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

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❯❯ Dirsko J. F. von Pfeil, Abstract: This article reviews nutritional and hormonal influences, diseases with uncertain etiol- Dr.med.vet, DVM, DACVS, ogy, and hereditary disorders affecting the growth and development of the long bones in dogs DECVS and cats. Veterinary Specialists of Alaska Anchorage, Alaska ❯❯ Charles E. DeCamp, utritional, hormonal, and genetic prevalence of musculoskeletal disorders is DVM, MS, DACVS factors play important roles in the reported to be 22% in dogs younger than 1 growth of animals.1–15 For example, year.12 Of these cases, 20% are thought to Sarah K. Abood, DVM, PhDa N 12 Michigan State University unbalanced or incomplete diets can result be nutrition related. Deficiencies in vita- in growth abnormalities.1–15 Hormonal fac- min D or trace elements, excessive calcium tors, such as prepubertal gonadectomy, or vitamin C, and high energy intake have have been associated with delayed closure been discussed as reasons for developmen- of growth plates in cats, which increases the tal growth abnormalities.12–15 Calcium and risk of slipped capital femoral epiphysiolysis energy are two of the most important fac- (SCFE) and may also affect the distal radius tors.16 Commercially prepared large-breed and femur.1,2 Documented hereditary disor- puppy diets that meet the nutritional guide- ders affecting the epiphyseal plate include lines of the Association of American Feed At a Glance ocular-skeletal dysplasia, dwarfism, canine Control Officials (AAFCO) and are labeled epiphyseal dysplasia, premature closure of “complete and balanced” should be fed to Nutrition Page E1 the ulna in Skye terriers, multiple cartilagi- growing large-breed dogs until they reach nous exostoses (MCE), and mucopolysaccha- approximately 80% of their mature size.18 Hormonal Influences ridosis (MPS).3–7 Osteochondrosis dissecans Smaller dogs can be fed puppy diets until Page E3 of the articular cartilage is a common dis- approximately 1 year of age and should Diseases With Uncertain ease in growing dogs, but diseases of the then be switched to an adult diet.12,18–20 Etiology epiphyseal cartilage, including hypertrophic Recommended levels of key nutrients in a Page E4 osteodystrophy, retained cartilaginous core, diet to prevent orthopedic disease in large- Hereditary Disorders and ununited anconeal process, can also be breed puppies are summarized in Table 1. Affecting the Epiphyseal observed.8,9 The etiology of these conditions Plate appears to be multifactorial,16,17 and further Calcium Page E6 research is warranted to better understand, Excess feeding (>3% of dry matter) of prevent, and treat these diseases. calcium increases the risk of slowing chondrocyte maturation, which can lead Nutrition to the development of retained cartilagi- a Dr. Abood discloses that she Musculoskeletal disorders are common in nous cores and, in some cases, angular has received financial support young dogs but uncommon in cats. The limb deformity.16 Osteochondrosis dissecans from Abbott Laboratories, Hill’s Pet Nutrition, and Nestlé Purina *A companion article, “The Epiphyseal Plate: Physiology, Anatomy, and Trauma,” is also available PetCare Company. on CompendiumVet.com.

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table 1 Recommended Ranges of Key Nutrients and Energy Content in a Diet for Large-Breed Puppies18

Nutrient Percentage on Dry Matter Basis Amount Fed as Canned Protein 29–34 6%–8% Fat 11–16 2%–4% Mean energy content 3.4–4.1 13.4–15.9 KJ/g DMB Calcium 0.8–1.4 — Phosphorus 0.7–1.2 — Fiber 2.4–5.6 1%

