Welcome to the all-new Vetlearn

  • What’s new on Vetlearn?
  • The latest issues of Compendium and
    Veterinary Technician
  • New CE articles for veterinarians and technicians
  • Expert advice on practice management
  • Care guides on more than 400 subjects
    to give to your clients
  • And more!

To access Vetlearn, you must first sign in or register.


Become a Member

Compendium August 2009 (Vol 31, No 8)

The Epiphyseal Plate: Nutritional and Hormonal Influences; Hereditary and Other Disorders

by Dirsko von Pfeil, Charles DeCamp, Sarah K. Abood Sarah K. Abood

    CETEST This course is approved for 3.0 CE credits

    Start Test


    This article reviews nutritional and hormonal influences, diseases with uncertain etiology, and hereditary disorders affecting the growth and development of the long bones in dogs and cats.

    Nutritional, hormonal, and genetic factors play important roles in the growth of animals.1-15 For example, unbalanced or incomplete diets can result in growth abnormalities.1-15 Hormonal factors, such as prepubertal gonadectomy, have been associated with delayed closure of growth plates in cats, which increases the risk of slipped capital femoral epiphysiolysis (SCFE) and may also affect the distal radius and femur.1,2 Documented hereditary disorders affecting the epiphyseal plate include ocular-skeletal dysplasia, dwarfism, canine epiphyseal dysplasia, premature closure of the ulna in Skye terriers, multiple cartilaginous exostoses (MCE), and mucopolysaccharidosis (MPS).3-7 Osteochondrosis dissecans of the articular cartilage is a common disease in growing dogs, but diseases of the epiphyseal cartilage, including hypertrophic osteodystrophy, retained cartilaginous core, and ununited anconeal process, can also be observed.8,9 The etiology of these conditions appears to be multifactorial,16,17 and further research is warranted to better understand, prevent, and treat these diseases.


    Musculoskeletal disorders are common in young dogs but uncommon in cats. The prevalence of musculoskeletal disorders is reported to be 22% in dogs younger than 1 year.12 Of these cases, 20% are thought to be nutrition related.12 Deficiencies in vitamin D or trace elements, excessive calcium or vitamin C, and high energy intake have been discussed as reasons for developmental growth abnormalities.12-15 Calcium and energy are two of the most important factors.16 Commercially prepared large-breed puppy diets that meet the nutritional guidelines of the Association of American Feed Control Officials (AAFCO) and are labeled "complete and balanced" should be fed to growing large-breed dogs until they reach approximately 80% of their mature size.18 Smaller dogs can be fed puppy diets until approximately 1 year of age and should then be switched to an adult diet.12,18-20 Recommended levels of key nutrients in a diet to prevent orthopedic disease in large-breed puppies are summarized in TABLE 1 .


    Excess feeding (>3% of dry matter) of calcium increases the risk of slowing chondrocyte maturation, which can lead to the development of retained cartilaginous cores and, in some cases, angular limb deformity.16 Osteochondrosis dissecans may also develop with a calcium-rich diet.14,21 Growing giant-breed dogs fed high-calcium diets (>3% of dry matter as calcium) experience greater development of osteochondrosis than control dogs.14,21,22 Even when dietary phosphorus is adjusted to maintain a physiologic calcium:phosphorus ratio, osteochondrosis can still occur.14,21


    Imbalances of dietary phosphorus intake can affect calcium homeostasis and may influence bone metabolism.21 Low dietary phosphorus is uncommon but has been reported to increase calcium and phosphorus absorption in the gut.20,23 Clinical signs can include poor weight gain and reduced growth rate.20,23 By contrast, excessively high phosphorus levels can stimulate hormone secretion (secondary hyperparathyroidism), which decreases calcium absorption.20 The result is poorly calcified, soft bones that are predisposed to pathologic fractures.15-18 It is therefore recommended to maintain a dietary calcium:phosphorus ratio between 1.1:1 and 2:1.12

    Vitamin D

    Vitamin D and its metabolites are important in the regulatory mechanism of calcium metabolism and skeletal development in dogs and cats. Vitamin D deficiency leads to a decreased plasma concentration of calcium.24 Chronic hypocalcemia, especially during growth, causes inadequate mineralization of bone so that the cartilaginous matrix in the growth plate fails to calcify.16 The resultant disease, rickets, is characterized by soft bones, lameness, pain, angular limb deformation, and pathologic fractures.13,25 Radiographs typically show thickened physeal cartilage plates and "cupping" of the metaphyseal bone with a dense sclerotic margin26 (FIGURE 1). Histology shows severe enlargement of the chondrocytes in the growth plate.27 Rickets is extremely rare in dogs and cats being fed commercially available pet foods.13 However, it may occur in other small companion animals.


