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See Latest ArticlesEfficacy of roxithromycin in adult patients with rheumatoid arthritis who had not received disease-modifying antirheumatic drugs: A 3-month, randomized, double-blind, placebo-controlled trial
Clinical Therapeutics, 10/15/09
Ogrendik M – It has been reported that antibodies to oral anaerobic bacteria are elevated in the serum and synovial fluids of patients with rheumatoid arthritis. Macrolide antibiotics are active against oral anaerobic bacteria...In these adult patients with rheumatoid arthritis, 3–month treatment with roxithromycin significantly improved the signs and symptoms of rheumatoid arthritis and was generally well tolerated. Future studies should investigate the relationship between disease activity and serum or joint antibodies to anaerobic bacteria.
Mesut Ogrendik, 10/15/09
| In this article, we have shown that 3-month treatment with roxithromycin significantly improved the signs and symptoms of rheumatoid arthritis (RA). We think that RA is an autoimmune disease caused by oral bacteria and roxithromycin can be used for the treatment of this disease with it is both antibacterial and immunomodulatory effects. Following findings indicate that RA is an autoimmune disease caused by oral bacteria: Porphyromonas gingivalis, Prevotella intermedia, Prevotella melaninogenica, and Tannerella forsythensis are Gram-negative anaerobic bacteria and are considered to be directly responsible for the periodontitis (periodontopathic bacteria) [1]. They are found commensally in the body flora, where they cause chronic sinusitis, chronic recurrent tonsillitis, bronchitis, pneumonia, chronic otitis media, parotitis, intra-abdominal infection, genitourinary infection, and wound infections in immune-suppressed individuals and when in conjunction with facultative anaerobic bacteria . Clinical studies of rheumatoid arthritis (RA) and periodontal disease have provided evidence for a significant association between the two disorders . Patients with long-standing active RA have a substantially increased frequency of periodontal disease compared to that among healthy subjects. Patients with periodontal disease have a higher prevalence of RA than patients without periodontitis[2-4]. Anaerobic bacterial DNAs and high levels of antibodies against these bacteria have been detected in the serum and synovial fluid from patients with the early or late stage of RA [5-7]. Ornidazole , levofloxacin, and clarithromycin have been shown to be effective against RA[8-10]. Ornidazole, levofloxacin, and clarithromycin are used in the treatment of infections caused by anaerobic bacteria. Effectiveness of antibiotics is independent of the stage or severity of RA. Alteration of bowel flora has been proposed as a mechanism of action for sulfasalazine, and it has been shown that patients with inflammatory bowel disease treated with sulfasalazine have decreased numbers of nonsporing anaerobes[11].Doxycycline and minocycline are members of the tetracycline family of broad-spectrum antibiotics[12]. Double blind, randomised controlled trials have shown that minocycline is an effective disease-modifying antirheumatic drug in RA, compared with placebo[13-16]. Deimination of arginine residues in autoantigenic proteins (profilaggrin/filaggrin, fibrinogen/fibrin, keratin, and vimentin) creates epitopes that are targeted by rheumatoid autoantibodies (anti-cyclic citrullinated peptide antibodies) . Arginine is the most important of the amino acids associated with autoantigenicity in proteins. There is one report of a peptidylarginine deiminase expression in the bacterium Porphyromonas gingivalis[17]. Tannerella forsythensis and Treponema denticola have arginine-specific proteinase. RF has been detected in the gingiva, subgingival plaque, saliva, and serum of patients with various periodontal diseases, particularly in patients with adult periodontitis[18-19]. Stastny[20] stated the relationship between the RA and HLA-DR4 in 1978. HLA-DR4 tissue antigens are found at high frequencies both in patients with periodontitis and in those with RA[21-23]. Some T-cell receptor (TCR) Vbeta genes (Vbeta-6,8,14,17) are present more frequently in patients with RA than in control subjects[24,25]. Similarly, P. intermedia specifically stimulates the expression of Vbeta-8 and Vbeta-17 genes in CD4(+) T cells[26]. Porphyromonas gingivalis and P. intermedia increase the expression of Vbeta-6 and Vbeta-8 (superantigens in RA) [27]. Finaly, RA is an autoimmune disease caused by oral bacteria. REFERENCES 1.Tatakis DN, Kumar PS. Etiology and pathogenesis of periodontal diseases. Dent Clin North Am. 2005;49:491-516. 