KJ/g = kilojoule per gram; DMB = dry matter basis

may also develop with a calcium-rich diet.14,21 Phosphorus Growing giant-breed dogs fed high-calcium Imbalances of dietary phosphorus intake can diets (>3% of dry matter as calcium) experi- affect calcium homeostasis and may influence ence greater development of osteochondrosis bone metabolism.21 Low dietary phosphorus is than control dogs.14,21,22 Even when dietary uncommon but has been reported to increase phosphorus is adjusted to maintain a physi- calcium and phosphorus absorption in the QuickNotes ologic calcium:phosphorus ratio, osteochon- gut.20,23 Clinical signs can include poor weight drosis can still occur.14,21 gain and reduced growth rate.20,23 By contrast, Disorders of the excessively high phosphorus levels can stim- growth plate and ulate hormone secretion (secondary hyper- FIGURE 1 diseases of young parathyroidism), which decreases calcium ab- bone and cartilage sorption.20 The result is poorly calcified, soft can be affected bones that are predisposed to pathologic 15–18 by unbalanced fractures. It is therefore recommended to maintain a dietary calcium:phosphorus ratio nutrition. 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, Rickets in a 5-year-old chimpanzee. Note the lameness, pain, angular limb deformation, extremely widened and radiolucent physes (arrows) of and pathologic fractures.13,25 Radiographs typi- the pelvis, femora, and tibiae, typical of this disease. cally show thickened physeal cartilage plates Excessive vitamin D deficiency may prevent the cal- and “cupping” of the metaphyseal bone with a cification process in the metaphyses. This disease is 26 Figure 1 extremely rare in dogs and cats in developed countries dense sclerotic margin ( ). Histology because of the availability of well-balanced commer- shows severe enlargement of the chondrocytes cial veterinary diets. (Courtesy of Dr. Tobias Schwarz, in the growth plate.27 Rickets is extremely rare University of Wisconsin-Madison) in dogs and cats being fed commercially avail-

E2 Compendium: Continuing Education for Veterinarians® | July 2009 | CompendiumVet.com FREE The Epiphyseal Plate: Influences and Disorders CE able pet foods.13 However, it may occur in been shown to promote the development of other small companion animals. thickened, short, disproportionate long bones; abnormal ossification of the skull; and otoliths Energy in the inner ear.36 However, no clinical cases The metabolic activity of growing bones is high of manganese deficiency have been reported. during an animal’s first year of life. Compared with mature bone, growing bone is softer and Hormonal Influences more predisposed to injury from minor trauma.28 As in people, congenital hypothyroidism has This risk increases when a high-calorie diet is fed, been documented to cause severe abnormali especially in fast-growing, large-breed dogs.15,29 t ie s i n d og s. 37–40 L ieb a nd c ol le a g ue s 39 described Foods high in dietary fat or protein have been a 4-year-old dog with congenital hypothyroid- shown to increase growth rate and affect hor- ism that presented with tetraparesis due to ver- monal regulatory mechanisms.12,30 Insulin-like tebral physeal fracture. This dog also showed growth factor, growth hormone, thyroid hor- skeletal immaturity in the long bones. Greco mone, and other hormones are overexpressed, et al38 reported congenital hypothyroid dwarf- reflecting an increased metabolic state and ism in five giant schnauzers of the same fam- increased bone formation.22 This leads to the ily. When treated with levothyroxine before 4 formation of a less dense spongiosa, and the months of age, puppies responded with com- comparably weak subchondral bone and thicker, plete remission.38 A similar report in toy fox weaker growth plate predispose these dogs to terriers described the heritability of congenital mechanical injuries.16 One study showed that hypothyroidism; a DNA-based carrier test has dogs fed ad libitum diets containing excessive been developed and is used to prevent breed- amounts of protein, calcium, phosphorus, and ing of affected dogs.40 vitamin D had slow cartilage maturation and Sex hormones influence the time of growth QuickNotes developed osteochondrosis.15 In contrast, more plate closure.41–43 Compared with animals that recent studies have shown that high amounts of do not undergo gonadectomy, male and female Commercially pre- dietary protein are unlikely to play a causative kittens and puppies neutered at the age of 7 pared canine foods role in the development of osteochondrosis in weeks can have significantly delayed physeal that meet the nutri- dogs.31 closure and greater radial length.44,45 Bone vol- tional guidelines Excessive dietary protein and fat also ume in these animals is also decreased, presum- of the Association 45 increase total body weight, which could lead to ably due to decreased osteoblast function. of American Feed obesity as well as secondary changes in joints32 and prolonged epiphyseal plate maturation. Slipped Capital Femoral Epiphysiolysis Control Officials for Adipocytes have been shown to be related The skeletal changes associated with prepu- all life stages and to the development of arthritis by the release bertal gonadectomy have been associated with that are labeled of adipokines, which are linked to immunity an increased risk for developing SCFE in cats “complete and and inflammation.33 Feeding commercial dry and, rarely, in dogs1,46,47 (Figure 2). Animals balanced” should diets with an energy density below 4.0 kcal/g are lame in the affected hindlimb; the dura- be fed until a can help minimize the negative effects of high tion and severity of the lameness vary.46 Serial large-breed puppy 12 calorie intake. Restricted total dietary intake radiographs are usually used to make the diag- reaches approxi- has been associated with decreased develop- nosis, and it has been demonstrated that dys- mately 80% of its ment of hip dysplasia and arthritis in several plasia can occur in multiple physes in the same joints, as well as with increased life span and animal. The distal femoral and distal radial epi- mature size. delayed onset of chronic disease.34 physes can be affected concurrent with SCFE.2 Histologic changes in the growth plate of cats Other Nutrients with SCFE include loss of normal columnar Copper, zinc, and manganese also affect epiphy- architecture of chondrocytes, chondrocyte seal growth.12 Although rare, copper deficiency clustering (Figure 3), granulation tissue within can impair the metabolism of collagen and the growth plate, physeal clefts with necrosis, elastin.35 Zinc deficiencies can lead to impaired and wider growth plates (up to twice normal).1,2 growth and skeletal development as well as skin These findings are similar to those in SCFE in problems and decreased immune function.12 people (obese, adolescent boys are most com- Experimentally, manganese deficiency has monly affected).1 In a study of SCFE in cats,1 all

