In the 1980s, an increase in the occurrence of foals with DOD coincided with the widespread introduction of supplementary feeding for broodmares and foals

Update on developmental bone diseases

Recent advances have added to our understanding of developmental bone diseases. DR JENNIFER STEWART updates us on what we now know.

Most of us choose to avoid anything described as skeletal abnormalities in our horses – especially when they are young and growing.

The term Developmental Orthopaedic Disease (DOD) is used to describe any orthopaedic (ie musculoskeletal) problem that involves tendon, joint, or bone tissue in growing horses. It was coined by the American Quarter Horse Association in 1986 when more and more young horses were developing growth issues. Today, across all breeds, the incidence of DOD is 10–65% and varies according to the number of risk factors.

Included under the umbrella of DOD (see Table 1) are flexural limb deformities

caused by contracted tendons; epiphysitis; physitis; Wobbler syndrome, or cervical vertebral malformation (CVM); and osteochondritis (OC). Common to all these conditions is a failure of the blood supply to the cartilage growing in the developing skeleton. It is generally accepted that these conditions can be congenital (present at birth) or acquired (developing after birth).

There are basically two forms of Osteochonditis dessicans (OCD): one is caused by defective cartilage maturation, the other is due to the mechanical overloading of normal cartilage. But for all types of DOD the causes are complex, multifaceted and comprise a combination of genetic predispositions, nutritional risk factors correlated with rapid growth, diet imbalances, exercise (biomechanical stress or trauma on immature joints and cartilage), and hormonal factors.

Genetics

It had been recognised by breeders that DOD seems to be more common in some breeds and bloodlines. Most breeds are susceptible although ponies and wild, free-ranging horses are less so, with an incidence in the latter of around 2%.

The prevalence and heritability vary between breeds and between joints. X-ray surveys found fetlock OC in 7–15% of Warmbloods and Thoroughbreds, 32% in French trotters and 54% in South German Coldbloods. Hock OC was found in 5–10% of Warmbloods and Thoroughbreds, 17–23% of Standardbreds, and 40% of South German Coldbloods; and stifle OCD reached prevalences of 4–10% in Thoroughbreds and Warmbloods. Several recent studies have estimated heritability for fetlock, hock and stifle lesions in different breeds (Table 2.).

With the completion of the horse whole genome sequencing project, several genes have been found that are associated with DOD and are linked to genes that relate to size. Breeding pressure often favours certain conformational traits – the height at the withers and high growth rate, for example – that are highly valued and known to be associated with the development of OC.

Nutritional risk factors

In the 1980s, an increase in the occurrence of foals with DOD coincided with the widespread introduction of supplementary feeding for broodmares and foals, which was precipitated by research showing that the nutrient levels in mares’ milk declined during lactation and that feeding concentrates increased foal growth rates. Subsequent research in 1989 demonstrated that skeletal abnormalities were higher in growing horses fed dietary energy at 129% of recommendations. The relationship between dietary energy and growth rate is analogous to fuel supply and speed in a car. When more fuel (energy from the diet) is available, speed (growth) will increase – but there is no brake on growth, and like maximum speed, maximum growth may not be optimal.

Foals with a genetic predisposition for rapid muscle development may develop greater muscle mass than their immature bones and joints can support. Those without the genetic potential for rapid musculoskeletal growth can quickly become fat if overfed and this can overload the immature, developing joints.

Young horses do not grow steadily in height and weight. Bone and muscle have their own windows of growth. The three most rapid growth periods for bone are:

from four months before, until one month after birth
between six to 12 months of age
just after puberty.

For muscles, the most rapid growth in terms of muscle cell size and number occurs between two and 24 months of age (Figure 1).

Major periods of bone. muscle and fat growth.

There is a link between above average weight gains and the onset of bone diseases. Muscle growth should not be pushed forward while the bones and joints are vulnerable. A lighter, leaner weanling with appropriate height (remember height is an indication of bone growth, not muscle) is the ideal.

