7: DevelopmentalOrthopedicDisease


Elizabeth Huynh

VCA West Coast Specialty and Emergency Animal Hospital, Fountain Valley, CA, USA


An understanding of normal radiographic anatomy and the pathogenesis of disease conditions is imperative when evaluating young dogs and cats for developmental orthopedic disease. There are unique factors that confound interpretation of orthopedic radiographs in juvenile patients. These include the presence of open physes, incomplete development of osseous structures, and variations of anatomy specific to species and breeds. A classic interpretation paradigm is not as helpful in developmental orthopedic disease, although specific diseases are associated with specific anatomic locations of the osseous structures.

One can develop a prioritized differential list based on some of the same questions asked of other orthopedic studies. These would include aggressive versus nonaggressive changes, position within the osseous structure (i.e., epiphysis, physis, metaphysis, diaphysis, joint centered, etc.), and number of bones involved (monostotic versus polyostotic).

Well‐positioned orthogonal radiographs are critical for accurate interpretation. At times, comparison views of contralateral limbs (or other age‐matched normal patients) provide a better understanding of normal developmental variations though some developmental orthopedic diseases may be bilateral. Unique radiographic views (i.e., oblique radiographs, etc.) will aid in interpretation for highlighting specific areas of the regional anatomy.

Finally, an awareness of the signalment and clinical signs associated with each developmental disease is imperative for the development of a prioritized differential list, as well as decisions around therapy (Table 7.1).

TABLE 7.1 Developmental orthopedic diseases with typical signalment, history, and imaging findings with recommended therapies.

Disease Common breeds Typical age of diagnosis Clinical signs Key radiographic changes Therapy
Hip dysplasia German shepherd, Labrador/golden retriever 24 mo Hip pain, lameness Coxal Incongruity, laxity, osteoarthritis Weight loss, pain management, hip replacement
Fragmented medial coronoid process (FMCP) Labrador/golden retriever 1 yr Elbow pain Flat or fragmented medial coronoid process, sclerosis of semilunar notch, osteoarthritis Weight loss, pain management, surgical debridement
Ununited anconeal process (UAP) German shepherd 5 mo Elbow pain Fissure between anconeal process and olecranon Surgical removal
Osteochondritis dissecans (OCD) Labrador/golden retriever, German shepherd 8–24 mo Location specific Flattening of humeral head, medial humeral condyle, medial or lateral femoral condyle, medial or lateral trochlear ridge of the talus Surgical debridement
TMJ dysplasia Basset hound, setter breeds, Cavalier King Charles spaniel Any age Asymptomatic, joint laxity, open mouth jaw locking, dental malocclusion Flat mandibular fossa, misshapen condylar process, short retroarticular process, TMJ subluxation Zygomatic arch ostectomy if jaw locking
Panosteitis German shepherd 5–12 mo Shifting leg lameness, pain over diaphysis Endosteal or subperiosteal new bone formation Supportive, steroids, NSAIDs
Hypertrophic osteodystrophy (HOD) Great Dane, Irish wolfhound, Rottweiler, Weimaraner 3–5 mo Shifting leg lameness, pain over metaphyses Double physis sign, metaphyseal flare, metaphyseal periosteal response Supportive, ± steroids, NSAIDs
Retained cartilage core Large to giant breeds, Great Dane 3–9 mo Angular limb deformities; may be asymptomatic Well‐defined, triangular lucency of the distal ulnar metaphysis Supportive
Incomplete ossification of the humeral condyle Spaniel breeds Any Asymptomatic or lameness Lucency of humeral intercondylar region, ± supracondylar fracture Surgical stabilization
Avascular necrosis of the femoral head Miniature to small‐breed dogs 5–8 mo Lameness Lucent, resorptive femoral head and neck, coxal osteoarthritis Femoral head and neck ostectomy
Capital femoral physeal fracture (Cats) Any 7 mo to 2 yr Traumatic or nontraumatic lameness Salter Harris type I fracture of the femoral head, coxal osteoarthritis Femoral head and neck ostectomy
Septic metaphysitis Any Young Lameness Soft tissue swelling, aggressive osseous proliferation and lysis Antibiotics
Multiple cartilaginous exostoses Great Danes, St Bernards, hounds 6 wk to 11 yr Lameness, firm masses Single/multiple osseous masses, metaphyses of long bones, axial skeleton Supportive
Multiple epiphyseal dysplasia Beagles, miniature poodles, others Young, adult Disproportionate size, lameness Shortened long bones, wide metaphysis, decreased epiphysis, vertebrae affected Supportive
Craniomandibular osteopathy West Highland white terriers 3–7 mo Difficult prehension Thickened mandibular cortex, bulla with periosteal proliferation Supportive, NSAIDs
Calvarial hyperostosis Bull mastiffs Any Pain Thickened external sagittal crest of the skull and frontal bone region Supportive, NSAIDs

NSAID, nonsteroidal antiinflammatory drug.

