Inflammatory Arthritis/Degenerative Cruciate Rupture

Over the past five years, the Comparative Orthopaedic Research Laboratory has studied the cruciate rupture syndrome in the dog.  This condition is estimated to cause 20% of all lameness in dogs.  The American public spends more than one billion dollars on the medical and surgical treatment of this condition.  It is currently estimated that 95% of cruciate ruptures in the dog are pathological, rather than accidental injuries.


Our long-term goal is to gain a fundamental understanding of the etiopathogenesis of cruciate rupture and to identify novel targets for therapy that will block joint degradation and pathological cruciate rupture.  Our research has shown that cruciate rupture is associated with the presence of chronic synovitis and up-regulation of antigen-specific immune responses within the synovium.  These findings suggest that this condition is an immune-mediated inflammatory arthritis.  Currently, our research is focused on identifying the antigen that triggers dysregulation of synovial immune responses, development of persistent synovitis, and development of progressive stifle joint degradation.  We are also focused on studying novel medical therapy for joint degradation and are currently conducting clinical trials in our hospital.

Figure:  Proposed mechanism for degenerative canine cruciate rupture, based on current research data.

Figure: Photomicrograph of frozen sections of cranial cruciate ligament (CCL) and synovial membrane from a dog with CCL rupture. (A) The cells staining red are activated macrophages infiltrating the epiligamentous tissue. (B) CCL rupture is associated with synovitis; in some instances lymphoid follicles can be seen with the synovium (arrows). Red-staining also indicates the presence of activated macrophages. Tartrate-resistant acid phosphatase histochemical stain, x200.
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