term experience is still lacking and, unfortunately, the new drugs will be far from affordable by all for some time to come.

Mactinin: a modulator of the monocyte response to inflammation.

During inflammatory processes, monocytes leave the blood stream at increased rates and enter inflammation tissue, where they undergo phenotypic transformation to mature macrophages with enhanced phagocytic activity. alpha-Actinin, a cytoskeletal protein, is present in focal adhesion complexes and left in the microenvironment as a result of cell movement. Mactinin, a 31 kDa amino-terminal fragment of alpha-actinin, is generated by the degradation of extracellular alpha-actinin by monocyte-secreted urokinase. We have previously demonstrated that mactinin promotes monocyte/macrophage maturation. We now report that 0.5-10 nM mactinin has significant chemotactic activity for monocytes. Mactinin seems to be present in inflammatory arthritis synovial fluid, because affinity-purified antisera reacted with a protein of the expected molecular mass in various types of arthritis fluids that were immunoaffinity-purified and subjected to Western analysis. Thus, six of seven samples from patients with psoriatic arthritis, reactive arthritis, gout, or ankylosing spondylitis contained mactinin at levels that are active in vitro. Initially, mactinin was not found in affinity-purified rheumatoid arthritis samples. However, it was detectable after the dissociation of immune complexes, suggesting that it was complexed to anti-microfilament auto-antibodies. In addition, mactinin was found in the lavage fluid from the arthritic knee joints of rabbits with antigen-induced arthritis and was absent from the contralateral control knee fluids. We conclude that mactinin is present in several types of inflammatory arthritis and might modulate mononuclear phagocyte response to inflammation.

Evidence for the Effects of a Superantigen in Rheumatoid Arthritis

While studying the alpha beta T cell receptor repertoire in rheumatoid arthritis (RA) patients, we found that the frequency of V beta 14+ T cells was significantly higher in the synovial fluid of affected joints than in the peripheral blood. In fact, V beta 14+ T cells were virtually undetectable in the peripheral blood of a majority of these RA patients. beta-chain sequences indicated that one or a few clones dominated the V beta 14+ population in the synovial fluid of individual RA patients, whereas oligoclonality was less marked for other V beta's and for V beta 14 in other types of inflammatory arthritis. These results implicate V beta 14-bearing T cells in the pathology of RA. They also suggest that the etiology of RA may involve initial activation of V beta 14+ T cells by a V beta 14-specific superantigen with subsequent recruitment of a few activated autoreactive v beta 14+ T cell clones to the joints while the majority of other V beta 14+ T cells disappear.

Jejunoileal bypass arthritis

Although intestinal bypass procedures are no longer performed, important lessons have been learned concerning clinical arthritides resulting from bacterial overgrowth and immune complex deposition. This information is of considerable value in patients who present with the clinical picture of intestinal bypass arthritis on the basis of other bowel abnormalities. Furthermore, the pathogenetic mechanisms involving bacterial overgrowth, release of bacterial antigens, and immune complex deposition may be pertinent to many types of inflammatory arthritis.

Intravascular degranulation of neutrophils: an important factor in inflammation?

Polymorphonuclear leukocytes are degranulated in the lumens of vessels in synovial membrane in humans with various types of inflammatory arthritis and in dogs with synovitis induced by urate crystals. This degranulation, accompanied by the release of lysosomal enzymes and vasoactive materials, may be an important part of the mechanism resulting in vascular injury.