Juvenile osteochondritis dissecans of the knee is a result of failure of the blood supply to growth cartilage and osteochondrosis.

OBJECTIVE: Juvenile osteochondritis dissecans (JOCD) is similar to osteochondrosis dissecans (OCD) in animals, which is the result of failure of the cartilage canal blood supply, ischemic chondronecrosis and delayed ossification, or osteochondrosis. The aim of the current study was to determine if osteochondrosis lesions occur at predilection sites for JOCD in children. METHOD: Computed tomographic (CT) scans of 23 knees (13 right, 10 left) from 13 children (9 male, 4 female; 1 month to 11 years old) were evaluated for lesions consisting of focal, sharply demarcated, uniformly hypodense defects in the ossification front. Histological validation was performed in 11 lesions from eight femurs. RESULTS: Thirty-two lesions consisting of focal, uniformly hypodense defects in the ossification front were identified in the CT scans of 14 human femurs (7 left, 7 right; male, 7-11 years old). Defects corresponded to areas of ischemic chondronecrosis in sections from all 11 histologically validated lesions. Intra-cartilaginous secondary responses comprising proliferation of adjacent chondrocytes and vessels were detected in six and two lesions, whereas intra-osseous responses including accumulation of chondroclasts and formation of granulation tissue occurred in 10 and six lesions, respectively. One CT cyst-like lesion contained both a pseudocyst and a true cyst in histological sections. CONCLUSION: Changes identical to osteochondrosis in animals were detected at predilection sites for JOCD in children, and confirmed to represent failure of the cartilage canal blood supply and ischemic chondronecrosis in histological sections.

Articular osteochondrosis: a comparison of naturally-occurring human and animal disease.

BACKGROUND: Osteochondrosis (OC) is a common developmental orthopedic disease affecting both humans and animals. Despite increasing recognition of this disease among children and adolescents, its pathogenesis is incompletely understood because clinical signs are often not apparent until lesions have progressed to end-stage, and examination of cadaveric early lesions is not feasible. In contrast, both naturally-occurring and surgically-induced animal models of disease have been extensively studied, most notably in horses and swine, species in which OC is recognized to have profound health and economic implications. The potential for a translational model of human OC has not been recognized in the existing human literature. OBJECTIVE: The purpose of this review is to highlight the similarities in signalment, predilection sites and clinical presentation of naturally-occurring OC in humans and animals and to propose a common pathogenesis for this condition across species. STUDY DESIGN: Review. METHODS: The published human and veterinary literature for the various manifestations of OC was reviewed. Peer-reviewed original scientific articles and species-specific review articles accessible in PubMed (US National Library of Medicine) were eligible for inclusion. RESULTS: A broad range of similarities exists between OC affecting humans and animals, including predilection sites, clinical presentation, radiographic/MRI changes, and histological appearance of the end-stage lesion, suggesting a shared pathogenesis across species. CONCLUSION: This proposed shared pathogenesis for OC between species implies that naturally-occurring and surgically-induced models of OC in animals may be useful in determining risk factors and for testing new diagnostic and therapeutic interventions that can be used in humans.

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.

Rabies in an Arctic fox on the Svalbard archipelago, Norway, January 2011.

We report a case of rabies in an Arctic fox. In January 2011 a fox attacked dogs belonging to a meteorological station in the Svalbard archipelago, Norway. Rabies virus was detected in the fox's brain post-mortem. The dogs had been vaccinated against rabies and their antibody levels were protective. Post-exposure prophylaxis was administered to staff at the station. Rabies vaccination is recommended for inhabitants and visitors to the Arctic who may be in contact with wild animals.

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 metatarsophalangeal 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.

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.

Bone dysplasia in the radial and ulnar metaphysis of a Newfoundland dog.

A recently described metaphyseal irregularity of the radius and ulna was diagnosed radiographically in a significant proportion of Newfoundland dogs during the course of a large study. This case report describes the pathological picture of a Newfoundland dog with these radiographic changes. The lesions in the distal radius and ulna were characterized by focal, longitudinal striations of sclerosis of the bone marrow cavity, surrounding thin trabeculae of primary spongiosa of the distal metaphysis. It is suggested that these lesions represent a sclerosing dysplasia not previously described in dogs, but with some similarities to the human disorder, osteopathia striata.

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.

Mesenteric chylothrombosis in hyperlipidaemic mink.

In the familial form of hyperlipoproteinaemia type I of mink (Mustela vison), mesenteric lipogranulomas are common findings in longstanding cases. Patho-morphological studies of early stages indicated that these lipogranulomas arose from stagnant chyle. The composition of fatty acids of a newly formed mesenteric granuloma was determined, together with fatty acids in liver, plasma and the feed. The results supported the pathological observations, as the fat of the granuloma differed from that of the liver and plasma, and contained only small amounts of the endogenous arachidonic acid, while the exogenous eicosenoic acid was present in amounts comparable with the dietary fat.

