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Developmental Orthopaedic Disease of Growing Horses Disclaimer
Developmental Orthopaedic Disease (DOD) is the most significant problem facing the modern horse breeder.

Until a cure or the exact cause of the problem of DOD is found, the best thing is to use good management and selection procedures, and feed a well-formulated feed in a conservative manner.

Through good management and proper nutrition, it is likely that the incidence of the problem of DOD on the farm can be reduced. Remember that the management of the late pregnant mare, wet mare, foal, weanling and yearling are all important in minimising the incidence and impact of DOD.

Types of DOD   Top
DOD includes epiphysitis (physitis), wobblers, osteochondritis dissecans (OCD), osteochondrosis, contracted flexor tendons, angular limb deformities (ALD) and juvenile arthritis. These are not new problems and it is unclear if there has been an increase in its incidence, or if there are simply more sophisticated techniques for its diagnosis.

The increased awareness of the problem has led to efforts to design feeding and management programs to decrease the incidence and severity of the disease. A single factor to prevent DOD has not been identified, but there are several areas that are known to be important (table 1). Nutrition is an important factor, but is not the only area of management that needs attention.

Table 1: Factors Which May Contribute to DOD in Young Horses
Mineral deficiencyRation analysisBalance ration e.g. add minerals
Mineral excessRation analysisBalance ration e.g. dilute legume hay with grass hay
1. Daily energy intakeMeasure growth rateMonitor condition score or weight;
Reduce feed to slow growth or if horse has access to great pasture
Increase exercise
2. Energy intake per mealMeasure amount fed per mealReduce grain intake; Feed 2 x per day.
EnvironmentHardness of groundSoften ground (by choice of paddock)
Excessive ConfinementLength of time stabledMinimise time in stable
Some daily exercise if boxed
Graded return to paddock
GeneticsObserve soundness, performance of offspringIntroduce new bloodlines or crosses
TraumaObserve horseSmall groups; segregate some horses
Treat injuries aggressively

Mineral deficiencies   Top
The NRC publication, Nutrient Requirements of Horses, suggest the copper and zinc requirements of the horse to be 10mg/kg and 50mg/kg, respectively. Research and field studies in various countries have shown that these levels are inadequate and foals on trace mineral levels this low, or lower, are inclined to develop more DOD problems. However, most natural feeds do not contain sufficient copper and zinc. Copper and zinc are cheap minerals, and copper especially is non toxic to horses, so higher levels of supplementation is good insurance.

Current practice is to formulate rations for late pregnant mares and young horses to provide daily intakes of copper and zinc of 150 and 450mg, respectively. You should check that your mineral supplement contains at least 150mg of copper and 400mg of zinc. Equivit Gold Pellets and Equivit All Phase Feed Balancer Pellets are examples of supplements that do contain sufficient trace minerals. A suitable fortified concentrate feed should contain 40mg/kg of copper and 120mg/kg of zinc – unfortunately many prepared feeds don’t.

New research from New Zealand has confirmed our belief that supplementation during late pregnancy is vital to minimise DOD. Copper supplementation together with zinc and selenium to pasture fed mares led to a significant reduction in the incidence and severity of physitis and articular cartilage lesions in weanlings. Interestingly, supplementation of mares and foals after birth did not reduce the development of DOD. Where the mare had been supplemented in late pregnancy, there was no need to supplement the foal. The supplementation during late pregnancy supplies the foal with trace minerals during a critical development phase and allows for adequate liver stores of trace minerals. After birth, milk is a relatively poor source of these important minerals. Supplying enough minerals to late pregnant mares is a critical step in preventing DOD in growing horses.

Other minerals such as manganese, sulphur and magnesium are also involved in the formation of bone and in the maturation of cartilage, and deficiencies of calcium and phosphorus can have devastating effects on skeletal development. Most breeders would be aware of the need for calcium, particularly when high grain diets are fed. Lucerne hay and chaff provides an important source of calcium for mares and growing horses.

Recent research has shown the low digestibility of many common phosphorus sources. A series of trials were conducted at KER in which horses were fed Yea-Sacc1026 live yeast culture which significantly improved fibre digestibility by about 7.5%. Phosphorus digestibility was increased by 22%. The addition of Yea-Sacc1026 to the diet of growing horses and late pregnant mares can help to provide adequate phosphorus and other minerals for rapid growth and improve feed utilisation.

Mineral excess   Top
A report from Texas showed that foals exhibiting severe DOD were consuming high levels of zinc in conjunction with marginally deficient levels of copper. The zinc interfered with the absorption and utilisation of copper, thus the deficiency of copper was caused by an interaction rather than an actual deficient level of copper in the diet.

Studies at the University of Melbourne have shown that excess phosphorus increases the risk of DOD. Where foals were fed diets containing 5 times the NRC recommendation for phosphorus, DOD occurred consistently in experimental foals. This situation is only likely in foals being fed very large amounts of grain bran and protein meals.

