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Osteochondrosis in six breeds of slaughter pigs. II. Data concerning carcass characteristics in relation to osteochondrosis.

Coefficients of correlation have been calculated between morphological lesion scores of osteochondrosis that were made on the bones of porcine fore and hind limbs and some carcass characteristics. It was found that carcass length, as well as the relative weights of the hams were significantly correlated with the lesions that were observed in the proximal site of the femur and the medial femoral condyle. Despite these significant correlations, the values of the correlation coefficients were too small to be of any use for selection purposes. This applies the whole animal population, consisting of 6 breeds of pigs. It is shown that the coefficients of correlation between the morphological lesion scores of the femur and the relative weights of the hams in some of the individual breeds were much higher, implying a possibility for the prediction of osteochondrosis based on carcass characteristics.

Animals↗

Osteochondrosis in six breeds of slaughter pigs. I. A morphological investigation of the status of osteochondrosis in relation to breed and level of feeding.

The severity and extent of osteochondral lesions have been examined, macroscopically, radiographically as well as histopathologically, in six different breeds of pigs (Belgian Landrace (B), Duroc (D), Dutch Landrace (N), Dutch Yorkshire (G), Hampshire (H) and Piétrain (P)). In these pigs three different levels of feeding were used. Duroc pigs had significantly more severe lesions in the fore limbs than Dutch Landrace (N), Dutch Yorkshire (G), Hampshire (H) and Piétrain (P) pigs, while Belgian Landrace pigs (B) had significant more severe lesions than Dutch Yorkshire (G) pigs. The differences between breeds related more to the degree of severity of the lesions in the articular surfaces of the distal humerus and proximal radius-ulna and in the distal ulnar growth plate than to the presence of the lesions per se. In the hind limbs Belgian Landrace pigs (B) had significantly more severe osteochondral lesions than all other breeds, while Dutch Landrace pigs (N) had significantly more severe lesions than Duroc (D), Dutch Yorkshire (G), Hampshire (H) and Piétran (P) pigs. Pigs with the highest growth rate showed significantly more severe osteochondral lesions in the distal ulnar growth plate and in the medial femoral condyle than pigs with a more restricted growth rate.

Animals↗

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.

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[Role of magnetic resonance in the evaluation of the normal and osteochondrosis hip in early and late childhood].

INTRODUCTION: Despite MR potentials, few studies investigate the features of normal hips and of hip osteochondrosis in early and late childhood. We report our personal experience with MRI of hip osteochondrosis in pediatric patients. MATERIAL AND METHODS: MR images were obtained with total body MR equipment at medium and high fields. The normal hips were studied in children aged 34 months to 6 years with abdominal-urinary tract disorders and in 9 patients of the same age with unilateral Perthes disease. Hip osteochondrosis was studied in 6 children with Catteral's type III and IV and in 3 with type I and II disease. General anesthesia was never necessary to perform MRI. RESULTS: MRI exactly defined the cephalic anatomic profiles of normal hips which are not depicted with conventional radiography before the femoral head cartilage ossifies completely. MR contrast resolution was very high in depicting the maturation of the epiphyseal nucleus and its exact site in the cartilagineous epiphyseal hemisphere proximal to the femur. The analysis of MR morphological and structural changes permitted to correlate MR findings with the histopathologic features described in the literature. In addition, MRI of childhood hip osteochondrosis showed maked structural changes of the epiphyseal nucleus which are usually missed with conventional radiography. MRI permits early location of the abnormal area and the recognition of growing disk abnormalities; it also shows the whole cephalic cartilage and the changes of the epiphyseal nucleus evolution, which permits to differentiate osteochondrosis evolution from recessive patterns. Finally, MRI clearly showed the increased equatorial diameters of the involved femoral heads and the associated decrease in polar diameters, which is essential to study the biomechanics of hip osteochondrosis and therefore to plan treatment. CONCLUSIONS: MRI, even with coronal sequences and T1-weighting only, permits: 1) to image normal hips and hip osteochondrosis, especially in early and late childhood; 2) to clearly define cephalocotyloid relationships; 3) to depict the actual anatomic margins of the head and its structure; 4) to investigate the head cartilage extent and to locate the ossification nucleus. These morphologic and structural data are very useful to diagnose and manage hip osteochondrosis in the evolutive age. MRI shows abnormal changes in anatomic structures which are not seen with conventional radiography and demonstrates the evolution of the osteochondrosis process over time. In children over six, at the end of the ossification process of the head cartilage, conventional radiography alone is often sufficient to depict cephalocotyloid relationships and the MR diagnostic criteria of bone-cephalic diseases are similar to those used in adult hip studies.