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FIGURE 2 FIGURE 3

Slipped capital femoral epiphysiolysis (SCFE) in a 10-month-old castrated Siamese cat. Note the obvious injury on the left (arrow) and mild mediodistal displace- ment of the femoral capital epiphysis on the right (ellipse).

affected animals were 5 to 24 months old, 85% Irregular chondrocyte clusters (ellipse) were male, 23% were Siamese, and 90% were attached to the metaphysis of a cat with obese. These cats were neutered between 4 SCFE secondary to dysplasia of the epiphyseal plate. and 8 months of age.46 Depending on the clini- (Hematoxylin–eosin stain; original magnification × 10; QuickNotes courtesy of Dr. Linden Craig, University of Tennessee) cal signs, conservative treatment or surgery The recommended (e.g., femoral head and neck ostectomy) may FIGURE 4 percentages, on a be indicated. dry matter basis, of key nutrients Diseases With Uncertain Etiology in a diet for large- Femoral Neck Metaphyseal Osteopathy in Cats breed puppies to Cats with metaphyseal osteopathy develop minimize the risk of necrosis in the proximal metaphysis, which orthopedic disease eventually results in a secondary, pathologic are as follows: pro- fracture of the femoral neck48 (Figure 4). The tein, 29% to 34%; condition may be unilateral or bilateral. Adult fat, 11% to 16%; male cats (neutered and intact) are overrep- mean energy, 3.4% resented. Lameness originates from the coxo to 4.1%; calcium, femoral joint. Unlike SCFE, radiographs show 0.8% to 1.4%; phos- characteristic chronic degenerative changes in the femoral neck region, including areas phorus, 0.7% to of radiolucency, bone resorption, an “apple- 1.2%; fiber, 2.4% to core” appearance, or an irregular radiolucent 5.6%. fracture line.48,49 Several etiologies have been proposed: traumatic fracture with secondary bone resorption, avascular necrosis, osteomy- Femoral neck metaphyseal osteopathy in a elitis, feline herpesvirus, and changes second- 2-year-old castrated cat. Note the severely irregular ary to SCFE.48,49 Histology does not show the changes around the femoral necks. This radiographic appearance may represent changes secondary to SCFE. typical features of SCFE but may include bone necrosis and microfracture, fibrosis, metaplasia, osteomyelitis, and synovitis of the surrounding Hypertrophic Osteodystrophy connective tissue.48,49 Excision of the femoral Hypertrophic osteodystrophy is seen in grow- head and neck carries a good prognosis.48,49 ing large- or giant-breed dogs with open

