Equine osteochondrosis in the '90s

Abstract

The International Seminar on Equine Osteochondrosis in the '90s was held September 28-30th at Girton College at Cambridge, England. Synopses of some of the presentations follow: Dr. R. R. Pool, of the School of Veterinary Medicine at Davis, California said the need for a more precise definition differentiating primary (idiopathic; genetic) from secondary (acquired) developmental lesions of the equine osteochondral complex is obvious. Truly primary equine osteochondrosis (EOCD) should be characterized by multiple random cartilage lesions in physes and articular surfaces in multiple skeletal sites. Lesions should not be bilaterally symmetrical. B. H. Thorp, of the Institute of Animal Physiology and Genetics Research, at Midlothian, Scotland described a potential model for EOCD, avian tibial dyschondroplasia (ATD). ATD and EOCD are both characterized by the presence of a largely avascular mass of cartilage composed mostly of partially hypertrophied (transitional) chondrocytes and abnormal interlacunar matrix. The hypothesis that ATD is a consequence of aberrant or incomplete chondrocyte differentiation may be supported by evidence that genetic selection forATD results in accumulations of transitional chondrocytes. Deficiencies in TGF-13 and c-myc gene products and a shift to increased fully hypertrophied chondrocytes resuits from a defect or defects in gene translation. It was suggested that similar metabolic approaches replace the current reliance on morphologic investigations in attempts to define the pathogenesis and possible etiology of EOCD. Dr. C.W. Mcllwraith, of Colorado State University said there are 3 classes of EOCD lesions: those showing both clinical and radiographic signs, those showing only arthroscopic signs, and those showing only radiographic signs. EOCD lesions are usually bilateral inthe femoropateUar and tarsocrural joints and quadrilateral in the fetlock joints, and occur most commonly at the margin of excursion of one articular surface on another. These findings are consistent with the existence of a window of vulnerability to biomechanical insult in the development of certain joints. N. E. Dolvik, Norwegian College of Veterinary Medicine reported that radiographic examination during 1989 of about 60% of all Standardbred trotters born in Norway in 1988 showed an incidence of tibiotarsal EOCD of 14.3% and of bony fragments in the palmar/ plantar portion of the metacarpophalangeal or metatarsophalangeal joints of 11.8%. The heritability coefficient of tibiotarsal EOCD was estimated to be 0.32 ± 0.12 (r 2 -0.13), and that of bony fragments in the palmar/plantar portion of the metacarpophalangeal or metatarsophalangeal joints was estimated to be 0.13 ± 0.08 (r 2 0.09). B. Sandren and J. Philipsson, of the Swedish University of Agricultural Sciences reported that radiographic examinations of the tarsocrural and metacarpophalangeal and metatarsophalangeal joints of 793 long yearling Standardbreds revealed an incidence of tarsocruununited palmar/plantar eminences in the fetlock joints of 4.2%. Most tarsocrural EOCD 95% occurred at the intermediate ridge of the tibia. Bony fragments and ununited eminences occurred mainly in the hind limbs. Most (75%) bony fragments were found in the medial regions of the fetlock joints, while ununited eminences were usually found laterally. Horses with ununited eminences had a much higher incidence of bony fragments within the fetlock joints. The heritability of tarsocrural EOCD was estimated to be 0.24 ± 0.18, and that of bony fragments in the fetlock joints was estimated to be 0.17 ± 0.13. Height at the withers was inversely correlated with the appearance of bony fragments in the fetlock joints (r ~= -0.12) and tarsocrural EOCD (r 2 = -0.51). Carpal circumference also was inversely correlated with the appearance of bony fragments in the fetlock joints (r ~ = 0.40); in contrast, carpal circumference was positively correlated with the presence of tarsocrural EOCD (r 2 = 0.91). TarsocruralEOCD and bony fragments in the fetlock joints were positively correlated (r 2 = 0.60), indicating that perhaps one-third of the genes involved as causative factors may be the same for both types of lesions. L.R. Bramlage, of Rood and Riddle Equine Hospital of Lexington, Kentucky said that foals followed from birth to 180 days of age exhibited little correlation between rates of increase in height (r = 0.24) or body weight (r = 0.14) and the number of EOCD-like cartilage defects discovered during gross examination at necropsy. Neither growth rates nor lesion frequency were correlated with dietary copper intake.