Although much knowledge has been gained regarding the nutrient requirements of the young growing horse, there are still many unanswered questions concerning optimum nutrition for growth and the avoidance of developmental orthopedic disease (DOD). What degree, if any, of DOD can be considered normal? If any DOD is abnormal, then what degree can be considered acceptable or recoverable, such that future athletic performance will not be compromised? Is there a perceived increase in the incidence due to a greater ability to detect DOD or due to changes in management practices that predispose horses to the disease, or both? Our ability to recognize and detect DOD has most likely increased, which leads back to the question of how much of what we detect is normal or inconsequential regarding the development and maturity of the tissue. Whether changes in management practices have affected the incidence of DOD is difficult to ascertain. Confounding factors of genetics, environment, non-nutritional management, and their interactions with nutrition make the establishment of accurate and precise optimal nutrient requirements for growth complex and difficult. The end goal is to grow individuals that will be more durable during their athletic career. Significant progress to the goal could be achieved by eliminating athletic events and strenuous training regimens to which young horses are subjected. Although this would be effective it is not a realistic solution given the current industry focus. So we will continue to work toward nutritional, management and medical practices that will help to develop earlier maturing horses and horses with improved skeletal strength and integrity.

Osteochondrosis is currently thought to be the result of a failure of endochondral ossification that may affect articular epiphyseal cartilage or the metaphyseal growth plate. Since extrapolation from studies in other species as well as the horse suggest that initial lesions are derived from growing cartilage and are associated with cartilage thickening and subchondral bone defects (28,32,31,33,41,15), dyschondroplasia may be considered to be a more accurate description of the condition (19). However, observations during surgery have indicated separation of cartilage and bone without cartilage thickening or defect in subchondral bone. It has been suggested that until the pathogenesis of DOD and the correlations with research models and clinical observations are better understood, the use of osteochondrosis would be most appropriate (18).

The term osteochondritis dissecans was used as early as 1887 in association with human knee injuries (4). Osteochondrosis, osteochondritis dissecans and osteochondrosis dissecans have often been used interchangeably and with some confusion. Osteochondrosis can be considered the disease, osteochondritis the inflammatory response and osteochondrosis dissecans the condition when a piece of cartilage is actually avulsed from the surface of a joint (27). In 1986 the term developmental orthopedic disease (DOD) was introduced as a heading for all orthopedic problems in growing horses (17). Today osteochondrosis, acquired limb deformities, physitis, subchondral cystic lesions, flexural deformities, cubiodal bone malformation and juvenile arthritis all fall under the heading DOD.

From a pathogenic standpoint osteochondrosis has been associated with various factors and interactions among these factors. Incomplete angiogenesis resulting in ischemic necrosis of subchondral bone has been one factor initially considered (1, 34). Other evidence suggested no association with cartilage necrosis and incomplete vascularization (33). However, studies in swine show a significant association with reduced blood supply and the pathogenesis of osteochondrosis (6). Some of these differences in observed pathologies may be due to the site of the lesion as well as the age of the animal. In addition, the influence of physical trauma that may shear vessels and thus contribute to cartilage necrosis and subsequent osteochondrosis lesions can also confound the issue regarding reduced blood supply and the pathogenesis of osteochondrosis (25, 26, and 14). Recent research also has focused attention on systemic and local growth factor effects on chondrocyte differentiation (13, 38).

We must define to what degree our nutritional management affects the horse during different stages of its growth. It would seem logical that nutrition would have the most profound effects during the most rapid periods of growth. Therefore, concerns have been directed toward the last third of gestation and the possible indirect effect brood mare nutrition has on fetal development. The early postnatal period is another period of rapid growth; thus, the effect of brood mare nutrition on lactation may affect the growth of the foal. Nutrition also will have a direct effect on growth and development from the initiation of creep feeding programs through maturity. Thus, the nutritional and management concerns regarding growth should start at conception and continue through maturity.

Genetics

There appears to be some degree of heritability for DOD, similar to milk yield and growth rate heritability in cattle. Heritability estimates could vary with specific joints and breeds since most of the studies only have addressed the hock in Standardbreds (11, 10, 24). Selection against DOD could be feasible; however, it would have to be based on progeny testing since stallions free of DOD have produced foals with a significant incidence of DOD lesions. As a population, feral horses have significantly less radiographic incidence of DOD than the domestic population (44). This may be related to natural selection pressures although nutrient intake differences between feral and domestic horses probably also plays a significant role.

The role of nutrition: Obviously nutrition does not have significant direct effects on genetics. However, knowing the possible genetic predisposition of a particular horse may allow adjustment to nutrition and management programs in order to reduce the risk of DOD.