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FIGURE 5 epiphyseal plates.9 until the cartilage becomes avascular. Studies Affected animals of pigs and chickens in which ischemia was present with intermit- induced have demonstrated that, at some point tent lameness, fever, during growth, the viability of cartilage cells and extremely pain- depends on the integrity of cartilage canal ful, swollen distal vessels.11 Aside from ischemia, other etiologies, metaphyses of the such as hereditary factors, rapid growth, and long bones. A radio- nutritional imbalances, have been suggested lucent line parallel to cause osteochondrosis.27 to the growth plate Osteochondrosis results in failure of matrix (pseudophyseal line) calcification, with retention of cartilage rather is the hallmark of than conversion to bone, leading to a thick- the disease. Possible ened, weaker growth plate. Excessive caloric causes of this line intake has been suggested to be a risk factor include increased leu- in the development of increased articular car- kocyte activity, bone tilage thickness, but high dietary protein alone lysis, and failure of is unlikely to be the cause of osteochondrosis ossification of the in dogs.22,54 Damage to the cartilage structures, hypertrophic zone.50 retained cartilaginous cores, and asymmetric Large, swollen, dense growth may be consequences of this process.27 m e t a p h y s e s a n d p e r i o - Histologic examination of the lesions may reveal steal exostosis com- areas of necrotic chondrocytes in the reserve plete the classic radio- zone, close to necrotic vascular channels.55 graphic appearance When osteochondrosis affects the articular Typical radiographic QuickNotes appearance of the dis- (Figure 5). surface, lesions consist of necrotic cartilage with tal radius and ulna of The etiology of hyper- a cleft extending from the subchondral bone to Clients feeding a a dog with hypertro- trophic osteodystrophy the articular surface, resulting in synovitis, joint growing dog or cat phic osteodystrophy. i s u n k n o w n . N u t r i t i o n a l effusion, and clinical signs of lameness.11 This a homemade diet Note the “double physeal (vitamin C deficiency) form of osteochondrosis is called osteochon- line” (arrows), extra- and (raw or cooked) and viral (distemper drosis dissecans (Figure 6). Treatment consists subperiosteal bone forma- should have the diet virus) factors have been of removal of loose cartilage and debridement tion at the metaphysis and evaluated and their suggested.50 However, of subchondral bone. The prognosis varies diaphysis, and widening of pet examined by a the epiphyseal plate of the these theories remain depending on the affected joint and advance- distal radius and ulna. unproven. The disease ment of arthritis. veterinarian at least is usually self-limiting, twice yearly. but affected dogs can be extremely ill. Treatment Retained Cartilaginous Core consists of supportive care. Permanent bone Retained cartilaginous cores are most com- changes, angular limb deformities second- monly seen in the distal ulna of growing large- ary to asymmetric or asynchronous growth and giant-breed dogs56 (Figure 7). These cores or bridging of bone, and retardation of axial are a developmental disorder of endochon- growth have been reported.9,50 dral ossification in which physeal calcification is disturbed, resulting in decreased bone Osteochondrosis growth of the ulna.57 The etiology is uncer- Osteochondrosis is a multifocal disease with tain; however, dietary imbalances and a form incomplete endochondral ossification of the of osteochondrosis have been suggested.10,57 articular-epiphyseal cartilage. It has also been Depending on the severity, affected dogs reported to affect the cartilage of the epiphy- present with variable degrees of lameness and seal growth plate.51,52 multiple deformities, including valgus defor- The etiology of osteochondrosis is not clear. mity of the carpus and cranial bowing of the Early in an animal’s development, blood ves- radius (with or without lameness). A radiolu- sels, nerves, and lymphatics supply the epiphy- cent cartilage core in the center of the dis- seal cartilage.53 As the animal ages and gains tal ulnar physis can be seen radiographically weight, the number of blood vessels decreases (Figure 7). Treatments include return to a com-

