Epiphyseal cartilage canal blood supply to the tarsus of foals and relationship to osteochondrosis

REASON FOR PERFORMING STUDY: Pathological changes in the blood supply to growth cartilage have been implicated in the pathogenesis of osteochondrosis (OC) in horses, but have not been reported using vascular perfusion techniques. OBJECTIVE: To describe the developmental pattern of cartilage canal vessels in the distal tibial epiphysis and talar growth cartilage of foals. METHODS: Nine foals bred from parents with OC were sacrificed between the ages of 0 and 7 weeks to undergo a barium perfusion procedure. The distal end of the tibia and the entire talus were cleared in methyl salicylate and perfused vessels studied in the intact bones. Slabs with a thickness of 4-5 mm from 3 predilection sites for OC were examined in the stereomicroscope and with light microscopy. RESULTS: Cartilage canals were present for a limited period of growth. Perfused vessels initially entered canals from the perichondrium. Vessels in the proximal portion of canals retained their perichondrial arterial source throughout. With time, the ossification front advanced to incorporate the mid-portion of canals; and anastomoses formed between canal vessels and subchondral vessels. A shift occurred and vessels in the distal terminus of canals came to use subchondral vessels as their arterial source. Twelve histological lesions were found in 7 foals. All contained necrotic vessels surrounded by necrotic growth cartilage and 3 caused macroscopically visible delay in endochondral ossification. Lesions were located where vessels traversed the ossification front to enter the distal terminus of canals. CONCLUSION: Cartilage canal vessels are particularly susceptible to failure at the point where they cross the ossification front, with consequences for the viability of those chondrocytes that depend on them. POTENTIAL RELEVANCE: A better understanding of how lesions of OC arise may improve the ability to identify, monitor, prevent and treat this disorder. Involvement of cartilage canals in the pathogenesis of equine tarsal OC plausibly explains several clinical features of this disease.     

Early lesions of articular osteochondrosis in the distal femur of foals

Failure of the cartilage canal blood supply to epiphyseal growth cartilage has been implicated in the pathogenesis of articular osteochondrosis in horses and other animal species. In a previous study of the developmental pattern of the blood supply in the tarsus of foals, early lesions of osteochondrosis were consistently found in regions where the cartilage canal vessels traversed the chondro-osseous junction. The developmental pattern of blood vessels has also been described in the distal femoral epiphysis; however, the group of foals examined in that study did not have lesions of osteochondrosis in this location. Therefore, the relationship between the occurrence of early lesions of osteochondrosis and the developmental pattern of the blood supply to epiphyseal growth cartilage in this site in foals has not been examined. Distal femora were collected from 30 fetuses and foals (up to 11 months old) submitted for postmortem examination. Sections from the lateral trochlear ridge and medial femoral condyle of both hind limbs were examined histologically. Sixteen cartilage lesions were found in 7 of the 30 fetuses and foals. All lesions contained evidence of cartilage canal necrosis and ischemic chondronecrosis. The lesions were located in regions where cartilage canal vessels traversed the chondro-osseous junction, as previously observed in the tarsus. The location and morphology of lesions indicated that a subclinical stage of ischemic chondronecrosis existed that preceded and predisposed to the development of osteochondrosis dissecans and subchondral bone cysts.     

The effects of copper supplementation on the prevalence of cartilage lesions in foals