High calcium diets have also been implicated in the onset of DOD, perhaps by reducing the availability of other minerals and creating deficiencies. Excessive calcium supplementation can occur in young horses eating large amounts of lucerne and calcium-only supplements, eg. limestone. The growing horse should receive a diet with the calcium:phosphorus ratio of 1.1:1 to 2:1. It also needs to meet the total daily requirements for calcium and phosphorus. The answer is to have your horse’s diet analysed by a veterinarian or nutritionist to check that these minerals are being supplied in the correct amounts and proportions.

There is a suggestion that excessive manganese may lead to problems if the diet is marginal for copper. The copper:manganese ratio needs to be considered if there is a higher than normal incidence of DOD. Some pastures appear to accumulate manganese and this will only be discovered by pasture testing.

In general, it is a good practice to ensure that any mineral is not fed at levels which far exceed requirements, in other words, you need to feed a balanced diet.

Overfeeding   Top
Maximum growth and optimum growth in young horses are mutually exclusive, and horses grown at a rapid rate are more prone to exhibit signs of DOD than are their more conservatively fed counterparts. From experience in humans and other species, there is reason to believe that fat, young horses will not become good athletes, and that excessive fat deposition in the young should be avoided.

A recent study of 10,000 Thoroughbred yearlings in the USA and England has shown that overweight and obese yearlings had substantially inferior racetrack performance. The ideal body weight yearlings won an average of nearly twice the stake money of the obese yearlings and similar trends were evident in numbers of stakes races won. Many breeders will have seen similar results when they compare the performance of horses given a sales preparation, with those retained for racing.

All breeders can monitor the body condition of growing horses and should not let them get too fat. A thick crest should be avoided and foals should not have a ‘gutter’ along the centre of the back or the rump. You should be able to easily feel the ribs of the foal.

Remember that exercise is important for young horses and that forced exercise can limit the side effects of a high energy diet. When weanlings and yearlings are confined or cannot exercise as a result of lameness, reduce the amount of grain being fed and reintroduce them to free choice exercise slowly.

One of the new theories on OCD development is sensitivity of cartilage to insulin. It appears logical that management changes which reduce post feeding insulin levels would be valuable, and the potential for its negative interaction with cartilage development be reduced as well. This includes small grain meals, dilution of grain with chaff, added fat and added chromium. This may lead to a reduction in the incidence or severity of OCD and other DOD.

Genetics   Top
Research in several countries and breeds has identified sires and sire lines in which the occurrence of DOD is significantly greater than average. Failure to consider the genetic component of the disease can be a severe management error.

The exact mechanism by which DOD is inherited is not clear, but the breeder should evaluate each case of DOD with the genetic component in mind and cull mares or choose matings carefully. The genetic influence may relate to rapid growth, body type, conformation, weight, early development or other factors.

Environment   Top
Environmental conditions, such as hard ground may contribute to physical or mechanical trauma to the growth plate. It is important to restrict exercise to those weanlings and yearlings with physitis or OCD by confining them in smaller paddocks or yards. However, confinement in a stable may be counter-productive. Foals and weanlings that are confined in a stable for extended periods have a higher incidence of OCD.

Confinement leads to reduced stress on bones which reduces bone strength. When the foal is let out into the paddock a period of excessive exercise is common and the combination of weaker bones and charging around may bring on an OCD problem. The answer is to only confine foals and weanlings in stables when it is really necessary, or allow some free exercise every day when they are in the box. A graded return to the paddock environment is very important.

A new perspective - Biomechanics   Top
Dr Roy Pool, a pathologist who recently retired from the University of California at Davis Veterinary School, has recently published articles addressing the question of what is the primary cause of skeletal lesion in growing horses. His conclusions may explain why dietary changes have not totally eliminated DOD from horses. Dr Pool maintains that these types of lesions are most likely the result of excessive biomechanical forces exerted on otherwise normal cartilage. These forces disrupt the blood supply to the cartilage and prevent its conversion to bone. There are several possible reasons why normal cartilage could not withstand these forces:

  1. Specific joints have ‘windows of vulnerability’ when they are particularly susceptible to damage. At this point in development, perhaps there is not adequate underlying bone to support the weight and force exerted on the joint. For example, stifles and hocks seem to be most vulnerable at six to eight months of age. At this point, excessive force may damage the underlying bone and vascular supply to the cartilage. The cartilage does not ossify and a lesion forms. The clinical expression of the lesion may not occur until later when the lesion becomes severe enough to cause lameness or swelling.
  2. Foals with genetic potential for rapid skeletal and muscle development may simply develop more muscle mass than the rapidly growing bone can support.
  3. Foals that don’t have the genetic potential for rapid growth become fat because of excessive energy intake and overload the joint.
  4. A conformation defect creates an uneven distribution of force upon the joint surface.
  5. Foals that have been confined due to illness do not develop enough subchondral bone to support their weight. When they are finally returned to the herd, the bone is too weak to support a normal amount of exercise and the joint cartilage collapses.
  6. Rapid changes in management that greatly alter the foal’s exercise patterns may overload the joint.

Authors: Dr Peter Huntington, Kentucky Equine Research Australasia
Dr Joe Pagan, Kentucky Equine Research, Lexington Kentucky USA

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