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FIGURE 6 FIGURE 8

Lateral radiograph of the shoulder joint Ununited anconeal process (arrowhead) in a showing osteochondrosis dissecans on 7-month-old German shepherd. Normal closure the caudal aspect of the humeral head (arrow) in a time is approximately 5 months of age. 10-month-old rottweiler. ing to the degree of deformity and lameness at QuickNotes FIGURE 7 initial presentation. Gonadectomy at Ununited Anconeal Process an early age can Unlike small-breed dogs, in large-breed dogs, lead to significantly the anconeal process develops from a sepa- delayed physeal rate center of ossification.55 Failure of this cen- closure and slipped ter to fuse with the proximal ulna by 5 months capital femoral epi- of age is characteristic of ununited anconeal process (Figure 8). Disturbance of endochon- physiolysis (SCFE) dral ossification, resulting in osteochondrosis, in cats and, rarely, is presumed to be the underlying etiology.8 dogs. The distal However, joint incongruity, growth plate femoral and distal trauma, excess calcium, excess weight, and radial epiphysis can genetic and hormonal factors have also been be affected concur- discussed.8,55 This disease is hereditary in rent with SCFE. 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 Lateral radiograph of the distal radius and anconeal process, attachment with a lag screw, 8,55,58 ulna in a 5-month-old Newfoundland with a and ulnar osteotomy. Combination of the retained cartilaginous core. Note the “flame-like” latter two methods possibly provides a better radiolucent area in the center of the ulnar growth plate prognosis than other treatment options.55 enclosed by two radiodense lines (box), which is diag- nostic for this condition. Hereditary Disorders Affecting the Epiphyseal Plate plete, balanced diet and cessation of excessive Incomplete Ossification dietary supplements in growing dogs. If clini- of the Humeral Condyle cally indicated, corrective osteotomy should Incomplete ossification of the humeral condyle be performed.10 The prognosis varies accord- (IOHC) was first described in 1990 by Drapé59

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FIGURE 9 FIGURE 10 A

QuickNotes Anteroposterior radiograph showing a fracture B of the lateral epicondyle of the humerus in a Osteochondrosis, 6-year-old cocker spaniel. This breed is predisposed to incomplete ossifica- incomplete ossification of the humeral condyle. tion of the humeral condyle, retained (Figures 9 and 10). Fusion of the two centers cartilaginous of ossification normally occurs at around 10 core, and ununited weeks of age. With IOHC, minor trauma may lead to condylar fracture and acute onset of anconeal process lameness. Although the disease occurs early should be on the dif- in life, the age at presentation is commonly ferential diagnosis between 3 and 8 years. This condition occurs for young animals mainly in spaniels, for which an autosomal with orthopedic recessive mode of inheritance has been sug- problems affecting gested.60 It is also described for rottweil- the growth plate. ers, English pointers, wachtelhunds, German wirehaired pointers, Bernese mountain dogs, Newfoundlands, giant schnauzers, Polish low- land sheepdogs, and Labrador retrievers.61–63 Radiographs should be obtained in 15° cran- iomedial to 15° caudolateral views.60 Both legs should be examined. The affected leg usually shows a fracture of the humeral condyle Images of the contralateral humeral condyle (Figure 9). If radiographs are not sufficient, of the dog in Figure 9. The dog was not lame or computed tomography or arthroscopy may help painful in this leg. (A) Anteroposterior radiograph. (B) While difficult to see on radiographs, a radiolucent line diagnose a bilateral condition (Figure 10). Lag separating the two condyles (ellipse) and minimal dis- screw fixation for the fractured leg or prophy- placement is visible on computed tomography. To pre- lactic transcondylar fixation for the contralateral vent fracture in the future, a prophylactic intercondylar leg is the best method of treatment; however, screw was placed.

