Rheumatoid arthritis (RA) is a chronic destructive arthritis of unknown etiology characterized
by various immune aberrations.
Mycoplasma, may serve as a cofactor that along with biological and/or chemical stressors
can induce proinflammatory cytokines (such as IL-6 and TNF alpha) and other immune abnormalities found in RA. Indeed, the occurrence of mycoplasma and Ureaplasma
species in joint tissues of RA and other forms of arthritis suggest that mycoplasma
might be significant cofactor that precipitates the symptomatology of RA. Moreover,
high levels of specific antibodies to Mycoplasma fermentans in synovial fluids of almost
50% of RA patients, was reported by Horowitz S et al., 2000, suggesting a local
production of antibodies inside the joints, namely – this bacteria was probably present
in the synovial cells, sometimes during development of the disease.
We have previously suggested that mycoplasma may trigger arthritis by means of a
chronic infection with a persistent low level bacterial load or by a “hit and run” phenomenon
in which mycoplasma is found in the joint for a short period of time and disappears
thereafter but initiates a cascade of events leading to an inflammatory process. It is also
possible that mycoplasma persist in other location of the body and occasionally reaches
the joint and causes exacerbation of arthritis.
More clinical efforts need to be made in identifying possible infections. Since
mycoplasma infections are found at significantly higher rates in RA, effective treatment
should be considered.