Etiology

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.

Pathogenesis

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.

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.

Pathogenesis

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.

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).

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.

Pathogenesis

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.

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].