title: Role of immune system, apoptosis and angiogenesis in pathogenesis of rheumatoid arthritis and joint destruction, a systematic review.
abstract: BACKGROUND
  Rheumatoid arthritis (RA) is a chronic inflammatory disorder of unknown cause that is notorious for the chronic polyarticular synovial inflammation and progressive destruction of affected joints. Understanding the pathogenesis of RA provides the basis for optimal management of that disease in patients. The pathogenesis of RA was largely explored in many studies in human as much as in mice models with collagen II induced arthritis, nevertheless the pathogenesis puzzle is still incomplete.
  
  
  OBJECTIVE
  The aim of this systematic review was to collect the results of many observations and to put them down into an original story of RA set up.
  
  
  METHODS
  An exhaustive electronic and library search of the relevant literature was carried out through "science direct" and "interscience wiley" web sites. The key words used for the search were "rheumatoid arthritis", "pathogenesis", "apoptosis", "angiogenesis", "immune response" and "joint destruction".
  
  
  RESULTS
  The suspected responsible antigen isn't yet determined although the great specificity of anti-CCP antibodies suggests that this antigen carries probably many citrullinated residues. The immuno-pathogenesis of RA involves both the innate and the adaptive immune system. In the other hand, apoptosis defect contribute to hyperplasia of rheumatoid synovium and in extended half life of fibroblast like synoviocytes (FLS), neutrophils and many other cells implied in rheumatoid synovitis. Hyperplasia of synovium leads to ischemia and that results in neo-angiogenesis with increase of proangiogenic factors such as VEGF. The last part of the pathogenesis of RA is the joint destruction resulting from increased MMP production and activation of osteoclasts which leads to the breakup of cartilage and to bone damage.
authors.affiliation: Laboratoire d'immunologie, EPS Charles Nicolle, Tunis, Tunisia.
authors.forename: Tarak
authors.initials: T
authors.lastname: Dhaouadi
authors.forename: Imen
authors.initials: I
authors.lastname: Sfar
authors.forename: Leila
authors.initials: L
authors.lastname: Abelmoula
authors.forename: Salwa
authors.initials: S
authors.lastname: Jendoubi-Ayed
authors.forename: Houda
authors.initials: H
authors.lastname: Aouadi
authors.forename: Taieb
authors.initials: T
authors.lastname: Ben Abdellah
authors.forename: Khaled
authors.initials: K
authors.lastname: Ayed
authors.forename: Rafik
authors.initials: R
authors.lastname: Zouari
authors.forename: Yousr
authors.initials: Y
authors.lastname: Gorgi
mesh_terms: D000818:Animals; D017209:Apoptosis; D001169:Arthritis, Experimental; D001172:Arthritis, Rheumatoid / Q000175:diagnosis / Q000209:etiology* / Q000276:immunology* / Q000473:pathology; D001402:B-Lymphocytes / Q000276:immunology; D006801:Humans; D007150:Immunohistochemistry; D007596:Joints / Q000473:pathology; D051379:Mice; D016688:Mice, Inbred NOD; D018345:Mice, Knockout; D009389:Neovascularization, Pathologic; D013601:T-Lymphocytes / Q000276:immunology; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology
chemical_list: D042461:Vascular Endothelial Growth Factor A