    The metabolic activity of growing bones is high during an animal's first year of life. Compared with mature bone, growing bone is softer and more predisposed to injury from minor trauma.28 This risk increases when a high-calorie diet is fed, especially in fast-growing, large-breed dogs.15,29 Foods high in dietary fat or protein have been shown to increase growth rate and affect hormonal regulatory mechanisms.12,30 Insulin-like growth factor, growth hormone, thyroid hormone, and other hormones are overexpressed, reflecting an increased metabolic state and increased bone formation.22 This leads to the formation of a less dense spongiosa, and the comparably weak subchondral bone and thicker, weaker growth plate predispose these dogs to mechanical injuries.16 One study showed that dogs fed ad libitum diets containing excessive amounts of protein, calcium, phosphorus, and vitamin D had slow cartilage maturation and developed osteochondrosis.15 In contrast, more recent studies have shown that high amounts of dietary protein are unlikely to play a causative role in the development of osteochondrosis in dogs.31

    Excessive dietary protein and fat also increase total body weight, which could lead to obesity as well as secondary changes in joints32 and prolonged epiphyseal plate maturation. Adipocytes have been shown to be related to the development of arthritis by the release of adipokines, which are linked to immunity and inflammation.33 Feeding commercial dry diets with an energy density below 4.0 kcal/g can help minimize the negative effects of high calorie intake.12 Restricted total dietary intake has been associated with decreased development of hip dysplasia and arthritis in several joints, as well as with increased life span and delayed onset of chronic disease.34

    Other Nutrients

    Copper, zinc, and manganese also affect epiphyseal growth.12 Although rare, copper deficiency can impair the metabolism of collagen and elastin.35 Zinc deficiencies can lead to impaired growth and skeletal development as well as skin problems and decreased immune function.12

    Experimentally, manganese deficiency has been shown to promote the development of thickened, short, disproportionate long bones; abnormal ossification of the skull; and otoliths in the inner ear.36 However, no clinical cases of manganese deficiency have been reported.

    Hormonal Influences

    As in people, congenital hypothyroidism has been documented to cause severe abnormalities in dogs.37-40 Lieb and colleagues39 described a 4-year-old dog with congenital hypothyroidism that presented with tetraparesis due to vertebral physeal fracture. This dog also showed skeletal immaturity in the long bones. Greco et al38 reported congenital hypothyroid dwarfism in five giant schnauzers of the same family. When treated with levothyroxine before 4 months of age, puppies responded with complete remission.38 A similar report in toy fox terriers described the heritability of congenital hypothyroidism; a DNA-based carrier test has been developed and is used to prevent breeding of affected dogs.40

    Sex hormones influence the time of growth plate closure.41-43 Compared with animals that do not undergo gonadectomy, male and female kittens and puppies neutered at the age of 7 weeks can have significantly delayed physeal closure and greater radial length.44,45 Bone volume in these animals is also decreased, presumably due to decreased osteoblast function.45

    Slipped Capital Femoral Epiphysiolysis

    The skeletal changes associated with prepubertal gonadectomy have been associated with an increased risk for developing SCFE in cats and, rarely, in dogs1,46,47 (FIGURE 2). Animals are lame in the affected hindlimb; the duration and severity of the lameness vary.46 Serial radiographs are usually used to make the diagnosis, and it has been demonstrated that dysplasia can occur in multiple physes in the same animal. The distal femoral and distal radial epiphyses can be affected concurrent with SCFE.2 Histologic changes in the growth plate of cats with SCFE include loss of normal columnar architecture of chondrocytes, chondrocyte clustering (FIGURE 3), granulation tissue within the growth plate, physeal clefts with necrosis, and wider growth plates (up to twice normal).1,2 These findings are similar to those in SCFE in people (obese, adolescent boys are most commonly affected).1 In a study of SCFE in cats,1 all affected animals were 5 to 24 months old, 85% were male, 23% were Siamese, and 90% were obese. These cats were neutered between 4 and 8 months of age.46 Depending on the clinical signs, conservative treatment or surgery (e.g., femoral head and neck ostectomy) may be indicated.

    Diseases with Uncertain Etiology

    Femoral Neck Metaphyseal Osteopathy in Cats

    Cats with metaphyseal osteopathy develop necrosis in the proximal metaphysis, which eventually results in a secondary, pathologic fracture of the femoral neck48 (FIGURE 4). The condition may be unilateral or bilateral. Adult male cats (neutered and intact) are overrepresented. Lameness originates from the coxofemoral joint. Unlike SCFE, radiographs show characteristic chronic degenerative changes in the femoral neck region, including areas of radiolucency, bone resorption, an "apple-core" appearance, or an irregular radiolucent fracture line.48,49 Several etiologies have been proposed: traumatic fracture with secondary bone resorption, avascular necrosis, osteomyelitis, feline herpesvirus, and changes secondary to SCFE.48,49 Histology does not show the typical features of SCFE but may include bone necrosis and microfracture, fibrosis, metaplasia, osteomyelitis, and synovitis of the surrounding connective tissue.48,49 Excision of the femoral head and neck carries a good prognosis.48,49


    Hypertrophic Osteodystrophy

    Hypertrophic osteodystrophy is seen in growing large- or giant-breed dogs with open epiphyseal plates.9 Affected animals present with intermittent lameness, fever, and extremely painful, swollen distal metaphyses of the long bones. A radiolucent line parallel to the growth plate (pseudophyseal line) is the hallmark of the disease. Possible causes of this line include increased leukocyte activity, bone lysis, and failure of ossification of the hypertrophic zone.50 Large, swollen, dense metaphyses and periosteal exostosis complete the classic radiographic appearance (FIGURE 5).