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FIGURE 11 FIGURE 12 A B

One-year-old Labrador retriever with ocular- skeletal dysplasia, showing the typical downhill conformation with bone shortening in the forelegs and Radiographs of the dog in Figure 11, showing carpus valgus. (Courtesy of Dr. Ullrich Reif, Tierklinik malformation of the humeral condyles, asynchronous Böbingen/Schwäbisch Gmünd, Germany) QuickNotes growth of the radius and ulna, and carpus valgus. (A) Lateral view. (B) Anteroposterior view. Genetic disorders nonunion is common with this disease.60,64 It such as epiphyseal has been suggested that dense cancellous bone, The ocular component of this disease may dysplasia, ocular- fibrous tissue, or undue motion may prevent present as night blindness. Ocular pathology skeletal dysplasia, appropriate or complete healing.60 includes cataracts, retinal dysplasia, and retinal chondrodysplasia, detachment. The degree of vision impairment 65–67 multiple cartilagi- Ocular-Skeletal Dysplasia depends on severity of the lesions. Carrig There are several reports of ocular-skeletal dys- and colleagues66 established a breeding colony nous exostoses, and plasia in dogs. 65–67 This condition occurs mainly in of Labrador retrievers to further investigate mucopolysaccha- Labrador retrievers, but it has also been described the mode of inheritance of this disorder. The ridosis should also for Samoyeds and German shepherds. Barnett heterozygotes were found to have a clinically be included in the and colleagues68 reported the mode of inheri- normal skeleton with mild ocular abnormali- differential diag- tance as an autosomal recessive defect. Affected ties, while homozygotes showed clinical signs nosis for growth dogs present with a typical “downhill conforma- of both ocular and skeletal dysplasia. It was con- abnormalities. tion” (front limbs shorter than hindlimbs; Figure cluded that abnormalities resulted from a single 11) and bony abnormalities, such as bone short- gene with recessive effects on the skeleton but ening in the forelegs with malformation of the with incomplete dominant effects on the eyes.66 humeral condyles, fracture of the lateral portion Depending on the degree of orthopedic and/ of the humeral condyle, asynchronous growth or ophthalmologic disease, surgical treatment may of the radius and ulna, varus deformity and sec- be beneficial. The prognosis for complete restora- ondary degenerative joint disease of the elbows, tion of normal orthopedic function is guarded to ununited and hypoplastic anconeal and/or coro- poor, and affected dogs should not be bred.67 noid process, and carpus valgus (Figure 12). Hip dysplasia and retarded tibial growth may also Chondrodysplasia occur.65–67 The degree of lameness varies with Chondrodysplasia, also commonly called dwarf- severity. Cortical thickness and density of the ism, has been described in Great Danes, Scottish bones can appear to be reduced, and the epiphy- deerhounds, Alaskan malamutes, Norwegian elk- ses and cuboid bones are larger and misshapen hounds, and miniature poodles.5 Other breeds compared with those of normal littermates. may be affected. In contrast to ocular-skeletal

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FIGURE 13 FIGURE 14

A 5-year-old golden retriever with chondrodysplasia (dwarfism). Note the short legs compared with the large body and head. 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 dwarf 5 (Figure 13). The disease is genetically transmitted as a simple autosomal recessive trait. In Alaskan malamutes, it is com- bined with a permanent macrocytic, hypochro- mic anemia.69,70 Affected animals are usually not Epiphyseal dysplasia in a 6-month-old cat lame. with chronic hindlimb lameness. Radiographic QuickNotes Chondrodysplasia appears radiographically changes are lack of radiopacity and ossification of similar to rickets and can easily be misin- cartilage (ellipse). Secondary joint degeneration can be Typical radiographic terpreted. Radiographic changes include flar- expected at a later stage. findings for epi- ing of the distal metaphyseal borders of the physeal dysplasia radii and ulnae. Prominent curvature of the Affected animals may present with painless include shortening front limbs and carpus valgus are present. For swelling, typically on the medial aspect of the of long bones and Great Danes, flaring of all metaphyses, includ- joint, limited range of motion, and recurrent widening of the ing a “trumpet-like” flaring of the distal tibia, locking of the joints. Radiographic findings has been described.6 Ossification of vertebral include shortening of long bones and widen- metaphysis, lack end plates and/or centers of ossification is ing of the metaphysis, lack of radiopacity, and of radiopacity, and delayed. Epiphyseal plates show delayed clo- ossification of cartilage3 (Figure 14). At later ossification of sure with shortened, disorganized columns of stages in the disease, irregular bony enlarge- cartilage. chondrocyte proliferation, swollen chondro- ments with secondary joint degeneration can cytes, and diminished endochondral ossifica- be observed.71 Several human cases have tion. Affected chondrocytes reveal a markedly been reported72–74; however, only one case has irregular dilatation of cisternae of the rough been reported in the veterinary literature.3 An endoplasmic reticulum.5 There may be a gen- unpublished feline case was seen at Michigan eralized defect involving all hyaline cartilage State University in 2006 (Figure 14). throughout the body. If no severe abnormali- Epiphyseal dysplasia develops secondary to ties occur, the quality of life of affected dogs an altered process of cell proliferation at the may be good. However, if animals show signs superficial zone of articular cartilage or a local- of osteopenia, kyphosis, joint laxity, reduced ized disturbance of the preaxial and postaxial diameter of the tracheal lumen, or angular part of the apical cap of the limb bud in early limb deformities, the prognosis is guarded.7 fetal development.75 The disease may also be a variant of MCE or osteochondroma arising Epiphyseal Dysplasia within a joint.74 Histologically, there is intra Epiphyseal dysplasia is a hereditary condi- cellular accumulation of predominantly chon- tion characterized by delayed and irregular droitin sulfate and glycoprotein, followed by ossification of the cartilage of the epiphysis. liquefaction of these materials and formation

