Rheumatoid arthritis pathophysiology: Difference between revisions

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==Overview==
==Pathophysiology==
==Pathophysiology==
[[Image:Rheumatoid arthritis joint.gif|thumb|left|Joint abnormalities in rheumatoid arthritis]]
[[Image:Rheumatoid arthritis joint.gif|thumb|left|Joint abnormalities in rheumatoid arthritis]]
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**Role of [[oral contraceptive]] pills and [[vitamin D]] is found to be equivocal.<ref name="pmid19318947">{{cite journal |author=Liao KP, Alfredsson L, Karlson EW |title=Environmental influences on risk for rheumatoid arthritis |journal=[[Current Opinion in Rheumatology]] |volume=21 |issue=3 |pages=279–83 |year=2009 |month=May |pmid=19318947 |pmc=2898190 |doi=10.1097/BOR.0b013e32832a2e16 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1040-8711&volume=21&issue=3&spage=279 |accessdate=2012-04-26}}</ref>
**Role of [[oral contraceptive]] pills and [[vitamin D]] is found to be equivocal.<ref name="pmid19318947">{{cite journal |author=Liao KP, Alfredsson L, Karlson EW |title=Environmental influences on risk for rheumatoid arthritis |journal=[[Current Opinion in Rheumatology]] |volume=21 |issue=3 |pages=279–83 |year=2009 |month=May |pmid=19318947 |pmc=2898190 |doi=10.1097/BOR.0b013e32832a2e16 |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1040-8711&volume=21&issue=3&spage=279 |accessdate=2012-04-26}}</ref>
==References==
==References==
{{reflist|2}}
{{Reflist|2}}


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[[Category:Aging-associated diseases]]
[[Category:Aging-associated diseases]]
[[Category:Arthritis]]
[[Category:Arthritis]]
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[[Category:Diseases involving the fasciae]]
[[Category:Diseases involving the fasciae]]
[[Category:Rheumatology]]
[[Category:Rheumatology]]
[[Category:Needs overview]]
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Revision as of 13:34, 18 March 2013

Rheumatoid arthritis Microchapters

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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]

Pathophysiology

Joint abnormalities in rheumatoid arthritis


  • Possible role of infections
  • 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
    • The factors that allow the inflammation, once initiated, to become permanent and chronic, are much more clearly understood. The genetic association with HLA-DR4 is believed to play a major role in this, as well as the newly discovered associations with the gene PTPN22 and with two additional genes [13] [14], all involved in regulating immune responses.
    • 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 [15]
  • 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.[16]
    • Pregnancy is associated with remission of the symptoms of RA throughout the three trimesters, whereas an increase in disease activity is noted in the first three months postpartum.[17]
    • 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

  1. 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 |month= ignored (help)
  2. 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 |month= ignored (help)
  3. 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 |month= ignored (help)
  4. 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 |month= ignored (help)
  5. 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 |month= ignored (help)
  6. 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 |month= ignored (help)
  7. 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 |month= ignored (help)
  8. 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 |month= ignored (help)
  9. 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 |month= ignored (help)
  10. 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 |month= ignored (help)
  11. 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 |month= ignored (help)
  12. Edwards JC, Cambridge G, Abrahams VM. Do self-perpetuating B lymphocytes drive human autoimmune disease? Immunology. 1999;97:188-96.
  13. Plenge RM, Seielstad M, Padyukov L et al. TRAF1-C5 as a risk locus for rheumatoid arthritis--a genomewide study. N Engl J Med. 2007;357:1199-209.
  14. Salliot C, Dawidowicz K, Lukas C; et al. (2011). "PTPN22 R620W genotype-phenotype correlation analysis and gene-environment interaction study in early rheumatoid arthritis: results from the ESPOIR cohort". Rheumatology (Oxford, England). 50 (10): 1802–8. doi:10.1093/rheumatology/ker224. PMID 21752868. Retrieved 2012-04-26. Unknown parameter |month= ignored (help)
  15. 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.
  16. 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 |month= ignored (help)
  17. Silman A, Kay A, Brennan P (1992). "Timing of pregnancy in relation to the onset of rheumatoid arthritis". Arthritis and Rheumatism. 35 (2): 152–5. PMID 1734904. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  18. 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 |month= ignored (help)
  19. 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 |month= ignored (help)
  20. 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 |month= ignored (help)
  21. 21.0 21.1 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 |month= ignored (help)

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