Ultrastructural histochemical evaluation of growth plate cartilage matrix from healthy and osteochondritic swine

A contributing factor to the lack of understanding the cause of osteochondritic syndromes has been incomplete knowledge of the morphology of lesions in subclinical stages of the disease. In osteochondritic growth plate cartilage from growing swine, the morphology of the pericellular matrix surrounding hypertrophic zone chondrocytes is abnormal and is characteristic of a matrix in which the ordered interactions of matrix macromolecules with each other and with the plasma membrane have been altered. In the present study, ultrastructural histochemical techniques were used to analyze the nature of macromolecular interactions in the pericellular matrix in normal growth plate cartilage, and selective enzyme digestions of normal growth plate cartilage were used to simulate the morphology found in osteochondritic lesions. Results showed that a pericellular macromolecular material which was both ferrocyanide positive and trypsin sensitive was essential for stabilizing the cell membrane/pericellular interface in normal growth plates. The highly variable morphology of this same material in osteochondritic lesions was simulated by hyaluronidase digestion. Since similar pericellular matrix abnormalities have not been described in other diseases of growth plate cartilage, they may represent a matrix abnormality unique to the vascularization failure of osteochondritic syndromes. Our ability to simulate the ultrastructural morphology of subclinical osteochondritic lesions enhances the potential for understanding the macromolecular changes found in the pericellular matrix of osteochondritic cartilage. Based on these results, a new hypothesis is presented for the early sequence of events in the pathogenesis of osteochondrosis.     

Changes in molecular expression of aggrecan and collagen types I, II, and X, insulin-like growth factor-I, and transforming growth factor-beta1 in articular cartilage obtained from horses with naturally acquired osteochondrosis.

OBJECTIVE: To determine molecular changes in the expression of insulin-like growth factor-I (IGF-I) and transforming growth factor-beta1 (TGF-beta1) in horses with osteochondrosis, and to characterize expression of matrix aggrecan and collagen types I, II, and X in articular cartilage of affected joints. SAMPLE POPULATION: Articular cartilage from affected stifle or shoulder joints of 11 horses with naturally acquired osteochondrosis and corresponding joints of 11 clinically normal horses. PROCEDURE: Harvested specimens were snap frozen in liquid nitrogen, and total RNA was isolated. Specimens were fixed in 4% paraformaldehyde for histologic examinations. Expression of matrix molecules was assessed by analysis of northern blots and in situ hybridization, using equine-specific cDNA probes and riboprobes, respectively. Expression of IGF-I and TGF-beta1 was assessed by use of noncompetitive quantitative polymerase chain reaction, in situ hybridization, and immunohistochemical analysis. RESULTS: Cartilage obtained from osteochondrosis lesions had significantly greater expression of IGF-I, compared with normal cartilage. Expression of TGF-beta1 and collagen type I were higher, but not significantly so, in affected tissues. Expression of aggrecan or collagen types II and X did not differ between affected and clinically normal cartilage. CONCLUSIONS AND CLINICAL RELEVANCE: Increased expression of growth factors and collagen type I was found in cartilage from osteochondrosis lesions. However, this probably reflects a healing response to injured tissue rather than a primary alteration. Therefore, methods aimed at altering concentrations of growth factors in cartilage of growing horses would be unlikely to alter the incidence or progress of the disease.     

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.     

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.     

Age related changes and osteochondrosis in swine articular and epiphyseal cartilage: light ane electron microscopy.

Age related changes and osteochondrosis in swine were studied using light microscopy and electron microscopy in articular cartilage and light microscopy and epiphyseal cartilage of swine from three days to 30 weeks of age. Thickness, cellularity and vascularity of both the epiphyseal and articular cartilage, decreased as the swine aged. Osteochondrotic changes included formation of "plugs" of cartilage indicating localized failure of ossification and separation and space formation in epiphyseal cartilage. Eosinophilic streaks and space formation in epiphyseal cartilage was observed in relation to epiphyseal separation. Electron microscopy showed a continuous fibrillar layer on the surface of the cartilage corresponding to the lamina splendens of light microscopy. This layer increased in the thickness and showed accumulation of amorphous material between the fibrils with aging. In the matrix, the orientation and distribution of the collagen fibers changed with growth and thicker fibers with clear sub banding were more common in older age groups. Also, necrotic cells, glycogen containing bodies and cellular debris were noticed in the matrix of normal cartilage in old animals. Chondrocytes in the younger cartilage showed accumulation of organelles responsible for protein synthesis; while Golgi bodies, vesicles, lysosomes, well developed foot processes and other inclusions were noticed in older cartilage. Cartilage erosions had a clumped and disrupted lamina splendens on the surface and electron lucent patches in the ground substances of the matrix and chondrocyte cytoplasm.     

