Development of an Equine Groove Model to Induce Metacarpophalangeal Osteoarthritis: A Pilot Study on 6 Horses

Abstract

The aim of this work was to develop an equine metacarpophalangeal joint model that induces osteoarthritis that is not primarily mediated by instability or inflammation. The study involved six Standardbred horses. Standardized cartilage surface damage or “grooves” were created arthroscopically on the distal dorsal aspect of the lateral and medial metacarpal condyles of a randomly chosen limb. The contralateral limb was sham operated. After 2 weeks of stall rest, horses were trotted 30 minutes every other day for 8 weeks, then evaluated for lameness and radiographed. Synovial fluid was analyzed for cytology and biomarkers. At 10 weeks post-surgery, horses were euthanized for macroscopic and histologic joint evaluation. Arthroscopic grooving allowed precise and identical damage to the cartilage of all animals. Under the controlled exercise regime, this osteoarthritis groove model displayed significant radiographic, macroscopic, and microscopic degenerative and reactive changes. Histology demonstrated consistent surgically induced grooves limited to non-calcified cartilage and accompanied by secondary adjacent cartilage lesions, chondrocyte necrosis, chondrocyte clusters, cartilage matrix softening, fissuring, mild subchondral bone inflammation, edema, and osteoblastic margination. Synovial fluid biochemistry and cytology demonstrated significantly elevated total protein without an increase in prostaglandin E2, neutrophils, or chondrocytes. This equine metacarpophalangeal groove model demonstrated that standardized non-calcified cartilage damage accompanied by exercise triggered altered osteochondral morphology and cartilage degeneration with minimal or inefficient repair and little inflammatory response. This model, if validated, would allow for assessment of disease processes and the effects of therapy.

Review of Soluble Biomarkers of Osteoarthritis: Lessons From Animal Models

“…In an equine metacarpophalangeal groove model, Manninchedda et al 76 showed that synovial fluid levels of C2C, COMP, CTX-I, osteocalcin (OC), and CS-846 were not significantly different between groups. 76 …”

Pro-inflammatory cytokines and structural biomarkers are effective to categorize osteoarthritis phenotype and progression in Standardbred racehorses over five years of racing career

“…Animal models, in which hyaline articular cartilage (HAC) was experimentally impacted [1–4] or joint instability was experimentally induced [5], showed rapid progression of joint damage, at the level of the cartilage and subchondral bone [2, 6–8]. Surgical management to achieve stabilization of the knee failed to abrogate the development of post-traumatic osteoarthritis (PTOA) [9, 10], indicating that a biochemical disturbance in the HAC of the affected joint is implicated in the accelerated rate of joint degeneration.…”

“…Considering animal models of PTOA, racehorses sustaining repetitive impact joint injuries, during their athletic career, are likely to develop DJD shortly after the initial inflammatory event affecting the joints [2, 4, 6, 7]. This progression was bound to occur at a much faster rate than in humans [22, 23], although there are currently not enough investigations and consensus about this statement.…”

Animal Models of Osteochondral Defect for Testing Biomaterials

“…e age of horses used ranges from 2 to 6 years. Defects have been created in the femoral trochlea [83], the medial femoral condyle [84], the lateral trochlear ridge [85], and the medial surface of lateral trochlea of the talus [86]. A 10 mm in diameter and 5 mm-10 mm deep defect has often been created to simulate osteochondral defects.…”