Developmental orthopedic disease can be broken down into three major categories.

  • Dysplasia (abnormal cartilage and/or bone development) [1]
  • Osteochondrosis (failure of normal endochondral ossification)
  • Miscellaneous idiopathic diseases that are often polyostotic and involve specific anatomic regions of the long bones


Joint dysplasias are best defined as growth disorders resulting in joint incongruity, laxity, or other malformations. These disorders often have multifactorial etiologies; however, genetic predisposition plays a role. Joints commonly affected by dysplasia are the coxal (coxofemoral), cubital (elbow), and temporomandibular joints (TMJ).

Generalized osseous dysplasias include epiphyseal and metaphyseal dysplasias, abnormalities associated with congenital hormonal underdevelopment (i.e., congenital panhypopituitarism, congenital hypothyroidism), or secondary to an underlying osseous structural disorder (i.e., osteogenesis imperfecta, mucopolysaccharidosis, etc.). Metabolic disorders of nutrition and renal dysplasia result in generalized osteopenia, pathologic folding fractures, and fibrous dysplasia of the skull.

Hip Dysplasia


Hip dysplasia is a developmental abnormality associated with the soft tissues and osseous structures of the coxal joint. Hip dysplasia is primarily a developmental disorder of large‐breed dogs but can affect small‐breed dogs and cats. It is usually bilateral but can be unilateral and asymmetric when comparing the right and left sides. Hip dysplasia is heritable, with environmental, nutritional, and conformational factors affecting rate of progression of degenerative changes and degree of lameness in the dog or cat [2]. The phenotypic expression of dysplastic changes, particularly degenerative changes, is not apparent early but progresses with age. Clinical signs of pelvic limb lameness can develop as early as 4–6 months and typically are documented radiographically at 24 months of age. Common breeds affected include the German shepherd, Labrador retriever, golden retriever, and other large‐breed dogs [1].


The underlying abnormality appears to be a laxity of the coxal joints resulting in incomplete development of the acetabular rim that leads to a shallow acetabulum and progressive coxal joint subluxation and resultant joint incongruity. This leads to secondary periarticular osteophyte formation associated with the acetabula and femoral heads. Enthesopathy will also develop over time in the region of the intertrochanteric fossa and femoral neck where a number of muscles and the coxal joint capsule insert. Other insertional abnormalities include lesser trochanter avulsion fractures associated with the iliopsoas muscle insertion and enthesopathy associated with the joint capsule. This is radiographically characterized by an osseous fragment immediately adjacent to the lesser trochanter of the femur in the region of the iliopsoas muscle insertion.

Radiographic Assessment and Indicators of Hip Dysplasia

There are five radiographic views that evaluate the coxal joint (Figure 7.1): (i) lateral pelvis view (with the pelvic limbs scissored so that the dependent limb is cranial and the pelvic limb further away from the table is positioned caudally), (ii) extended limb ventrodorsal pelvis view, (iii) flexed limb ventrodorsal pelvis view, (iv) dorsal acetabular rim (DAR) view [3], and (v) PennHip evaluation view using a distraction device for determining degree of subluxation/laxity. The first two listed are obtained for routine evaluation of the pelvis. The other views may be obtained for evaluation of specific conditions as clinically warranted (Table 7.2).

Photos depict evaluation of the canine pelvis and coxal joints.

FIGURE 7.1 Evaluation of the canine pelvis and coxal joints. (A) Ventrodorsal extended limbs, (B) ventrodorsal flexed limb, (C) lateral, (D) craniocaudal dorsal acetabular rim, and (E) PennHip radiographs. In (D), the dorsal acetabular rim () point is the lateral aspect of the dorsal acetabular rim that is seen in this radiograph (arrow).

TABLE 7.2 Radiographic views for evaluation of the canine and feline pelvis.