    The etiology of hypertrophic osteodystrophy is unknown. Nutritional (vitamin C deficiency) and viral (distemper virus) factors have been suggested.50 However, these theories remain unproven. The disease is usually self-limiting, but affected dogs can be extremely ill. Treatment consists of supportive care. Permanent bone changes, angular limb deformities secondary to asymmetric or asynchronous growth or bridging of bone, and retardation of axial growth have been reported.9,50


    Osteochondrosis is a multifocal disease with incomplete endochondral ossification of the articular-epiphyseal cartilage. It has also been reported to affect the cartilage of the epiphyseal growth plate.51,52

    The etiology of osteochondrosis is not clear. Early in an animal's development, blood vessels, nerves, and lymphatics supply the epiphyseal cartilage.53 As the animal ages and gains weight, the number of blood vessels decreases until the cartilage becomes avascular. Studies of pigs and chickens in which ischemia was induced have demonstrated that, at some point during growth, the viability of cartilage cells depends on the integrity of cartilage canal vessels.11 Aside from ischemia, other etiologies, such as hereditary factors, rapid growth, and nutritional imbalances, have been suggested to cause osteochondrosis.27

    Osteochondrosis results in failure of matrix calcification, with retention of cartilage rather than conversion to bone, leading to a thickened, weaker growth plate. Excessive caloric intake has been suggested to be a risk factor in the development of increased articular cartilage thickness, but high dietary protein alone is unlikely to be the cause of osteochondrosis in dogs.22,54 Damage to the cartilage structures, retained cartilaginous cores, and asymmetric growth may be consequences of this process.27 Histologic examination of the lesions may reveal areas of necrotic chondrocytes in the reserve zone, close to necrotic vascular channels.55

    When osteochondrosis affects the articular surface, lesions consist of necrotic cartilage with a cleft extending from the subchondral bone to the articular surface, resulting in synovitis, joint effusion, and clinical signs of lameness.11 This form of osteochondrosis is called osteochondrosis dissecans (FIGURE 6). Treatment consists of removal of loose cartilage and debridement of subchondral bone. The prognosis varies depending on the affected joint and advancement of arthritis.

    Retained Cartilaginous Core

    Retained cartilaginous cores are most commonly seen in the distal ulna of growing large- and giant-breed dogs56 (FIGURE 7). These cores are a developmental disorder of endochondral ossification in which physeal calcification is disturbed, resulting in decreased bone growth of the ulna.57 The etiology is uncertain; however, dietary imbalances and a form of osteochondrosis have been suggested.10,57 Depending on the severity, affected dogs present with variable degrees of lameness and multiple deformities, including valgus deformity of the carpus and cranial bowing of the radius (with or without lameness). A radiolucent cartilage core in the center of the distal ulnar physis can be seen radiographically (FIGURE 7). Treatments include return to a complete, balanced diet and cessation of excessive dietary supplements in growing dogs. If clinically indicated, corrective osteotomy should be performed.10 The prognosis varies according to the degree of deformity and lameness at initial presentation.

    Ununited Anconeal Process

    Unlike small-breed dogs, in large-breed dogs, the anconeal process develops from a separate center of ossification.55 Failure of this center to fuse with the proximal ulna by 5 months of age is characteristic of ununited anconeal process (FIGURE 8). Disturbance of endochondral ossification, resulting in osteochondrosis, is presumed to be the underlying etiology.8 However, joint incongruity, growth plate trauma, excess calcium, excess weight, and genetic and hormonal factors have also been discussed.8,55 This disease is hereditary in some German shepherd lines, in which three dominant genes have been suggested for this trait.58 Treatment options are controversial and include medical management, excision of the anconeal process, attachment with a lag screw, and ulnar osteotomy.8,55,58 Combination of the latter two methods possibly provides a better prognosis than other treatment options.55

    Hereditary Disorders Affecting the Epiphyseal Plate

    Incomplete Ossification of the Humeral Condyle

    Incomplete ossification of the humeral condyle (IOHC) was first described in 1990 by Drapé59 (FIGURE 9 and FIGURE 10). Fusion of the two centers of ossification normally occurs at around 10 weeks of age. With IOHC, minor trauma may lead to condylar fracture and acute onset of lameness. Although the disease occurs early in life, the age at presentation is commonly between 3 and 8 years. This condition occurs mainly in spaniels, for which an autosomal recessive mode of inheritance has been suggested.60 It is also described for rottweilers, English pointers, wachtelhunds, German wirehaired pointers, Bernese mountain dogs, Newfoundlands, giant schnauzers, Polish lowland sheepdogs, and Labrador retrievers.61-63

    Radiographs should be obtained in 15° craniomedial to 15° caudolateral views.60 Both legs should be examined. The affected leg usually shows a fracture of the humeral condyle (FIGURE 9). If radiographs are not sufficient, computed tomography or arthroscopy may help diagnose a bilateral condition (FIGURE 10). Lag screw fixation for the fractured leg or prophylactic transcondylar fixation for the contralateral leg is the best method of treatment; however, nonunion is common with this disease.60,64 It has been suggested that dense cancellous bone, fibrous tissue, or undue motion may prevent appropriate or complete healing.60

    Ocular-Skeletal Dysplasia

    There are several reports of ocular-skeletal dysplasia in dogs.65-67 This condition occurs mainly in Labrador retrievers, but it has also been described for Samoyeds and German shepherds. Barnett and colleagues68 reported the mode of inheritance as an autosomal recessive defect. Affected dogs present with a typical "downhill conformation" (front limbs shorter than hindlimbs;FIGURE 11) and bony abnormalities, such as bone shortening in the forelegs with malformation of the humeral condyles, fracture of the lateral portion of the humeral condyle, asynchronous growth of the radius and ulna, varus deformity and secondary degenerative joint disease of the elbows, ununited and hypoplastic anconeal and/or coronoid process, and carpus valgus (FIGURE 12). Hip dysplasia and retarded tibial growth may also occur.65-67 The degree of lameness varies with severity. Cortical thickness and density of the bones can appear to be reduced, and the epiphyses and cuboid bones are larger and misshapen compared with those of normal littermates.

