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foals, and was associated with a focal delay in endochondral ossification, i.e. OC in three out of five foals examined 21 days or more after transection. Pathological cartilage fracture through the area of ischaemic chondronecrosis, i.e. OCD, occurred in one foal examined 42 days after transection (Olstad et al. 2013) (Fig 6).
Fig 2: Microphotograph of a femur of a 114-day-old foal. A necrotic cartilage vessel, surrounded by an area of necrotic matrix can be seen (arrow). Scale bar: 1 mm. (From Olstad et al. 2011.)
to lesions were surrounded by mineral opacity and compatible with separate centres of endochondral ossification (Fig 5, Supplementary Item 2) that, combined with phagocytosis of necrotic cartilage and intramembranous ossification of granulation tissue, could lead to filling of lesions with bone (Olstad et al. 2008a). This would explain how even major lesions can heal without leaving traces at a very early age (Dik et al. 1999). Finally, the hypothesis that vascular failure could lead to
OC and OCD was tested experimentally by surgical transection of vessels supplying the epiphyseal cartilage canals of the lateral trochlear ridge of the distal femur in 10 Fjord pony foals at age 13–15 days (Olstad et al. 2013) (Supplementary Item 3). Vascular transection resulted in cartilage canal and chondrocyte necrosis in all operated
a)
The early pathogenetic mechanism of osteochondrosis It can thus be concluded that there is at present compelling evidence for a crucial mechanistic role in the early pathogenesis of OC in the horse of failure of vascularisation of the growth cartilage via the cartilage canals. This mechanism can explain many features of equine OC, such as the joint-specific time windows (related to joint-specific patterns in the progress of the ossification front and subsequent vascular rearrangements), and the frequent bilateral occurrence. However, these complex vascular rearrangements that take place during the process of endochondral ossification and the related vulnerability are common to all horses and not only to those developing osteochondrotic lesions. There are, therefore, other aetiological factors that incite or predispose to lesion formation during this vulnerable period. Biomechanical loading is obviously one of them, but differences in the biochemical and/or biomechanical characteristics of key tissue components may play a role as well. These factors are partly genetically, but to a large extent environmentally determined and may hence be heavily influenced by the management of the young horse.
Aetiological factors
As pointed out, there is now convincing evidence for a common pathogenetic mechanism for osteochondrotic lesions. However, this is not equivalent to a single aetiology. There is common agreement that the background of OC is
b)
Fig 3: Images of three-dimensional volume-rendered models of micro-computed tomography scans of a tissue block (approximately 2 3 2 3 2 cm) from the cranial part of the distal intermediate ridge of the tibia of a 3-week-old foal. The block contained a permanent barium angiogram, and only the greyscale segments representing barium and bone are shown. a) A vessel originating from the perichondrial plexus on the cranial aspect of the distal tibia courses into the subchondral bone towards the cranial apex of the distal intermediate ridge (black arrow). Distal and caudal to this, towards the distal articular surface of the intermediate ridge, vessels emerge into the growth cartilage directly from subchondral bone (white arrow). b) The greyscale segment for bone has been rendered more translucent than in a), illustrating how the midsection of cartilage canal vessels is incorporated into the advancing ossification front during growth. This traversing of junctions between tissues of different plasticity (e.g. bone and cartilage) is believed to render vessels particularly vulnerable to failure.
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