312 Canine Sports Medicine and Rehabilitation
decreased osteocyte density, has been
strongly linked with the presence of microda
mage after fatigue loading, and may play an
important role in the pathogenesis of TFCP
(Verborgt et al., 2000). A second theory specu
lates that these dogs are predisposed due to
underlying elbow dysplasia, in particular
incongruency. Elbow incongruity such as
radioulnar step defects, humeroulnar incon
gruency/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 (Punke et al., 2009). The third theory
proposes that microfractures of the bone
below the cartilage (subchondral fractures)
result from abnormal repetitive loading, such
as landing from jumps, or hitting contacts or
flyball boxes (Boettcher et al., 2009). Recent
research may elicit some clarification on these
competing theories.
One study excluded dogs that showed any
radiographic or arthroscopic evidence of FCP
due to elbow dysplasia or other intra‐articular
pathological changes. Dogs under 2 years of
age were also excluded because elbow dyspla
sia related to medial compartment disease,
osteochondrosis, or osteochondritis dissecans
may not present until 18 months of age.
Clinical records of dogs that experienced
acute unilateral non‐weight‐bearing lameness
associated with a traumatic and concussive
event were reviewed. Arthroscopy of these
dogs revealed a single, large, displaced or
nondisplaced fragment with no other lesions
or elbow pathological changes present (Figure
12.21). This research suggests that while TFCP
can accompany elbow disease and dysplasia
as a secondary condition, TFCP itself can pre
sent in dogs with no genetic predisposition
and should be deemed a clinically distinct
disease unrelated to elbow dysplasia (Tan et
al., 2016). Secondary osteoarthritis will pro
gress if left untreated. Damage to the cartilage
such as softening, fibrillation, fissuring, ero
sions, and additional subchondral bone
microcracks and fragmentation may occur.
Over time, frictional abrasion (kissing lesions)
may occur as a result of free fragments dis
rupting opposing surfaces, including the
medial aspect of the humeral condyle and
radial head.
Diagnosis
Patients with TFCP present with a history of
subtle intermittent lameness to significant acute
unilateral lameness. Bilateral presentation is
uncommon. The lameness is exacerbated with
increased activity and exercise. Onset is insidi
ous, although, on occasion, acute onset follow
ing a jump‐down may be reported. Severity of
the lameness may be progressive. Affected
dogs gait in a manner consistent with elbow
pain. A lack of response to rest and NSAIDs is
common.
Discomfort is elicited on direct palpation of
the medial compartment of the elbow joint, spe
cifically the medial coronoid process. Patients
are reluctant to allow full elbow flexion, and
discomfort is noted on hyperflexion. In chronic
cases, full flexion may not be obtained. Crepitus
is rare. Carpal flexion with external rotation
while extending the elbow may exacerbate the
pain response. Joint effusion distal to the lateral
or medial epicondyle of the humerus may be
detected.
Misdiagnosis as biceps tendinopathy is com
mon, based on the pain response to shoulder
extension or the biceps stretch test. This pain
response may be due to the simultaneous
hyperextension of the elbow when the shoulder
is placed in extension. Elbow extension causing
tension in the biceps/brachialis muscle com
plex may exert pressure on the medial coronoidFigure 12.21 Arthroscopic image of a traumatic
fragmented medial coronoid process (arrow).