The potential role of dietary copper in the development of cartilage defects in foals was investigated. Twenty-one mares were fed rations containing 13 ppm copper (CuC, control) or 32 ppm copper (CuS, supplemented) during the last three to six months of gestation and first three months of lactation. Their foals were fed pelleted concentrate containing 15 or 55 ppm Cu and were destroyed at 90 (5 CuC and 5 CuS foals) or 180 (6 CuC and 5 CuS foals) days. Focal cartilage lesions were found at multiple sites on necropsy. In foals killed at 90 days, there were over twice (9 versus 4) as many lesions of osteochondrosis and more than four times (9 versus 2) as many articular lesions of osteophyte formation or thinning in CuC foals compared with CuS foals. These differences were due predominantly to a higher number of lesions in one CuC foal. Two 90-day CuC foals had osteochondrosis of articular-epiphyseal (A-E) complex, one with thickenings and separation from subchondral bone and one with subchondral fibrosis. One 90-day CuS foal had a cartilage thickening of the A-E complex in the tibiotarsal joint with separation from subchondral bone. In foals killed at 180 days, there were seven times more articular lesions (21 versus 3) of osteophyte formation or thinning, nearly twice as many lesions of osteochondrosis (13 versus 8) [corrected] in the physis and over five times as many involving the A-E complex (11 versus 2) in six CuC foals compared with five CuS foals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Osteochondrosis in the horse--searching for the key to pathogenesis

This paper reviews current developments in equine osteochondrosis complex and the clinical syndromes associated with it. Although the primary lesion has been defined as a failure of endochondral ossification, its definitive cause is unknown and appears to involve heredity, growth rate, nutrition, mineral imbalance, endocrinological dysfunction and biomechanical trauma. Despite the international importance of osteochondrosis in horses, surprisingly few controlled investigations have been performed on its pathogenesis. The studies that have been conducted suggest that local effects on differentiating growth cartilage are the key to a more complete understanding of the problem. Gaps in the current knowledge include in-depth understanding of the life cycle of chondrocytes in growth cartilage, the process of mineralisation and the use of a standard experimental model for the induction of osteochondrosis. The ultimate goal of osteochondrosis research must be to prevent or reduce the incidence of the condition in horses.     

Epiphyseal cartilage canal blood supply to the distal femur of foals

REASONS FOR PERFORMING STUDY: The developmental pattern of the cartilage canal blood supply to epiphyseal growth cartilage has been linked to osteochondrosis (OC) in the tarsus of foals. This pattern has not yet been described in the distal femur, another site frequently affected by OC. OBJECTIVE: To describe the developmental pattern of the blood supply to the distal femoral epiphyseal growth cartilage in 8 Standardbred foals age 0-7 weeks. METHODS: One foal was sacrificed weekly from birth to age 7 weeks (n=8) to undergo a barium perfusion procedure to demonstrate vessels within cartilage canals of one hindlimb. The distal end of the femur was cleared in methyl salicylate and perfused vessels were studied in the intact bones. Each distal femur was then sawed into 5 mm thick slabs in the transverse plane, and the slabs decalcified and radiographed. Finally, the lateral trochlear ridge was separated from each slab and examined histologically. RESULTS: The cartilage canal blood supply regressed with increasing age, but several regions remained vascularised in the oldest foal at age 7 weeks. Vessels arose from perichondrial and subchondral arterial sources, and coursed perpendicular or parallel to the ossification front. The midsection of parallel vessels became incorporated into the ossification front during growth. Anastomoses formed and vessels within the distal portion of canals with an original perichondrial source shifted to use subchondral vessels as their arterial source. Both parallel and perpendicular vessels therefore traversed the ossification front to enter cartilage canals. No histological lesions were observed in sections from any of the foals. CONCLUSION: The same anatomical feature (traversing the ossification front to enter cartilage canals) reported to render vessels vulnerable to failure in the tarsus was also present in the distal femur of foals. POTENTIAL RELEVANCE: OC may occur by the same pathogenetic mechanism in the distal femur as in the tarsus of foals.     

