Animal models of infectious arthritis.

Abstract

The results from animal studies of bacterial joint infection have demonstrated pathogenic changes in synovium, cartilage, and bone which lead to joint destruction. Mechanisms responsible for the changes in these articular components remain to be more completely defined in order to develop methods to prevent articular destruction. Eradication of the active infectious process with early institution of antibiotics and adequate drainage is required but is not sufficient to prevent chronic destructive processes initiated by the acute bacterial infection. Biochemical effects of changes in the anabolic and catabolic functions of the cells in bone, cartilage, and synovium and the control mechanisms for these functions undoubtedly hold the key to prevention of destruction in infectious arthritis. Much less is understood about the pathogenic changes and mechanisms in infections caused by anaerobic bacteria, mycobacteria, fungi or viruses. Application of advances in immunological, morphological and biochemical techniques to animal models of infectious arthritis provides the opportunity to increase understanding of pathogenic mechanisms and to develop innovative methods of treatment.