Developmental Orthopaedic Diseas

As many as 10% of Thoroughbred foals are not eligible to be sold through yearling sales because of developmental orthopaedic disease, with total costs arising from angular limb deviations and OCD being in the order of $9.8 million per year in the Hunter Valley alone.

Developmental orthopaedic disease is a multifactorial problem. Some of the factors which may contribute to this disease include:

Nutrition of the brood mare, foal, weanling and yearling
Genetics
Environment (season, locality, paddock vs box)
Exercise
Pasture quality and area
Ground hardness
Diseases resulting in catch-up nutrition and growth spurts
Biomechanics-abnormal limb loading
Body mass and growth rate (body score)
Endocrine factors/administration of external steroids

Nutritional causes of developmental orthopaedic disease may include:

Energy levels
Copper deficiency (primary)
Zinc excess (causing a secondary copper deficiency)
Calcium and phosphorus levels
Feed size and frequency of feeding
Time of weaning (early vs late)
Creep feeding (detrimental?)

Copper and zinc imbalances as a cause of developmental orthopaedic disease in growing foals

A correlation between the occurrence of DOD in horses and reduced amounts of calcium, phosphorus, zinc and copper, but not with the amount of other nutrients in weanling’s diets has been observed (Knight et al., 1985). The incidence of these diseases decreased significantly when these minerals, particularly copper, were increased in the diet.

Copper is involved in stabilising bone collagen and elastin synthesis. A copper deficiency impairs these functions, resulting in developmental orthopaedic disease (DOD) (Lewis, 1995). It is suggested that copper supplementation of mares may be a useful treatment in situations where the incidence and severity of DOD are of concern (Pearce et al., 1998). Supplementation of mares at 0.5mg Cu/kg liveweight/day significantly (P<0.01) decreased radiographic indices of physitis in the distal third metatarsal bone of the foals at 150 days and the prevalence of articular cartilage lesions (P<0.05) compared to control animals grazing 4.4-8.6 mg Cu/kg dry matter. However, copper supplementation of the mares did not abolish DOD in the growing foals, emphasising the probable multifactorial nature of this condition.

Copper supplementation has also been shown to reduce the prevalence of cartilage lesions in foals. In a study investigating the effects of copper supplementation on the prevalence of cartilage lesions in foals, mares were fed rations containing 13 ppm copper (control group) or 32 ppm (supplemented group). Foals were fed a pellet containing 15 or 55 ppm Cu and were destroyed at 90 or 180 days. In foals killed at 90 days, there were over twice as many lesions of osteochondrosis and more than four times as many articular lesions of osteophyte formation in the control group versus the supplemented group. In foals killed at 180 days, there were seven times more articular lesions of osteophyte formation or thinning, nearly twice as many lesions of osteochondrosis in the physis and over five times as many involving the A-E complex in control foals compared to supplemented foals (Knight et al., 1990). In another study, five of nine foals fed from 4 to 10 months of age a diet containing 7 ppm copper developed osteochondritis dissecans (OCD) and subchondral bone cysts (SBC), whereas no DOD occurred in any of nine foals fed 30 ppm dietary copper (Hurtig et al., 1990). The liver copper content was six times lower in the low copper-fed foals, but there was no difference in their plasma copper, calcium, phosphorus or zinc concentration or their plasma alkaline phosphatase activity. In another report, seven of eight nursing foals with osteochondrosis had plasma copper concentrations below normal (Bridges et al., 1984). A more recent study however showed that there was no relationship between foal or mare liver copper concentration and osteochondrosis status at either 5 or 11 months. However, osteochondrotic lesions in foals with low-level copper status at birth decreased significantly less in number and severity than those in foals with high-level copper status at birth. The authors of this paper concluded that copper is not likely to be an important factor in the aetiopathogenesis of osteochondrosis, but there may be a significant effect of high copper status on the natural process of repair of early lesions (van Weeren et al., 2003). Radiographically visible OCD lesions present at weaning resolved in foals fed a diet containing 30 ppm copper, whereas in those fed a 7 ppm copper-containing diet, the lesions worsened and mild angular and flexure deformities, intermittent lameness, and joint effusions occurred (Hurtig, 1993). In addition, their growth plates and metaphyseal bone contained microfractures, and they had wider zones of provisional calcification and higher rates of metaphyseal bone accretion as compared to the weanlings fed the high copper diets.

Dietary zinc deficiency has also been postulated as a cause of DOD (Knight et al., 1985). In an unpublished report, it was stated that three-month old foals fed a diet containing 152 ppm zinc had less cartilage defects at 6 months of age than those fed 42 ppm (Lewis, 1995). This diet also contained 35 ppm copper. In another study, foals with osteodystrophy administered 200mg Zn/day (equivalent to increasing their dietary zinc from 25 to 65 ppm) increased their rate of recovery as compared to those not given additional zinc (Spais, et al., 1976).

The NRC (1989) recommends that all horses receive 40ppm zinc and 10 ppm copper in the diet. Research indicates that growing horses consuming these levels (or lower) are more likely to develop DOD. Despite other studies suggesting that lower amounts of dietary copper and zinc may be adequate, because of studies suggesting that increasing copper and zinc in the growing horse’s diet may decrease the risk and occurrence of DOD, and because there is no risk of harm from doing so, it has been recommended that copper and zinc be added to the growing horse’s diet to the amounts shown in Table 1 (Lewis, 1995). More recently, a RIRDC publication has also revised the recommended levels of these nutrients, as shown in Table 2. These publications recommend that zinc levels be increased to at least 40ppm (dry matter in diet) and between 25 and 40ppm copper. The NRC (1989) original recommendations are shown in Table 3.

