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.