    The ocular component of this disease may present as night blindness. Ocular pathology includes cataracts, retinal dysplasia, and retinal detachment. The degree of vision impairment depends on severity of the lesions.65-67 Carrig and colleagues66 established a breeding colony of Labrador retrievers to further investigate the mode of inheritance of this disorder. The heterozygotes were found to have a clinically normal skeleton with mild ocular abnormalities, while homozygotes showed clinical signs of both ocular and skeletal dysplasia. It was concluded that abnormalities resulted from a single gene with recessive effects on the skeleton but with incomplete dominant effects on the eyes.66

    Depending on the degree of orthopedic and/or ophthalmologic disease, surgical treatment may be beneficial. The prognosis for complete restoration of normal orthopedic function is guarded to poor, and affected dogs should not be bred.67


    Chondrodysplasia, also commonly called dwarfism, has been described in Great Danes, Scottish deerhounds, Alaskan malamutes, Norwegian elkhounds, and miniature poodles.5 Other breeds may be affected. In contrast to ocular-skeletal dysplasia, in which limb shortening is mild, chondrodysplasia is characterized by severely shortened limbs, normal body length, and normally sized skull, leaving the impression of a disproportionate dwarf5 (FIGURE 13). The disease is genetically transmitted as a simple autosomal recessive trait. In Alaskan malamutes, it is combined with a permanent macrocytic, hypochromic anemia.69,70 Affected animals are usually not lame.

    Chondrodysplasia appears radiographically similar to rickets and can easily be misinterpreted. Radiographic changes include flaring of the distal metaphyseal borders of the radii and ulnae. Prominent curvature of the front limbs and carpus valgus are present. For Great Danes, flaring of all metaphyses, including a "trumpet-like" flaring of the distal tibia, has been described.6 Ossification of vertebral end plates and/or centers of ossification is delayed. Epiphyseal plates show delayed closure with shortened, disorganized columns of chondrocyte proliferation, swollen chondrocytes, and diminished endochondral ossification. Affected chondrocytes reveal a markedly irregular dilatation of cisternae of the rough endoplasmic reticulum.5 There may be a generalized defect involving all hyaline cartilage throughout the body. If no severe abnormalities occur, the quality of life of affected dogs may be good. However, if animals show signs of osteopenia, kyphosis, joint laxity, reduced diameter of the tracheal lumen, or angular limb deformities, the prognosis is guarded.7

    Epiphyseal Dysplasia

    Epiphyseal dysplasia is a hereditary condition characterized by delayed and irregular ossification of the cartilage of the epiphysis. Affected animals may present with painless swelling, typically on the medial aspect of the joint, limited range of motion, and recurrent locking of the joints. Radiographic findings include shortening of long bones and widening of the metaphysis, lack of radiopacity, and ossification of cartilage3 (FIGURE 14). At later stages in the disease, irregular bony enlargements with secondary joint degeneration can be observed.71 Several human cases have been reported72-74; however, only one case has been reported in the veterinary literature.3 An unpublished feline case was seen at Michigan State University in 2006 (FIGURE 14).

    Epiphyseal dysplasia develops secondary to an altered process of cell proliferation at the superficial zone of articular cartilage or a localized disturbance of the preaxial and postaxial part of the apical cap of the limb bud in early fetal development.75 The disease may also be a variant of MCE or osteochondroma arising within a joint.74 Histologically, there is intracellular accumulation of predominantly chondroitin sulfate and glycoprotein, followed by liquefaction of these materials and formation of cysts, which finally calcify.71 Alterations of bone and cartilage with hyperplastic chondrocytes and fibrous tissue interrupted by phases of normal endochondral ossification can also be seen.76 This condition may lead to pain and interference with function or to angular limb deformity. Corrective surgery may be required to restore function.75

    Premature Closure of the Distal Ulnar Physis in Skye Terriers

    Thirty years ago, Lau4 described premature closure of the distal ulnar physis in Skye terriers as a hereditary disease. Twenty-three dogs, all the offspring of two females and four males, presented with forelimb lameness between 3 and 5 months of age. Radiographic and physical examination findings included carpus valgus, lateral subluxation of the radial head, circumduction of the elbows, and decreased range of motion of the elbow joint. Lau provided evidence of a recessively inherited trait as the etiology for this disease. A similar syndrome, although not well described in genetic terms, is seen in Welsh corgis, basset hounds, and other chondrodystrophic breeds.