Hind limb skeletal lesions in 12-month-old bulls of beef breeds

In the present study, right hind limb bones from 46 12-month-old bulls with no clinical signs were examined to identify and describe lesions that could predispose the stifle and tarsal joints to osteoarthritis. The bulls came from a performance testing station and were slaughtered due to a low index at the end of the testing period 1996-97. Differences in frequency of lesions among breeds as well as the relationship between lesions and growth rate were evaluated. Forty-five (97.8%) of the 46 bulls had lesions in the joints and/or growth plates. Prevalence of lesions was 100% in the Charolais (22/22), the Hereford (8/8), and the Limousin (4/4) breeds, and 85.7% (6/7) in the Simmental breed. The stifle was affected in 37, the tarsus in 33, and the growth plates in 34, of the 46 bulls. Lesions found in the stifle joint were: osteochondrosis of the articular-epiphysical cartilage complex (AECC) (25), subchondral bone cyst of the distal femur (1), fragmentation of the medial intercondylar eminence of the tibia (20), cleft in the distal part of the patellar groove (28), and an avulsion fracture of the lateral condyle together with a partial tear of the cranial cruciate ligament (1). Lesions found in the tarsal joint were: osteochondrosis of the AECC (23), ulcerative lesions of the articular cartilage of the talus (25), and fracture of the medial malleolus (4). Twenty-eight bulls had lesions of osteochondrosis at the AECC and 37 at the growth plates. When osteochondrosis at the AECC and thickening of the growth plates were combined, 44 of the 46 bulls had at least one lesion at the AECC and/or the growth plate. Prevalence of bulls with at least one lesion was similar between breeds, but the number of lesions per bull was significantly higher in Charolais followed by Simmental, Hereford, and Limousin. Number of lesions per bull was significantly correlated with daily weight gain, carcase weight, and the width of the proximal tibial epiphysis. Lesions were statistically independent, indicating that local biomechanical factors within the joints are important in the pathogenesis. In conclusion, we suggest that the high incidence of hind limb osteoarthritis reported in the Swedish beef bull population can be explained by the high prevalence of skeletal lesions found in the present material. The lesions appeared to be related to high growth rate and to the breed.     

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)     

Osteochondrosis — An international problem for the horse industry

Osteochondrosis is one of the most important skeletalproblems affecting young horses and is one of the conditions included in the syndrome of developmental orthopedic disease. It occurs worldwide in many different breeds and its incidence appears to be steadily increasing. The primary lesion of osteochondrosis is attributed to focal damage of endochondral ossification. When occurring in the articular/epiphyseal cartilage complex, there may be bone formation within the retained cartilage, resulting in “bony fragments.” These are often seen in the tarsocrural articulation on the cranial aspect of the tibia. Focal retention of necrotic cartilage into the subchondral bone may eventually lead to cleft formation resulting in osteochondrosis dissecans. Other lesions associated with osteochondrosis are subchondral cysts, fractures and osteoarthrosis.The definitive cause of osteochondrosis is unknown,but there is evidence that it is the response in growth cartilage to a number of different challenges. It appears to be multifactorial in origin, involving heredity, growth rate, body size, nutrition, mineral imbalance, endocrinological dysfunction and biomechanical trauma. Recent studies have shown cases of osteochondrosis to be preceded by radiographically detectable disturbances of endochondral ossification during the first three months of life. This early appearance of disturbed ossification necessitates further studies into the importance of nutrition/management of the pregnant and lactating mare. Whether these early disturbances will lead to fully developed osteochondrosis or if they will recede obviously depends on a number of factors such as nutrition and exercise. High energy diets have been shown in weaning foals to consistently produce lesions of osteochondrosis. If, however, foals fed a high energy diet are subjected to forced exercise, the incidence of osteochondrosis is reduced dramatically.The prevention of osteochondrosis must rate as a highpriority for the horse industry, but to achieve this more data on the mechanisms of endochondral ossification and how this process is influenced by different intrinsic and environmental factors are required. Recent research into osteochondrosis has involved studies of chondrocyte metabolism in growth cartilage, the influence of growth factors, the extent of degradation of extracellular matrix and endochondral ossification.     

