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growth rate, at least a high growth rate during certain periods of time, most probably those coinciding with the various windows of vulnerability of specific joints, is a factor associated with more, or more severe, OC lesions (Lepeule et al. 2013). Mechanistically, a high growth rate may just put the physiological process of endochondral ossification under excessive pressure and thereby increase the risk of lesion development. However, when the high growth rate is caused by the use of high-energy diets, especially when fed in the form of easily digestible carbohydrates, also another mechanism comes into action, as these diets result in a strong post prandial hyperinsulinaemia (Glade 1986, 1987). Horses with OC have been shown to have higher post prandial glucose and insulin responses to feeding with high- grain ratios than normal horses (Ralston 1996). Imbalances of insulin and its derivatives insulin-like growth factor (IGF)-I and IGF-II have a direct effect on the process of endochondral ossification and OC-positive foals have been shown to have significantly lower IGF-I activity than OC-negative foals (Sloet van Oldruitenborgh-Oosterbaan et al. 1999). Insulin also stimulates the rapid removal of the thyroid hormones T3 and T4 from the circulation (Glade et al. 1984), which are involved in chondrocyte differentiation and in the invasion of growth cartilage by blood vessels before its conversion to bone. The effect of carbohydrates on thyroid hormone levels is present in weanlings, but not in yearlings (Glade and Reimers 1985), which may be a factor in the determination of the specific time windows for OC. It is clear that nutrition-related hormonal imbalances may play a role in the development of equine OC, but they are, like unfavourable exercise conditions, a risk factor and not a sole aetiological factor.
Imbalances in trace elements and minerals There has been a strong interest in nutritional copper since a relationship was reported between low serum copper, ceruloplasmin level and OC in the early 1980s (Bridges et al. 1984). Incriminating low copper levels as the main cause of OC seemed very attractive, as there was a very plausible mechanism (decreased levels of lysyl-oxidase, a copper- dependent enzyme involved in collagen cross-linking), and because there was epidemiological evidence emerging that low nutritional copper was linked to higher levels of developmental orthopaedic diseases on stud farms in Kentucky and Ohio (Knight et al. 1985). Further, excessive intake of cadmium or zinc, both copper antagonists by displacing it from the sulfhydryl binding sites on metallothionein, was shown to result in OC-like lesions (Gunson et al. 1982). However, the reality was more complicated than that. In experimental studies it was shown that copper or zinc imbalances had to be huge to exert any effect and the resulting lesions were often much more severe than seen clinically (Bridges and Harris 1988; Bridges and Moffitt 1990). Copper intake recommendations were raised from the original National Research Council (NRC) recommendation of 10 ppm (NRC 1989) to 20–25 ppm (Hurtig et al. 1993) or even 50 ppm (Lewis 1995), but the rationale of these measures became questionable when it was shown that in New Zealand, a country where horses tend to stay out on grass all year round and the OC prevalence is traditionally low, the natural copper level in grass was 4.3–8.6 ppm (Pearce et al. 1998). Foals are, as many mammalian species, born with a large stock of copper in the liver that they need during the first
months of life, as milk contains hardly any copper. The copper level in the liver declines gradually to normal levels at the moment they eat enough grass to ensure sufficient daily intake (Egan and Murrin 1973). In a study in Thoroughbreds mean liver copper concentrations were shown to decline from 374 mg/kg dry matter at birth to 21 mg/kg dry matter at 160 days (Gee et al. 2000). Liver copper concentrations in foals appeared not to be related to the formation of osteochondrotic lesions, but foals with higher liver copper concentrations showed better lesion resolution, and thus may result in better final clinical outcome (Van Weeren et al. 2003).
Mechanistically, copper may have a chondroprotective
effect through reduction of the activity of the proteinases cathepsin B and cathepsin D (Davies et al. 1996), rather than act via lysyl oxidase (Jeffcott and Davies 1998). The calcium/phosphorus balance is of importance too.
High calcium levels were found to have no influence on the incidence of OC in foals, but four times the NRC recommendation of phosphorus resulted in a significantly increased number of lesions (Savage et al. 1993). The supposed mechanism was via the induction of secondary hyperparathyroidism, which would cause increased osteoporosis and hence weakening of the subchondral bone. This is an interesting study, as 2.5–6.5 month-old-foals were studied, which is an age that much later was identified as an age interval when the dynamic process of OC is very active and animals are very susceptible to the disorder.
Osteochondrosis in the equine industry
Equine OC is a complex and multifactorial disorder that is intricately linked to the physiological processes that are going on in the young, growing horse. The disorder is of great relevance to the equine industry. It has been estimated that in North-Western Europe alone, each year 20,000–25,000 foals are born that will manifest some form of OC during their life (Van Weeren and Barneveld 1999). The direct loss of animals may be limited, as only few foals are so heavily affected that they need to be subjected to euthanasia (Fig 7), but many of the other animals will require surgery at some stage. This means substantial economic loss to the equine industry and is also a serious welfare issue. A more indirect effect is the elimination from the population of many otherwise very attractive potential sires because of OC. This loss may easily be up to 30% of potential breeding stock. Both genetics and a multitude of environmental factors
play a role. It lies at hand, therefore, that no simple ‘one size fits all’ management strategies exist that can remediate,
let alone eradicate, the disorder. For a better appreciation of OC in the larger picture of the equine industry and to understand the implications of modern horse management for OC, it may be good to place equine osteochondrosis in its historical perspective.
Osteochondrosis – a ‘modern’ disease Unlike many other equine diseases of which written reports go back hundreds or even thousands of years, OC in the horse is a relatively new phenomenon. Nilsson’s report from 1947 is generally seen as the first publication on equine OC (Nilsson 1947), but it is not until the early 1970s that the disease is mentioned more frequently (Birkeland 1972; De Moor et al. 1972) and only from the 1980s onwards the disorder is
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