    Multiple Cartilaginous Exostoses

    MCE are "mini growth plates" found in random areas of metaphyseal bone50 (FIGURE 15). They are identified in cats and dogs of any age as bony proliferations on the body and spinous processes of the vertebrae; the processes of the scapula, sternum, ribs, and ischii; and the petrous portion of the temporal bones.77,78 The disease is commonly an incidental finding because animals do not usually show clinical signs. This condition was formerly called osteochondromatosis. Currently, a solitary lesion is described as osteochondroma, whereas multiple lesions are referred to as MCE.79 These malformations are a result of disturbed endochondral ossification at the periphery of the growth plate with abnormal, "benign" development of cartilage and fibrous connective tissue. MCE seem to be associated with FeLV infection in cats.80,81

    MCE are reported to occur predominantly in Siamese cats, in which the temporal bone, vertebral bodies, and spinous processes of the scapula, vertebrae, sternum, ribs, and ischium can be affected.82 The disease is a heritable entity in dogs and has been identified in the vertebrae, ribs, and long bones.83-85 Interestingly, lesions are not observed to affect long bone growth. Dogs and cats may have no clinical signs, unless the exostoses cause dysfunction of a joint or vital structure such as the trachea or spinal cord.86,87 Affected animals may present with myelopathy, commonly at younger than 1 year.80 Depending on the severity of the lesion, progressive neurologic signs may be seen. Histologically, lesions are consistent with a site of endochondral ossification.85 Clinical presentation and radiographic and histologic findings help to differentiate MCE from other benign polyostotic exostoses such as tumoral calcinosis or canine disseminated idiopathic skeletal hyperostosis.80 While the disease is often aggressive and carries a poor prognosis in cats, dogs usually have a good prognosis because the process ceases at maturity.88 However, in rare cases, transformation into malignant neoplasia several years after initial diagnosis has been reported.80


    MPS is a rare storage disease in which different lysosomal enzyme defects result in the inability to degrade glycosaminoglycans.5 Endochondral ossification is disturbed, resulting in skeletal abnormalities.

    Six subtypes of MPS (I, II, IIIA, IIIB, VI, VII) have been described in dogs and cats.89,90 Mixed-breed dogs, German shepherds, Plott hounds, rottweilers, Labrador retrievers, wirehaired dachshunds, New Zealand huntaways, miniature poodles, Chesapeake Bay retrievers, and miniature schnauzers have been reported to be affected by different types of MPS.89 The only MPS disorder with mostly neurologic signs is MPS IIIA, reported in wirehaired dachshunds and New Zealand huntaways.89 MPS I, MPS VI, and MPS VII have also been observed in cats.89,90 MPS VI occurs in Siamese cats and follows an autosomal recessive inheritance.90

    Animals present with dwarfism, a disproportionately small and broad maxilla, small ears, large paws, hip dysplasia, crepitus and hypermotility in multiple joints, and fusion of vertebral bodies with subsequent neurologic deficiencies5 (FIGURE 16 and FIGURE 17). Affected cats excrete high amounts of dermatan sulfate in their urine.90 Dermatan sulfate glycosaminoglycan (formerly called mucopolysaccharide) accumulates abnormally in several of the different subtypes of MPS disorders and is found mostly in skin tissue but also in blood vessels, heart valves, tendons, and the lungs.90 Breed-specific DNA tests have been established for the diagnosis of affected animals and for carrier detection.89 Treatment and prognosis depend on the type and severity of MPS. MPS III is usually incurable, and most animals are euthanized before 5 years of age.89


    A thorough understanding of the anatomy and physiology of the growth plate is necessary to understand the effect of nutritional imbalances, hormonal influences, and hereditary disorders on developing long bones. Early correction of each specific condition is warranted to avert permanent damage. Dogs and cats that are affected with a familial or potentially heritable problem should not be considered for breeding purposes.

    Read the companion article, "The Epiphyseal Plate: Physiology, Anatomy, and Trauma."


    To Dr. Cheri Johnson, DVM, MS, DACVIM, for editorial work, and Sandra Schallberger, Dr.med.vet., for technical support.


    Downloadable PDF

    aDr. Abood discloses that she has received financial support from Abbott Laboratories, Hill's Pet Nutrition, and Nestlé Purina PetCare Company.

    1. Craig LE. Physeal dysplasia with slipped capital femoral epiphysis in 13 cats. Vet Pathol 2001;38:92-97.

    2. Newton AL, Craig LE. Multicentric physeal dysplasia in two cats. Brief communications and case reports. Vet Pathol 2006;43:388-390.

    3. Vignoli M, Sarli G, Rossi F, et al. Dysplasia epiphysealis hemimelica in a Boxer puppy. Vet Radiol Ultrasound 2002;43(6):528-533.

    4. Lau R. Inherited premature closure of the distal ulnar physis. JAAHA 1977;13:609-612.

    5. Sande RD, Bingel SA. Animal models of dwarfism. Vet Clin North Am Small Anim Pract 1982;13(1):71-89.

    6. Bingel SA, Sande RD. Chondrodysplasia in five Great Pyrenees. JAVMA 1994;205(6):845-848.

    7. Breur GJ, Slocombe RF, Padgett GA, et al. Clinical, radiographic, pathologic and genetic features of osteochondroplasia in Scottish Deerhounds. JAVMA 1989;195(9):606-612.

    8. Piermattei DL, Flo GL, DeCamp CE. Osteochondrosis of the elbow. In: Brinker, Piermattei, and Flo's Handbook of Small Animal Orthopedics and Fracture Repair. 4th ed. St. Louis: Saunders Elsevier; 2006:339-344.

    9. Piermattei DL, Flo GL, DeCamp CE. Hypertrophic osteodystrophy. In: Brinker, Piermattei, and Flo's Handbook of Small Animal Orthopedics and Fracture Repair. 4th ed. St. Louis: Saunders Elsevier; 2006:781-784.