Maternal Influences on Growth

Linear increase in fetal body weight occurs after 200 days of gestation, and increases in length are greatest during mid-gestation. Growth in length of the cannon bones continues rapidly until eight to nine months of gestation and then slows; however, the pastern bones reach almost adult length by the time of birth. In general the more distal the bone the sooner it reaches its mature size and shape. At birth the third phalanx no longer has an active growth plate and post-natal growth proceeds perichondral

Concerns regarding the maternal effects on foal growth and development should include the prenatal period, particularly during the last two thirds of gestation. Evidence suggest neuroendocrine control of growth hormone secretion in the horse may occur before parturition, which is earlier than in other species and may emphasize the importance of broodmare nutrition during gestation and lactation. This may be of significance due to recent research exploring the role of the growth hormone – IGF-1 axis and a possible role in chondrocyte differentiation. At this time no research has been done to examine the role of brood mare nutrition on fetal growth hormone secretion. A series of studies have shown copper supplementation in the mare is reflected in increased copper concentrations in the liver of the foal and also resulted in reduced radiographic indices for physitis in the distal third metatarsal (21,23,22). However, more recent research showed no difference in the incidence of osteochondritic lesions in foals from mares given injectable supplementation of copper compared to mares not receiving copper supplementation (8).

The role of nutrition: Increasing the amount of nutrients available to the broodmare during the last third of gestation and during lactation is well accepted. Such increases help insure proper fetal growth and development. In the mare it provides for adequate milk production and maintains broodmare body condition, which enhances rebreeding efficiencies. However, we do not know how the intricacies of broodmare nutrition may affect the skeletal soundness of the foal. Feeding for growth starts at conception, thus the broodmare should be fed a well balanced diet throughout gestation/lactation such that a condition score of 5-7 is maintained.

Growth Rate

The association with rapid rates of growth and OCD has been long recognized in other species (12, 32). Such conditions were reported in the horse as early as 1979, as well as many observational opinions offered before that time (41). Several studies have reported height and weight measurements of a horse’s growth rate when compared to estimated mature body size. At 6 months of age a horse has obtained approximately 83% of mature height and 46% of mature weight, at 12 months 90% and 67%, and at 18 months 95% and 80%. Much of the growth in length from the knee and hock to the ground has occurred by 4 to 6 months of age. Growth data shows that Thoroughbreds from 1989 to 1990 grew slightly heavier and taller compared to Thoroughbreds from 1958 to 1976 (43). This may be related to genetic selection for larger, faster growing horses and/or increased nutrient intake, better defined nutrient requirements, improved nutritional management and improved health management. Data from 1979 showed that colts of the same age were heavier and taller than fillies and this difference persisted to maturity. However, data from Quarter horses showed no difference in height between colts and fillies after 48-60 months of age. Interestingly, growth patterns of horses seem to be similar across breeds, geography and diet (9). Studies in Thoroughbreds and Standardbreds indicate an increased incidence of OCD lesions, particularly in the shoulder, stifle and tibiotarsal joints in horses with greater than average weight gains. Lesions in the fetlock were not associated with weight gain prior to weaning (20, 35). It has been suggested that DOD lesions occur in the first three months of life, which is the most intense postnatal growth phase. In addition, the hind limbs of the horse tend to grow at a more accelerated rate that the front limbs and there is a greater frequency of DOD associated with the hind limbs. Also, timing may play a role in the development of DOD in that there may be a “window of opportunity” along some point of the growth curve or at some transition period that allows for a greater susceptibility to DOD.

The role of nutrition: The effects of supplemental feeding programs for young, growing horses may be most profound during the transition period when the young horse begins receiving most of its nutrients from feed sources rather than mare’s milk. This transition period is usually associated with weaning (3 to 5 months of age), a period of rapid growth that may compound the effects of feeding programs on growth. Creep fed foals (at approximately 1.5% of body weight) generally show a greater growth response than non-creep fed foals. However, differences in weight and height between creep and non-creep fed horses that may be evident at the weaning to yearling stage are not maintained provided the non-creep fed horses receive adequate nutrition for growth until maturity. Growth in the foal has been expressed in a curvilinear fashion as it relates to age. Studies in other species have shown that daily growth is variable and may not follow a precise growth curve. Growth in children has been suggested to be a series of 0.5 to 1 centimeter spurts, each approximately lasting less than twenty-four hours and separated by periods of stasis. Daily measurements of growth in horses suggest similar fluctuations may exist. Thus, a horse’s growth curve would represent a more stair step type of pattern with a negative rate of gain for 2-3 days post weaning. Where on the growth curve a horse should be at a given point in time is dependant on breed, the growth potential of the individual horse, and the desired growth rate. It is generally accepted that moderate (based on 1989 NRC standards for light breeds of horses) or less rates of growth contribute less to the incidence of DOD than rapid rates of growth. Horses that may be predisposed to DOD (i.e. large framed individuals with an apparent potential for rapid growth) may benefit from diets of lower caloric density. This is sometimes confused with nutrient deprivation (starvation), which is counter-productive to reducing the potential for DOD. Protein, vitamins and minerals are needed to insure sound tissue development, but do not accelerate growth rate. Even protein concentrations at 126% of NRC recommendations have not been shown to result in an increased incidence of DOD (36, 37). However, deficiencies of these nutrients will certainly retard growth rate and effect quality of growth. Managing the growth rate of predisposed horses is best achieved by reducing the calories provided while still providing at least 100% NRC of protein, vitamins and minerals.

