Traumatic Fragmented Medial Coronoid Process
Traumatic fragmented medial coronoid process (TFMCP) is a condition in the elbow joint of dogs that appears to occur commonly
in performance dogs. Unlike the classic condition of fragmented medial coronoid process (FMCP) affecting the elbow joints
of skeletally immature large to giant breed dogs, jump down syndrome (TFMCP) appears to have no age or size limitations.
Cause
The cause and pathogenesis of TFMCP are poorly understood. It is possible that abnormal repetitive loading, such as landing
from a jump, hitting contacts or a flyball box, and so on, may lead to microfractures of the bone underneath the cartilage
(subchondral fractures). Additionally, increased repetitive loading can arise from contraction of the biceps/ brachialis muscle
complex. When the biceps/brachialis contracts, a force is generated that rotates the medial coronoid into the radius. These
microcracks disturb the mechanical properties of bone, and if not repaired properly through normal body mechanisms, fatigue
fractures develop. Additionally, loss of osteocytes (bone cells), indicated by decreased osteocyte densities, has been strongly
associated with the presence of microdamage after fatigue loading. These studies imply that excess load may lead to fatigue
microdamage of the subchondral trabecular bone and eventual fracture, which we believe may play an important role in the pathogenesis
of TFMCP. Dogs may be further predisposed to this condition if they have elbow dysplasia. Dogs with elbow dysplasia had asymmetric
growth of the radius and ulna during development, resulting in elbow joint incongruity. Elbow incongruity such as radioulnar
step defects, humeroulnar incongruence/conflict, and varus deformity of the humerus causes abnormal contact patterns in the
elbow, specifically at the coronoid trochlear articulation, which is theorized to increase the load on the medial coronoid
process (MCP). Regardless of the etiology, if left untreated as a continual lameness, secondary osteoarthritis may progress
as noted by damage to the cartilage such as softening, fibrillation, fissuring, and erosions as well as additional subchondral
bone microcracks and fragmentation. The free fragments contribute to frictional abrasion ("kissing lesions") of the opposing
surface including the medial aspect of the humeral condyle and radial head.
Diagnosis
History and Clinical Signs
Dogs with TFMCP may present with a history ranging from a subtle intermittent offloading of the forelimb to significant unilateral
or bilateral forelimb lameness. This lameness is typically exacerbated with exercise and heavy activity. The onset of lameness
is insidious. As lameness persists, it may increase in severity. Affected dogs often place the carpus in an exaggerated valgus
position (turned out) when sitting or standing, and circle the foreleg outward and move the elbow away from the midline (circumduct
the antebrachium and abduct the elbow) during the swing phase of the stride. The history of dogs with TFMCP typically includes
a lack of response to rest and non-steroidal anti-inflammatory drugs (NSAIDs). Many dogs with TFMCP are mistakenly treated
for shoulder pathology because the attending veterinarian elicits a pain response when the shoulder is extended. The authors
believe the pain response actually arises from the elbow because when the veterinarian performs an extension maneuver of the
shoulder, the elbow is usually simultaneously extended. Extension of the shoulder and elbow causes tension in the biceps/brachialis
muscle complex. Tension in the biceps/brachialis exerts pressure on the medial coronoid and overlying inflamed joint capsule
causing the pain response.
Orthopedic Examination
On physical examination discomfort is usually noted on direct palpation of the medial compartment of the elbow joint, specifically
the medial coronoid process. Discomfort may also be noted on hyperflexion of the elbow. Most dogs with TFMCP are reluctant
to allow for full endrange flexion. In chronic cases, full flexion may not be obtained. Crepitus may be noted when placing
the elbow through range of motion. Some investigators suggest that the carpus should be placed in a flexed, externally rotated
position while the elbow is extended. Joint effusion may be detected as a fluctuant swelling beneath the lateral or medial
epicondyle of the humerus. Depending on the chronicity, atrophy may be noted in the affected forelimb.
Advanced Diagnostics
In addition to history, gait analysis, physical examination, orthopedic and neurologic examinations, further diagnostic tests
used to differentiate causes of elbow pathology currently consist of hematology, biochemical profile, urinalysis, arthrocentesis,
imaging modalities, and arthroscopy. Unfortunately, radiographs have been shown to be of little value because of difficulty
identifying the fragment or line of separation using standard radiography. In some chronic cases, however, radiographs may
reveal secondary evidence of bony remodeling consistent with osteoarthritis. These changes may include sclerosis within the
ulnar notch, and remodeling along the anconeal process and MCP. Advanced diagnostic imaging modalities such as CT scans,
MRI, nuclear scans, and arthroscopy may allow confirmation of the condition. Arthroscopic evaluation of the elbow joint
allows direct observation of all major intra-articular structures with magnification, "dynamic" evaluation of tissues during
elbow range-of-motion tests, and "palpation" of intra-articular tissues using arthroscopic instrumentation. Arthroscopic
exploration of the elbow provides a definitive diagnosis of TFMCP when a fragment or cartilage fissure. In a small percentage of cases, advanced imaging (nuclear scan, CT, MRI) indicates fragmentation of the coronoid but arthroscopic
observation does not reveal a fissure or fragment. In such cases, the fissures (microcracks) are believed to be within the
coronoid bone beneath the cartilage surface.