    10. Piermattei DL, Flo GL, DeCamp CE. Retained cartilaginous cores. In: Brinker, Piermattei, and Flo's Handbook of Small Animal Orthopedics and Fracture Repair. 4th ed. St. Louis: Saunders Elsevier; 2006:780-781.

    11. Ekman S, Carlson CS. The pathophysiology of osteochondrosis. Vet Clin North Am Small Anim Pract 1998;28(1):17-32.

    12. Richardson DC, Zentek J. Nutrition and osteochondrosis. Vet Clin North Am Small Anim Pract 1998;28(1):115-135.

    13. Kallfelz FA, Dzanis DA. Overnutrition: An epidemic problem in pet animal practice? Vet Clin North Am Small Anim Pract 1989;19(3):433-446.

    14. Hazewinkel HAW, Goedengebuure SA, Poulos PW, et al. Influences of chronic calcium excess on the skeletal development of growing Great Danes. JAAHA 1985;21:377-391.

    15. Hedhammar A, Wu FM, Krook L, et al. Overnutrition and skeletal disease. An experimental study in growing Great Dane dogs. Cornell Vet 1974;64(2):Suppl 5:5-160.

    16. Fascetti AJ. Food for thought on canine developmental orthopedic disease.Vet Surg 2006;35(3):211-213.

    17. Lopez MJ, Quinn MM, Markel MD. Associations between canine juvenile weight gain and coxofemoral joint laxity at 16 weeks of age. Vet Surg 2006;35(3):214-218.

    18. Remillard RL. Practical nutritional and dietary recommendations: minimizing clinical aspects of orthopedic diseases. Proc Western Vet Conf 1995:25-28.

    19. Association of American Feed Control Officials (AAFCO). Official Publication Association of American Feed Control Officials Incorporated. Washington, DC: AAFCO; 2009:147.

    20. Lauten SD. Nutritional risks to large-breed dogs: from weaning to geriatric years. Vet Clin North Am Small Anim Pract 2006;36(6):1345-1359.

    21. Hazewinkel HAW, Van den Brom WE, Van T Klooster AT, et al. Calcium metabolism in Great Dane dogs fed diets with various calcium and phosphorus levels. J Nutr 1991;121(11 suppl):99-106.

    22. Nap RC, Hazewinkel HA, Voorhout G, et al. Growth and skeletal development in Great Dane pups fed different levels of protein intake. J Nutr 1991;121(11 Suppl):107-113.

    23. Tanaka Y, DeLuca HF. The control of 25-hydroxyvitamin D metabolism by inorganic phosphorus. Arch Biochem Biophys 1977;154:566-574.

    24. Hall JE. Parathyroid hormone, calcitonin, calcium and phosphate metabolism, Vitamin D, bone, and teeth. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology. 11th ed. Philadelphia: Elsevier Saunders; 2006:978-995.

    25. Braden TD. Histophysiology of the growth plate and growth plate injuries. In: Smeak DD, Bojrab JM, Bloomberg MS, eds. Disease Mechanisms in Small Animal Surgery. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1993:1027-1041.

    26. Morgan JP. Radiographic diagnosis of bone disease. In: Morgan JP, ed. Radiology of Veterinary Orthopedics: Features of Diagnosis. 2nd ed. Iowa City: Iowa State University Press; 2000:116, 119.

    27. Olsson SE, Ekman S. Rickets and nutritional secondary hyperparathyroidism. In: Sumner-Smith G, ed. Bone in Clinical Orthopedics. 2nd ed. Stuttgart: Thieme; 2002:139, 142.

    28. Carter DR, Spengler DM. Biomechanics of fracture. In: Sumner-Smith G, ed. Bone in Clinical Orthopedics. 2nd ed. Stuttgart: Thieme; 2002:275.

    29. Kealy RD, Olsson SE, Monti KL, et al. Effects of limited food consumption on the incidence of hip dysplasia in growing dogs. JAVMA 1992;201(6):857-863.

    30. Glade MJ, Gupta S, Reimers TJ. Hormonal responses to high and low planes of nutrition in weanling thoroughbreds. J Anim Sci 1984;59(3):658-665.

    31. Nap RC, Hazewinkel HAW, Voorhout G, et al. The influence of the dietary protein content on growth in giant breed dogs. J Vet Comp Orthop Trauma 1993;6:1-8.

    32. Smith GK, Paster ER, Powers MY, et al. Lifelong diet restriction and radiographic evidence of osteoarthritis of the hip joint in dogs. JAVMA 2006;229:690-693.

    33. Trayhurn P, Bing C, Wood IS. Adipose tissue and adipokines—energy regulation from the human perspective. J Nutr 2006;136(7):1935S-1939S.

    34. Kealy RD, Lawler DF, Ballam JM, et al. Effects of diet restriction on life span and age-related changes in dogs. JAVMA 2002;220(9):1315-1320.

    35. Danks DM. Copper deficiency in humans. In: Biological Roles of Copper. Proceedings of the CIBA Foundation Symposium 79. Amsterdam: Excerpta Medica; 1980:163-182.

    36. Hurley LS, Keen CL. Manganese. In: Mertz W, ed. Trace Elements in Human and Animal Nutrition. Orlando, FL: Academic Press; 1986:185-223.

