[Biomechanical studies on the pathogenesis of ochronotic arthropathy].
The enzymatic defect leading to alcaptonuria is well known. However, the pathogenesis of the associated arthropathy is poorly understood. From clinical and morphological observations it is assumed that the breakdown of ochronotic cartilage is due to an increased fragility. To test the hypothesis that polymerisation products of homogentisic acid change the biomechanical behaviour of hyalin cartilage, investigations on natural ochronotic cartilage and tissues following in vitro incubation with homogentisic acid were performed. It could be demonstrated that the "ochronotic situation" is associated with an increased hardness and a decreased elasticity of the hyalin cartilage. For the pathogenesis of ochronotic arthropathy it is assumed that these alterations, in association with mechanical stress to the joints, lead to cartilage destruction.
D000293:Adolescent; D000328:Adult; D000368:Aged; D000474:Alkaptonuria / Q000503:physiopathology*; D001168:Arthritis / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D002358:Cartilage, Articular / Q000503:physiopathology; D005260:Female; D005270:Femur Head / Q000503:physiopathology; D006713:Homogentisic Acid / Q000378:metabolism*; D006801:Humans; D008875:Middle Aged; D009794:Ochronosis / Q000503:physiopathology*
D006713:Homogentisic Acid
Biomechanische Untersuchungen zur Pathogenese der ochronotischen Arthropathie.