FIGURE LEGENDS
Figure 1: US images of Foal 2 (a) on admission with moderate effusion (*) and fibrin formation of the L LFTJ. The LM was abnormal in shape, protruding beyond the level of the tibial/femoral condyles, with a diffuse hypoechoic region within it (arrowhead). Screening radiographs of the L stifle of Foal 2 were taken on admission, findings were unremarkable (b & c). Plain CT of the L stifle of Foal 2 revealed marked distension of the LFTJ with irregularity and sclerosis of the subchondral bone of the LFC and the lateral tibial condyle (d). Contrast CT-arthrogram revealed disruption of the LM caudally, with lateral displacement (e). At its attachment to the caudal horn of the LM, disruption of the meniscofemoral ligament could be seen (Figure 2 f). F = lateral femoral condyle; POP = popliteus tendon; T = lateral tibial condyle.
Figure 2: US images of Foal 1 on admission (a) with marked effusion and fibrin formation within L LFTJ (*). The LM was abnormal in shape, protruding beyond the level of the tibial/femoral condyles (covered by epiphyseal cartilage), with a horizontal hypoechoic line running through it (arrowheads). Figure (b) shows normal R LFTJ for comparison. Figure (c) shows arthroscopic image of the cranial aspect of the L LFTJ of Foal 1, the LM can be seen prolapsed and displaced craniolaterally, with fibrin accumulation (*), meniscal hyperhemia and synovial proliferation. Figure (d) shows probe revealing Grade III tear of LM (#) extending beyond the margin of the lateral femoral condyle. F = lateral femoral condyle; T = lateral tibial condyle.
Figure 3: CT images of Foal 3, left (normal) stifle (a) for comparison with right (abnormal) stifle (b). The LM was diffusely abnormal with multiple tears in multiple orientations, primarily within the lateral and caudal aspects (Figure 3 b). A large, pyramidal shaped tear of the axial aspect of the caudal horn of the LM was present, resulting in marked irregularity of the axial margin of the meniscus (Figure 3 c). There was a small tear of the distal substance of the cranial cruciate ligament. The margin of the caudal cruciate ligament was minimally fibrillated (Figure 3 d). Figure (e) shows an arthroscopic image of R LFTJ of Foal 3, the LM can be seen prolapsed and displaced craniolaterally, with fibrin accumulation. Figure (f) shows Grade III tear (arrow) of LM extending beyond the margin of the lateral femoral condyle (F – femoral condyle; T – tibia).
Figure 4: US images of Foal 3 R LFTJ 3 days after initial presentation (a) and 6 months after initial presentation (b). US 6 months after initial presentation revealed increased synovial effusion within the LFTJ (*) (Figure 4 b). The LM position continued to be displaced laterally and was abnormal in appearance with areas of increased echogenicity suggestive of forming mineralization (arrows) (Figure 4 b). There was a marked palpable thickening and fibrosis over the region of the LM (Figure 4 c). Radiographs of the L stifle 6 months after initial presentation showed the LFC was flattened in appearance with remodeling of the lateral tibial condyle (Figure 4 d). A small radiolucent area (4 x 3 mm) was evident on the lateral tibial plateau, surrounded by a rim of sclerosis (arrow) (Figure 4 e).
Figure 5: Radiograph showing a Jamshidi needle approaching the sternebra for bone marrow aspiration performed under general anesthesia. This is the first step for production of autologous bone marrow-derived mesenchymal stem cells (BMSCs) (a). Foals 2 & 3 received 3 US-guided injections of autologous BMSCs, in the SER of the affected LFTJs post initial discharge. T = tibia.
Figure 6: Gross post-mortem images of Foal 2 showing left stifle joint (a). Image showing ventral/tibial surface of the menisci of L LFTJ (b), with medial meniscus (left side) and LM (right side). The LM showed marked thinning with loosening of collagen fibers, especially caudally (b). Figure (c) shows the posterior articular surface of the lateral condyle of the proximal tibia, revealing the presence of diffuse gray-white lesions in the subchondral bone, immediately below the articular cartilage. Figure (d) shows synovitis with diffuse villous proliferation and infiltration of inflammatory cells in the villous stroma. Figure (e) shows meniscitis with irregular arrangement of collagen fibers, infiltration of inflammatory cells and capillary angiogenesis. Figure (f) shows a septic cartilage canal with inflammatory cell infiltration and deposition of fibrin-like material within the cartilage canal of the articular cartilage. Bar=200 µm.