Evaluation of serum concentrations of biomarkers of skeletal metabolism and results of radiography as indicators of severity of osteochondrosis in foals

OBJECTIVE: To determine whether serum concentrations of biomarkers of skeletal metabolism can, in conjunction with radiographic evaluation, indicate severity of osteochondrosis in developing horses. ANIMALS: 43 Dutch Warmblood foals with varying severity of osteochondrosis. PROCEDURE: 24 foals were monitored for 5 months and 19 foals were monitored for 11 months. Monthly radiographs of femoropatellar-femorotibial and tibio-tarsal joints were graded for osteochondral abnormalities. Serial blood samples were assayed for 8 cartilage and bone biomarkers. At the end of the monitoring period, foals were examined for macroscopic osteochondrosis lesions. RESULTS: Temporal relationships were evident between certain serum biomarkers and osteochondrosis severity in foals during their first year. Biomarkers of collagen degradation (collagenase-generated neoepitopes of type-II collagen fragments, type-I and -II collagen fragments [COL2-3/4C(short)], and cross-linked telopeptide fragments of type-I collagen) and bone mineralization (osteocalcin) were positive indicators of osteochondrosis severity at 5 months of age. In foals with lesions at 11 months of age, osteochondrosis severity correlated negatively with COL2-3/4C(short) and osteocalcin and positively with C-propeptide of type-II procollagen (CPII), a collagen synthesis marker. Radiographic grading of osteochondrosis lesions significantly correlated with macroscopic osteochondrosis severity score at both ages and was strongest when combined with osteocalcin at 5 months and CPII at 11 months. CONCLUSIONS AND CLINICAL RELEVANCE: The ability of serum biomarkers to indicate osteochondrosis severity appears to depend on stage of disease and is strengthened with radiography. In older foals with more permanent lesions, osteochondrosis severity is significantly related to biomarker concentrations of decreased bone formation and increased cartilage synthesis.     

Etiology and pathogenesis of osteochondrosis

Osteochondrosis is a common and clinically important joint disorder that occurs in human beings and in multiple animal species, most commonly pigs, horses, and dogs. This disorder is defined as a focal disturbance of enchondral ossification and is regarded as having a multifactorial etiology, with no single factor accounting for all aspects of the disease. The most commonly cited etiologic factors are heredity, rapid growth, anatomic conformation, trauma, and dietary imbalances; however, only heredity and anatomic conformation are well supported by the scientific literature. The way in which the disease is initiated has been debated. Although formation of a fragile cartilage, failure of chondrocyte differentiation, subchondral bone necrosis, and failure of blood supply to the growth cartilage all have been proposed as the initial step in the pathogenesis, the recent literature strongly supports failure of blood supply to growth cartilage as being the most likely. The term osteochondrosis has been used to describe a wide range of different lesions among different species. We suggest a refinement of this terminology to include the modifiers latens (lesion confined to epiphyseal cartilage), manifesta (lesion accompanied by delay in endochondral ossification), and dissecans (cleft formation through articular cartilage). The purpose of this review is to provide an overview of the disease, focusing on the most commonly cited theories, recent research findings, and our own views regarding the etiology and pathogenesis of osteochondrosis, in order to provide a better understanding of this apparently complex disease.     

Hypertrophy and physiological death of equine chondrocytes in vitro

REASON FOR PERFORMING STUDY: Equine osteochondrosis results from a failure of endochondral ossification during skeletal growth. Endochondral ossification involves chondrocyte proliferation, hypertrophy and death. Until recently no culture system was available to study these processes in equine chondrocytes. OBJECTIVE: To optimise an in vitro model in which equine chondrocytes can be induced to undergo hypertrophy and physiological death as seen in vivo. METHODS: Chondrocytes isolated from fetal or older (neonatal, growing and mature) horses were cultured as pellets in 10% fetal calf serum (FCS) or 10% horse serum (HS). The pellets were examined by light and electron microscopy. Total RNA was extracted from the pellets, and quantitative PCR carried out to investigate changes in expression of a number of genes regulating endochondral ossification. RESULTS: Chondrocytes from fetal foals, grown as pellets, underwent hypertrophy and died by a process morphologically similar to that seen in vivo. Chondrocytes from horses age >5 months did not undergo hypertrophy in pellet culture. They formed intramembranous inclusion bodies and the cultures included cells of osteoblastic appearance. Pellets from neonatal foals cultured in FCS resembled pellets from older horses, however pellets grown in HS underwent hypertrophy but contained inclusion bodies. Chondrocytes from fetal foals formed a typical cartilage-like tissue grossly and histologically, and expressed the cartilage markers collagen type II and aggrecan mRNA. Expression of Sox9, collagen type II, Runx2, matrix metalloproteinase-13 and connective tissue growth factor mRNA increased at different times in culture. Expression of fibroblast growth factor receptor-3 and vascular endothelial growth factor mRNA decreased with time in culture. CONCLUSIONS: Freshly isolated cells from fetal growth cartilage cultured as pellets provide optimal conditions for studying hypertrophy and death of equine chondrocytes. POTENTIAL RELEVANCE: This culture system should greatly assist laboratory studies aimed at elucidating the pathogenesis of osteochondrosis.     

