From Arthroscopy to Gene Therapy—30 Years of Looking in Joints

Equine degenerative arthritis was reported as an entity in 1938 by Kelser and Callender based on a comparison of the pathological changes in humans and horses by the same authors. Equine osteoarthritis (OA; the common name now) was reviewed by Mackay-Smith in 1962, and it received its first clinical attention at AAEP in 1966 with a presentation on pathophysiology of equine degenerative joint disease and lameness by the clinical pioneers Raker et al. Until this stage, the studies had been postmortem studies, with little correlation to clinical signs or clinical significance, and there had been considerable extrapolation from human literature. Clinical problems in the fetlock joint were considered to correlate with articular cartilage lesions by Rooney, but in another study in Standardbred fetlocks, although there was good correlation between lameness and pathologic change in the synovial membrane and fibrous joint capsule, degenerative cartilage lesions were not well correlated with evidence of pain, and wear lines were commonly seen. Degenerative cartilage lesions were not considered to be painful if they did not involve subchondral bone. Therefore, in 1975, articular cartilage lesions were considered the indispensable criteria of OA, but it was also recognized that they may not be the centrally important cause of clinical disease. Today, equine OA may be considered as a group of disorders characterized by a common end stage: progressive deterioration of the articular cartilage accompanied by changes in the bone and soft tissues of the joint. The deterioration of the articular cartilage is characterized by local splitting and fragmentation (fibrillation) of articular cartilage. Synovitis and joint effusion are often associated with the disease, and, clinically, the disease is characterized by pain and dysfunction of the affected joint. In the early days, there was considerable extrapolation of equine OA to human OA, but the literature could be confusing, and, retrospectively, extrapolation was not appropriate. Human OA was initially classified conventionally into primary and secondary varieties. The term “primary” was used when the causes were unidentified and was typified by the insidiously developing disease of old people. The term “secondary” was used when an etiologic factor could be demonstrated. The term degenerative joint disease was used as a synonym for primary OA. However, as etiologic factors were identified, the distinction between primary and secondary lesions became difficult, and OA and degenerative joint disease are now used synonymously for