2. Greenwald RA, Kirkwood K . Adult periodontitis as a model for rheumatoid arthritis (with emphasis on treatment strategies). J Rheumatol. 1999;26:1650-3. 3. Mercado FB, Marshall RI, Klestov AC, Bartold PM . Relationship between rheumatoid arthritis and periodontitis. J Periodontol. 2001;72:779-87. 4. Rosenstein ED, Greenwald RA, Kushner LJ, Weissmann G. Hypothesis: the humoral immune response to oral bacteria provides a stimulus for the development of rheumatoid arthritis. Inflammation. 2004;28:311-8. 5.Moen K, Brun JG, Madland TM, Tynning T, Jonsson R. Immunoglobulin G and A antibody responses to Bacteroides forsythus and Prevotella intermedia in sera and synovial fluids of arthritis patients. Clin Diagn Lab Immunol. 2003;10:1043-50. 6. Ogrendik M, Kokino S, Ozdemir F, Bird PS, Hamlet S. Serum antibodies to oral anaerobic bacteria in patients with rheumatoid arthritis. MedGenMed. 2005 Jun 16;7(2):2. Avaliable at: http://www.medscape.com/viewarticle/505458 . Accessed June 16, 2005. 7.Moen K, Brun JG, Valen M, et al. Synovial inflammation in active rheumatoid arthritis and psoriatic arthritis facilitates trapping of a variety of oral bacterial DNAs. Clin Exp Rheumatol. 2006;24:656-63. 8. Ogrendik M, Hakguder A, Keser N. Treatment of rheumatoid arthritis with ornidazole. A randomized, double-blind, placebo-controlled study. Rheumatology(Oxford). 2006;45: 636-7. 9.Ogrendik M. Levofloxacin treatment in patients with rheumatoid arthritis receiving methotrexate. South Med J. 2007;100:135-9. 10.Ogrendik M. Effects of clarithromycin in patients with active rheumatoid arthritis. Curr Med Res Opin. 2007;23:515-22. 11. Das KM. Sulfasalazine therapy in inflammatory bowel disease. Gastroenterol Clin North Am. 1989 ;18:1-20. 12. Amin AR, Attur MG, Thakker GD, et al. A novel mechanism of action of tetracyclines: effects on nitric oxide synthases. Proc Natl Acad Sci U S A. 1996 ;93:14014-9. 13.Tilley BC, Alarcon GS, Heyse SP, et al. Minocycline in rheumatoid arthritis. A 48-week, double-blind, placebo-controlled trial. MIRA Trial Group. Ann Intern Med. 1995;122:81–9. 14. Kloppenburg M, Breedveld FC, Terwiel JP, Mallee C , Dijkmans BA. Minocycline in active rheumatoid arthritis. A double-blind, placebo-controlled trial. Arthritis Rheum. 1994;37:629–36. 15.O’Dell JR, Haire CE, Palmer W , et al. Treatment of early rheumatoid arthritis with minocycline or placebo: results of a randomized, double-blind, placebo-controlled trial. Arthritis Rheum. 1997;40:842–8. 16.O’Dell JR, Paulsen G , Haire CE, et al. Treatment of early seropositive rheumatoid arthritis with minocycline: four-year followup of a double-blind, placebo-controlled trial. Arthritis Rheum. 1999;42:1691–5. 17. McGraw WT, Potempa J, Farley D, Travis J. Purification, characterization, and sequence analysis of a potential virulence factor from Porphyromonas gingivalis, peptidylarginine deiminase. Infect Immun. 1999 ;67:3248-56. 18. Gargiulo AV Jr, Robinson J, Toto PD, Gargiulo AW. Identification of rheumatoid factor in periodontal disease. J Periodontol. 1982;53:568-77. 19. Thé J, Ebersole JL. Rheumatoid factor (RF) distribution in periodontal disease. J ClinImmunol. 1991;11:132-42. 20.Stastny P. Association of the B-cell alloantigen DRw4 with rheumatoid arthritis. N Engl J Med. 1978;298:869–871. 21. Katz J, Goultschin J, Benoliel R, Brautbar C. Human leukocyte antigen (HLA) DR4. Positive association with rapidly progressing periodontitis. J Periodontol.1987;58:607-10. 22. Gran JT, Husby G, Thorsby E. The association between rheumatoid arthritis and HLA antigen DR4. Ann Rheum Dis. 1983;42:292-6. 23. Bonfil JJ, Dillier FL, Mercier P, et al. A "case control" study on the role of HLA DR4 in severe periodontitis and rapidly progressive periodontitis. Identification of types and subtypes using molecular biology (PCR.SSO).J Clin Periodontol. 1999;26:77-84. 24.Cuesta IA, Sud S, Song Z, Affholter JA, et al. T-cell receptor (V beta) bias in the response of rheumatoid arthritis synovial fluid T cells to connective tissue antigens. Scand J Rheumatol. 1997;26:166-173. 25.Hall FC, Thomson K, Procter J, McMichael AJ, Wordsworth BP.TCR beta spectratyping in RA: evidence of clonal expansions in peripheral blood lymphocytes. Ann Rheum Dis. 1998;57:319-22. 26.Leung KP, Torres BA. Prevotella intermedia stimulates expansion of Vbeta-specific CD4(+) T cells. Infect Immun. 2000;68:5420-5424. 27.Mathur A, Michalowicz B, Yang C, Aeppli D. Influence of periodontal bacteria and disease status on V beta expression in T cells. J Periodontal Res. 1995;30:369-373. |
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