Osteochondrosis and juvenile spavin in equids

Thirty-six of 50 young equids examined at necropsy for gross pathologic and histopathologic evidence of osteochondrosis were determined to have lesions characteristic of this disorder in the distal joints of the tarsus. Abnormalities ranged from retained endochondral cores underlying undisturbed articular cartilage surfaces to clefts, subchondral osseous cyst-like lesions, and cartilage ulceration. Our findings supported the conclusion that osteochondrosis may cause spavin in the juvenile equid.     

Skeletal disease in a hypothyroid foal

Hypothyroidism was diagnosed in a 5-month-old Thorough-bred colt by clinical and clinico-pathology examinations, thyroid stimulating hormone response test and by microscopic evaluation of the thyroid gland. Skeletal lesions included delayed appearance of ossification centers and delayed development of bone in cartilage models, delayed closure of epiphyseal plates, transverse trabeculation in metaphyses, osteochondrosis dissecans and subchondral cysts.     

Effect of diet on longitudinal bone growth and osteochondrosis in swine

Weanling gilts were fed either a 12% or 16% protein diet for 10 weeks. Animals fed the 12% protein diet had reduced body weights and reduced longitudinal bone growth as measured in the distal radial growth plate. There was no difference in the growth plate widths between the two animal groups, but there was a significant reduction in the daily rate of cell production in the proliferative zone of animals fed the 12% protein diet. No effect of diet on the rate of expansion of the epiphysis at the articular-epiphyseal junction of the distal femur or humerus could be detected. All animals in both groups had morphologic cartilage lesions consistent with early changes associated with osteochondrosis (OCD), and there was no difference in the lesion morphology between the dietary groups. Areas of disorderly endochondral ossification in the radial growth plate were associated with perpendicular growth cartilage infractions. Growth plate lesions were characterized by increased widths of the maturing cartilage zone without increased width of the proliferative zone or an increase in the daily rate of cell production. Focal growth plate lesions developed because of a transitory inhibition of cartilage mineralization and resorption. Disorderly foci of endochondral ossification beneath articular cartilage were characterized by an area of chondrocyte necrosis which prevented normal cartilage matrix mineralization. Lamellae of cartilage necrosis were also present within the reserve zone of the articular cartilage. These were associated with abnormalities of the cartilage canal vessels, and chondrocyte necrosis was considered to precede degenerative changes in articular cartilage matrix.(ABSTRACT TRUNCATED AT 250 WORDS)     

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

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.     

Osteochondrosis and arthrosis in pigs. I. Incidence in animals up to 120 kg live weight

Joint and bone lesions in growing pigs are described on the basis of post-mortem examination of 341 gilts, boars or castrates from 10 to 120 kg live weight, and 869 separate bones from pigs between 80 and 115 kg live weight at slaughter. No evidence of rickets or generalized osteodystrophia fibrosa was found. Lesions occurred in both sexes. The typical osteochondral lesions were most often symmetrical, occurred at certain sites in joints and epiphyseal plates and were most obvious in the elbow and stifle joint, and in the distal epiphyseal plate of the ulna. Lesions of varying degree could be demonstrated in most pigs at 90–100 kg live weight. The use of the diagnosis osteochondrosis is suggested for local primary non-inflammatory disturbances which lead to a failure of endochondral ossification in joint cartilage as well as in epiphyseal plates. The diagnosis arthrosis is used when the superficial layer of the joint cartilage is affected. Investigations of the early changes in the medial condyle of the femur suggest that the osteochondral lesions start in the deep layers of the joint cartilage. Arthrosis occurred frequently in the lumbar intervertebral joints of Norwegian pigs. Otherwise the lesions appeared to be identical with those described from other countries.     