Radiographic view Positioning Comments When used
Right (or left) lateral Patient in right (left) lateral recumbency with the right (left) pelvic limb cranial and the left (right) pelvic limb caudal; coxal joints should be superimposed over each other for straight radiographic positioning; collimation is open to the stifle joints from the dorsal aspect of the pelvis Useful for luxations of the coxal joints that are commonly cranial and dorsal (femoral head position relative to the acetabulum). Useful for evaluation of the lumbosacral joint and acute traumatic injuries Routine view of the pelvis
Extended leg ventrodorsal radiograph of the pelvis Dog/cat is in dorsal recumbency and the stifle joints and pelvic limbs are extended so that the stifle joints are internally rotated (patella in a central position and femoral condyles equal in size); pelvic limbs should be taped equidistant from the table Useful for evaluation of the coxofemoral joints, coverage of the femoral heads, presence of degenerative changes of the coxal joint; joint space collapse; subluxation to luxation; presence of eburnation Routine view of the pelvis
Flexed or neutral pelvic limb ventrodorsal radiograph of the pelvis Dog/cat in dorsal recumbency with pelvic limbs flexed to the side; the pelvis should be straight; no tension on the coxofemoral joint compared with the extended leg view Evaluation of the femoral head/physis and femoral neck for acute trauma or aggressive osteolytic changes Follow‐up image if acute trauma is suspected based on other views; however, fracture not confirmed
Dorsal acetabular rim (DAR) view Dog in sternal recumbency with the pelvic limbs flexed under the pelvis and the x‐ray collimation centered over the coxofemoral joints Documents degree of development of the dorsal acetabular rim and coverage of the femoral heads Fallen out of favor as triple pelvic osteotomies are not routinely performed any more
PennHip neutral, compression, traction views Dog is in dorsal recumbency with the pelvic limbs in a neutral position (stifle joints pointing up toward the collimator) and the distraction device between the pelvic limbs Allows for early detection of laxity and subluxation of the coxofemoral joints; can be done as early as 4 months for review and comparison with national/international database for a joint laxity score called the distraction index Images are sent away for review and distraction index created and compared with database for interpretation

Multiple radiographic abnormalities are seen with hip dysplasia (Figure 7.2). Coxal joint laxity is manifested as decreased coverage of the femoral head by the DAR resulting in incongruency of the femoral head and acetabular surfaces. Additionally, osseous proliferation is associated with the acetabulum, femoral head, and femoral neck. An early indicator of degenerative joint disease associated with osseous proliferation of the femoral neck has been termed the “Morgan line,” which represents enthesophyte formation of the insertion of the coxal joint capsule.

Photo depicts canine hip dysplasia.

FIGURE 7.2 Canine hip dysplasia. Ventrodorsal radiograph of the pelvis of a 3‐year‐old German shepherd dog. There is severe osteophyte formation of the acetabular rims and femoral heads. The femoral heads are misshapen. There is severe enthesophyte formation of the femoral necks, causing marked femoral neck irregularity and thickening, representing joint capsule insertion osteoproliferation. There is marked subchondral sclerosis of the coxal joints, worse on the right. The acetabular rims are shallow, worse on the right. There is decreased acetabular coverage of the femoral heads, representing coxal joint subluxation. Within the soft tissues surrounding the right coxal joint, there are multifocal, well‐defined, amorphous, mineral opaque structures, which may represent synovial osteochondromas or chronic avulsion fractures.

Elbow Dysplasia

Elbow dysplasia causes variable degrees of lameness in affected dogs and cats and is a multifactorial disease composed of one or more of the following developmental abnormalities: fragmented medial coronoid process (FMCP), ununited anconeal process (UAP), osteochondritis dissecans (OCD) of the medial humeral condyle, elbow joint incongruity, and secondary elbow joint osteoarthrosis [4]. FMCP and UAP can be related to asynchronous growth of the radius and ulna leading to joint incongruity, whereas osteochondrosis and osteoarthrosis can be primary disease conditions or secondary to elbow incongruity. To diagnose elbow dysplasia, knowledge of normal elbow anatomy is important (Figure 7.3).

Photos depict elbow radiographic anatomy.

FIGURE 7.3 Elbow radiographic anatomy. (A) Mediolateral radiograph of the elbow. (B) Caudocranial radiograph of the elbow.

Fragmented Medial Coronoid Process of the Ulna


Fragmented medial coronoid process is characterized by fragmentation or fissuring of the cartilage and bone over the craniolateral aspect of the medial coronoid process of the ulna. A recent change in terminology groups a number of related pathologies under the term “medial compartment syndrome”: coronoid process sclerosis, coronoid eburnation and microfissuring, and coronoid fragmentation with or without documented incongruity. The frequency of disease and the commonality of breeds it affects have led to much investigation into this disease process and its underlying etiologies, including osteochondrosis, joint incongruities, and biomechanical force mismatch. Dog breeds commonly affected by FMCP include the Labrador retriever, golden retriever, Rottweiler, and Bernese mountain dog.


