This article is the first of a three-part series covering elbow disease in dogs. This first part reviews a new subset of elbow
dysplasia, traumatic fragmented medial coronoid process (TFMCP). Part 2 will cover rehabilitation therapy for the elbow after
surgical treatment. The final article will discuss intra-articular medical treatment options for dogs.
TFMCP is a condition of the elbow joint that commonly occurs in active dogs. It appears that affected dogs can be any size
or age, in contrast to the classic fragmented medial coronoid process (FMCP) that affects the elbows of skeletally immature
large- or giant-breed dogs.
Dogs with TFMCP have a history ranging from intermittent offloading of the affected forelimb to marked lameness, and they
often show little response to rest and nonsteroidal anti-inflammatory drugs (NSAIDs). Onset of clinical signs is insidious
and exacerbated by exercise. Also, as the lameness persists, its severity may increase. An affected dog often places its carpus
in a slightly exaggerated valgus position when it sits or stands, and it may circumduct its antebrachium and abduct its elbow
during the swing phase of its stride. Because pain is elicited when the shoulder is extended, many affected dogs are mistakenly
treated for shoulder pathology. But this pain is more likely caused by simultaneous elbow extension. Extending the shoulder
and elbow causes tension in the biceps-brachialis muscle complex, which exerts pressure on the medial coronoid and overlying
inflamed joint capsule and results in pain.
TFMCP's cause and pathogenesis are not well understood. Abnormal repetitive loading (e.g., landing from a jump, hitting contacts
or a flyball box) may cause subchondral microfractures to develop. Increased repetitive loading can also occur from contracting
the biceps-brachialis muscle complex, generating a force that rotates the medial coronoid into the radius. The microcracks
that develop disturb the bone's mechanical properties, and if the microcracks are not repaired properly through normal body
mechanisms, fatigue fractures may arise. Additionally, osteocyte loss, indicated by decreased osteocyte densities, is associated
with microdamage after fatigue loading. Excess load can lead to fatigue microdamage of the subchondral trabecular bone and
subsequent fracture, which may play an important role in the pathogenesis of TFMCP. Dogs with elbow dysplasia may be further
predisposed because of asymmetric growth of the radius and ulna during development, resulting in elbow joint incongruity.
This joint incongruity 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. Regardless of the cause of the condition, if TFMCP
is left untreated, it will likely lead to progression of secondary osteoarthritis.
A complete diagnostic evaluation involves a history taking, gait analysis, a physical examination and orthopedic and neurologic
examinations. In patients with TFMCP, physical examination reveals discomfort when the medial compartment of the elbow joint,
specifically the medial coronoid process, is directly palpated and with elbow hyperflexion. The patient may be reluctant to
allow full end-range flexion, and crepitus may be noted when the elbow is put through its range of motion. Joint effusion
may be detected as a fluctuant swelling beneath the lateral or medial epicondyle of the humerus, and, depending on how long
the condition has existed, muscle atrophy may be noted in the affected forelimb.
Photo 1: A "clean" lateral elbow radiograph of a dog with TFMCP.