Epiphyseal cartilage canal blood supply to the metatarsophalangeal joint of foals

Reasons for performing study: It is presently unknown whether cartilage ischaemia plays any part in the pathogenesis of osteochondral fragmentation within the equine metatarsophalangeal joint, as no detailed studies on microcirculation in the area have been reported. Objective: To describe the developmental pattern of the blood supply to the epiphyseal growth cartilage in the metatarso‐phalangeal joint of foals. Methods: Eight Standardbred foals were sacrificed between birth and age 7 weeks to undergo a barium perfusion procedure to demonstrate vessels within growth cartilage canals of one hindlimb. The metatarso‐phalangeal joint was cleared in methyl salicylate and perfused vessels studied in the intact bones. The bones were sawed into 5 mm thick slabs, decalcified and radiographed. Selected slabs were cleared in methyl salicylate for a second time and examined at low magnification. The dorsal half of the sagittal ridge of the distal third metatarsal bone and the plantar half of the proximal phalanx were examined histologically. Results: Regions of the epiphysis with thick cartilage contained a greater number of perfused vessels than regions with thin cartilage. The cartilage canal vessels were oriented either parallel or perpendicular to the underlying ossification front. Cartilage canal vessels were incorporated into the ossification front during growth and became reliant on a subchondral arterial source. Macroscopically visible lesions were not detected in the current group of foals. On histological examination, pathological changes consisting of an area of chondronecrosis surrounded by fibrovascular granulation tissue were found in sections from the lateral proximo‐plantar eminence of the proximal phalanx in the 7‐week‐old foal. Conclusion: The same anatomical feature (traversing the ossification front to enter cartilage canals) reported to render vessels vulnerable to failure in the tarsus was also present in the metatarso‐phalangeal joint of foals. Potential relevance: Osteochondrosis may occur by the same pathogenetic mechanism in the metatarso‐phalangeal joint as in the tarsus of foals.     

Osteochondritis dissecans in the dog: diagnosis and therapy.

Osteochondritis dissecans (OCD) is a manifestation of osteochondrosis. It is thought to be a metabolic disease of cartilage maturation and endochondral ossification. Therefore, any disturbance affecting the differentiation of growth cartilage constitutes osteochondrosis. When this disturbance affects the articular cartilage so that a piece detaches, it is called OCD. Osteochondritis dissecans is well recognized but poorly understood. The etiology remains controversial. Osteochondritis dissecans is most commonly recognized in the shoulder but can occur in other areas which makes it difficult to differentiate from other disease entities. Diagnosis of OCD is based on signalment (age, breed, and sex), history, and physical and radiographic evidence. Therapy must be individualized and based on the patient's clinical signs and not on the severity of the radiographic lesion. Therapy can be effective only when applied correctly.     

肉鸡骨骼发育的调控机制

肉鸡骨骼发育主要是通过软骨内骨化完成的。在软骨内骨化的进程中,生长板软骨细胞经历增殖、肥大、转分化和软骨基质矿化等,最终成骨逐渐取代软骨原基,实现骨骼的线性延长。软骨内成骨是一个复杂精密的过程,由SOX9、RUNX2、MEF2C、OSX、TGF-β、BMP2、FGFs、IHH和PTHrP等多种信号因子和转录因子协调调控,这些调控因子由生长板不同区的软骨细胞表达或特异性的调控软骨细胞的增殖、分化及血管侵入等过程。在家禽养殖中,肉鸡常发腿病且治疗难度大,而有关肉鸡腿病发病机制的研究报道相对较少。本文综述了骨形成过程及具体的分子调控机制,为了解肉鸡腿病的发生以及提供有效治疗方案提供参考。     

