Osteochondrosis Dessicans, Developmental Orthopedic Disease, OCD and DOD in Horses
As the bone grows, the border between the cartilage on the end and the calcified (hard) bone continually differentiates. One side becomes cartilage that lines the joints and the other becoming bone. In OCD, the cartilage formed is abnormal. There is argument over how it is abnormal and there probably are several types of OCD. Many cases fit the "abnormally thick" hypothesis. The cartilage becomes too thick in a region and this causes problems because the cartilage does not have blood vessels to feed it. It receives nutrition by diffusion from the joint fluid. If the cartilage becomes too thick it cannot receive adequate nutrition by this mechanism and becomes weakened at its base. This may result in a defect that goes all the way to the joint space. This defect results in abnormal joint function, inflammation, and pain. A frequent sequelae to OCD is arthritis and degenerative joint disease.
OCD in shoulder joimt
Osteochondritis dissecans (OCD) or osteochondrosis is a failure of the bone underlying the smooth articular cartilage inside the joints, i.e. the subchondral bone, to form properly from the skeleton’s cartilage template. This weakness results in cracking and fissure formation in the articular cartilage, when the foal, yearling or young horse takes weight on its joints during exercise. Flaps and fragments of cartilage consequently form within the joint, some of which are transformed from cartilage into bone and are termed ‘joint mice’. Chemicals that cause joint inflammation (synovitis) are released during the development of the flaps and fragments, or as a consequence of exercise on the abnormal surfaces. The affected joints may become visibly enlarged and distended with fluid and the horse may become lame, but there is no doubt that many cases never show symptoms of abnormality, are never recognised and resolve in time of their own accord.
Often OCD does not cause recognisable symptoms and may be found coincidentally on radiographic examinations (x-ray pictures). However, the more typical presentation is seen in young horses (weanlings or yearlings) that have rapidly grown and are increasing their exercise levels. There may or may not be lameness with a swollen, fluid filled joint (synovial effusion). Following flexion of the joint the lameness may be exacerbated and palpation of the joint may cause pain.
Clinical signs: depends on anatomical location
1.Early physeal closure and angulation. 12-18 months
2.Enlarged flared metaphysis. 3-4 months of age
a.Distention of joints involved
b.Lameness when horses begin training
4.All OCD lesions don't cause a lameness
a.Lameness evaluation important
a.Males 2 times more prevalent than females
Common sites of OCD formation in Horses
Normal bone formation
I.Long bones formed from cartilagenous modelsa.Formation starts in center of the model and extends toward either end.b.Cartilage cap is left at the bone ends.c.Second center of ossification begins in the cartilage caps and forms the epiphysis.d.Epiphysis and diaphysis remain separate to allow for long bone extension as animal matures. This is known as the physis.e.Separate physis develops adjacent to the articular cartilage.II.Physis is highly organized aggregation of cartilage cells with new cartilage proliferated at epiphyseal and articular surface and trabecular bone formed on the opposite surface.1.Physeal cartilage organizationa.Resting zoneb.Proliferating zonec.Hypertrophied zoned.Provisional calcification zone2.Calcifaction occurs at hypertrophied zone3.OCD occurs in this region
Diagram of pathogenesis of osteochondritis dissecans and subchondral cystic lesions in relation to the generalized condition of osteochondrosis.
Pathophysiology of OCD
I.Focal failure of endochondral ossificationa.Cartilage is retained and physis increases in widthb.These areas are weakc.Weight bearing causes articular changeII.Molecular and biochemical causes of OCDa.Abnormal proteoglycan core protein formationb.Abnormal organization of type II collagenc.Failure of appropriate transfer of glycoproteinsIII.Metaphyseal lesionsa.Physeal thickeningb.Microfractures of trabeluar bonec.Periosteal new bone formation in metaphysisd.Severe lesions may lead to osseus bridgingIV.Articular lesionsa.Fissures in thickened cartilageb.Cartilage flapsc.Involuted cartilage over subchondial cystic lesionsd.Joint inflammation due to products of cartilenous matrix and underlying trabecular bonee.Loose bodies form from cartilage flapV.Multifocal disease. If one lesion is found, suspect other lesions in other locations.
Diagnosis is made on the basis of detailed radiographic examination (x-ray pictures) of the suspected joints, sometimes performing a nuclear bone scan (scintigraphy) or by looking inside the joint with keyhole surgery (arthroscopy) to find the typical signs of abnormal bone shape, bone cysts, flaps, chips or fragments.