Fragmented medial coronoid process is thought to represent a form of osteochondrosis, which has been histologically reported in one study [5] and more suggestive of an osteochondral fracture of the medial coronoid process in another study [6]. In the latter study, FMCP was determined to be more consistent with a fibrous nonunion, nonhealed osteochondral fracture. The medial coronoid process ossifies between 12 and 22 weeks and may be susceptible to osteochondrosis during this time.

The most recent research suggests that asynchronous growth of the radius and ulna leads to incongruity of the elbow joint and altered forces on the medial aspect of the elbow joint [7, 8]. The disease process begins as the radius and ulna are lengthening with onset of clinical signs between 6 and 9 months of age. A shortened radius, with respect to the ulna, subjects the medial coronoid process to increased weight‐bearing load from the humeral condyle. This altered load causes microfractures of the medial coronoid, leading to alteration in bone density. Secondary subchondral bone sclerosis of the trochlear notch of the ulna develops.

Underdevelopment and the small size of the ulnar trochlear notch and relatively increased size of the proximal ulna could result in loading at the anconeal and medial coronoid processes of the ulna, which has also been proposed as the cause of elbow joint incongruity [7, 9]. Changes associated with the medial coronoid process, regardless of the underlying cause, cause secondary periarticular osseous proliferation associated with the radial head, anconeal process, and humeral epicondyles.

Radiographic Assessment and Indicators

Radiographic diagnosis of FMCP is challenging. Secondary osseous proliferation of the elbow joint is commonly seen with or without radiographic changes associated with the medial coronoid process. Radiographically, the medial coronoid process is normally triangular shaped and well defined on both craniocaudal and mediolateral views. FMCP is characterized by indistinct or irregular margination of the medial coronoid process on mediolateral and craniocaudal views. Blunting of the cranial margin of the medial coronoid process on mediolateral views may also be present (Figure 7.4) [10]. Secondary FMCP changes include ulnar subtrochlear sclerosis and periarticular osseous proliferation associated with the radial head, anconeal process, and humeral epicondyles. Humeral condylar “kissing lesion” with subchondral sclerosis of the medial humeral condyle with or without associated articular margin lucency can also be seen.

Photo depicts fragmented medial coronoid process of the ulna.

FIGURE 7.4 Fragmented medial coronoid process of the ulna. Mediolateral radiograph of the elbow with flattening (arrow) and sclerosis of the medial coronoid process with a well‐defined triangular shaped osseous fragment (arrowhead). There is also moderate cubital joint osteoarthrosis, further characterized by osteophyte formation of the humeral condyle, humeral epicondyle, anconeal process, and radial head.

At a minimum, standard orthogonal mediolateral and craniocaudal radiographic views are required for assessment of the elbow. The cranio15° lateral‐caudomedial oblique view (Cr15L‐CdMO) is the best radiographic view to completely evaluate the cranial margin of the medial coronoid process for the detection of FMCP [11]. Distomedial‐proximolateral oblique views can also be helpful; however, the utility of oblique views is dependent on the viewer’s familiarity with reading oblique projections which can be difficult to completely assess. A maximally flexed mediolateral projection identifies osteophytes on the proximal anconeal process without superimposition of the humerus.

Ununited Anconeal Process of the Ulna


Similar to FMCP, UAP has been described as a manifestation of osteochondrosis. Multiple theories of the pathogenesis of UAP are proposed, which include an inherited developmental anomaly, metabolic defect, nutritional deficiencies, trauma, and radioulnar mismatch and growth asynchrony secondary to radial lengthening. This causes increased proximal pressure on the humeral condyle, and subsequent excessive load on the anconeal process. The altered pressure causes proximal displacement of and lack of fusion of the anconeal process to the parent bone. The prompt healing of UAP reported after ulnar osteotomy further supports the hypothesis that asynchronous growth between the radius and ulna is the underlying cause of UAP. Lucency of the tip of the anconeal process representing a normal secondary center of ossification should not be confused with a pathologic UAP (Figure 7.5) [12]. As a location for separate center of ossification, the tip of the anconeal process should fuse to the parent bone by 150 days.

Photos depict secondary center of ossification of the anconeal process.

FIGURE 7.5 Secondary center of ossification of the anconeal process. Note the small triangular‐shaped secondary center of ossification of the anconeal process (arrow). The ossification center is small and poorly defined with an irregular line of separation from the ulnar diaphysis.

Source: Jean K. Frazho DVM et al. [12] / with permission of John Wiley & Sons.