Table 1. Recommended levels of nutrients in the growing horse diet (Lewis, 1995)
	ppm in Dry Matter		% in Dry Matter
	Zinc^a	Copper^a	Calcium^b	Phosphorus^b
Nursing foal (0-4)	60	50	0.9	0.6
Weanling (4-12)	60	25	0.8	0.5
Yearling (12-18)	40	25	0.5	0.4
Long yearling (18-24)	40	10	0.4	0.25

^a It is stated that these amounts may be added to the grain mix without regard to that naturally present in normal feeds without risk of harmful excess. This is often done rather than determining the amount present in the feed and adding just enough copper and zinc containing mineral to attain these concentrations, as should be done for calcium and phosphorus.

^b Amounts of calcium and phosphorus are also more than recommended by NRC because the amount necessary to maximise bone strength and ash content is higher than that required to maximise growth rate and because the incidence of developmental orthopaedic diseases has been reported to be lower with higher amounts (Knight et al., 1985, from Lewis, 1995)

Table 2. Recommended levels of nutrients in the growing horse diet (Kohnke et al., 1999)
	ppm in Dry Matter		% in Dry Matter
	Zinc	Copper	Calcium	Phosphorus
Nursing foal (4)	40	40	0.68	0.43
Weanling (6-12)	40	40	0.61	0.39
Yearling (12-18)	40	40	0.44	0.28
Long yearling (18-24)	40	40	0.36	0.23

Table 3. Recommended levels of nutrients in the growing horse diet (NRC, 1989)
	ppm in Dry Matter		% in Dry Matter
	Zinc	Copper	Calcium	Phosphorus
Nursing foal (0-4)	40	10	0.68	0.38
Weanling (6-12)	40	10	0.56-0.61	0.31-0.34
Yearling (12-18)	40	10	0.43-0.45	0.24-0.25
Long yearling (18-24)	40	10	0.34-0.36	0.19-0.20

The upper safe concentrations of copper and zinc are 800 ppm and 500 ppm respectively (Lewis, 1995; NRC, 1989).

Most pastures in Australia are deficient in copper, if a copper deficiency (or any other deficiency) is suspected it would be wise to have a diet evaluation done on the feeding program of young growing stock. In these circumstances, if inadequate volumes of a complete feed are fed (i.e. if you are feeding less than the recommended levels which is often the case when horses are “good doers”), a supplement containing good levels of calcium, phosphorus, copper and zinc may be required.

Folactin Red Plus: Specifically designed to meet higher nutrient demands of growing foals and broodmares

Folactin Red Plus is a premium fortified supplement providing essential vitamins and minerals for healthy bone growth. Folactin Red Plus has been formulated in response to recent increased recommendations for calcium, phosphorus, copper and zinc in broodmares and foals at stud and is also appropriate for use in adult horses where calcium, phosphorus, copper and zinc deficiencies or imbalances exist. Folactin Red PLUS now also contains magnesium. Please note Folactin Red Plus is a new product and may not yet be available in your area, please contact Ranvet on 1800 727 217 (free call number) if you are interested in this product and we will arrange delivery to your local supplier.

References

Bridges, C.H., Womack, J.E., Harris, E.D. et al (1984). Considerations of copper metabolism in osteochondrosis of suckling foals. J. Am. Vet. Med. Assoc. 185, 173-178.
Hurtig, M.B. (1993). Equine osteochondrosis in the 90’s. As reported by MJ Glade. J. Equine Vet Sci. 13, 13.
Hurtig, M.B., Green, S.L., Dobson, H. et al (1990). Defective bone and cartilage in foals fed a low copper diet. Am. Assoc. Equine Pract. Proc., pp 637-644.
Knight, D.A., Gabel, A.A., Reed, S.M. et al (1985). Correlation of dietary mineral to incidence and severity of metabolic bone disease in Ohio and Kentucky. Am. Assoc. Pract. Proc, 445-461.
Knight, D.A., Weisbrode, S.E., Schmall, L.M., Reed, S.M., Gabel, A.A., Bramlage, L.R., Tyznik, W.I. (1990). The effects of copper supplementation on the prevalence of cartilage lesions in foals. Equine Vet J. 22, 426-432.
Kohnke, J.R., Kelleher, F., Trevor-Jones, P. (1999). Feeding Horses in Australia. RIRDC Publication No 99/49.Lewis, L.D. (1995). Developmental orthopaedic diseases in horses. In: Equine Clinical Nutrition: Feeding and Care. Williams & Wilkins, USA, p431.
National Research Council (1989). Nutrient requirements of horses. 5th Edition. National Academy Press. Washington DC.
Pearce, S.G., Firth, E.C., Grace, N.D., Fennessy, P.F. (1998). Effect of copper supplementation on the evidence of developmental orthopaedic disease in pasture-fed New Zealand Thoroughbreds. Equine Vet J. 30, 183-185.
Spais, A.G., Papasteriadis, A., Zafracas, A. et al. (1976). Osteodystrophy associated with a zinc deficiency in foals. Proc. World. Vet. Cong. 3, 2103-2106.
Van Weeren, P.R., Knaap, J., Firth, E.C. (2003). Influence of liver copper status of mare and newborn foal on the development of osteochondrotic lesions.