Adult↗

Clinical and radiographic findings, treatment, and outcome in cattle with osteochondrosis: 29 cases (1986-1996).

OBJECTIVE: To summarize the radiographic and clinical findings, treatment, and outcome in cattle with osteochondrosis diagnosed radiographically. DESIGN: Retrospective case series. SAMPLE POPULATION: 29 cattle with radiographic evidence of osteochondrosis. PROCEDURES: Medical records were reviewed, and owners or referring veterinarians were contacted for outcome assessment. Data were analyzed for potential interactions between osteochondrosis classification (osteochondritis dessicans vs subchondral cyst-like lesions), clinical and radiographic findings, treatment, and outcome, using Fisher's exact test and descriptive statistics. RESULTS: Osteochondrosis was associated with young, male, purebred cattle, clinical evidence of lameness, and radiographic evidence of concurrent degenerative joint disease. Osteochondritis dissecans and subchondral cyst-like lesions had similar clinical findings and outcomes but varied significantly in their radiographic distribution among joints. Osteochondrosis often manifests clinically as a unilateral condition, but bilateral lesions were often found (88%) when limbs were radiographically examined. Cattle managed conservatively tended to be culled (within 6 months of diagnosis because of lameness) more often than those managed surgically, despite the lack of treatment bias. CLINICAL IMPLICATIONS: Osteochondrosis in cattle is often associated with lameness or degenerative joint disease. Conservative management does not result in a favorable clinical prognosis for long-term, lameness-free survival, and more studies need to be completed to evaluate the efficacy of surgical treatment of osteochondrosis in cattle.

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The pathophysiology of osteochondrosis.

Osteochondrosis is a disorder of epiphyseal cartilage about which there is considerable confusion in the literature. We believe that this is due to the fact that osteochondrosis has been studied in the chronic stage when the lesions are morphologically complicated and the initial causative insult is impossible to determine. The etiology of osteochondrosis appears to be multifactorial, with trauma, hereditary factors and rapid growth, nutritional factors, and ischemia all having a role in its pathogenesis. Although predilection sites are variable among species, the morphology of the early lesions is strikingly similar, strongly suggesting that the pathogenesis of osteochondrosis is the same, regardless of the species affected. Based on recent studies in pigs and horses, and supported by observations in dogs and cattle, we believe that local ischemia secondary to defects in cartilage canal blood supply is a key factor in the initiation of lesions of osteochondrosis and explains many of the features of this disease. Local ischemia to the epiphyseal cartilage of the articular-epiphyseal cartilage complex leads to the formation of highly vulnerable zones of necrotic epiphyseal cartilage which later cause a delay in endochondral ossification, with extension of necrotic cartilage into the subchondral bone. Trauma, whether major or minor, to the overlying articular cartilage leads to cartilage cleft formation, clinical signs of pain and lameness, and other chronic sequelae. Studies aimed at further elucidating the pathogenesis of osteochondrosis should attempt to determine the cause of the vascular defect and whether or not it may be modified by experimental manipulations.

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Hormones, growth factors and other plasma variables in relation to osteochondrosis.

Osteochondrosis (OC) is a multifactorial disorder with endocrinological dysfunction and mineral imbalance having a role in pathogenesis. The present study focused on a possible relationship between insulin-like growth factor I (IGF-I), insulin-like growth factor II (IGF-II), parathyroid hormone (PTH), 1,25-dihydroxy-vitamin D (1,25(OH)2D), cortisol, copper, zinc, calcium, ionised calcium, magnesium and phosphorus and 5 different postmortem and radiographical osteochondrosis scores of hock and stifle joints in foals age 0-11 months. Osteochondrosis-positive foals showed a significantly lower IGF-I activity than osteochondrosis-negative foals. PTH, 1,25(OH)2D, cortisol, copper, zinc and calcium also showed significant differences between osteochondrosis-positive and osteochondrosis-negative foals.

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The role of cumulative physical work load in lumbar spine disease: risk factors for lumbar osteochondrosis and spondylosis associated with chronic complaints.

