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Osteochondritis Dissecans in the Dog David Novotny Iowa State University Volume 48 | Issue 1 Article 12 1986 Osteochondritis Dissecans in the Dog David Novotny Iowa State University Caroline L. Runyon Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/iowastate_veterinarian Part of the Skin and Connective Tissue Diseases Commons, and the Small or Companion Animal Medicine Commons Recommended Citation Novotny, David and Runyon, Caroline L. (1986) "Osteochondritis Dissecans in the Dog," Iowa State University Veterinarian: Vol. 48 : Iss. 1 , Article 12. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol48/iss1/12 This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. Osteochondritis Dissecans in the Dog David Novotny, BS, DVM* Caroline L. Runyon, DVM, MS** Introduction drocytes near the joint surface. As the carti­ Osteochondritis dissecans (OeD) is a mani­ 1age continues to grow, these chondrocytes festation of osteochondrosis characterized by a hypertrophy, vesiculate, degenerate, and be­ focal thickening of joint cartilage and subse­ come calcified. This calcified layer of the car­ quent dissection of a flap of this thickened car­ tilage is invaded by vessels from the bone tilage away from the underlying subchondral marrow. Some of the calcified cartilage is re­ bone. 1 The etiology of this condition remains sorbed, but remnants of cartilage are used as somewhat of a mystery; trauma, nutrition, is­ a framework upon which osteoblasts lay down chemia, and hereditary abnormalities of ossi­ bone. This process is called endochondral os­ fication have all been suggested.2 The disease sification. 4 is usually seen in the faster growing members In osteochondrosis, the normal chondro­ of large and giant breed dogs. The first clini­ cytes differentiation process is disturbed. 5 Ve­ cal signs of lameness are usually noted when siculation, degeneration, and calcification do the dog is between 5 and 9 months of age. not occur in a normal fashion, and the carti­ OCD is most commonly recognized in the lage gets thicker than normal. Vessels from proximal humerus, but is also found in the the bone marrow cannot penetrate this thick­ distal humerus, distal femur, and tibial tarsal ened cartilage, and bone is not formed. Re­ bone. One case of OeD of the distal radius sorption of the basal layers of cartilage and has been reported. 3 Other manifestations of replacement by bone on the diaphyseal side of osteochondrosis include ununited anconeal the joint cartilage ceases. The chondrocytes process, fragmented coronoid process, and re­ continue to proliferate near the joint surface, tained cartilage of metaphyseal growth resulting in a thickening of the joint carti­ plates. 1 Current research suggests there may lage. 4 If this process is localized to only a por­ be some relationship between osteochondrosis tion of the joint cartilage, and formation of and the development of cervical spondylolis­ bone continues in the calcified layer of the thesis, slipped femoral capital epiphysis, and surrounding cartilage, the radiographic ap­ hip dysplasia. 1 pearance will be that of an osseous defect. If the thickening of the joint cartilage is the only Pathogensis pathological change, there are no apparent OeD is a pathological condition in rapidly clinical signs. There is little inflammatory growing cartilage caused by a disturbance of reaction in the subchondral bone at this stage. endochondral ossification. Growth of the After the thickened cartilage is resorbed and epiphysis occurs in the articular cartilage in endochondral ossification then proceeds nor­ the same manner that growth of the long mally. bones occurs in the cartilage of the metaphy­ Since joint cartilage nutrition depends seal growth plates.4 Normal growth of the upon simple diffusion of nutrients from the epiphysis takes place by proliferation of chon- synovial fluid, the deeper layers of the thick­ ened cartilage are insufficiently nourished. These deeper layers of thickened articular car­ *Dr. Novotny is a 1985 graduate of the College of Vet­ tilage die, necrose, and serve as a' starting erinary Medicine at Iowa State University. point for fissures. 