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/osteoarthrosis and claw disorders in sows, associated with leg weakness

The objective of this study was to investigate the associations between different leg weakness symptoms and osteochondrosis/osteoarthrosis and claw disorders in sows together with the influence of age on these findings. One hundred and seventeen sows in one herd were followed from 6 months of age until culling and judged for leg weakness once in every gestation using a scale from 1 (normal) to 4 (severe changes). At slaughter changes in joints, growth plates and claws were scored on a scale from 1 (normal) to 5 (very severe changes). Osteoarthrotic changes were strongly associated with osteochondral changes in humeral and femoral condyles. The clinical signs of osteochondrosis and osteoarthrosis were found to be: buck-kneed forelegs, turn out of fore and hind legs, upright pasterns on hind legs, stiff locomotion, lameness and tendency to slip. The clinical signs of claw lesions were found to be: buck-kneed forelegs, upright pasterns, steep hock joints, turn out of hind legs, standing under position on hind legs, stiff movements, swaying hindquarters, goose-stepping hind legs, tendency to slip and lameness. Overgrown claws were strongly associated with leg weakness indicating the need for claw trimming in sow populations.     

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.     

Immunohistochemical study of matrix metalloproteinase‐3 (MMP‐3) at the articular cartilage in osteochondrotic pigs

In order to understand the mechanism of osteochondrosis in the pig, articular cartilage was taken from the distal femoral condyles of Duroc pigs exhibiting leg weakness and then examined immunohistochemically for the localization of matrix metalloproteinases‐3 (MMP‐3), one of the enzymes involved in the resolution of cartilage matrix. The articular cartilage had the typical characteristics of osteochondrotic lesions, such as abnormal calcification, clefts of cartilage, disappearance of proteoglycan, and necrotic chondrocytes. The immunoreaction of MMP‐3 was observed in chondrocytes at the boundary between normal cartilage and proteoglycan‐deficient area. Moreover, chondrocytes expressing MMP‐3 showed normal morphology, but the surrounding cartilage matrix did not stain with toluidine blue, which indicated a lack of glycosaminoglycans. These results suggest that MMP‐3 is highly involved in the appearance and expansion of osteochondrotic lesions.     

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.     

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

REASONS FOR PERFORMING STUDY: The earliest osteochondrosis (OC) microscopic lesion reported in the literature was present in the femorotibial joint of a 2-day-old foal suggesting that OC lesions and factors initiating them may arise prior to birth. OBJECTIVE: To examine the developing equine epiphysis to detect histological changes that could be precursors to OC lesions. METHODS: Osteochondral samples from 21 equine fetuses and 13 foals were harvested from selected sites in the scapulohumeral, humeroradial, metacarpophalangeal, femoropatellar, femorotibial, tarsocrural and metatarsophalangeal joints. Sections were stained with safranin O and picrosiruis red to assess cartilage changes and structural arrangement of the collagen matrix. RESULTS: Extracellular matrix changes observed included perivascular areas of paleness of the proteoglycan matrix associated with hypocellularity and, sometimes, necrotic chondrocytes. These changes were most abundant in the youngest fetuses and in the femoropatellar/femorotibial (FP/FT) joints. Indentations of the ossification front were also observed in most specimens, but, most frequently, in scapulohumeral and FP/FT joints. A cartilage canal was almost always present in these indentations. The vascular density of the cartilage was higher in the youngest fetuses. In these fetuses, the most vascularised joints were the metacarpo- and metatarsophalangeal joints but their cartilage canals regressed quickly. After birth, the most vascularised cartilage was present in the FP/FT joint. Articular cartilage differentiated into 4 zones early in fetal life and the epiphyseal cartilage also had a distinct zonal cartilage structure. A striking difference was observed in the collagen structure at the junction of the proliferative and hypertrophic zones where OCD lesions occur. CONCLUSION: Matrix and ossification front changes were frequently observed and significantly associated with cartilage canals suggesting that they may be physiological changes associated with matrix remodelling and development. The collagen structure was variable through the growing epiphysis and a differential in biomechanical properties at focal sites may predispose them to injury.     

Use of histochemical techniques in the characterisation of osteochondroses affecting pigs

Growth cartilages with dyschondroplastic foci (osteochondrosis) or areas of chondrolysis were selected from the ribs and bones of the appendicular skeleton of 132 commercial pigs euthanased between one and 169 days old or at a liveweight of 100 kg. Histochemical staining techniques that identified proteoglycans, collagen and deposits of calcium enhanced the visualisation of the lesions, were valuable for recognising the distribution of lesions, and helped to elucidate the development of the lesions. On the basis of the histochemical and morphological differences, it was considered that the lesions associated with growth plates and the lesions associated with articular-epiphyseal cartilage complexes should be considered as different entities. Lesions were identified in the articular-epiphyseal cartilage complexes of pigs at 15 days old, earlier than has been reported previously. Toluidine blue and safranin O were more useful than alcian blue and, in terms of staining intensity, toluidine blue gave more consistent results than safranin O.     