OBJECTIVES: To investigate the relation with a case-control study between symptomatic osteochondrosis or spondylosis of the lumbar spine and cumulative occupational exposure to lifting or carrying and to working postures with extreme forward bending. METHODS: From two practices and four clinics were recruited 229 male patients with radiographically confirmed osteochondrosis or spondylosis of the lumbar spine associated with chronic complaints. Of these 135 had additionally had acute lumbar disc herniation. A total of 197 control subjects was recruited: 107 subjects with anamnestic exclusion of lumbar spine disease were drawn as a random population control group and 90 patients admitted to hospital for urolithiasis who had no osteochondrosis or spondylosis of the lumbar spine radiographically were recruited as a hospital based control group. Data were gathered in a structured personal interview and analysed using logistic regression to control for age, region, nationality, and other diseases affecting the lumbar spine. To calculate cumulative forces to the lumbar spine over the entire working life, the Mainz-Dortmund dose model (MDD), which is based on an overproportional weighting of the lumbar disc compression force relative to the respective duration of the lifting process was applied with modifications: any objects weighing >or=5 kg were included in the calculation and no minimum daily exposure limits were established. Calculation of forces to the lumbar spine was based on self reported estimates of occupational lifting, trunk flexion, and duration. RESULTS: For a lumbar spine dose >9 x 10(6) Nh (Newton x hours), the risk of having radiographically confirmed osteochondrosis or spondylosis of the lumbar spine as measured by the odds ratio (OR) was 8.5 (95% confidence interval (95% CI) 4.1 to 17.5) compared with subjects with a load of 0 Nh. To avoid differential bias, forces to the lumbar spine were also calculated on the basis of an internal job exposure matrix based on the control subjects' exposure assessments for their respective job groups. Although ORs were lower with this approach, they remained significant. CONCLUSIONS: The calculation of the sum of forces to the lumbar spine is a useful tool for risk assessment for symptomatic osteochondrosis or spondylosis of the lumbar spine. The results suggest that cumulative occupational exposure to lifting or carrying and extreme forward bending increases the risk for developing symptomatic osteochondrosis or spondylosis of the lumbar spine.

Adult↗

Frequency and severity of osteochondrosis in horses with cervical stenotic myelopathy.

We compared the frequency and severity of osteochondrosis lesions in young Thoroughbred horses with cervical stenotic myelopathy (CSM) vs that in clinically normal Thoroughbreds of the same age. All lesions of the cervical vertebrae and appendicular skeleton were classified histologically as osteochondrosis or nonosteochondrosis and were measured for severity. Minimal sagittal diameter was significantly smaller in horses with CSM from C2 through C6; no difference was detected at C7. Severity of cervical vertebral osteochondrosis was greater in the horses with CSM, however frequency was not different. Frequency and severity of nonosteochondrosis lesions were not different in cervical vertebrae or appendicular skeleton. Frequency and severity of appendicular skeleton osteochondrosis lesions were both greater in horses with CSM. Osteochondrosis and nonosteochondrosis lesions were more severe on facets at sites of compression than on facets at noncompressed sites in horses with CSM. However, compression was also observed at sites with no articular facet lesions. The association of widespread osteochondrosis and spinal canal narrowing with CSM suggests CSM may represent a systemic failure in the development or maturation of cartilage and bone.

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Osteochondrosis in growing bulls. Pathology, frequency and severity on different feedings.

Lesions typical for osteochondrosis were found in the joint cartilage and metaphyseal growth plates of growing bulls, of which many showed clinical signs of so-called leg weakness. Of 48 bulls included in the investigation, 23 were on intensive feeding and they all were found to have osteochondrosis at several locations. Of the 25 bulls of lower intensity feeding, only 13 had osteochondrosis. The lesions in those bulls were less severe than in the bulls on the high intensity feeding. At slaughter, when the lesions were inspected, the bulls on high energy feeding were much younger than the ones on the lower energy feeding. This must be kept in mind, when a comparison is made. As the bulls of the high intensity feeding were growing more rapidly, frequency and severity of osteochondrosis seemed to be correlated with rapid growth. Other etiological factors were, however, considered. A comparatively low intake of calcium in relation to daily weight increase may be one explanation for the high frequency in the bulls in high intensity feeding. Lack of exercise and large amounts of concentrates were possible explanations for the overall high frequency of osteochondrosis in the present material. The lesions in the joints and growth plates in the bulls were similar to those seen in pigs and horses. The reason why some partly or completely detached bodies contained bone is discussed. A possible connection between osteochondrosis and so-called subchondral bone cysts, as previously described in horses, is mentioned.

Animal Feed↗

Morphology of osteochondrosis and sequelae in pigs.