The other aspect of the growing horse’s diet that is often neglected is the forage component, which can vary from 30% of the diet or less to 70% or more. Depending on the quality of the hay or pasture, this aspect of the diet will have a greater impact on the amount of calories consumed than the concentrate portion of the diet and thus should be considered in the overall calorie reduction and management of the growth rate of predisposed horses.

Exercise / mechanical stress

Although exercise contributes positively to bone density (30, 42), exercise seems to have a dual role regarding DOD depending on the circumstance. One role is as a contributing factor to DOD. Researchers have suggested that non-clinical lesions present at an early age manifest into clinical signs with the increased trauma of exercise (41, 16, 5). Another role serves as a potential prophylactic to the development and severity of DOD as more recent research suggests (45, 46, 2). Horses with access to free exercise or subjected to forced exercise (trotting five miles/day five days/week) in addition to free exercise tended to have less incidence and had less severity of DOD lesions.

The role of nutrition: Feed to meet the additional demands of exercise so that the nutrient intake for quality of growth is not compromised.

Hormonal interactions

Initial research regarding the role of hormones and their relationship with DOD suggested episodic transient hypothyroidism resulting from increased concentrations of insulin as a predisposing factor (8). However, more recent research suggests that increased concentrations of insulin in response to dietary induced elevations in blood glucose may be more directly associated with DOD than the unsubstantiated hypothesis of transient hypothyroidism. Increases in glycemic response measurements have been associated with increased incidence of DOD (29). Increases in glycemic response may affect directly and indirectly hormonal responses that may affect cartilage metabolism. Other more recent research has focused on the systemic and local hormonal influences as well as some molecular aspects that may contribute to DOD. Much of this research has focused on the suppression of differentiation of chondrocytes. Without differentiation chondrocytes do not allow for proper matrix formation and subsequent calcification and thus resulting in retained cartilage. Chondrocytes at lesion sites have a deficient concentration of TGF-alpha and cMyc, as well as type X collagen. In addition, mRNA expression for TGF-alpha 1 was reduced in the mid and lower hypertrophic zones of epiphyseal cartilage at focal lesion sites (13). IGF-1 and TGF-beta may also play a role in changes of cartilage protein and proteoglycan seen in osteochondritic lesions (38).

The role of nutrition: How nutrition interacts with various hormonal theories associated with DOD is not well understood at this time. It is generally accepted that feeding large amounts of caloric dense diets to achieve rapid rates of growth can contribute to the development of DOD. However, the source of those calories also may play a contributory role particularly as it relates to possible hormonal interactions. The association between a high glycemic response, insulin concentration and increased potential for DOD may implicate diets that are higher in their overall digestible sugar content. However, such interpretations may be complicated since glycemic response may be affected by rate of consumption, physical form of the diet and diet composition. Substituting fat and fiber calories for sugar calories has been shown to effect systemic concentrations of IGF-1 in foals (40). Other studies addressing the effect of added fat to the concentrate portion of the diet did not see any significant effects on systemic IGF-1 or TGF-beta (3, 39). The optimal amount of calories and the form in which they are presented to reduce the potential of DOD is not known at this time. However, an old management rule of thumb that may be very applicable regarding nutrition and DOD would be: the more of the nutrient requirements of a horse that can be met with long stem roughage the better will be their overall health. In addition, what is not met with roughage should be compensated for with a well formulated, research based, high quality concentrate. When feeding with such concentrates their nutritional balance and quality should not be compromised with added supplements.

Other nutrient considerations

There has been little work addressing possible connections to vitamin status and DOD. The pathology of the various forms of DOD does not suggest a vitamin deficiency or excess issue. Vitamin K deficiency has been investigated recently as having a possible role in DOD but the normal diet of the horse appears to have adequate amounts of vitamin K. Deficiencies of calcium, phosphorus and copper have been implicated in DOD. Inverted calcium to phosphorous ratios (normal 2:1, Ca: P) and excesses of specific minerals that render other minerals deficient due to binding activities also have been implicated as contributors to DOD. Of all the minerals, copper requirements have been most studied and seemingly well established, however, it should not be considered a prescription for DOD given the multifactorial nature of the disease (7).

Summary

Genetics is the primary determinant factor for risk of DOD
Meet as much of a growing horses nutrient needs as possible with good quality roughage (test forage quality)
Feed for moderate or less growth rates
Provide abundant free exercise or a well constructed and controlled forced exercise program
Concentrates should be research based, well formulated and manufactured under the highest quality control standards
For horses with incidence of DOD reduce caloric intake but maintain adequate amounts and quality of protein, vitamin and mineral intake.

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