Consequences of capital femoral dyschondroplasia in young adult and skeletally mature broilers

Radiographs revealed defective endochondral ossification in proximal femora of 52 lame broilers. Cartilage retention either involved epiphyseal cartilage close to the articular surface or growth plate cartilage (dyschondroplasia). In at least seven birds proximal femoral lesions were the only abnormalities detected which could have caused lameness. In cases of moderate or severe cartilage retention, fracture lines traversed necrotic cartilage to undermine part or all of the femoral head. Evidence of reparative fibrosis was seen with augmentation of metaphyseal trabeculae by woven bone apposition. Foveal blood vessels aided repair by re-establishing a new ossification centre but in many cases attempts at repair were inadequate.     

Articular / epiphyseal osteochondrosis in Thoroughbred foals at 5 months of age: influences of growth of the foal and prenatal copper supplementation of the dam

AIMS: To determine the influence of copper (Cu) supplementation by injection of mares in late gestation on the frequency and severity of osteochondrosis (OC) lesions in their foals at around 160 days of age. To determine if there was any influence of the concentration of Cu in the liver, growth rate, birthweight, weight at 160 days of age, fatness, sex, or year of birth of the foal on the frequency and severity of OC lesions. To determine the influence of dam's age, and sex and birthweight of the foal on the growth rate from birth to 160 days of age, and weight at 160 days of age. METHODS: Thirty-three Thoroughbred foals, born in two consecutive years, were weighed every 2 weeks from birth. The dams had been supplemented with parenteral Cu or saline during late gestation, and the supplementation regimens were different in each year. Foals had liver biopsies harvested at birth for determination of Cu concentration. Pasture samples were collected every 4-8 weeks for analysis of concentration of Cu and zinc (Zn). At 160 days of age, articular cartilage of long bones was examined. Gross lesions were counted and scored, then sawn and radiographed, and processed for histopathology. Lesions were given radiographic scores and histopathological scores. Maximum scores for each lesion were combined to give a total OC score for each joint and each foal. The fatness of 20 foals (10 each from Years 1 and 2) at 160 days of age was determined chemically. RESULTS: Supplementation of dams with Cu had no significant effect on the concentration of Cu in the liver of foals at birth, or on the frequency or severity of lesions in articular cartilage at 160 days of age. The Cu and Zn concentrations of pasture were similar in Years 1 and 2, and were lower than current recommendations. All foals in Year 2, and 9/10 foals in Year 1 had irregularities in cartilage that was confirmed histologically to be indicative of OC. The average number of lesions per foal was 4.7 (SD 1.1) and 5.7 (SD 1.1) in Years 1 and 2, respectively. However, the severity of the lesions was considered mild, and no foals showed any clinical evidence of OC while alive. The number of lesions in the tarsocrural (TC) joint and the TC OC score at 160 days were positively associated with average daily weight gain (ADG) in the previous 4 weeks (p=0.005 and p=0.001, respectively). There was no significant effect of sex, fatness, birthweight, weight at 160 days of age, or year of birth of the foal on the frequency and severity of OC lesions. CONCLUSIONS: Many of the lesions classified as OC, using classification systems described by other authors, were likely to be normal variations of the process of endochondral ossification. Despite the high frequency of such lesions, they were considered to be of minor significance and none were clinically evident. The distribution of lesions was not typical, and most probably reflected the subtlety of the lesions. These results support the hypothesis that Cu is an over-emphasised factor in the aetiopathogenesis of OC. The relationship between subtle macroscopic lesions and lesions resulting in clinical signs of disease requires further investigation.     

