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Part 1: Musculoskeletal Development & Pediatric Bone Diseases Peer Reviewed JUVENILE ORTHOPEDIC DISEASE IN DOGS & CATS JUVENILE ORTHOPEDIC DISEASE IN DOGS & CATS Part 1: Musculoskeletal Development & Pediatric Bone Diseases Ingrid Balsa, MEd, DVM, and Duane Robinson, DVM, PhD, Diplomate ACVS (Small Animal) University of California–Davis Juvenile orthopedic diseases affect the musculoskel- conditions have a genetic basis and, thus, can be etal system of immature animals, and most of these inherited diseases can be traced to pathologic events (eg, • Careful and thorough physical and orthopedic diseases, toxins, inappropriate nutrition, trauma) examinations. occurring in this period. Treatment options depend on the disease, and This 2-part series addresses the most common range from medical/nonsurgical management to pathologic conditions affecting juvenile dogs and surgical treatment. Similarly, prognosis is disease cats, including: dependent and can vary from one patient to the • Congenital and neonatal orthopedic diseases: next. Defined, for these articles, as diseases that occur in the prenatal period or within the first 3 to 4 MUSCULOSKELETAL DEVELOPMENT weeks of life Embryonic Development • Pediatric bone, cartilage, and joint diseases: During embryonic development, mesenchymal Diseases that occur in the skeletally immature cells—capable of developing into lymphatic, dog. circulatory, and connective tissues—coalesce in the Part 1 of this series presents an overview of regions of future bones, progressing from cartilage musculoskeletal development and pediatric bone diseases (diseases that occur after 1 month of age FIGURE 1. Anatomy of and before skeletal maturity), which generally have an immature long bone a good prognosis. Part 2 will discuss pediatric joint (tibia) in the dog: The and cartilage diseases, as well as congenital and immature long bone is characterized by neonatal orthopedic diseases. radiolucent lines that represent the proximal DIAGNOSTIC APPROACH and distal physeal In juvenile patients, determining the correct growth plates (primary diagnosis can be challenging because the clinician centers of ossification; must understand developmental physiology (Tables the epiphyses are the 1 and 2) and how errors in development affect locations of secondary particular body systems. centers of ossification). A = proximal epiphysis; To properly diagnose juvenile orthopedic disease, B = distal epiphysis; it is important to obtain key information: C = apophysis; D = • Patient signalment: Age, breed, and sex proximal physeal plate • Accurate history, including: or physis; E = distal » Origin of the dog, which can indicate the physeal plate or physis; general care the dam and puppies received F = metaphysis; G = » History of any known trauma, which can help diaphysis determine the presence of fractures or soft Courtesy Veterinary Medical Teaching tissue injuries. Hospital, University of • Information about dam, sire, and siblings: California–Davis Evidence suggests that many juvenile orthopedic 38 TODAY’s VeTERINARY PRACTICE | May/June 2016 | tvpjournal.com JUVENILE ORTHOPEDIC DISEASE IN DOGS & CATS Peer Reviewed TABLE 1. TABLE 2. Approximate Closure Times of Major Approximate Closure Times of Major Growth Plates in Long Bones of Average Growth Plates in Bones of Average Cats7 2 (25- to 30-kg) Dogs AGE AT CLOSURE (MONTHS) AGE AT CLOSURE (MONTHS) GROWTH PLATE Earliest Latest GROWTH PLATE Earliest Latest Hindlimb Hindlimb Proximal femur 8 14 Greater trochanter 6 11 Distal femur 14 20 Proximal femur 6 12 Proximal tibia 14 20 Distal femur 6 11 Distal tibia 8 14 Proximal tibia 6 12 Proximal fibula 14 20 Tibial tuberosity 10 12 Distal fibula 8 14 Distal tibia 5 11 Ilioischial 4 8 Medial malleolus 4 5 Forelimb Proximal fibula 6 11 Proximal humerus 14 20 Distal fibula 5 11 Distal humerus 4 8 Tuber calcaneus 11 wks 8 Proximal ulna 8 14 Forelimb Scapula 4 8 Supraglenoid 12 wks 5 Distal ulna 14 20 tuberosity Proximal radius 4 8 Proximal humerus 10 12 Distal radius 14 20 Distal humerus 5 8 Spine 14 20 Proximal ulna 5 8 Anconeal process 4 5 characterized as lamellar bone with Haversian Distal ulna 6 11 systems.3 In most long bones, physeal growth Proximal radius 5 8 represents 75% to 80% of the final bone length, Distal radius 6 11 whereas epiphyseal growth represents 20% to 25%.1,2 By the end of this period, mineralization of the to bone via endochondral and intramembranous epiphyseal centers of ossification is complete and ossification.1-3 Formation of joints and intraarticular growth continues at the physes at a much slower rate. structures follows; mesenchyme surrounding the The cessation or closure of the physeal growth plates bones and joints then gives rise to muscles. Tendinous occurs at predetermined times and varies widely from insertions develop