Abstract

BackgroundYoung Standardbred horses frequently develop fragments in joints. Some fragments represent osteochondrosis; others are considered developmental, but it is uncertain whether they result from preceding osteochondrosis. Osteochondrosis occurs as a consequence of failure of the cartilage canal blood supply and ischaemic chondronecrosis. In heritably predisposed foals, failure was associated with incorporation of vessels into bone. However, bacterial vascular failure was also recently documented in foals suffering spontaneous infections, proving that bacteria can cause osteochondral lesions in foals up to 150 days old. The aim was to determine prevalence of fetlock and hock lesions at screening age in Standardbred horses that survived infections before 6 months of age, and compare this to prevalence reported in the literature.MethodsThe material consisted of 28 Standardbred horses; 17 males and 11 females that presented and were diagnosed clinically with bacterial infections from 1 to 150 days of age (average: 41.3 days). A screening set of 8 radiographic projections was available from all 28 horses at 7–85 months of age (average: 23.6 months). Lesion prevalence was compared to three previously reported Standardbred cohorts.ResultsOsteochondral lesions were detected in one or more joints of 19/28 horses (67.9%); in the fetlock joint of 14/28 horses (50%) and the hock joint of 11/28 horses (39.3%). These prevalences were ≥ 2 x higher than the corresponding prevalences in the comparison cohorts, and statistically significantly so in 5:6 comparisons (p-values from < 0.00001 to 0.01). In the sepsis cohort, there were an average of 2.3 affected joints and 2.5 lesions per affected horse, whereas there in the one comparable literature cohort were an average of 1.5 affected joints and 1.7 lesions per affected horse.ConclusionsStandardbred horses that survived bacterial infections before 6 months of age had more osteochondral lesions than literature comparison cohorts at screening age. The implication was that some of the lesions in this group were caused by bacteria. It may become necessary to develop methods for differentiating between acquired, septic and aseptic, heritably predisposed lesions.

Highlights

  • Young Standardbred horses frequently develop fragments in joints

  • The pathogenesis of articular osteochondrosis in horses has been documented at three levels of evidence: changes are present at predilection sites prior to clinical lesions [1, 2], identical changes occur in more than one species [2, 3], and lesions can be experimentally reproduced [4, 5]

  • Lesions can resolve [7,8,9], or pathologic fracture can occur through the infarct, leading to fragments in joints known as osteochondrosis dissecans (OCD) [5, 10]

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Summary

Introduction

Young Standardbred horses frequently develop fragments in joints. Some fragments represent osteochondrosis; others are considered developmental, but it is uncertain whether they result from preceding osteochondrosis. The morphology of spontaneous lesions in both heritably predisposed foals [2] and pigs [3] indicates that failure occurs where the mid-portion of blood vessels is incorporated into the advancing ossification front. This results in ischaemic necrosis of chondrocytes at mid-depth of the growth cartilage [2, 3]. Fragments at predilection sites in the hock and stifle are referred to as OCD because it has been confirmed that they are the result of preceding osteochondrosis [1, 2]. Heritability has been estimated for all hock and fetlock fragments [17,18,19] except UPEs, omitted due to low prevalence

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