Cartilage canals in the distal intermediate ridge of the tibia of fetuses and foals are surrounded by different types of collagen

Abstract

Some epiphyseal growth cartilage canals are surrounded by a ring of hypereosinophilic matrix consisting of collagen type I. Absence of the collagen type I ring may predispose canal vessels to failure and osteochondrosis, which can lead to fragments in joints (osteochondrosis dissecans). It is not known whether the ring develops in response to programming or biomechanical force. The distribution that may reveal the function of the ring has only been described in the distal femur of a limited number of foals. It is also not known which cells are responsible for producing the collagen ring. The aims of the current study were to examine fetuses and foals to infer whether the ring forms in response to biomechanical force or programming, to describe distribution and to investigate which cell type produces the ring. The material consisted of 46 fetuses and foals from 293 days of gestation to 142 days old, of both sexes and different breeds, divided into three groups, designated the naïve group up to and including the day of birth, the adapting group from 2 days up to and including 14 days old, and the loaded group from 15 days and older. The distal tibia was sawn into parasagittal slabs and the cranial half of the central slab from the intermediate ridge was examined by light microscopy and immunohistochemical staining for collagen type I. Presence, completeness and location of the collagen ring was compared, as was the quantity of perivascular mesenchymal cells. An eosinophilic ring present on HE‐stained sections was seen in every single fetus and foal examined, which corresponded to collagen type I in immunostained sections. A higher proportion of cartilage canals were surrounded by an eosinophilic ring in the naïve and adapting groups at 73 and 76%, respectively, compared with the loaded group at 51%. When considering only patent canals, the proportion of canals with an eosinophilic ring was higher in the adapting and loaded than the naïve group of foals. The ring was present around 90 and 81% of patent canals in the deep and middle layers, respectively, compared with 58% in the superficial layer, and the ring was more often complete around deep compared with superficial canals. The ring was absent or partial around chondrifying canals. When an eosinophilic ring was present around patent canals, it was more common for the canal to contain one or more layers of perivascular mesenchymal cells rather than few to no layers. It was also more common for the collagen ring to be more complete around canals that contained many as opposed to few mesenchymal cells. In conclusion, the proportion of cartilage canals that had an eosinophilic ring was similar in all three groups of fetuses and foals, indicating that the presence of the collagen ring was mostly programmed, although some adaptation was evident. The ring was more often present around deep, compared with superficial canals, indicating a role in preparation for ossification. The collagen ring appeared to be produced by perivascular mesenchymal cells.

Biomechanical loading of the porcine femorotibial joint during maximal movements: An exploratory, ex vivo study

“…Concomitant damage to the vessels (Tóth et al, 2013;Nissi et al, 2014;Tóth et al, 2015) would support our hypothesis that maximal joint excursions experienced for example during slipping and simulated in this ex vivo study, would cause high peak pressures in the femorotibial (FT) joint, biomechanically contributing to the development of OC lesions in pigs (Olstad et al, 2015;Hellings et al, 2017). Interestingly, De Koning et al (2014) found that a bedding of wood shavings at a relatively young age increases the odds for severe OC, similar to that observed in free ranged pigs (Etterlin et al, 2014(Etterlin et al, , 2015.…”

“…Osteochondrosis (OC) in pigs develops after initial injury to the subchondral blood vessels, and leads via extracellular matrix thickening, lack of ossification of the necrotic cartilage, and splitting of the diseased cartilage with cracks, to loose cartilage flaps and fragments on the articular surface (Weisbrode, 2007;Olstad et al, 2015;Hellings et al, 2017). It has been estimated that around 80% of the pigs in today's porcine industry show superficial to mild signs of OC (Crenshaw, 2006).…”

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

“…In a review about cartilage cell clusters it was stated that “Such cell‐cell interactions are likely to also occur in cell clusters but this has not been formally demonstrated.” The current study gave further support to the existence of such connections. Cells with processes have been associated with progenitor characteristics and were also observed at the articular surface and in cartilage canals . Specific markers for progenitor cells were observed in chondrocyte clusters adjacent to severe cartilage degeneration .…”

Evaluation of the appearance of osteochondrosis lesions by two radiographic examinations in sport horses aged from 12 to 36 months

“…Furthermore, histopathological observations of the epiphyseal cartilage, particularly in foals, have shown that cartilage thickness, the number of vessels and their direction follow a heterogeneous distribution which could explain, in part, the susceptibility of specific sites within the joint to develop OC(D) [14][15][16]. However, processes leading to a vascular failure remain poorly elucidated and various hypotheses persist -specifically an implication of the forces (compression, shearing) exerted at the level of the osteochondral junction of the ossification front [1,12], extracellular matrix alteration [17,18], involvement of energetic metabolism [19,20], alteration of the chondrocyte proteome [21,22], hormonal dysregulation [23,24] and, in foals which suffered from bacterial infection during the first months of their lives, a process of septic ischemic chondronecrosis (9). Although the understanding of pathogenic processes leading to OC(D) has been the subject of much research, the dynamic aspect remain poorly studied.…”