Radiographic analysis in Thoroughbreds reveals morphological changes in healthy maturing stifle joints and possible association between subchondral lesions and femoral condyle width.

OBJECTIVE: Assess femorotibial features in foals with and without medial femoral condyle (MFC) subchondral radiolucencies (SR+ and SR-). METHODS: 3 independent, sequential radiographic studies were performed. Study 1 retrospectively measured femorotibial morphological parameters in repository radiographs (SR- and SR+). Study 2 qualitatively compared drawings of intercondylar notch shape in postmortem radiographs (SR-). Study 3 prospectively measured femorotibial parameters in 1-month-old foals (SR-). In studies 1 and 3, 13 morphologic parameters were measured. Limb directional asymmetry was assessed in 2 age groups (< 7 or ≥ 7 months). RESULTS: Study 1 (SR- group; n = 183 radiographs) showed increased femoral measurements with maturation, except the distal femoral intercondylar notch width (FINwal), which decreased. In contrast, in SR+ stifles (53 radiographs), 3 femoral parameters (MFC width [MFCwpf], MFC height, or FINwal) showed no changes. Tibial plateau width alone increased with maturation in both groups. Interobserver reliability was good to excellent. Study 2 (n = 53 radiographs) confirmed a distal FINw decrease in SR- foals. In study 1, left SR- stifles in greater than or equal to 7-month-old fillies had significantly larger femoral bicondylar width and FINw, while right SR+ stifles in fillies greater than or equal to 7 months had a significantly larger MFCw. In study 3 of 1-month-old foals (n = 94 SR- radiographs), the MFCw, femoral condyle bicondylar width, and lateral femoral condyle height were all greater on the left, whereas the intercondylar intereminence space width was larger on the right. CLINICAL RELEVANCE: In SR+ stifles, the distal femur exhibited divergent maturation, indicating a wider MFC in the right stifle in older foals. As SR lesions are more common on the right, this suggests a potential association with MFC morphology.

Osteoclast density is not increased in bone adjacent to radiolucencies (cysts) in juvenile equine medial femoral condyles.

BACKGROUND: There is a knowledge gap about how equine MFC subchondral radiolucencies (SR) arise and evolve. Osteoclasts are believed to have a role but have not been studied in situ. OBJECTIVES: To measure and compare osteoclast density and the percentage of chondroclasts in healthy and MFC SR specimens from juvenile Thoroughbreds. STUDY DESIGN: Cadaveric study. METHODS: Medial femoral condyles (MFC) from a tissue bank of equine stifles were studied. Inclusion criteria were MFCs (≤8 months old) with a computed tomography SR lesion and histological focal failure of endochondral ossification (L group). Contralateral, lesion-free, MFCs were a control group (CC). Osteochondral slabs were cut through the lesion (L), a healthy site immediately caudal to the lesion, (internal control; IC) and the contralateral, site-matched controls (CC). Histological sections were immunostained with Cathepsin K for osteoclast counting. Osteoclasts in contact with the growth cartilage (chondroclasts) were also counted. The sections were segmented into regions of interest (ROI) at different depths in the subchondral bone: ROI1 (0-1 mm), ROI2 (1-3 mm) and ROI3 (3-6 mm). Osteoclasts were counted and the bone area was measured in each ROI to calculate their density. Chondroclasts were counted in ROI1 . RESULTS: Sections were studied from L and IC (n = 6) and CC sites (n = 5). Osteoclast density was significantly higher in ROI1 when compared with ROI3 in all groups. Although higher osteoclast density was measured in ROI1 in the L group, no significant differences were detected when compared with control ROIs. The proportion of chondroclasts in ROI1 was lower in the L sections when compared with controls but no significant differences were detected. MAIN LIMITATIONS: Limited sample size. CONCLUSIONS: Osteoclasts are important actors in MFC subchondral bone development, digesting both growth cartilage (chondroclasts) and bone, but the pathophysiology of early MFC SRs cannot be explained solely by an increased osteoclast presence in the subchondral bone.