Scientific StudiesEquine Vet J 2000 May;32(3):217-21 Functional adaptation of equine articular cartilage: the formation of regional biochemical characteristics up to age one year. Brama PA, Tekoppele JM, Bank RA, Barneveld A, van Weeren PR Department of Equine Sciences, Faculty of Veterinary Medicine, Utrecht University, The Netherlands.Biochemical heterogeneity of cartilage within a joint is well known in mature individuals. It has recently been reported that heterogeneity for proteoglycan content and chondrocyte metabolism in sheep develops postnatally under the influence of loading. No data exist on the collagen network in general or on the specific situation in the horse. The objective of this study was to investigate the alterations in equine articular cartilage biochemistry that occur from birth up to age one year, testing the hypothesis that the molecular composition of equine cartilage matrix is uniform at birth and biochemical heterogeneity is formed postnatally. Water content, DNA content, glycosaminoglycan content (GAG) and biochemical characteristics of the collagen network (collagen content, hydroxylysine content and hydroxylysylpyridinoline [HP] crosslinks) were measured in immature articular cartilage of neonatal (n = 16), 5-month-old foals (n = 16) and yearlings (n = 16) at 2 predefined differently loaded sites within the metacarpophalangeal joint. Statistical differences between sites were analysed by ANOVA (P<0.01), and age correlation was tested by Pearson's product moment correlation analysis (P<0.01). In neonatal cartilage no significant site differences were found for any of the measured biochemical parameters. This revealed that the horse has a biochemically uniform joint (i.e. the cartilage) at birth. In the 5-month-old foals and yearlings, significant site differences, comparable to those in the mature horse, were found for DNA, GAG, collagen content and hydroxylysine content. This indicates that functional adaptation of articular cartilage to weight bearing for these biochemical parameters takes place during the first months postpartum. Water content and HP crosslinks showed no difference between the 2 sites from neonatal horses, 5-month-old animals and yearlings. At both sites water, DNA and GAG decreased during maturation while collagen content, hydroxylysine content and HP crosslinks increased. We propose that a foal is born with a uniform biochemical composition of cartilage in which the functional adaptation to weight bearing takes place early in life. This adaptation results in biochemical and therefore biomechanical heterogeneity and is thought to be essential to resist the different loading conditions to which articular cartilage is subjected during later life. As collagen turnover is extremely low at mature age, an undisturbed functional adaptation of the collagen network of articular cartilage at a young age may be of significant importance for future strength and resistance to injury.--------------------------------------------------------------------------------Dietary carbohydrates and fat influence radiographic bone mineral content of growing foals.Hoffman RM, Lawrence LA, Kronfeld DS, Cooper WL, Sklan DJ, Dascanio JJ, Harris PA Department of Animal Science, University of Connecticut, Storrs 06269-4040, USA. Rhonda.M.Hoffman@uconn.eduHydrolyzable carbohydrate intake in horse diets may become excessive when rapidly growing pastures are supplemented with grain-based concentrates. The substitution of fat and fiber for hydrolyzable carbohydrate in concentrates has been explored in exercising horses but not in young, growing horses. Our objective was to compare bone development in foals that were fed pasture and concentrates rich in sugar and starch (corn, molasses) or fat and fiber (corn oil, beet pulp, soybean hulls, oat straw). Forty foals were examined, 20 each in 1994 and 1995. In each year, 10 mares and their foals were fed a corn and molasses supplement (SS) and 10 others were fed a corn oil and fiber supplement (FF). The concentrates were formulated to be isocaloric and isonitrogenous, and mineral content was balanced to complement the pastures and meet or exceed NRC requirements. Dorsopalmar radiographs were taken of the left third metacarpal monthly from birth to weaning and then every other month until 1 yr of age. Bone density was estimated using imaging software and an aluminum stepwedge. Radiographic examination indicated differences in medial, lateral, and central bone mineral content of the metacarpal III. Bone mineral content increased with age, and a plateau was observed during winter. Bone mineral content was lower in weanlings and yearlings fed the FF supplement than in those fed SS. Subjective clinical leg evaluations indicated differences in physitis, joint effusion, and angular and flexural limb deformities in response to age, and possibly to season. Regression analysis indicated positive relationships between bone mineral content and body weight, age, and body measurements. Nutrient and chemical interactions, such as the binding of calcium by fat