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.

Pancreatitis associated with hyperlipoproteinaemia type I in mink (Mustela vison): earliest detectable changes occur in mitochondria of exocrine cells.

Pancreatic tissue from young mink homozygous for a mutation in the lipoprotein lipase gene was studied by light and electron microscopy, with the aim of describing the earliest detectable changes in a process which rapidly progresses into overt pancreatitis. The mutation leads to hyperlipoproteinaemia, corresponding to hyperlipoproteinaemia type I in man. Assessment of relevant hepatic and pancreatic enzymes were included in the investigation. The earliest detectable changes consisted of widespread swelling and vacuolation of exocrine cells, arising mainly from swollen mitochondria. To a lesser extent, vesiculation of endoplasmic reticulum occurred. Mitochondria exhibited various changes, including cavitation and dilution of the matrix, with shortened and disorganized cristae displaced towards the periphery. Lamellar figures that developed within mitochondria were numerous. Acinar lumina were somewhat dilated, while plasma membranes were relatively well preserved and secretory granules seemed unchanged. Exfoliative processes progressively occurred, resulting in total necrosis of groups of parenchymal cells, while intercalated ducts were spared. The necrosis was rapidly followed by inflammatory reactions. The activity of the mitochondrial enzyme carnitine O-palmitoyltransferase, essential for the transport of fatty acids into the mitochondria, was lower in the pancreas than in the liver. The activity of the peroxisomal fatty acid beta-oxidation was high in the liver and low in the pancreas of both lipoprotein lipase-deficient and control mink. It is concluded that pancreatic lesions associated with hyperlipoproteinaemia start in exocrine cells, and are most probably the result of a metabolic disturbance, possibly a toxic effect of an excess of free fatty acids.

The effect of parentage on the prevalence, severity and location of lesions of osteochondrosis in swine.

The aims of this study were to determine the effects of parentage and gender on the prevalence, severity and location of lesions of osteochondrosis manifesta (OCM) and osteochondrosis dissecans (OCD) in offspring from different Norwegian Landrace boars and to examine the relationships between lesion characteristics and selected growth parameters. Fifteen sires were selected based on their high breeding value for osteochondrosis. Seven locations in the distal humerus and the distal femur from 1680 offspring of these animals were evaluated for severity of OCM and presence of OCD by gross examination of serially sectioned humeri and femora. Osteochondrosis manifesta was most prevalent in the trochlea of humerus, the sagittal ridge of humerus, the medial condyle of femur and the medial sulcus obliquus of femur. The severity of the lesions and the prevalence of OCD were highest in the trochlea and the sagittal ridge of humerus. Castrates had significantly higher OCM scores than sows. There were significant effects of both sire and dam on the OCM scores of the offspring in most locations; however, growth rate and weight at slaughter did not influence the OCM score.

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.

Spinal cord astrocytoma in a cat.

A nine-year-old neutered male domestic shorthaired cat with a history of spinal pain and progressive hindlimb dysfunction was presented to the Norwegian School of Veterinary Science. Following neurological and myelographic examination, an intramedullary mass affecting several lumbar spinal cord segments was diagnosed. A neoplastic lesion was suspected and a poor prognosis was given. On postmortem examination, the spinal cord was found to be dorsally flattened from the 12th thoracic vertebra to the fifth lumbar vertebra and severely thickened with a dorsal cleft from the fifth to the seventh lumbar vertebra. Histologically, the tumour was diagnosed as an anaplastic astrocytoma.

Osteoporosis, bone mineralization, and status of selected trace elements in two populations of moose calves in Norway.

This study was conducted to clarify the etiology of a high frequency of bone fractures and osteoporosis in the moose (Alces alces) population in southern Norway. Liver samples, both metacarpi, and carcass data were collected from 21 and 22 moose calves shot in 1994 in Birkenes (southern Norway), and Naerøy (central Norway), respectively. The liver samples were analyzed for copper, manganese, zinc, cobalt, chromium, molybdenum, and selenium. Bone samples were subject to histologic, radiologic, and chemical examinations. Three of the calves from Birkenes and one calf from Naerøy showed histologic and radiologic evidence of generalized osteoporosis consistent with osteoporosis due to starvation. The calves with osteoporosis had the lowest carcass weights and radio-opacities recorded. There was a positive correlation between carcass weight and bone radio-opacity. Density, ash content, phosphorus, and calcium contents and phosphorous/calcium ratio in bone samples, as well as hepatic trace element status, were within the normal range for all calves in both populations. Two of the osteoporotic calves, were reported to have been orphaned. Our results indicate that the high frequency of bone fractures reported in moose in southern Norway is not associated with regional differences in trace element status or bone mineral balance. We propose that the occurrence of osteoporosis in moose calves in Birkenes may have resulted from inadequate nutrition following general overcrowding and high pressure on feed resources in the southernmost part of Norway.