EQUINE

A NEW LOOK AT OSTEOCHONDROSIS

Last year atthe Bain Fallon lectures, in Australia, Dr. Roy Pool, presented an argument that subchondral bone cysts are not always a manifestation of osteochondrosis, and that the various manifestations of so-called developmental bone dis- ease may not necessarily have the same etiology. In Pool's experience with hundreds of horses submitted to the Pathol- ogy Service of the Veterinary Medical Teaching Hospital, UC Davis, for necropsy because of a crippling spontaneous lesion, very few of the horses he has examined had general- ized articular and physeal lesions of osteochondrosis similar to the pattern found in swine and poultry. Since the swine and poultry form of osteochondrosis has served as the model for the pathogenesis of osteochondrosis, or developmental bone disease (DOD), in horses, Pool's findings may be important in determining the actual pathogenesis of the condition in horses.

According to Pool, "There is growing concern among equine practitioners that all disorders of growing homes characterized by abnormalities in cartilage maturation are being inappropriately or prematurely regarded as variants of osteochondrosis, at a time when there is no general agreement on what constitutes the fundamental lesion and the etiopathogenesis ofosteochondrosis in horses. The proposals that this group ofosteochondral lesions in growing horses are all part of one entity is based on studies in swine and poultry where osteochondrosis is a systemic disease with a genetic basis. In response to that concern, it has become current practice by equine practitioners to group the disorders of endochondral ossification under the term developmental or- thopedic disease (DOD), until their true nature is determined. DOD usually includes" 1) osteochondrosis/OCD and its spec- trum of lesions; 2) acquired angular limb deformity; 3) flexural deformities ofthe limbs; 4) aseptic physitis (epiphysi- tis); 5) subchondral bone cysts not associated with OCD; 6) cuboidal bone malformation; and 7) cervical vertebral mal- formation.

"To understand the etiopathogenesis ofosteochondrosis, it is important that, where possible, the precise cause or causes of osteochondrosis be identified realizing that both primary

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and secondary factors may be involved in the pathogenesis of osteochondrosis. Major factors supposedly predisposing to development of osteochondrosis are" genetic susceptibilities including abnormalities in endocrine control of growth or in metabolic requirements for cartilage matrix production, nutri- tional excesses, dietary imbalances or trace element deficien- cies, and mechanical stress.

"If current practices continue, the recognizing of all noninfectious disturbances of osteochondral junctions in im- mature homes as lesions ofosteochondrosis regardless of their cause, it becomes very important that the cause of the lesion, where known, must be included in the naming ofthe particular lesion, eg. traumatic osteochondrosis, osteochondrosis due to flexural deformity, osteochondrosis due to faulty conforma- tion, nutritional osteochondrosis, genetic osteochondrosis, etc. Using this approach, veterinarians concerned with under- standing and treating this disease would eventually be able to distinguish between the primary and secondary factors initi- ating and promoting lesions of osteochondrosis.

"They could then begin to develop strategies, based on scientific fact, for reducing the incidence of the disease. Genetic/nutritional factors involved in the pathogenesis of osteochondrosis ofjoints and physitis should be distinguished so that, if their etiopathogenesis is different, rational recom- mendations can be made for breeding and dietary manage- ment."

It is a general tendency to want to simplify problems by categorizing them, or lumping them into groups. Then as facts are determined about various members of the group, the conclusion can be made that the facts apply to all in the group. This certainly simplifies the scientific process, but often leads to false conclusions. There seems to be some aspects in common between the various manifestations of DOD, but that does not mean they have a common etiopathogenesis. Ac- cording to Pool, it would be wise for everyone concerned to use caution in drawing too many conclusions about the cause or pathogenesis of any manifestation of DOD, until we learn more specifics about this perplexing group of maladies.

In October, a symposium on osteochondrosis will be held at Cambridge University, under the direction of Dr. Leo Jeffcott. Researchers from around the world who have made significant contributions on the subject of osteochondrosis will meet to inform and update each other. A proceedings of the meeting will be published in the Equine Veterinary Journal. WEJ

Volume 12, Number 5, 1992 319