5 When a developing fissure **Dr. Runyon is a Professor of Veterinary Clinical Sciences at Iowa State University. reaches the joint cartilage surface, synovial 46 Iowa State University Veterinarian fluid enters the fissure and contacts the basal and development, and are "pushed" nutri­ layers of the joint cartilage and the subchon­ tionally during their most active growth pe­ dral bone. An inflammatory reaction then riod have the greatest risk of developing takes place in the defect. The dog becomes OCD. 1 painful and starts to limp. It is at this stage that the lesion becomes osteochondritis disse­ oeD of the Shoulder cans. Osteochondritis refers to the inflamma­ OCD of the shoulder joint is seen in large tion in the joint cartilage and subchondral and medium size dogs, predominantly in the bone, and dissecans refers to the flap of carti­ male. The clinical signs are first noticeable 1age that is dissected away fron1 the underly­ between 4 to 7 months of age and are usually ing subchondral bone. This flap may remain insidious in onset. Lameness on one or both in the defect, or it may detach and form an forelegs, which worsens after exercise, is the intraarticular body. The fate of the flap is of n10st prominent clinical sign. Stiffness after great importance to further development of periods of rest is also an important clinical clinical signs. 5 sign. Pain can usually be elicted by palpation, hyperflexion or hyperextension of the Etiology shoulder joint. The clinical signs may vary in A number of factors have been incrimi­ severity over periods of weeks to months. The nated as the cause of OCD, but the etiology condition is often bilateral. remains controversial and appears to be The definitive diagnosis of OCD is made multifactorial. The most common factor in­ by radiology. The view that best demonstrates criminated in experimental and clinical stud­ the lesion is the medial-lateral with slight ex­ ies is rapid growth and weight gain. In one tension ofthe limb. 13 The affected limb should study of nearly 300 patients with only a few be placed down on the film cassette and pulled dogs were not of medium or larger size. There cranial. The unaffected or upper limb should were twice as many males as females in these be pulled caudally. The image of the humeral cases. This difference may be explained by the head will thereby be superimposed over the fact that male dogs usually grow more rapidly radiolucent lumen of the trachea to enhance than female dogs.1 delineation of any lesions present. Radio­ There is probably a hereditary predisposi­ graphs will demonstrate a defect, usually in tion for OCD in the dog, although this has not the caudal aspect of the humeral head. In been proven. A higher incidence of OCD was mild or early cases only a flattening of the found in offspring of certain dogs and there dorso-caudal contour of the humeral head is were litters in which several or all of the pup­ seen. In advanced lesions there may be 12 6 9 pies were affected. - Genetic factors that sclerosis of the subchondral bone and calcifi­ affect growth rate and weight gain, sexual de­ cation of the cartilagenous flap. A radiograph velopment, behavior, and conformation un­ of the shoulder taken with the primary beam doubtedly playa role in the etiology.10 directed at a slightly oblique angle from the Nutrition seems to be an important factor lateral may be needed to visualize the lesion. in the development of OCD. In an experi­ This view may assist in a diagnosis because in mental study in Great Dane puppies, free many cases the lesion is slightly to the caudo­ choice feeding resulted in increased growth lateral instead of the caudal side of the hu­ rate accompanied by skeletal abnormalities meral head. 13 Both shoulders should be radio- similar to those seen with OCD.ll graphed, even if there is no history or clinical Trauma may also contribute to the develop­ sign of bilateral lameness.1 ment of OCD. Biomechanical studies have It is generally easier to diagnose OCD of shown that OCD lesions typically develop in the shoulder than it is to decide what therapy those areas of the joint cartilage that are most to use. If the flap mineralizes, it is usually subjected to the stress and trauma of weight visible on radiographs. The cartilagenous flap bearing. Trauma probably enhances the op­ may remain connected to the adjacent normal portunity for the abnormally thickened and articular cartilage and within the defect. If the slow-to-mature cartilage to cleave further flap remains cartilagenous, radiographs will once a fissure is formed. 12 reveal only the defect in the subchondral In conclusion, most evidence indicates that bone. Because animals show pain and lan1e­ dogs with a genetic capacity for rapid growth ness, restriction of exercise has been recom- VOL. 48) No. 1 47 mended as a part of the therapy by many in­ with functional fibrocartilage and restore a vestigators. In contrast, another researchers smooth contour over the articular defect. This believes that a dog with OCD of the shoulder fibrocartilage is not as biomechanically stable should be allowed to move around as much as as the hyaline cartilage that was originally possible because this will increase the chances present, but is functionally adequate. Re­ that the flap will become dislodged. 1 If neces­ moval of the diseased tissue allows for better sary, the dog can be given analgesics. In cases healing, and greater freedom from lame­ in which clinical signs are not severe or may ness.
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