and fiber, may alter the availability of elements necessary for bone development.Measurement of synovial fluid and serum concentrations of the 846 epitope of chondroitin sulfate and of carboxy propeptides of type II procollagen for diagnosis of osteochondral fragmentation in horses. Frisbie DD, Ray CS, Ionescu M, Poole AR, Chapman PL, McIlwraith CW OBJECTIVE: To determine whether serum or synovial fluid concentrations of chondroitin sulfate epitope 846 and carboxy propeptides of type II collagen (CPII) can be used to diagnose osteochondral fragmentation (OC) in horses. ANIMALS: 38 horses with unilateral OC of the radiocarpal (n = 31) or intercarpal (33) joints and 8 clinically and radiographically normal horses. Procedures-For horses with OC, serum and synovial fluid concentrations of epitope 846, CPII, and keratan sulfate (KS) were determined, along with synovial fluid WBC counts and total protein concentrations. Serum epitope 846, CPII, and KS concentrations were measured in control horses. RESULTS: Synovial fluid epitope 846 and total protein concentrations were significantly higher in the joints with OC than in unaffected joints, but CPII and KS concentrations and WBC counts were not. Synovial fluid total protein and 846 epitope concentrations were linearly related to grade of OC. Serum epitope 846 and CPII concentrations were significantly higher in horses with OC than in control horses. Discriminant analysis allowed 27 of 34 (79%) horses to be correctly classified as having or not having OC on the basis of serum epitope 846 and CPII concentrations. CONCLUSIONS: Results suggest that serum and synovial fluid concentrations of epitope 846 and CPII are associated with OC. Increases in concentrations of epitope 846 and CPII suggest that increased synthesis of cartilage aggrecan and type II procollagen may be associated with OC. CLINICAL RELEVANCE: Measurement of serum epitope 846 and CPII concentrations may be useful in the diagnosis of OC in horses. Studies on growth cartilage in the horse and their application to aetiopathogenesis of dyschondroplasia.Vet J 1998 Nov;156(3):177-92Jeffcott LB, Henson FM The importance of osteochondrosis (dyschondroplasia) to the horse industry has been well documented since 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 cartilage 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 that there 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. Progression of femoropatellar osteochondrosis in nine young horses. Clinical, radiographic and arthroscopic findings. Dabareiner RM, Sullins KE, White NA 2dVet Surg 1993 Nov;22(6):515-523Marion duPont Scott Equine Medical Center, Virginia-Maryland Regional College of Veterinary Medicine, Leesburg, Virginia. The clinical and radiographic progression, and arthroscopic findings for nine young horses (less than 1 year of age) with femoropatellar osteochondrosis (OCD) are presented. Horses had a 2 to 12 week history of bilateral (8 horses) or unilateral (1 horse) hindlimb lameness. The most consistent clinical signs included femoropatellar joint distention and bilateral hindlimb lameness. At the onset of clinical signs, radiographic lesions were not present (4 horses) or subtle (5 horses), but were easily identified on radiographs taken 4 to 24 weeks later. Arthroscopic surgery was delayed until radiographic changes became obvious. Surgical findings in 20 femoropatellar joints were most commonly osteochondral "flaps" located on the proximal lateral trochlear ridge of the femur and were larger than had been indicated by the radiographs. Eight horses were being used for their intended purpose, which was racing (3 horses were racing and 3 were in race training), dressage (1 horse) or pleasure riding (1 horse). One horse required a second surgery when similar lesions developed on the opposite stifle, and was euthanatized 2 months later because of persistent lameness. One clinical signs are observed, osteochondrosis lesions of the distal femur can progress in foals younger than 9 months of age and the full extent of the radiographic lesion may take several weeks to develop. --------------------------------------------------------------------------------Racing performance of standardbreds after conservative and surgical treatment for tarsocrural osteochondrosis.Equine Vet J 1993 May;25(3):199-202Laws EG, Richardson DW, Ross MW, Moyer WDepartment of Clinical Studies, University of Pennsylvania School of Veterinary Medicine, Kennett Square 19348. A retrospective study of 114 Standardbred horses diagnosed with osteochondrosis (OC) of the cranial intermediate ridge of the distal tibia was carried out, and their subsequent race records were compared with 456 control horses. Each OC-affected horse was compared with 4 horses randomly selected from a list of horses matched to it by year of birth, sex and sire. The horses with OC were treated by arthroscopic removal of osteochondral fragments (N = 58) or managed conservatively (N = 56). The clinical presentation of these two groups was similar, although joint effusion was a more common presenting