Breeds commonly affected by UAP include the German shepherd, St Bernard, Great Dane, Labrador retrievers, and others. The disease process is typically seen in dogs between 3 and 4 months of age, and is documented at 5 months of age, when the anconeal process secondary ossification center should have fused to the parent bone. Occasionally, UAP can be diagnosed in older dogs with an acute onset of lameness or considered incidental [13].

Radiographic Assessment and Indicators

Radio‐graphically, UAP is characterized by radioulnar incongruity with proximal displacement of the radial head with respect to the trochlear notch, a well‐delineated lucency of the anconeal process and proximal displacement and lack of fusion of the anconeal process in relation to the parent bone (Figure 7.6).

Photo depicts ununited anconeal process.

FIGURE 7.6 Ununited anconeal process. Mediolateral radiograph of the elbow with a well‐defined, irregular lucency (arrow) at the level of the anconeal process. There is also mild cubital joint osteoarthrosis, further characterized by osteophyte formation of the radial head (arrowhead).

The flexed mediolateral projection best evaluates for UAP, as there is no superimposition of the humerus with the anconeal process. Projections of both limbs are recommended as UAP is commonly bilateral.

Osteochondrosis or Osteochondritis Dissecans of the Medial Humeral Condyle


Osteochondrosis or osteochondritis dissecans (OC/OCD) is an erosive cartilage defect caused by disturbed endochondral ossification of the articular or epiphyseal cartilage which can be seen in conjunction with FMCP. OC/OCD of the medial humeral condyle may be categorized as primary or secondary. OC/OCD of the humeral condyle is of similar etiology to OC/OCD lesions in other anatomic regions: failure of endochondral ossification with thinning and flattening of the cartilage surface. More common is secondary erosion of the medial humeral condyle articular surface, as a result of altered forces such as incongruity between the ulnar trochlear notch and the humeral trochlea, leading to eburnation of the opposing cartilaginous surfaces. The resultant lesions are commonly known as “kissing lesions” and are better classified as a form of joint degeneration than osteochondrosis.

The most common dog breed affected by OC/OCD with a combination of FMCP is the Labrador retriever. Males are more commonly affected, which may be due to their quicker rate of overall growth or a sex‐linked factor [14].

Radiographic Assessment and Indicators

Radiographic changes associated with OC/OCD of the medial part of the humeral condyle include subchondral sclerosis of the medial humeral condyle with or without a concave articular margin lucency/defect (Figure 7.7). Small OC/OCD lesions may be difficult to evaluate radiographically. Diagnosing the concave articular margin defect is also dependent on the angle of the radiographic view. Severe joint erosion may result in secondary subchondral defects that can appear similar to OC/OCD on imaging.

Photo depicts osteochondritis dissecans of the medial part of the humeral condyle and fragmented medial coronoid process of the ulna.

FIGURE 7.7 Osteochondritis dissecans of the medial part of the humeral condyle and fragmented medial coronoid process of the ulna. Caudocranial radiograph of the cubital joint. Within the medial aspect of the cubital joint, there are two ovoid to rounded, smoothly marginated, osseous fragments, partially superimposed over one another (arrow). There is a large, irregularly marginated, concave defect of the medial humeral condyle with regional subchondral sclerosis (arrowhead). The adjacent soft tissues are markedly thickened, representing joint effusion and/or synovial proliferation.

OC/OCD of the medial part of the humeral condyle is most readily seen on the craniocaudal view. The best radiographic view includes the craniocaudal (CC) and Cr15L‐CdMO (Figure 7.8) [15].

Photo depicts cranio15 degrees lateral-caudomedial oblique (Cr15L-CdMO) radiograph for the detection of osteochondrosis or osteochondritis dissecans of the medial part of the humeral condyle.

FIGURE 7.8 Cranio15°lateral‐caudomedial oblique (Cr15L‐CdMO) radiograph for the detection of osteochondrosis or osteochondritis dissecans of the medial part of the humeral condyle. A mineralized fragment (arrow) is seen distal to the lucency. There is surrounding subchondral sclerosis of the medial part of the humeral condyle (arrowhead).

Source: Cristi R. Cook DVM et al. [4] / with permission of John Wiley & Sons.

Temporomandibular Joint Dysplasia

See also Chapter 12, Imaging of the Head.


Temporomandibular joint dysplasia is a congenital disease with an unclear underlying etiology; however, the underlying cause may be attributable to the rapid growth of chondrodystrophic breed dogs, prognathism, and laxity of the mandibular symphysis [16]

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Jul 15, 2023 | Posted by in ANIMAL RADIOLOGY | Comments Off on 7: DevelopmentalOrthopedicDisease

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