Articular/epiphyseal osteochondrosis in Thoroughbred foals at 5 months of age: Influences of growth of the foal and prenatal copper supplementation of the dam

AIMS: To determine the influence of copper (Cu) supplementation by injection of mares in late gestation on the frequency and severity of osteochondrosis (OC) lesions in their foals at around 160 days of age. To determine if there was any influence of the concentration of Cu in the liver, growth rate, birthweight, weight at 160 days of age, fatness, sex, or year of birth of the foal on the frequency and severity of OC lesions. To determine the influence of dam's age, and sex and birthweight of the foal on the growth rate from birth to 160 days of age, and weight at 160 days of age.

METHODS: Thirty-three Thoroughbred foals, born in two consecutive years, were weighed every 2 weeks from birth. The dams had been supplemented with parenteral Cu or saline during late gestation, and the supplementation regimens were different in each year. Foals had liver biopsies harvested at birth for determination of Cu concentration. Pasture samples were collected every 4–8 weeks for analysis of concentration of Cu and zinc (Zn). At 160 days of age, articular cartilage of long bones was examined. Gross lesions were counted and scored, then sawn and radiographed, and processed for histopathology. Lesions were given radiographic scores and histopathological scores. Maximum scores for each lesion were combined to give a total OC score for each joint and each foal. The fatness of 20 foals (10 each from Years 1 and 2) at 160 days of age was determined chemically.

RESULTS: Supplementation of dams with Cu had no significant effect on the concentration of Cu in the liver of foals at birth, or on the frequency or severity of lesions in articular cartilage at 160 days of age. The Cu and Zn concentrations of pasture were similar in Years 1 and 2, and were lower than current recommendations. All foals in Year 2, and 9/10 foals in Year 1 had irregularities in cartilage that was confirmed histologically to be indicative of OC. The average number of lesions per foal was 4.7 (SD 1.1) and 5.7 (SD 1.1) in Years 1 and 2, respectively. However, the severity of the lesions was considered mild, and no foals showed any clinical evidence of OC while alive. The number of lesions in the tarsocrural (TC) joint and the TC OC score at 160 days were positively associated with average daily weight gain (ADG) in the previous 4 weeks (p=0.005 and p=0.001, respectively). There was no significant effect of sex, fatness, birth-weight, weight at 160 days of age, or year of birth of the foal on the frequency and severity of OC lesions.

CONCLUSIONS: Many of the lesions classified as OC, using classification systems described by other authors, were likely to be normal variations of the process of endochondral ossification. Despite the high frequency of such lesions, they were considered to be of minor significance and none were clinically evident. The distribution of lesions was not typical, and most probably reflected the subtlety of the lesions. These results support the hypothesis that Cu is an over-emphasised factor in the aetiopathogenesis of OC. The relationship between subtle macroscopic lesions and lesions resulting in clinical signs of disease requires further investigation.     

Differential distribution of cathepsins B and L in articular cartilage during skeletal development in the horse

REASONS FOR PERFORMING STUDY: This study was designed to examine a new role for cysteine proteinases in the process of endochondral ossification. OBJECTIVES: The aim of the present study was to investigate the presence and distribution of cathepsin B and cathepsin L in equine articular cartilage during development. METHODS: Full-depth cartilage samples from a total of 40 horses (age range: 4 month fetuses to 2 years) were examined and enzymes detected by immunocytochemical localisation. RESULTS: Observations on the presence of cathepsins B and L revealed significant age-related differences, resulting in clear division of the animals into 2 age groups: i) fetuses and neonates; ii) young growing horses (age 4 weeks to 2 years). Cathepsin B was not detected in cartilage from the majority of fetuses and neonates but was located characteristically in chondrocytes at the articular surface and hypertrophic zone in all growing horses. In contrast, cathepsin L was predominantly present in fetal and neonatal cartilage, located primarily in proliferating chondrocytes. CONCLUSIONS: This study is the first to demonstrate differential and site-specific roles for cathepsin B and cathepsin L in skeletal development in the horse. Potential relevance: The demonstrated involvement of cathepsins B and L in endochondral ossification is of relevance to developmental orthopaedic diseases such as osteochondrosis in which there is a focal failure of bone formation.