What is Developmental Orthopedic Disease?

Developmental Orthopedic Disease (DOD) is a broad term representing a number of clinical syndromes affecting the musculoskeletal (muscles and skeleton) system of the horse during growth and development.

DOD is multifactorial, meaning more than one factor plays a role in the development of these syndromes. These factors are:

  • Nutrition
  • Exercise
  • Hormones
  • Heredity
  • Trauma
  • Combination of any or all of the above.

There is likely a range of susceptibilities to DOD, ranging from horses that will not develop DOD under any circumstances, to horses that will develop DOD unless well managed (nutrition, exercise etc.) to those that will develop DOD no mater what is done. The latter are the horses to eliminate from the breeding herd.

Syndromes included under the term “DOD” are:

  • Physitis (“epiphysitis”)
  • Osteochondrosis (“Osteo” = bone;“chondro” = cartilage)
    • Osteochondritis dessicans (OCD)
    • Subchondral bone cysts (SBC)
  • Angular limb deformities
  • Flexural deformities (“contracted tendons”)
  • Cervical compressive myelopathy (CCM – “wobblers”);
    “cervical” = neck; “myelo” = nerve; “path” = disease

Let's take a look at the factors involved in the development of DOD in more detail:

Nutrition
To determine the impact of the nutritional program on DOD, it is most appropriate to assess the composition of the diet, not blood levels of nutrients. This is because the horse’s body will try to maintain blood levels of most nutrients within a certain range by the process of “homeostasis” (“homeo” = same; “stasis” = stand). Also, time of feeding prior to blood sampling can affect the levels of nutrients in the blood. They may be high soon after feeding or low after a long overnight fast.

Two major areas of nutrition tend to contribute to DOD:

  1. Excess energy intake (especially high starch/sugar and/or protein)
  2. Inadequate or imbalanced Calcium/Phosphorous and/or Copper/Zinc

Excess energy intake, especially from starch and sugar, can come from many sources. Consumption of feeds high in cereal grains, most notably, corn, and molasses will results in the horse taking in high levels of starch and sugar, which will drive up blood insulin levels. High insulin levels have been shown to decrease growth hormone, critical for the development of normal cartilage and bone, and will contribute to DOD.

Intake of high levels of protein, as is common when horses are fed straight alfalfa hay, will also cause problems. Straight alfalfa hay can provide over 2-times the protein required by a growing horse. Such excess protein will be, in essence, turned in to sugar in the horse’s body I with the same results as if it had been fed molasses!! In addition, excess protein requires the body to rid itself of excess nitrogen, which is excreted in the urine, resulting in increased urine output, wetter stalls and the ammonia smell in the barn with which we are all familiar!!!!!

Too much time on lush pasture can also result in high intake of calories, starch and protein.

Historically, many thought that the early pregnant mare could be fed like an open mare until the last 3-4 months of gestation. Research has shown that this practice may actually predispose the foal to Developmental Orthopedic Diseases (DOD). Trace nutrients, many of which are critical to normal bone development, are stored in the liver of the developing fetus. Mares not receiving adequate nutrition during gestation may not be able to shunt enough nutrients to support the developing foal during the last trimester - the most rapid growth phase.

Special attention must be given to the diet of the pregnant mare from conception to foaling, especially for essential amino acid balance and the levels of copper, zinc and possibly manganese. Current NRC (2007) recommendations for copper and zinc are 100- 125 mg and 400 mg/day, respectively. Some research suggests copper levels of 350 mg and zinc levels near 800-1,000 mg/day may reduce the incidence of D.O.D. The current NRC (2007) only addresses a single amino acid, lysine. The lysine requirements have been increased somewhat from previous publications without a correlating change to the overall protein requirement, suggesting increased attention to protein “quality” or amino acid balance instead of protein “quantity”. Researchers will learn more about other essential amino acids as our knowledge base increases.

It is important to note that, while a foal is nursing on its Mother, the mare’s intake of energy will also affect the foal and the likelihood of developing DOD.

Another problem with high levels of alfalfa in the horse’s diet is the calcium (Ca) to phosphorous (P) ratio. The ideal Ca:P ratio for the growing horse is 1.5:1. Young horses can probably tolerate ratios slightly over 2:1. The Ca:P ratio in alfalfa hay can be as high as 6 or 7 to 1!!!!!!! The P content in grain will adjust this somewhat, but comes at the cost of hundreds of starch calories.

To correct the imbalance requires a well-designed concentrate, like Tribute Equine Nutrition’s Alfa Essentials, with more P than Ca to correct the Ca:P ratio in the entire diet. Tribute’s Alfa Assist Mineral also corrects the Ca:P ratio created by alfalfa hay or pasture.

Grass hay will have a Ca:P ratio closer to 1:1 and usually needs no adjustment. Hay that is part grass and part alfalfa (or other legume, like clover) will have a Ca:P ratio that correlates to the percent of each in the mix. When you get to a mix that is about halfgrass and half-alfalfa, hay analysis is warranted to make sure the Ca:P ratio in the diet is acceptable. In fact, hay analysis is a good idea whenever it is fed to breeding animals.

Another important concern is the levels of copper (Cu) and zinc (Zn) in the growing horse’s diet. The current National Research Council’s recommendations (NRC, 2007) for Cu and Zn are 10 and 40 parts per million (ppm) in the total diet, respectively. Recent research suggests those levels should be more like 35-50 and 80-100 ppm, respectively. Tribute Equine Nutrition is formulating to the new levels and results have shown dramatic reductions in DOD on many breeding farms!!! Products designed for the breeding farm, such as Essential KAlfa EssentialsGrowth and Alfa Growth address Ca:P balance, copper and zinc levels and amino acids balance. For foals of mares that were not adequately fed during pregnancy, foals expected to grow fast or those showing signs of DOD, Tribute’s ADVANCE paste will supply a concentrated dose of chelated copper, zinc and other vitamins and minerals to help the healing process. ADVANCE paste also has encapsulated probiotics to help establish a normal bacterial population in the foal’s hindgut.

