Studies on growth cartilage in the horse and their application to aetiopathogenesis of dyschondroplasia (osteochondrosis)

• Published in: The veterinary journal (1997) 1998-11, Vol.156 (3), p.177-192
• Main Authors: Jeffcott, L.B., Henson, F.M.D.
• Format: Article
• Language: English
• Subjects: Animals; Cartilage, Articular - growth & development; dyschondroplasia; endochondral ossification; growth cartilage; Growth Plate - growth & development; Horse; Horse Diseases - etiology; Horses - growth & development; Osteochondritis - etiology; Osteochondritis - veterinary; osteochondrosis; Osteogenesis; Physical Conditioning, Animal
• ISSN: 1090-0233; 1532-2971
• DOI: 10.1016/S1090-0233(98)80121-4

The importance of osteochondrosis (dyschondroplasia) to the horse industry has been well documentedsince it was first recorded 50 years ago. The condition is known to be multifactorial in origin, arising from focal failure of endochondral ossification at predilection sites in articular/epiphyseal growth cartilage, but specific information on its aetiopathogenesis is sparse. This paper reviews the current knowledge of growth cartilate metabolism and the process of normal endochondral ossification in the horse. It highlights the localization of various protein products of chondrocytes and the differences in the zones of articular cartilage. In the early focal lesions (referred to as dyschondroplasia) there are alterations in the chondrocytes, extracellular matrix and some of the local protein products. The most obvious feature is an alteration in matrix metabolism which may be responsible for triggering a range of other factors leading to the development of a retained core of cartilage and a primary lesion of dyschondroplasia. Based on available evidence, a preliminary hypothesis for pathogenesis is presented. This suggests thatthere are a number of factors capable of initiating the condition. One of these involves high circulating insulin levels from high energy feeding which may affect chondrocyte maturation leading to altered matrix metabolism and faulty mineralization resulting in the formation of cartilage cores which characterize the condition. Further research to test this hypothesis is needed before there can be a rational basis for prophylaxis.