The morphologic features of osteochondrosis were studied in skeletons of 176 pigs of different ages. Macroscopic and histologic as well as radiologic and microradiographic methods were used. Osteochondrosis was found to be a generalized disease, characterized by a disturbance of endochondral ossification. It was concluded that early changes occur at about 4 months of age in the growth cartilage. Both the metaphyseal growth cartilage (growth plates) and epiphyseal growth cartilage (joint cartilage) were affected. Abnormal hypertrophy and hyperplasia of cartilage as well as focal degeneration were seen in the early cases. Osteochondrosis was found to lead to abnormal skeletal growth and change in shape of various bones and joints. Serious manifestations of osteochondrosis were epiphyseolysis and osteochondritis dissecans. A quantitative difference was found between different individuals in development of osteochondrosis. The onset of clinical signs was thought to depend on degree and localization of osteochondrosis.

Animals↗

[Histological study of cartilage channels in the epiphyseal cartilage of young dogs and their relationship to that of osteochondrosis dissecans in the most frequently affected locations].

Osteochondrosis is a disease occurring in many species of domestic animals. There are different factors like genetic predisposition, housing and feeding, trauma and stress, which are thought to be the causes or part of the causes of the disease. There have been studies about swine, finding a connection between cartilage channels in juvenile epiphyseal cartilage and the development of osteochondrosis. The aim of the study was to find out whether those connections exist in dogs as well. Special interest has been laid upon the localisation, the contents and the surroundings of cartilage channels as well as their relationship to the localisation of osteochondrosis. Joint surfaces, that are most often subject to osteochondrosis in the dog, have been examined macroscopically and histologically, e.g. the caput humeri, the medial part of the humeral condyle, the lateral condyle of the os femoris, the cochlea tibiae and the trochlea tali of 31 dogs at the age of three days to nine months. According to this examination cartilage channels can disturb the process of ossification of cartilage in the secondary centre of ossification, causing a thickening of cartilage layers. These changes can often be seen in locations, where osteochondrosis usually develops, especially in the caput humeri. Altogether they could be located more often in male animals and large breeds than in female animals and small breeds. To a certain degree these changes can be considered as normal in the development and growth of a young dog, but combined with other factors like trauma or stress, they may play a favoring role in the pathogenesis of osteochondrosis as well.

Animals↗

Alterations in cartilage type-II procollagen and aggrecan contents in synovial fluid in equine osteochondrosis.

The etiology and pathophysiology of osteochondrosis remain poorly understood because it is difficult to obtain material from lesions in the early stage of this disease and because there is no satisfactory experimental animal model. We wished to determine whether there are changes in articular cartilage turnover in equine osteochondrosis, which closely resembles the human disease, by assaying cartilage matrix molecules in synovial fluids. We used immunoassays that measure a keratan sulfate epitope and the epitope 846 on the cartilage proteoglycan aggrecan and the C-propeptide of cartilage type-II procollagen, which is released following the synthesis of this molecule, to analyse synovial fluids from equine tarsocrural joints with and without osteochondrosis. In young horses with osteochondrosis, there was a significant increase of C-propeptide of type-II procollagen accompanied by a decrease in the 846 and keratan sulfate epitopes. The results identify differential alterations in aggrecan and type-II collagen turnover in the cartilage matrix in young animals with osteochondrosis that may contribute to the pathological degeneration of articular cartilage in this disease.

Aggrecans↗

Vascularisation and osteochondrosis of the epiphyseal growth cartilage of the distal femur in pigs--development with age, growth rate, weight and joint shape.

Until recently, the cartilage canals of the epiphyseal growth cartilage have not been associated with any specific disease. However, data support the hypothesis that osteochondrosis could be related to inadequate blood supply from vessels in these channels. We have done a study to investigate the relationship between the regression of cartilage canals and the formation of osteochondrosis latens in the epiphyseal growth cartilage of the distal femur in pigs, and the relationship between these events and age, growth rate, weight and femoral shape of the individual animals. This involved, in part, a comprehensive study of the distribution and pattern of regression of the cartilage canals. We found that the regression is a highly predictable process that follows an age-dependent pattern. However, we failed to prove any association between overall vascular regression and osteochondrosis, between vascular regression and weight, growth rate or femoral shape or between osteochondrosis and weight, growth rate or femoral shape. This may indicate that osteochondrosis latens is not caused by a general failure of vascular supply or general factors such as growth rate, but rather a consequence of local conditions affecting a limited number of vessels. A factor fitting this description is local compression.

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