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FIGURE 15 processes of the scapula, sternum, ribs, and ischii; and the petrous portion of the temporal bones.77,78 The disease is commonly an inci- dental 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 Multiple cartilaginous exostoses in a dog. Note the bony changes on the spinous processes of the cranial thoracic vertebral bodies (ellipse) and at the sixth and the scapula, vertebrae, sternum, ribs, and 82 seventh ribs (arrow). ischium can be affected. The disease is a heritable entity in dogs and has been identi- of cysts, which finally calcify.71 Alterations of fied in the vertebrae, ribs, and long bones.83–85 bone and cartilage with hyperplastic chondro- Interestingly, lesions are not observed to affect cytes and fibrous tissue interrupted by phases long bone growth. Dogs and cats may have QuickNotes of normal endochondral ossification can also no clinical signs, unless the exostoses cause be seen.76 This condition may lead to pain and dysfunction of a joint or vital structure such Multiple cartilagi- interference with function or to angular limb as the trachea or spinal cord.86,87 Affected ani- nous exostoses are deformity. Corrective surgery may be required mals may present with myelopathy, commonly “mini growth plates” to restore function.75 at younger than 1 year.80 Depending on the in random areas of severity of the lesion, progressive neurologic metaphyseal bone. Premature Closure of the Distal Ulnar signs may be seen. Histologically, lesions are Physis in Skye Terriers consistent with a site of endochondral ossifi- Thirty years ago, Lau4 described premature cation.85 Clinical presentation and radiographic closure of the distal ulnar physis in Skye terri- and histologic findings help to differentiate ers as a hereditary disease. Twenty-three dogs, MCE from other benign polyostotic exostoses all the offspring of two females and four males, such as tumoral calcinosis or canine dissemi- presented with forelimb lameness between 3 nated idiopathic skeletal hyperostosis.80 While and 5 months of age. Radiographic and physi- the disease is often aggressive and carries a cal examination findings included carpus poor prognosis in cats, dogs usually have a valgus, lateral subluxation of the radial head, good prognosis because the process ceases circumduction of the elbows, and decreased at maturity.88 However, in rare cases, transfor- range of motion of the elbow joint. Lau pro- mation into malignant neoplasia several years vided evidence of a recessively inherited trait after initial diagnosis has been reported.80 as the etiology for this disease. A similar syndrome, although not well described in genetic Mucopolysaccharidosis terms, is seen in Welsh corgis, basset hounds, MPS is a rare storage disease in which dif- and other chondrodystrophic breeds. ferent lysosomal enzyme defects result in the inability to degrade glycosaminoglycans.5 Multiple Cartilaginous Exostoses Endochondral ossification is disturbed, result- MCE are “mini growth plates” found in ran- ing in skeletal abnormalities. dom areas of metaphyseal bone50 (Figure Six subtypes of MPS (I, II, IIIA, IIIB, VI, 15). They are identified in cats and dogs of VII) have been described in dogs and cats.89,90 any age as bony proliferations on the body Mixed-breed dogs, German shepherds, Plott and spinous processes of the vertebrae; the hounds, rottweilers, Labrador retrievers, wire-