from cartilaginous primordia and bone to bone and across breeds of dogs and cats secondarily connect to developing muscle masses 4-6 during limb elongation.1 (Tables 1 and 2). Postnatal Development The most physeal activity and, thus, the During postnatal skeletal development, the Effect of majority of longitudinal bone growth, occurs cartilaginous skeletal components enlarge, and from 12 to 26 weeks of age.1 However, timing of Gonadectomy mineralization occurs via intramembranous and long bone physeal closure is controlled, in part, 1,3 on Bone endochondral ossification. by gonadal hormones, particularly estrogen, in Longitudinal bone development results from both sexes.4 Therefore, in both dogs and cats, Growth growth of the secondary centers of ossification in gonadectomy before physeal closure delays the epiphyses and the primary centers of ossification this closure and is associated with significantly in the physes (Figure 1).1 In these regions, new greater final length of associated long bones.4–6 cartilage forms, increasing the area in length and The role that delayed physeal closure plays in width.2 the development of orthopedic disease is an Endochondral ossification then occurs, area of current research and discussion. transforming the cartilage into bone, which is tvpjournal.com | May/June 2016 | TODAY’s VeTERINARY PRACTICE 39 Peer Reviewed JUVENILE ORTHOPEDIC DISEASE IN DOGS & CATS Weight is a contributing factor, and young dogs weighing more than 23 kg are at increased risk compared with those weighing less than 23 kg. Females and males over 23 kg are 3 and 5 times, respectively, at greater risk.9 Diagnosis Diagnosis is based on signalment, history, physical examination findings, and radiographic findings. There are generally no systemic signs of illness. Physical examination findings include a shifting leg FIGURE 2. Ventrodorsal pelvic radiograph of a juvenile dog with panos- lameness and pain on palpation of the long bones. teitis affecting the left femur (A); the arrow identifies nodular opacity In some patients, pain is so severe that it impedes similar to cortical bone opacity in the medullary canal. Transverse CT im- age of the femur of the same patient (B); the arrow identifies increased ambulation and can also result in hyporexia or opacity/medullary sclerosis of the diaphysis of the left femur (compared unwillingness to eat and drink. Note that care must with the right femur), which is consistent with panosteitis. Courtesy Veter- be taken during palpation to avoid eliciting pain by inary Medical Teaching Hospital, University of California–Davis palpating/compressing a nerve or other structure. In the acute phase, radiographs may be normal or PEDIATRIC BONE DISEASES show circumscribed cortical bone opacities within Panosteitis the medullary canal adjacent to the nutrient foramina Overview (Figure 2). As the disease progresses, the medullary Panosteitis—also known as enostosis, eosinophilic pattern changes to a coarser than normal trabecular panosteitis, juvenile osteomyelitis, and osteomyelitis pattern, and a progressive periosteal reaction may be of young German shepherd dogs—is a self-limiting present (Figure 3). Severity of radiographic signs disease of the long bones of large- and giant-breed does not necessarily parallel severity of clinical signs. dogs. It most commonly affects the ulna, followed by Differential diagnoses include hypertrophic the radius, humerus, femur, and tibia. osteodystrophy, osteochondritis dissecans, hip The cause of panosteitis is unknown, but it may be the result of excessively high dietary protein dysplasia, fragmented medial coronoid process, and or calcium administration that causes protein united anconeal process. accumulation and/or vascular proliferation and local bone formation at nutrient foramina, which increases intraosseous pressures.1 In one study, incidence was estimated at 2.6 per 1000 patients.8 Panosteitis also has regional and seasonal distribution differences, with more cases in the Northeast and north-central United States and in the summer and fall. Signalment Age at diagnosis is most often 5 to 12 months; however, panosteitis may affect younger dogs and those up to 5 years of age. Males are more commonly affected than females. Breeds at risk of developing panosteitis include FIGURE 3. Orthogonal projections of the left the Airedale terrier, Irish setter, German shorthaired humerus of a juvenile dog with a shifting limb pointer, Doberman pinscher, Afghan, Great lameness of 1.5 months’ duration that was Dane, Saint Bernard, Bernese mountain dog, diagnosed as panosteitis; note the patchy Newfoundland, golden and Labrador retrievers, and increased medullary opacities that are visible German shepherd dog. Some small and medium- throughout the length of the humeral diaphysis
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