RA is a heterogeneous autoimmune disease of unknown cause that presents with diverse clinical symptoms.1
However, there appears to be a strong genetic component to the aetiology of RA1,2
The HLA (human leukocyte antigen) region on chromosome 6 has been identified as a major genetic risk locus.3
A number of environmental influencers have been described as risk factors for developing RA.4,5
Investigations have failed to associate RA with any specific infectious agent, but it is possible that infection may trigger RA in individual cases.6
References:
van der Helm-van Mil AH, et al. Emerging patterns of risk factor make-up enable subclassification of rheumatoid arthritis. Arthritis Rheum 2007; 56:1728–1735.
Begovich AB, et al. A missense single-nucleotide polymorphism in a gene encoding a protein tyrosine phosphatase (PTPN22) is associated with rheumatoid arthritis. Am J Hum Genet 2004; 75:330–337.
Lee HS, et al. Genetic risk factors for rheumatoid arthritis differ in Caucasian and Korean populations. Arthritis Rheum 2009; 60:364–371.
Sugiyama D, et al. Impact of smoking as a risk factor for developing rheumatoid arthritis: A meta-analysis of observational studies. Ann Rheum Dis 2009 [epub].
Pedersen M, et al. Environmental risk factors differ between rheumatoid arthritis with and without auto-antibodies against cyclic citrullinated peptides. Arthritis Res Ther 2006; 8:R133.
Symmons D & Harrison B. Early inflammatory polyarthritis: results from the Norfolk arthritis register with a review of the literature. I. Risk factors for the development of inflammatory polyarthritis and rheumatoid arthritis. Rheumatology (Oxford) 2000; 39:835–843.