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between joints can be substantial. Patent cartilage canals had disappeared in the proximal phalanx after age 3 weeks, but in the femoral condyle they were still present at 4.5 months and had all regressed at age 7 months. The distal tibia was in between (Carlson et al. 1995).
Vascular events in early osteochondrosis: pioneering work in the pig Much of the initial work on the early pathogenetic mechanisms of OC has been conducted in the pig, a species in which the disease has a high prevalence and presents major economic and welfare concerns (Jørgensen and Andersen 2000). In this species it was shown that areas of chondronecrosis related to necrotic cartilage canals could be found, which were much larger in commercial pig breeds than in miniature pigs of wild hog ancestry (Ekman et al. 1990). Artificial devascularisation led to the formation of areas of ischaemic chondronecrosis (Carlson et al. 1991; Ytrehus et al. 2004). These observations led to the hypothesis that local biomechanical damage to cartilage canals, especially to the vulnerable anastomosing branches that run through the ossification front, would be the first step in the pathogenesis of OC (Ytrehus et al. 2007). The earliest lesion following vascular failure was an area of ischaemic chondronecrosis located at intermediate depth of the epiphyseal growth cartilage, designated as OC latens. With time, the area became surrounded by the ossification front and clinically apparent, at which stage it is called OC manifesta (Ytrehus et al. 2004).
Vascular events in early osteochondrosis: the situation in the horse Later work in the horse provided evidence for a similar pathogenetic mechanism in this species. Material was collected from the distal tibia of 100 foals submitted for post mortem examination between 191 days of gestation and 153 days post partum (Olstad et al. 2007). Identical lesions to those that were previously identified in pigs, i.e. areas of ischaemic chondronecrosis (Fig 2) were observed in the cranial intermediate ridge predilection site for osteochondrosis in nine of the 100 foals (Olstad et al. 2007).
a) b)
The blood supply to the distal tibia was then studied in
nine Standardbred foals aged 0–7 weeks by a technique involving arterial perfusion with barium, followed by clearing of the cartilage with methyl salicylate, which renders the perfused vessels visible to the naked eye (Olstad et al. 2008a, b). The age window for the presence of cartilage canal vessels fitted with the age window for development of radiographically detectable lesions (Dik et al. 1999). During the age window when vessels were present, epiphyseal cartilage canals were initially supplied by vessels originating from the perichondrium (Olstad et al. 2008a). With time, the ossification front advanced to surround the middle portion of the cartilage canal, after which time vessels in the distal portion became reliant on an arterial source that was obliged to traverse the ossification front in order to enter the cartilage canal (Fig 3). Lesions (n = 12) were consistently located at the point where vessels should have entered cartilage canals from bone after being incorporated into it. This prompted the suggestion that vessels might be particularly vulnerable to failure at the point where they traversed the ossification front (Olstad et al. 2008a), i.e. where tissues of highly different plasticity meet and create a sharp stiffness gradient (Fig 4a,b). In the femoropatellar joint, regression of blood vessels was
less advanced at this early age than in the tarsocrural joint (Olstad et al. 2008b). This agrees with the observation that the femoropatellar joint matures later with respect to most other joints (Lecocq et al. 2008) and is in line with earlier work showing that the peak of osteochondrotic lesion development is later in this joint than in most other joints (Dik et al. 1999). This means that there is no difference in pathogenetic mechanism of OC in different joints, but there may be a difference in timing. Indeed, in older foals (aged 31–336 days, mean 148 days), similar chondronecrotic areas as in the tarsal joint were found (Olstad et al. 2011). Also, in the metacarpophalangeal/metatarsophalangeal joints, a similar pattern was observed (Olstad et al. 2009). Early lesions in the tarsus were studied by micro-computed
tomography (Olstad et al. 2008c) (Supplementary Item 1). In still-mineralised samples, viable proliferating vessels adjacent
c)
Fig 1: a) Semischematic drawing of the ossification process of the long bones in mammals. After ossification of the originally totally cartilaginous anlagen and closure of the growth plates, only articular cartilage is left. b) Section of the femur of an 11-week-old Warmblood foal, showing the richly vascularised subarticular growth cartilage. c) Section of the tarsus of the same foal as b). The tarsus matures earlier than the stifle and here the layer of subarticular growth cartilage has become much thinner and lost its blood supply. (Fig 1a from Van Weeren 2006.)
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