The risk for skeletal abnormalities is highest during periods of rapid growth and early this century, this was determined to be the major factor causing DOD. More recently, records have shown that Warmblood foals positive for stifle OC had a significantly higher rate of weight gain at three and five months of age, weighed more at 11 months, and were taller at the withers and croup. Lusitano yearlings with DOD had higher daily body weight gains from six to 18 months of age. This and other recent studies have revealed that all breeds and ages of horses positive for OC had higher blood glucose and insulin levels.

Diet imbalances

A balanced diet with the correct amount and ratio of minerals, essential amino acids and energy will assist in preventing lesions that result from defective cartilage formation. The incidence of OCD is much higher in horses fed unbalanced diets than those on a balanced nutrient intake. In the biomechanical induced forms of OCD and in foals with a genetic potential for rapid growth, correct dietary management will assist in regulating growth and preventing excess condition.

Exercise

In the 1970s, Dr Roy Pool found that many cases of OCD are likely the result of excessive biomechanical force on the developing cartilage. These forces disrupt the blood supply to the cartilage and prevent its conversion to bone. Possible reasons why the cartilage does not withstand these forces include conformation defects which can lead to uneven and abnormal loading of the joint surface. Another reason lies with foals who have had their exercise restricted due to illness, and consequently have reduced bone density. When returned to pasture, the bone is not strong enough to support a normal amount of exercise, the joint cartilage collapses, and the sudden changes in exercise patterns can lead to fatigue and joint overload.

Hormonal

Over 40 years ago studies examining the effect of different feeds on blood glucose and insulin in horses appeared – and throughout this century the role of insulin in DOD has been explored. The consistent finding is that although the amount of energy (calories) fed to mares and foals is important, the source of that energy is even more so because raised blood glucose and insulin are implicated in the pathogenesis of osteochondrosis.

Foals with a genetic predisposition for rapid skeletal and muscle development may develop greater muscle mass than the rapidly growing bone can support.

Insulin has a profound effect on blood vessels and those in the developing bones and joints are especially susceptible. Insulin also influences the thyroid hormone, which impacts cartilage integrity and growth, and can result in faulty mineralisation. In addition, feeding pregnant mares high starch/sugar feeds increases insulin resistance, low-grade inflammation, and osteochondrosis lesions in foals and yearlings until 18 months of age. Both starch and sugar increase blood glucose and insulin levels, and low starch/sugar feeds are recommended for pregnant mares, foals, weanlings and yearlings.

So, what is ‘low’ starch and how much starch is too much? Research published in the last two years has found that in normal healthy horses, insulin rises dramatically when starch intake reaches 0.3g/kg body weight per meal. Importantly, insulin-dysregulated horses are nine times more sensitive to non-structural carbohydrate (NSC) and a limit to starch intake of between 0.02 and 0.05g/kg body weight per meal has been proposed.

For example, if a feed is 15% starch, a 500kg normal healthy horse could eat around 1kg per meal without adversely affecting blood glucose and insulin levels. However, for insulin-sensitive or insulin dysregulated horses, the amount of a 15% starch feed that could be safely consumed would be between 65g and 150g.

Take the time to read feed labels and do the maths, or have the diet analysed for starch, or have your vet check insulin levels

The exact causes of each type of DOD are unknown, but in all cases disturbance in the maturation of the joint cartilage and weakening of the bone is associated with high energy intakes, traumatic injuries and a genetic predisposition – it’s a case of genetics loading the gun (25% risk) and the environment pulling the trigger (75% risk).

When you search Google Scholar, there are articles dating much further back than the 1986 introduction of the term developmental orthopaedic disease. With the mapping of the equine genome and advanced imaging techniques it is now possible to study in minute detail the influences on the tiny blood vessels growing with and providing nutrition to the developing cartilage. As studies progress, we will learn even more about how to protect the young skeleton – but in the meantime, we can apply the existing knowledge to avoid feeding and dietary mistakes, and to protect developing joints from the damaging effects of elevated insulin.

Dr Jennifer Stewart BVSc BSc PhD is an equine veterinarian, a member of the Australian Veterinary Association and Equine Veterinarians Australia, CEO of Jenquine and a consultant nutritionist in Equine Clinical Nutrition.

All content provided in this article is for general use and information only and does not constitute advice or a veterinary opinion. It is not intended as specific medical advice or opinion and should not be relied on in place of consultation with your equine veterinarian.