Physitis is a developmental orthopedic problem involving disruption of the normal process of endochondral ossification. Endochondral ossification is a process through which bone grows during the development stage of life.
On the ends of the bones, there exist a layer of cartilage. As the bone grows, the cartilage layer provides a "scaffolding" or "meshwork" into which osteoblasts (bone cells) can attach themselves. As the bone cells are laid down on the cartilage matrix, the cartilage eventually develops into bone. This process is called endochondral ossification, or mineralization of cartilage, and occurs within the growth plates (physes). Meanwhile, a new layer of cartilage is forming on the newly-formed end of the bone. And the process continues until the bones have reach their predetermined length.
For a variety of reasons, some of which are known and some of which are unknown, there may occur a defect in the process of endochondral ossification. This especially occurs in bones that are growing very quickly. The faster the bone grows, the more "finely-tuned" this process must be in order for normal ossification of the cartilage to occur.
Therefore, fast-growing horses are especially susceptible to physitis.
Defective areas may predispose the underlying subchondral bone to microfracture, which is typically implicated as the cause of pain, swelling, and lameness that often accompanies physitis. As the severity of the lesions worsen, partial loss of the structural integrity of the physis stimulates periosteal new bone formation in the distal metaphysis. As periosteal new bone is formed, the metaphysis acquires a flared appearance, which is typical of the physitis syndrome. Further remodeling of the surrounding metaphysis in response to subchondral microfracture is seen radiographically as increased radiolucency, giving the appearance of widening at the physeal growth cartilage, which is bordered by a margin of sclerotic bone formed in the surrounding metaphysis.
I. The primary goal of treatment is to limit the foal's rate-of-growth as much as possible.
There are many factors that dictate a foal's rate-of-growth. Two of the most important include:
1) Genetics, and
2) Energy Intake During Growth
Obviously, we cannot manipulate the foal's genetics after it is born. We can, however, adjust the quantity and type of feed that it ingests. Our goal is to provide the least amount of energy possible, especially in the form of carbohydrate. The primary source of carbohydrate for horses is sweet feed and grains. Alfalfa hay is also somewhat high in carbohydrates.
Fat, on the other hand, is generally stored after consumption. It is later broken down into sugar as energy is required, but does not make energy readily available to the horse. Therefore, decreasing the carbohydrate/ starch percentage of the diet and increasing fat while maintaining a comparable caloric intake may prove beneficial.
II. Depending on the feed that you choose, copper supplementation may also be necessary to reduce the likelihood of copper deficiency, which has also been linked to developmental orthopedic disease (DOD).
III. Restriction of exercise (i.e. stall confinement) is recommended when moderate to severe pain/ lameness is evident to prevent further injury to the affected physes.
IV. Palliative use of non-steroidal antiinflammatory medications (e.g. Phenylbutazone) may also be necessary to reduce pain, although these drugs should be administered with caution due to the foal's propensity for developing gastric ulcers. Adjunctive antiulcerative medication (such as Omeprazole) and/or use of specific Cox-2 inhibiting NSAIDs (such as Equioxx or Previcox) may be a safer approach in very young animals or those with history of gastric irritation.
Fortunately, physitis is self-limiting and rarely results in any permanent issues. Physitis can be expected to spontaneously resolve as the process of endochondral ossification ceases as the bone reaches it mature length.