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FIGURE 16 FIGURE 17

QuickNotes Mucopolysaccharidosis is associated with Typical phenotype of mucopolysaccharido- dwarfism, small ears, sis in a cat. Note the small ears and large head. This cat also had crepitus and hypermotility in several joints. large paws, pathologic changes in multiple joints, and neurologic haired dachshunds, New Zealand huntaways, miniature poodles, Chesapeake Bay retrievers, deficiencies. 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 dachs- Mucopolysaccharidosis in a cat showing 89 hunds and New Zealand huntaways. MPS I, dysplastic hip joints with generalized radiolucency MPS VI, and MPS VII have also been observed of the acetabulum, head, neck, and subtrochanteric in cats.89,90 MPS VI occurs in Siamese cats and area of the femur. Also note generalized radiolucency follows an autosomal recessive inheritance.90 of the distal femoral condyles and tibiae and the mild Animals present with dwarfism, a dispro- varus deformity (medial bowing) at the level of the knee joints. (Courtesy of Drs. Van Knox, Susquehanna portionately small and broad maxilla, small Veterinary Imaging, LLC, and Mark Haskins, University ears, large paws, hip dysplasia, crepitus and of Pennsylvania) hypermotility in multiple joints, and fusion of vertebral bodies with subsequent neurologic deficiencies5 (Figures 16 and 17). Affected cats heart valves, tendons, and the lungs.90 Breed- excrete high amounts of dermatan sulfate in specific DNA tests have been established for their urine.90 Dermatan sulfate glycosamino- the diagnosis of affected animals and for glycan (formerly called mucopolysaccharide) carrier detection.89 Treatment and prognosis accumulates abnormally in several of the dif- depend on the type and severity of MPS. MPS ferent subtypes of MPS disorders and is found III is usually incurable, and most animals are mostly in skin tissue but also in blood vessels, euthanized before 5 years of age.89

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Conclusion affected with a familial or potentially heritable A thorough understanding of the anatomy and problem should not be considered for breed- physiology of the growth plate is necessary to ing purposes. understand the effect of nutritional imbalances, hormonal influences, and hereditary disorders Acknowledgments on developing long bones. Early correction of To Dr. Cheri Johnson, DVM, MS, DACVIM, for edito- each specific condition is warranted to avert rial work, and Sandra Schallberger, Dr.med.vet., for permanent damage. Dogs and cats that are technical support.

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1. What is the recommended percentage of c. a circular defect in the articular cartilage 8. ______has/have been implicated in the calcium on a dry matter basis in food for d. flaring of the distal metaphyseal bor- etiology of osteochondrosis. large-breed puppies? ders of the radius and ulna a. Nutritional factors a. 0.3% to 1.5% d. 7.4% to 8.1% e. endosteal proliferation b. Hereditary factors b. 0.8% to 1.4% e. 25% to 30% c. Rapid growth c. 3.2% to 3.8% 5. Ocular-skeletal dysplasia occurs most d. Vascular impairment commonly in e. all of the above 2. What could be the effect of feeding a. basset hounds. ad libitum diets with high amounts of b. German shepherds. 9. ______has/have been associated with protein, calcium, phosphorus, and c. Welsh corgis. MCE in cats. vitamin D? d. rottweilers. a. FeLV a. retarded cartilage maturation and e. Labrador retrievers. b. Feline infectious viremia osteochondrosis c. A single dominant autosomal gene b. ocular-skeletal dysplasia d. Multiple genes 6. ______is a finding in dogs with c. rickets e. A single gene with recessive effects on chondrodysplasia. d. chondromalacia the skeleton a. Osteopenia and angular limb deformity e. kidney failure b. Kyphosis 10. Which is not a clinical sign of MPS? c. Joint laxity 3. Prepubertal gonadectomy has been a. large ears d. Reduced diameter of tracheal lumen associated with which of the following? b. dwarfism a. diabetes mellitus e. all of the above c. disproportionate and broad maxilla b. MPS d. hip dysplasia c. hypothyroidism 7. Which statement regarding hypertrophic e. fusion of vertebral bodies with subse- d. SCFE osteodystrophy is false? quent neurologic signs e. hair loss a. It is a self-limiting disease. b. The hallmark is a double physeal line. 4. Epiphyseal dysplasia is characterized by c. Swollen, extremely painful distal meta- which of the following? physes are common. a. a double physeal line d. It is common in chondrodystrophic b. lack of opacity and ossification of breeds. cartilage e. The etiology is unknown.

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