    37. Loder RT, Aronson DD, Bollinger RO. Seasonal variation of slipped capital femoral epiphysis. J Bone Joint Surg [Am] 1990;72(3):378-381.

    38. Greco DS, Feldman EC, Peterson ME, et al. Congenital hypothyroid dwarfism in a family of giant schnauzers. J Vet Intern Med 1991;5(5):306-307.

    39. Lieb AS, Grooters AM, Tyler JW, et al. Tetraparesis due to vertebral physeal fracture in an adult dog with congenital hypothyroidism. J Small Anim Pract 1997;38(8):364-367.

    40. Fyfe JC, Kampschmidt K, Dang V, et al. Congenital hypothyroidism with goiter in toy fox terriers. J Vet Intern Med 2003;17(1):50-57.

    41. Caruso-Nicoletti M, Cassorla F, Skerda M, et al. Short term, low dose estradiol accelerates ulnar growth in boys. J Clin Endocrinol Metab 1985;61(5):896-898.

    42. Lloyd HM, Meares JD, Jacobi J, et al. Effects of stilboestrol on growth hormone secretion and pituitary cell proliferation in the male rat. J Endocrinol 1971;51(3):473-481.

    43. Cutler GB Jr, Cassorla FG, Ross JL, et al. Pubertal growth: physiology and pathophysiology. Recent Prog Horm Res 1986;42:443-470.

    44. Salmeri KR, Bloomberg MS, Scruggs SL, et al. Gonadectomy in immature dogs: effects on skeletal, physical, and behavioral development. JAVMA 1991;198(7):1193-1203.

    45. Root MV, Johnston SD, Olson PN. The effect of prepuberal and postpuberal gonadectomy on radial physeal closure in male and female domestic cats. Vet Radiol Ultrasound 1997;38(1):42-47.

    46. McNicholas Jr WT, Wilkens BE, Blevins WE, et al. Spontaneous femoral capital physeal fractures in adult cats: 26 cases (1996-2001). JAVMA 2002;221(12):1731-1736.

    47. Dupuis J, Breton L, Drolet R. Bilateral epiphysiolysis of the femoral heads in two dogs. JAVMA 1997;210(8):1162-1165.

    48. Queen J, Bennet D, Carmichael N. Femoral neck metaphyseal osteopathy in the cat. Vet Rec 1998;142:159-162.

    49. Ridge PA. What is your diagnosis? J Small Anim Pract 2006;47:291-293.

    50. Montgomery R. Miscellaneous orthopedic diseases. In: Slatter D, ed. Textbook of Small Animal Surgery. Philadelphia: Saunders; 2003:2251-2260.

    51. Olsson SE, Reiland S. The nature of osteochondrosis in animals. Summary and conclusions with comparative aspects on osteochondritis dissecans in man. Acta Radiol Suppl

    52. Reiland S, Stromberg B, Olsson SE, et al. Osteochondrosis in growing bulls. Pathology, frequency and severity on different feedings. Acta Radiol Suppl 1978;358:179-196.

    53. Gilmore RS, Palfrey AJ. A histological study of human femoral condylar articular cartilage. J Anat 1987;155:77-85.

    54. Schulz KS, Krotscheck U. Canine elbow dysplasia. In: Slatter D, ed. Textbook of Small Animal Surgery. Philadelphia: Saunders; 2003:1930-1935, 1936.

    55. Carlson CS, Meuten DJ, Richardson DC. Ischemic necrosis of cartilage in spontaneous and experimental lesions of osteochondrosis. J Orthop Res 1991;9(3):317-329.

    56. Riser WH, Shirer JF. Normal and abnormal growth of the distal foreleg in large and giant breed dogs. J Am Vet Radiol Soc 1965;VI:50-64.

    57. Corley EA, Sutherland TM, Carlson WD. Genetic aspects of canine elbow dysplasia. JAVMA 1968;153(5):543-547.

    58. Johnson KA. Retardation of endochondral ossification at the distal ulnar growth plate in dogs. Aust Vet J 1981;57:474-478.

    59. Drapé J. Pathogénie des fractures du condyle latéral de l'humérus. Prat Méd Chir

    60. Marcellin-Little DJ, DeYoung DJ, Ferris KK, et al. Incomplete ossification of the humeral condyle in spaniels. Vet Surg 1994;23(6):475-487.

    61. Rovesti GL, Fluckiger M, Margini A, et al. Fragmented coronoid process and incomplete ossification of the humeral condyle in a Rottweiler. Vet Surg 1998;27(4):354-7.

    62. Meyer-Lindenberg A, Heinen V, Fehr M, et al. Incomplete ossification of the humeral condyle as the cause of lameness in dogs. Vet Comp Orthop Traumatol 2002;15(3):187-194.

    63. Gnudi G, Martini FM, Zanichelli S, et al. Incomplete humeral condylar fracture in two English pointer dogs. Vet Comp Orthop Traumatol 2005;18(4):243-245.

    64. Marcellin-Little DL, Roe SC, DeYoung DJ. What is your diagnosis? Faint vertical condylar radiolucency, secondary to incomplete ossification of the humeral condyle. JAVMA 1996;209(4):727-728.

    65. Meyers VN, Jezyk PF, Aguirre GD, et al. Short-limbed dwarf-ism and ocular defects in the Samoyed dog. JAVMA 1983;183(9):975-979.