sign in the group that received surgical treatment. There was no association between presence of lameness and the type of treatment used. Data from the race records of treated and control horses (including the number of starts, lifetime earnings and record racing times) were compared. Overall, horses treated for OC had significantly fewer starts than, but earnings similar to, those in the control group. However, when stratification by sex was performed, females with OC made fewer starts and had lower earnings than did their control group. There was no significant difference in record time between OC-affected horses and controls. These results indicate that horses treated for osteochondrosis of the cranial intermediate ridge of the distal tibia performed as well as matched controls. J Am Vet Med Assoc 1997 Jun 1;210(11):1649-1652 --------------------------------------------------------------------------------Evaluation of cartilage lesions on the medial femoral condyle as a cause of lameness in horses: 11 cases (1988-1994).Schneider RK, Jenson P, Moore RMDepartment of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman 99164, USA. OBJECTIVE: To evaluate clinical findings and response to treatment in horses in which cartilage lesions on the medial femoral condyle were a cause of lameness. DESIGN: Retrospective case series. SAMPLE POPULATION: Medical records of 11 horses that had cartilage lesions on the medial femoral condyle detected during arthroscopy of the stifle. PROCEDURE: Signalment, history, lameness examination, response to intra-articular anesthesia, radiographs of the stifle, observations during diagnostic arthroscopy, and treatment were extracted from the medical record of each horse. Follow-up examinations and outcome were available for all horses. RESULTS: All horses in the study had lameness, but their gait improved after intra-articular injection of anesthetic. Abnormalities were not observed on radiography of the stifle. Diagnostic arthroscopy was performed on 12 affected joints in 11 horses. Cartilage was dimpled, wrinkled, and infolded, and a blunt arthroscopic probe could be inserted into the subchondral bone. In addition to focal lesions, 4 horses had generalized damage to cartilage on the medial femoral condyle. Focal cartilage lesions on the femoral condyle were debrided. In 2 horses, debridement was not performed because of extensive generalized damage to the cartilage. Six of 7 horses with focal cartilage lesions treated by debridement recovered completely and resumed previous activities. CLINICAL IMPLICATIONS: Cartilage lesions on the medial femoral condyle can cause lameness in performance horses. Diagnostic arthroscopy is necessary to make an accurate diagnosis. Debridement of focal cartilage lesions may allow some horses to successfully resume performance activities. J Am Vet Med Assoc 1986 Oct 1;189(7):802-803 --------------------------------------------------------------------------------Osteochondrosis-like lesion of the anconeal process in two horses.Hardy J, Marcoux M, Eisenberg H A suspected lesion of osteochondrosis dissecans involving the anconeal process of the humeroradial joint (elbow) was found in 2 horses. In horse 1, the lesion was found during routine lameness examination, during which alleviation of the lameness was achieved after intra-articular anesthesia of the elbow. In horse 2, the lesion was found at necropsy. Horse 1 responded satisfactorily to intra-articular treatment with hyaluronic acid. Both horses also had other joints affected with osteochondrosis dissecans.
- Pain, neck, cervical, throat
- Forelimb pain, front leg
- Hindlimb pain, hind leg
- Decreased mobility of hindlimb joint, arthrogryposis rear leg
- Contracture fore limb, leg
- Decreased mobility of forelimb joint, arthrogryposis front leg
- Forelimb swelling, mass in fore leg joint and/or non-joint area
- Hindlimb swelling, mass in hind leg joint and/or non-joint area
- Forelimb atrophy, wasting
- Hindlimb atrophy, wasting
- Stiffness or extended neck
- Forelimb lameness, stiffness, limping fore leg
- Hindlimb lameness, stiffness, limping hind leg
- Generalized lameness or stiffness, limping
- Reluctant to move, refusal to move
Once a foal becomes lame from OCD there are two treatment options:
1. Enforced rest at a lower plane of nutrition.
2. Surgical debridement of the defect. Arthroscopy
Controversy exists over the necessity of surgery in most cases. Many cases respond to stall rest until the lameness resolves, intrarticular hyaluronic acid and phenylbutazone. The diet should be looked at to be sure it is well balanced with respect to protein, calcium, phosphorous, copper and zinc. Also, it has been suggested that a balanced diet at 75% of NRC requirements helps, but no strong evidence exists for this recommendation.
Surgery may help in cases of large lesions or OCD in areas that seem to cause more trouble such as the shoulder etc.
What treatment options are there?
What is the outcome if OCD is left untreated?
What is the prognosis for OCD following treatment?
How can OCD be prevented?