Circumferential hoof clamp method of lameness induction in the horse.

A circumferential hoof clamp method to induce controlled and reversible lameness in the forelimbs of eight horses was assessed. Peak vertical forces and vertical impulses were recorded using a force plate to verify induced lameness. Video recordings were used by blinded observers to determine subjective lameness using a 0-5 scale and any residual lameness following clamp loosening. Tightening of clamps resulted in consistent, visible lameness in the selected limbs in all horses. Lameness was confirmed by significant decreases from baseline in the peak vertical force (P <0.01). Lameness was also confirmed subjectively by elevated median scores (0 at baseline and 2 during lameness). Lameness was not immediately reversible after clamp loosening (median score 1.5), but horses were not obviously lame after clamp removal and were no different from initial baseline (median score 0.5) approximately 3 days later.

Non-terminal animal model of post-traumatic osteoarthritis induced by acute joint injury.

OBJECTIVE: Develop a non-terminal animal model of acute joint injury that demonstrates clinical and morphological evidence of early post-traumatic osteoarthritis (PTOA). METHODS: An osteochondral (OC) fragment was created arthroscopically in one metacarpophalangeal (MCP) joint of 11 horses and the contralateral joint was sham operated. Eleven additional horses served as unoperated controls. Every 2 weeks, force plate analysis, flexion response, joint circumference, and synovial effusion scores were recorded. At weeks 0 and 16, radiographs (all horses) and arthroscopic videos (OC injured and sham joints) were graded. At week 16, synovium and cartilage biopsies were taken arthroscopically from OC injured and sham joints for histologic evaluation and the OC fragment was removed. RESULTS: OC fragments were successfully created and horses were free of clinical lameness after fragment removal. Forelimb gait asymmetry was observed at week 2 (P = 0.0012), while joint circumference (P < 0.0001) and effusion scores (P < 0.0001) were increased in injured limbs compared to baseline from weeks 2 to 16. Positive flexion response of injured limbs was noted at multiple time points. Capsular enthesophytes were seen radiographically in injured limbs. Articular cartilage damage was demonstrated arthroscopically as mild wear-lines and histologically as superficial zone chondrocyte death accompanied by mild proliferation. Synovial hyperemia and fibrosis were present at the site of OC injury. CONCLUSION: Acute OC injury to the MCP joint resulted in clinical, imaging, and histologic changes in cartilage and synovium characteristic of early PTOA. This model will be useful for defining biomarkers of early osteoarthritis and for monitoring response to therapy and surgery.