Local Morphological Response of the Distal Femoral Articular–Epiphyseal Cartilage Complex of Young Foals to Surgical Stab Incision and Potential Relevance to Cartilage Injury and Repair in Children

Abstract

Objective: Describe the local morphological response of the articular–epiphyseal cartilage complex to surgical stab incision in the distal femur of foals, with emphasis on the relationship between growth cartilage injury, enchondral ossification, and repair. Design: Nine foals were induced into general anesthesia at the age of 13 to 15 days. Four full-thickness stab incision defects were created in the cartilage on the lateral aspect of the lateral trochlear ridge of the left distal femur. Follow-up examination was carried out from 1 to 49 days postoperatively, including examination of intact bones, sawed slabs, and histological sections. Results: Incision defects filled with cells displaying fibroblast-, chondrocyte-, and osteoblast-like characteristics, potentially validating the rationale behind the drilling of stable juvenile osteochondritis dissecans lesions in children. Incisions induced necrosis within the cartilage on the margins at all depths of the defects. Sharp dissection may therefore be contraindicated in cartilage repair in young individuals. Incisions caused a focal delay in enchondral ossification in 2 foals, apparently related to the orientation of the incision defect relative to the direction of ossification. Defects became progressively surrounded by subchondral bone, in which granulation tissue containing clasts and foci of osteoblast-like cells was observed. Continued enchondral ossification was therefore likely to result in healing of uncomplicated defects to morphologically normal bone. Conclusions: Epiphyseal growth cartilage injury had the potential to exert a negative effect on enchondral ossification. Enchondral ossification exerted a beneficial effect on repair. This relationship warrants consideration in future studies of cartilage injury and repair within the articular–epiphyseal cartilage complex of all species.

Transection of vessels in epiphyseal cartilage canals leads to osteochondrosis and osteochondrosis dissecans in the femoro-patellar joint of foals; a potential model of juvenile osteochondritis dissecans

“…The number of foals and time to follow-up examination was based on previous studies in piglets 20,29 . Local morphological changes at the site of transecting incisions are described separately 30 .…”

An Update on the Pathogenesis of Osteochondrosis

“…8). 85,88,130 Chondrocyte proliferation was observed in response to both surgical incisions 80 and ischemic chondronecrosis 78 and is considered a response that is nonspecific with respect to the inciting insult. Vascular proliferation has, however, only been observed adjacent to lesions that include necrosis of vessels and may therefore be specific to ischemic insult.…”

“…Vascular proliferation has, however, only been observed adjacent to lesions that include necrosis of vessels and may therefore be specific to ischemic insult. 78,80 Vascular proliferation was first noted in histological sections cut from decalcified tissue. 85,130 The micro-CT was carried out prior to decalcification of the tissue, and in scans, proliferating vessels were surrounded by focal mineral opacity and compatible with formation of separate centers of endochondral ossification (Fig.…”

Characterization of cellular and matrix alterations in the early pathogenesis of osteochondritis dissecans in pigs using second harmonic generation and two‐photon excitation fluorescence microscopy

“…There was a linear relationship between the number of cells in the largest cluster and the ratio of average SHG intensity in a lesion to the average SHG intensity in the adjacent deep resting zone. Because cluster size previously was shown in experimental studies to increase with time after appearance of lesion, the same may also be concluded about changes in the collagen matrix. The lesions showing fewer responses were located most superficially in the growth cartilage, whereas lesions located at the ossification front had more changes.…”

“…Proliferation is seen as increased numbers of cells within a single lacuna, which is then referred to as a cluster, proliferative nest, or chondrone . Clusters have been observed in response to ischemic necrosis, experimental incisions . and in conjunction with osteoarthritis and are therefore regarded as a non‐specific response to insult.…”