In addition, Cu and Zn are two minerals that have shown improved absorption when they are CHELATED. Chelated minerals are bound to a protein or polysaccharide (complex sugar), which prevents other substances in the diet from binding them before they can be absorbed by the horse. Don’t worry!!! The levels of polysaccharides used for chelating minerals are EXTREMELY low and will not cause the issues discussed above.

Thus, we must consider the Ca:P ratio and intake, as well as the Cu and Zn intake in the TOTAL diet, hay and concentrate combined. Consult an Equine Nutritionist for help.

Exercise
Another important factor in preventing DOD is avoiding excessive forced exercise (like lounging for long periods). Each horse is individual in what amount of exercise it can tolerate, but if the horse’s knees are shaking after he is worked, you probably worked him too hard, and will aggravate DOD.

Research has shown that voluntary exercise is critical for normal bone development. Restriction to a stall for most of the day will contribute to the development of DOD. Afford as much free-exercise as possible for the growing horse.

Hormonal
Hypothyroidism (low thyroid hormone levels) has been correlated to DOD. Though uncommon, having a veterinarian check the DOD foal’s thyroid level may be a benefit.

We discussed above the negative effect high insulin levels, caused by high starch/sugar diets, will have on Growth hormone.

The important message here is that just assessing calories does not tell the whole story – the hormonal impact of starch and sugar need to be evaluated.

Heredity
Conditions that are inherited will affect the propensity of a horse to develop DOD.

Such conditions include:

  • Poor conformation (upright pasterns, toed-in or out, calf-kneed etc.)
  • Fine-boned legs
  • High body weight (muscle and/or fat)
  • Rapid growth

Trauma
Injury to the affected leg(s), lameness in opposing leg putting pressure on the affected leg, obesity in mares leading to fetal malpositioning (foals legs bent in the mare’s uterus) can all lead to DOD.

How does DOD develop?


The process of cartilage maturation and ossification (turning into bone) is defective, due to one or more of the factors previously discussed. Blood supply to the long-bones generally comes from the middle of the bone and moves towards the end of the bone. Cartilage at the growth plate, near the end of long bones, thickens and prevents adequate blood supply to deeper tissues, like the cartilage in joints, causing further tissue abnormalities or death.

Underlying Causes of DOD Syndromes


Physitis

  • Growth plate does not mineralize properly
  • Growth plate widens
  • Swelling and pain occur
  • Flexural deformities may follow due to pain

Osteochondrosis (OC)

  • Abnormality of the articular cartilage
  • Can affect development of bone below (subchondral):

Can lead to:
Osteochondritis Dessicans (OCD) – cartilage flaps or fragments
Subchondral Bone Cysts (SBC) – lesions in bone below articular cartilage

Angular Limb Deformity
Asymmetrical development of growth plate (physes) or collapse of knee or hock bones

  • Congenital – foal is born with deformity; due to malposition in uterus
  • Acquired – foal is born with straight legs; deformity develops over time

Flexural Deformity
Due to pain in the limb from other DOD syndromes. Tendons may appear “contracted” but they are not. Can also be Congenital or Acquired.

  • Contracted tendons – tendons are not actually contracted!.affects coffin joint in foals & weanlings; knees & hock in older horses
  • Club foot – raised heel; hoof turned in

Cervical Compressive Myelopathy (CCM) “Wobblers Syndrome”

  • Swelling of vetebral bone and joints causes narrowing of vetebral canal.
  • Pressure on spinal cord causes ataxia (incoordination), base-wide stance, spasticity.
  • Most common cause of Wobbler’s in horses < 4 years old
  • Other causes:
    • EDM (equine degenerative myeloencephalopathy
    • EPM (equine protozoal myelitis)

Summary


DOD covers a number of growth-related abnormalities.

DOD’s can be caused by a number of factors and combinations of factors.

Nutritional and management practices can reduce incidence.

  • Pay attention to the diet of the broodmare from early pregnancy forward
  • Begin to increase the mare’s nutrient intake AFTER she foals until 6-8 weeks post-foaling to match her milk production
  • Creep feeding foals with a milk-based foal feed will help the foal get used to solid food and reduce milk production stress on the mare
  • Ensure proper intake and balance of calcium and phosphorous and intake of copper and zinc

Genetic contributors are more difficult to detect and control.

Assess diet, not blood levels for deficiencies/imbalances!!!!

Ca/P levels and ratio (< 3:1)

  • Legumes can have Ca:P ratios as high as 7:1
  • Thus, must add P to diet to balance
  • Levels not likely to be too low – ratio is usually the issue

Cu (35-50 ppm) and Zn levels (80-100 ppm) in total diet

  • Most forages very low in Cu/Zn (< 15 ppm)
  • Critical to supply in concentrate

Low (< 30%) starch/sugar in diet

  • Insulin response disrupts growth hormone

Protein

  • High quality (lysine good indicator, but not the whole story)
  • Total diet 16-18%
  • Excessive protein converted to glucose

In face of DOD

  • Reduce grain intake – ESSENTIAL K and minerals alone
  • Reduce weight on horse
  • Eliminate forced exercise
  • Stall rest, minimal turnout, hand-walking – work with veterinarian
D.J. Burke, Ph.D.