Unified theory of the origins of erosive arthritis: conditioning as a protective/directing mechanism?
- PMID: 14528501
Unified theory of the origins of erosive arthritis: conditioning as a protective/directing mechanism?
Abstract
Objective: To validate the western Tennessee River limits of the originally described rheumatoid arthritis (RA) catchment area and to assess the possibility that absence of tuberculosis allowed the original development of RA. The hypothesis that RA was related to tuberculosis was once a driving force in treatment approach. RA initially was very limited in geographic distribution, in contrast to tuberculosis. Classical tubercular lesions were not observed in the rheumatoid catchment area in ancient times. Similarities between clinical and radiologic manifestations of spondyloarthropathy (SpA) and adjuvant arthritis raised the possibility of a potential conditioning role for occurrence of nonrheumatoid erosive arthritis.
Methods: Skeletal samples from ancient RA catchment and non-catchment areas were compared for frequency of tubercular-relatable pathologies.
Results: Tubercular-relatable osseous pathologies were found only outside the rheumatoid catchment area (p < 0.0001). The original RA catchment area was confirmed not to extend beyond the western portion of the Tennessee River.
Conclusion: There is an inverse relationship between occurrence of tuberculosis and RA in the Archaic and Early Woodland periods of North America. The virtually universal presence of tuberculosis in contiguous Amerindian populations contrasts dramatically with its absence in the ancient catchment area for RA. Conversely, SpA and tuberculosis do occur in the same populations. Tuberculosis may represent a conditioning agent for development of SpA, but at least potentially provides protection against development of RA.
Comment in
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Origins of erosive arthritis.J Rheumatol. 2004 Jul;31(7):1463-4; author reply 1464-5. J Rheumatol. 2004. PMID: 15229977 No abstract available.
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Origins of erosive arthritis.J Rheumatol. 2005 Aug;32(8):1632; author reply 1632-3. J Rheumatol. 2005. PMID: 16078349 No abstract available.
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