Rheumatoid arthritis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
Overview
Pathophysiology
- Possible role of infections
- Some infectious organisms mentioned in this context have been Mycoplasma, Erysipelothrix, Epstein-Barr virus, parvovirus B19 and rubella, adenovirus, Herpesvirus, have been implicated in the pathophysiology of RA.[1] [2] [3] [4]
- Periodontitis and Rheumatoid arthritis
- Various studies have elucidated the co-relation between periodontitis and Rheumatoid arthritis because of the similarities .[5]
- It was found to be more common and severe in patients with RA, but did not correlate with the disease severity. The presence of periodontitis in these patients was also associated with seropositivity for Rheumatoid factor, the anti-cyclic citrullinated peptide antibody (anti-CCP)and antibodies to Porphyromonas gingivalis as well. [6] [7]
- Smoking
- Smoking is one of the most important independent risk factors for radiographic progression of RA. It is associated with an earlier disease onset and shared epitope HLA DRB1.[8] [9] However, short term cessation in smoking does not appear to alter the progression of disease activity over time.[10]
- Genetic variations in NAT2 appear to mediate the risk RA imposed by smoking in African American population.[11]
- Effects of lifestyle
- There is also no clear evidence that physical and emotional effects, stress and improper diet could be a trigger for the disease. The many negative findings suggest that either the trigger is different from patient to patient, or that the trigger might in fact be a chance event. [12]
- Genetic associations
- It has also become clear from recent studies that these genetic factors may interact with the most clearly defined environmental risk factor for rheumatoid arthritis, namely cigarette smoking [13]
- Hormonal factors
- Sex hormones also appear to play a role in pathophysiology of RA, partly the reason for increased incidence of RA in women.
- The symptoms of RA may alleviate during the luteal phase of the menstrual cycle when the progesterone levels peak.[14]
- Breast feeding also appears to exacerbate symptoms. As the immediate postpartum period also imposes a risk for disease activity flare up, the exact role of breast feeding in RA is difficult to delineate.
- Occupational risks
- Other factors
References
- ↑ Kozireva SV, Zestkova JV, Mikazane HJ; et al. (2008). "Incidence and clinical significance of parvovirus B19 infection in patients with rheumatoid arthritis". The Journal of Rheumatology. 35 (7): 1265–70. PMID 18484700. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Davis JM, Knutson KL, Skinner JA; et al. (2012). "A profile of immune response to herpesvirus is associated with radiographic joint damage in rheumatoid arthritis". Arthritis Research & Therapy. 14 (1): R24. doi:10.1186/ar3706. PMID 22293286. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Pierer M, Rothe K, Quandt D; et al. (2011). "Anti-cytomegalovirus seropositivity in rheumatoid arthritis is associated with more severe joint destruction and more frequent joint surgery". Arthritis and Rheumatism. doi:10.1002/art.34346. PMID 22183424. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Goldstein BL, Chibnik LB, Karlson EW, Costenbader KH (2012). "Epstein-Barr virus serologic abnormalities and risk of rheumatoid arthritis among women". Autoimmunity. 45 (2): 161–8. doi:10.3109/08916934.2011.616557. PMID 22011088. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Mercado FB, Marshall RI, Bartold PM (2003). "Inter-relationships between rheumatoid arthritis and periodontal disease. A review". Journal of Clinical Periodontology. 30 (9): 761–72. PMID 12956651. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Dissick A, Redman RS, Jones M; et al. (2010). "Association of periodontitis with rheumatoid arthritis: a pilot study". Journal of Periodontology. 81 (2): 223–30. doi:10.1902/jop.2009.090309. PMID 20151800. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Mikuls TR, Payne JB, Reinhardt RA; et al. (2009). "Antibody responses to Porphyromonas gingivalis (P. gingivalis) in subjects with rheumatoid arthritis and periodontitis". International Immunopharmacology. 9 (1): 38–42. doi:10.1016/j.intimp.2008.09.008. PMC 2748386. PMID 18848647. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Ruiz-Esquide V, Gómez-Puerta JA, Cañete JD; et al. (2011). "Effects of smoking on disease activity and radiographic progression in early rheumatoid arthritis". The Journal of Rheumatology. 38 (12): 2536–9. doi:10.3899/jrheum.110410. PMID 22045838. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Bang SY, Lee KH, Cho SK, Lee HS, Lee KW, Bae SC (2010). "Smoking increases rheumatoid arthritis susceptibility in individuals carrying the HLA-DRB1 shared epitope, regardless of rheumatoid factor or anti-cyclic citrullinated peptide antibody status". Arthritis and Rheumatism. 62 (2): 369–77. doi:10.1002/art.27272. PMID 20112396. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Fisher MC, Hochberg MC, El-Taha M, Kremer JM, Peng C, Greenberg JD (2012). "Smoking, Smoking Cessation, and Disease Activity in a Large Cohort of Patients with Rheumatoid Arthritis". The Journal of Rheumatology. doi:10.3899/jrheum.110852. PMID 22422494. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Mikuls TR, Levan T, Gould KA; et al. (2012). "Impact of interactions of cigarette smoking with NAT2 polymorphisms on rheumatoid arthritis risk in African Americans". Arthritis and Rheumatism. 64 (3): 655–64. doi:10.1002/art.33408. PMID 21989592. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Edwards JC, Cambridge G, Abrahams VM. Do self-perpetuating B lymphocytes drive human autoimmune disease? Immunology. 1999;97:188-96.
- ↑ Padyukov L, Silva C, Stolt P, Alfredsson L, Klareskog L. A gene-environment interaction between smoking and shared epitope genes in HLA-DR provides a high risk of seropositive rheumatoid arthritis. Arthritis Rheum. 2004;50:3085-92.
- ↑ Case AM, Reid RL (1998). "Effects of the menstrual cycle on medical disorders". Archives of Internal Medicine. 158 (13): 1405–12. PMID 9665348. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Stolt P, Yahya A, Bengtsson C; et al. (2010). "Silica exposure among male current smokers is associated with a high risk of developing ACPA-positive rheumatoid arthritis". Annals of the Rheumatic Diseases. 69 (6): 1072–6. doi:10.1136/ard.2009.114694. PMID 19966090. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Stolt P, Källberg H, Lundberg I, Sjögren B, Klareskog L, Alfredsson L (2005). "Silica exposure is associated with increased risk of developing rheumatoid arthritis: results from the Swedish EIRA study". Annals of the Rheumatic Diseases. 64 (4): 582–6. doi:10.1136/ard.2004.022053. PMC 1755463. PMID 15319232. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ Crowson CS, Matteson EL, Davis JM, Gabriel SE (2012). "Obesity fuels the upsurge in rheumatoid arthritis". Arthritis Care & Research. doi:10.1002/acr.21660. PMID 22514156. Retrieved 2012-04-26. Unknown parameter
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ignored (help) - ↑ 18.0 18.1 Liao KP, Alfredsson L, Karlson EW (2009). "Environmental influences on risk for rheumatoid arthritis". Current Opinion in Rheumatology. 21 (3): 279–83. doi:10.1097/BOR.0b013e32832a2e16. PMC 2898190. PMID 19318947. Retrieved 2012-04-26. Unknown parameter
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ignored (help)