A. Sulphonamides like sulfasalazine were used against RA in the 1930s and 1940s, and showed some effectiveness (2, 3). This treatment later evolved into the so-called triple DMARD therapy (combination of sulfasalazine, hydroxychloroquine and methotrexate) for treating RA (4, 5).
B. In the 1970s, McPherson Brown revived the long-held view that RA was triggered by an infection and suggested long-term antibiotics, particularly tetracycline (6) for RA treatment. Tetracyclines are protein synthesis inhibitors with broad spectrum antibiotic action. More recently, minocycline, a new generation tetracycline, was shown to be efficacious against RA in 4 different clinical trials (7, 8, 9, 10).
C. Macrolides are another class of antibiotic, also protein synthesis inhibitors. Macrolides like clarithromycin (11, 12, 13) and roxithromycin (14, 15) have also shown effectiveness in treating RA.
D. Fluoquinolones are another class of antibiotic which inhibit cell division by inhibiting enzymes such as DNA gyrase. Levofloxacin, a fluoroquinolone, has also been shown in at least one study (16) to be effective against RA.
Currently, one of the most intensively investigated hypotheses to understand RA etiology (cause) suggests that there is a causative link between periodontal disease and RA (17, 18, 19, 20, 21, 22, 23, 24). Periodontal disease is triggered by infection leading to inflammation of the periodontium, and it can lead to tooth loss. Porphyromonas gingivalis, Prevotella intermedia and Tannerella forsythia are among the bacteria most commonly associated with periodontal disease.
The history for an infectious disease origin for RA is quite long standing. In fact,, a man commonly described as ” the father of modern medicine”, first proposed an infectious disease origin for RA as far back as 1909.