THE SUPINATED MEDIOLATERAL RADIOGRAPH FOR DETECTION OF HUMERAL HEAD OSTEOCHONDROSIS IN THE DOG

Mediolateral and supinated mediolateral radiographs of the shoulder joint were compared in 19 dogs. Twenty shoulders, representing 15 dogs (5 had bilateral lesions), had osteochondrosis of the humeral head. The flattened humeral head and subchondral defect were detectable in both views in all affected shoulders. The lesions were slightly more easily detected in the supinated view. The supinated view more consistently demonstrated the presence of a calcified cartilage flap and therefore, could be useful in determining a course of therapy. In four dogs (8 shoulders) without osteochondrosis and six normal shoulders from affected dogs, there were no instances in which a shoulder appeared normal on one view, but demonstrated a lesion on the other. The supinated view should be obtained in addition to the mediolateral view in dogs with osteochondrosis of the humeral head.     

Articular cartilage blood vessels in swine osteochondrosis

Perfusion studies in swine with early lesions of osteochondrosis demonstrated that lamellar areas of chondrocyte necrosis within reserve zones of growth areas occurred only in regions of nonperfused articular cartilage. Articular cartilage with a similar anatomical location was perfused in some animals. Occasionally, nonperfused articular cartilage showed vascular alterations within cartilage canals without evidence of significant perivascular or lamellar necrosis. By light microscopy, some vessels within or adjacent to nonperfused articular cartilage had normal morphology; however, ultrastructural abnormalities were found in some vessels of all cartilage canals adjacent to necrotic cartilage lamella. Minimal alterations were in the few cartilage canal vessels that appeared normal by light microscopy, and the surrounding chondrocytes showed only minimal alterations. Early cartilage canal alterations were seen in the endothelium of cartilage canal capillaries, and ultrastructural changes in these vessels were similar to those described with experimentally induced, direct vascular injury. Vascular injury was followed by leakage of plasma and cells into the interstitial space of the cartilage canal. Necrosis of the vessel wall and interstitial tissue caused the cartilage canals to appear empty or to be filled with fibrin-like material. Although the vascular changes could be considered as part of the normal process of cartilage maturation and cartilage canal chondrification, observations suggest that in domestic swine the attendant cartilage necrosis and chondrolysis is exuberant. It is suggested that alterations in cartilage canal vessels play a major role in the pathogenesis of articular cartilage lesions that are found in osteochondrosis of swine.     

ULNAR METAPHYSEAL OSTEOCHONDROSIS IN SEVEN CAPTIVE BRED CHEETAHS (ACINONYX JUBATUS)

Distal ulna metaphyseal osteochondrosis was identified in seven captive bred cheetahs raised in Australia between 1984 and 2005. The disorder was characterized by bilateral carpal valgus conformation. In the metaphyseal region of the distal ulnae, an osteolucent defect that appeared as a proximal extension of the lucent physis was identified radiographically between 6 and 10 months of age. Ulna ostectomy was done to correct the angular limb deformity. Histologically, changes were identified in the osteolucent lesion that resembled osteochondrosis. We propose that the condition is probably familial and/or dietary in origin.     

A SACRAL LESION RESEMBLING OSTEOCHONDROSIS IN THE GERMAN SHEPHERD DOG

More than 30% (21 of 65) of German Shepherd dogs with clinical signs of cauda equina compression had radiographic and pathologic abnormalities compatible with osteochondrosis of the sacral endplate. Most of these dogs had a defect in the dorsal part of the sacral endplate and a detached bone fragment in the vertebral canal. Similar lesions were also found in growing and young adult dogs without clinical signs. The dogs with clinical signs of cauda equina compression also had severe degenerative disc disease with protrusion of the lumbosacral disc and compression of the cauda equina, suggesting that the signs of cauda equina compression more likely were related to the secondary degenerative changes (disc protrusions) rather than the primary disease. Clinically normal German Shepherds with sacral osteochondrosis usually were younger than 18 months, the dogs with cauda equina compression and sacral osteochondrosis older than 18 months (mean age 4.8 years). On the average, these dogs were two years younger as compared to dogs with cauda equina compression without sacral osteochondrosis. Male dogs are more often affected than females (5:1). There is a breed predisposition: in dogs other than German Shepherds, osteochondrosis of the sacral endplate seems to be extremely rare.     

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.