EQUINE VETERINARY EDUCATION / AE / MARCH 2016


155


Review Article


Pathogenesis of osteochondrosis dissecans: How does this translate to management of the clinical case?


P. R. van Weeren†* and K. Olstad‡ †Department of Equine Sciences, Faculty of Veterinary Medicine, Utrecht University, The Netherlands; and ‡Department of Companion Animal Clinical Sciences, Faculty of Veterinary Medicine and Biosciences,


Norwegian University of Life Sciences, Oslo, Norway. *Corresponding author email: r.vanweeren@uu.nl


Keywords: horse; osteochondrosis dissecans (OCD); osteochondrosis (OC); aetiology


Summary Osteochondrosis (OC) is the most prevalent developmental orthopaedic disease in the horse. It is a complex disorder because of the interplay of factors that influence the formation of lesions and the ensuing natural healing process, the end result of which determines clinical outcome. The early pathogenetic mechanism of OC has long remained elusive, but recent research has provided compelling evidence for vascular disturbances leading to areas of ischaemic necrosis in the subarticular growth cartilage as the primary event. The aetiological factors that influence the process of the development of lesions are many and comprise both genetic and environmental factors. The genetic background of OC (dissecans) is highly complex with quantitative trait loci associated with some form of OC found on not fewer than 22 of the 33 chromosomes of the horse, and different manifestations and locations of OC having probably different genetic backgrounds. The environmental factors can be divided into nutritional factors and factors influencing the biomechanical loading of joints. Feeding large quantities of easily digestible carbohydrates is a clear risk factor and also the availability of sufficient copper for mares in the last part of pregnancy is important. Factors influencing the biomechanical loading of joints include the exercise regimen of foals, paddock size and roughness of terrain, and conformation. Equine OC is rarely a life- threatening disease and the prognosis of (surgical) treatment is good to very good. However, the impact on economics of the equine industry and on horse welfare is large. This impact can only be lessened by the judicious management of both horse breeding and horse husbandry. Some of the measures that would alleviate the burden of OC conflict with (commercial) pressures from the industry and a balance between human-imposed breeding and performance goals and the interest of the animal itself should be sought.


Introduction


The term ‘osteochondritis dissecans’ (inflammation of bone and cartilage with formation of loose fragments) was coined by the German surgeon Franz K€


onig (1832–1910). In his study


on loose bodies in joints he discussed three possible causes. The first two were traumatic in origin: severe trauma directly causing breaking off of fragments and lesser trauma causing necrosis of subchondral bone, indirectly leading to fragment formation. In the third category lesions were formed without any substantial trauma, but because of some (unidentified)


underlying lesion (K€ onig 1887). Later, this lesion was shown to


be a focal disturbance of the process of endochondral ossification (Barrie 1987). It is this last category for which the terms ‘osteochondrosis’ (OC) and ‘OC dissecans’ (OCD) are used in the veterinary literature. In the horse, the term OC was already used in the 1960s


(Baker 1960), but a substantial stream of reports on the condition did not start until the early to mid-1970s. From the beginning there has been controversy about the (aetio)pathogenesis. Despite many attempts to do so, no single causative factor, environmental or genetic, could be pinpointed, and the disease is now generally acknowledged to be multifactorial. The pathogenetic mechanism was long thought to be of primary biomechanical nature, but original work in pigs and horses by Scandinavian groups has now provided convincing evidence for a predominantly vascular pathogenetic mechanism. A large problem in the research in this field is that samples were often taken from long-existing lesions that had undergone extensive secondary processes, which had long effaced any possible traces of primary events (Pool 1993). In almost all studies using clinical material it is unfortunately not possible to say whether any abnormalities are primary or the expression of a secondary response, as it is known that the reactive repair process starts soon after initial lesion formation. The evidence for a vascular pathogenetic mechanism for OC comes from both observational and experimental studies. These studies conclude that osteochondrosis occurs as a consequence of ischaemic chondronecrosis (necrosis of cartilage that is dependent on blood supply, i.e. growth cartilage). This overview focuses on (early) pathogenesis of OC, the aetiological factors that have been identified and the practical implications for clinical management that follow from these.


Pathogenesis of osteochondrosis


Changes in vascularisation during the process of endochondral ossification The thick layer of epiphyseal cartilage of the growing joint that is destined to change into bone via the process of endochondral ossification is irrigated by vessels running through so-called cartilage canals (Wheeler Haines 1933) (Fig 1). During growth, the canals regress by a physiological process called chondrification. The timing of this process varies between different joints, as not all joints mature simultaneously, as also exemplified by the large differences in closure times of physes (Butler et al. 2011). The time lag


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