    66. Carrig CB, Sponenberg DP, Schmidt GM, et al. Inheritance of associated ocular and skeletal dysplasia in Labrador retrievers. JAVMA 1988;193(10):1269-1272.

    67. Cook JL, Jordan RC. What is your diagnosis: retinal dysplasia with concurrent developmental skeletal abnormalities in Labrador retrievers. JAAHA 1997;210(3):329-330.

    68. Barnett KC, Bjork GR, Kock E. Hereditary retinal dysplasia in the Labrador retriever in England and Sweden. J Small Anim Pract 1970;10:755-759.

    69. Fletch SM, Pinkerton PH, Brueckner PJ. The Alaskan malamute chondrodysplasia syndrome in review. JAAHA 1975;11:149-152.

    70. Fletch SM, Smart ME, Pennock PW, et al. Clinical and pathological features of chondrodysplasia (dwarfism-anemia) syndrome in review. JAVMA 1973;162:357-361.

    71. Rasmussen PG. Multiple epiphyseal dysplasia. Morphological and histochemical investigation of cartilage matrix, particularly in the pre-calcification stage. Acta Pathol Microbiol Scand 1975;83(5):493-502.

    72. Azouz EM, Slomic AM, Marton D, et al. The variable manifestations of dysplasia epiphysealis hemimelica. Pediatr Radiol 1985;15(1):44-49.

    73. Acquaviva A, Municchi G, Marconcini S, et al. Dysplasia epiphysealis hemimelica in a young girl: role of MRI in the diagnosis and follow-up. Joint Bone Spine 2005;72(2):183-186.

    74. Hensinger RN, Cowell HR, Ramsey PL, et al. Familial dysplasia epiphysealis hemimelica, associated with chondromas and osteochondromas. Report of a kindred with variable presentations. J Bone Joint Surg [Am] 1974;56(7):1513-1516.

    75. Kuo RS, Bellemore MC, Monsell FP, et al. Dysplasia epiphysealis hemimelica: clinical features and management. J Pediatr Orthop 1998;18(4):543-548.

    76. Martens M, Tanghe W, Mulier JC. Hemimelic epiphyseal dysplasia. Acta Orthop Belg 1968;34(4):625-644.

    77. Riddle WE, Leighton RL. Osteochondromatosis in a cat. JAVMA 1970;156:1428-1430.

    78. Pool RR, Carrig CB. Multiple cartilaginous exostoses in a cat. Vet Pathol 1972;9:350-359.

    79. Franch J, Font J, Ramis A, et al. Multiple cartilaginous exostosis in a golden retriever cross-bred puppy. Clinical, radiographic and backscattered scanning microscopy findings. Vet Comp Orthop Traumatol 2005;18(3):189-193.

    80. Jacobson LS, Kirberger RM. Canine multiple cartilaginous exostoses: unusual manifestations and a review of the literature. JAAHA 1996;32(1):45-51.

    81. Alexander JW. Selected skeletal dysplasia: craniomandibular osteopathy, multiple cartilaginous exostoses, and hypertrophic osteodystrophy. Vet Clin North Am Small Anim Pract 1983;13:55.

    82. Brown JH, DeLuca SA. Growth plate injuries: Salter-Harris classification. Am Fam Phys 1992;46(4):1180-1184.

    83. Goldschmidt MH, Thrall DE. Benign bone tumors in the dog. In: Newton CD, Nunamaker DM, eds. Textbook of Small Animal Orthopaedics. Philadelphia: Lippincott; 1985:900.

    84. Chester DK. Multiple cartilaginous exostoses in two generations of dogs. JAVMA 1971;159(7):895-897.

    85. Gambardella PC, Osborne CA, Stevens JB. Multiple cartilaginous exostoses in the dog. JAVMA 1975;166(8):761-768.

    86. Beck JA, Simpson DJ, Tisdall PL. Surgical management of osteochondromatosis affecting the vertebrae and trachea in an Alaskan malamute. Aust Vet J 1999;77(1):21-23.

    87. Prata RG, Stoll SG, Zaki FA. Spinal cord compression caused by osteocartilaginous exostoses of the spine in two dogs. JAVMA 1975;166(4):371-375.

    88. Dewey C, Coates JR. Cartilagenous exostoses. In: Slatter D, ed. Textbook of Small Animal Surgery. 3rd ed. Philadelphia: Saunders; 2003:1211.

    89. Wang P, Seng A, Huff A, et al. Mucopolysaccharidosis in dogs and cats: clinical signs to DNA tests. Proc Canine Feline Breeding Genetics Conf 2005. Accessed June 2009 at vin.com/proceedings/Proceedings.plx?CID=TUFTSBG2005&PID=10662&Category=1485&O=Generic.

    90. Haskins ME, Jezyk PF, Patterson DF. Mucopolysaccharide storage disease in three families of cats with arylsulfatase B deficiency: Leukocyte studies and carrier identification. Pediatr Res 1979;13(11):1203-1210.

    References »

    NEXT: The Epiphyseal Plate: Physiology, Anatomy, and Trauma

    CETEST This course is approved for 3.0 CE credits

    Start Test


    Did you know... Metacarpal and metatarsal fractures are common in small animal practice, accounting for 8.1% to 11% of all fractures in dogsRead More

    These Care Guides are written to help your clients understand common conditions. They are formatted to print and give to your clients for their information.

    Stay on top of all our latest content — sign up for the Vetlearn newsletters.
    • More