The "soft collagen" hypothesis in the pathogenesis of the inflammatory bowel disease and the seronegative spondylarthritides.

Seronegative spondylarthritides (SpAs) and inflammatory bowel disease (IBD) are disorders with a complex and elusive etiology. Current research has focused on downstream events and mechanisms of autoimmunity and inflammation but the primary etiologic factor is still unknown. We present a new hypothesis for the role of collagen into the pathogenesis of SpAs and IBD based on the assumption that they represent deferent phenotypes of the same disease. We gathered information on humans and animals which fit to the current evidence based concepts into their pathogenesis. We developed a logical hypothesis for the contribution of the individual's connective tissue profile among with the well known contribution of other genetic factors. The presence of a specific collagen or tissue matrix, which for abbreviation will be called the "soft collagen" (SC) is the basis for the pathogenesis of SpAs and the IBD. It seems that a triplet consisted of the "soft collagen", the genetic predisposition (such as the presence of HLA-B27, PSORS1 genes, NOD2/CARD mutations) and the triggering event (trauma or infection) are necessary for the development of these particular disorders. The "soft collagen" hypothesis may explain the pathogenesis as well as the various clinical aspects of these particular disorders which affect mostly young individuals.