Cartilage matrix changes in the developing epiphysis: Early events on the pathway to equine osteochondrosis?

Lecocq, Michèle; Girard, Christiane; Fogarty, Ursula; Beauchamp, Guy; Richard, Hélène

doi:10.2746/042516408x297453

Cited by 59 publications

(82 citation statements)

References 53 publications

(79 reference statements)

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“…Collagen was organized differently around, compared with between, cartilage canals, 43,64 but is there any evidence to suggest that collagen is organized differently between adjacent individual canals, which could then explain why vessels within one canal fail at the same time as vessels in neighboring canals remain intact? Copper deprivation was associated with reduced crosslinking of collagen, 45 but is there any evidence that crosslinking of elastin in blood vessel walls is affected also, 45,54 resulting in weakening and vascular failure?…”

Section: Not Applicablementioning

confidence: 99%

“…17,89 There is some evidence to suggest that a high copper status at birth is associated with an increased proportion of lesions undergoing spontaneous resolution, 54,118 but the conclusion of the most recently published study was that the role of copper in the pathogenesis of osteochondrosis remains poorly understood. 30 Independent of copper, Lecocq et al 64 detected changes in collagen structure, and studies reviewed by Laverty and Girard 60 indicate that the biomarker change that is most frequently detected in young horses is an increase in type II collagen synthesis. Both author groups suggest that collagen changes could be involved in the initiation of lesions.…”

Section: What Is the Relationship Between The Studies Of Ischemic Chomentioning

confidence: 99%

“…Both author groups suggest that collagen changes could be involved in the initiation of lesions. 60,64 Chondrocytes that have undergone necrosis are unable to perform their role in matrix homeostasis, and reduced number and thickness of collagen fibrils were observed in areas of ischemic chondronecrosis in pigs. 13,25 Whether changes in collagen structure 64 or synthesis 60 are capable of causing vascular failure remains to be determined (see ''Causes of Vascular Failure,'' below).…”

Section: What Is the Relationship Between The Studies Of Ischemic Chomentioning

confidence: 99%

“…42,104 Further studies have confirmed that the ossification front is generally irregular in young animals. 64,77,82,85 The irregularities that are associated with osteochondrosis contain chondrocytes that are necrotic, and it is possible to distinguish between such lesions and general irregularities in histological sections 85 and CT scans. 77,79,82 What Is the Relationship Between Ischemic Chondronecrosis and the Pathogenesis of Osteochondrosis in Species Other Than Pigs and Horses?…”

Section: What Is the Relationship Between The Studies Of Ischemic Chomentioning

confidence: 99%

“…42,61,62,103,113 From 2008 onward, there was a shift from looking at collagen as the direct cause of osteochondrosis 42,61,62,103,113 to considering whether collagen disease is capable of causing vascular failure. 60,64 With reference to what has been discussed for biomechanical force and primary disease of collagen above, it may be pertinent to investigate the following questions:…”

Section: Not Applicablementioning

confidence: 99%

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An Update on the Pathogenesis of Osteochondrosis

2015

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Osteochondrosis is defined as a focal disturbance in endochondral ossification. The cartilage superficial to an osteochondrosis lesion can fracture, giving rise to fragments in joints known as osteochondrosis dissecans (OCD). In pigs and horses, it has been confirmed that the disturbance in ossification is the result of failure of the blood supply to epiphyseal growth cartilage and associated ischemic chondronecrosis. The earliest lesion following vascular failure is an area of ischemic chondronecrosis at an intermediate depth of the growth cartilage (osteochondrosis latens) that is detectable ex vivo, indirectly using contrast-enhanced micro-and conventional computed tomography (CT) or directly using adiabatic T1r magnetic resonance imaging. More chronic lesions of ischemic chondronecrosis within the ossification front (osteochondrosis manifesta) are detectable by the same techniques and have also been followed longitudinally in pigs using plain CT. The results confirm that lesions sometimes undergo spontaneous resolution, and in combination, CT and histology observations indicate that this occurs by filling of radiolucent defects with bone from separate centers of endochondral ossification that form superficial to lesions and by phagocytosis and intramembranous ossification of granulation tissue that forms deep to lesions. Research is currently aimed at discovering the cause of the vascular failure in osteochondrosis, and studies of spontaneous lesions suggest that failure is associated with the process of incorporating blood vessels into the advancing ossification front during growth. Experimental studies also show that bacteremia can lead to vascular occlusion. Future challenges are to differentiate between causes of vascular failure and to discover the nature of the heritable predisposition for osteochondrosis.

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