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A fibrin based model for rheumatoid synovitis
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  1. O Sánchez-Pernaute,
  2. R Largo,
  3. E Calvo,
  4. M A Alvarez-Soria,
  5. J Egido,
  6. G Herrero-Beaumont
  1. Inflammation Research Unit, Rheumatology Section, Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Spain
  1. Correspondence to:
    Dr O Sánchez-Pernaute
    Rheumatology Section, Fundación Jiménez Díaz, Avda Reyes Católicos 2, 28040 Madrid, Spain; OSanchezfjd.es

Abstract

Intracavitary fibrin clots may initiate pannus formation and the immunopathology of RA. Two critical steps, probably host dependent, may determine the development of RA: an altered regulation of extravascular haemostasis or an aberrant reactivity of synovial fibroblasts to the adhered fibrin clots. Current treatments for RA target events downstream of fibrin deposition, perhaps agents acting at an earlier stage should be tried.

  • fibrin
  • fibronectin
  • fibroblasts
  • rheumatoid arthritis
  • MMPs, matrix metalloproteinases
  • PA, plasminogen activator
  • RA, rheumatoid arthritis
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