P. 576

An Urban Experience
A. Pozzi1
1Clinic for Small Animal Surgery, Department of Small Animals, Vetsuisse-Faculty, University of Zurich
Hereditary musculoskeletal disorders include several diseases, such as elbow dysplasia, osteochondrosis,
hip dysplasia, medial patellar luxation and less common diseases such as hemimelia and ectrodactyly syndrome. The notes will focus on elbow dysplasia, as other lectures (and proceedings notes form the same author) include hip dysplasia, medial patellar luxation and cranial cruciate ligament rupture. The lectures will also mention less common pathologies. Elbow dysplasia is an umbrella term grouping four developmental disease processes of the elbow joints of dogs: fragmented coronoid process (FCP), ununited anconeal process (UAP), osteochondritis dissecans of the medial aspect of the distal humeral condyle (OCD) and elbow incongruity (INC). FCP is the most frequently diagnosed form of elbow dysplasia.
It is most commonly  rst recognized in growing, large and giant breed dogs between seven and nine months
of age. Bernese Mountain dogs, Labrador retrievers
and Golden retrievers are the breeds most commonly affected. Males are more commonly affected than females, although this may be a re ection of differential rate of growth. Resultant elbow osteoarthritis is the third most common orthopedic condition affecting adult dogs, after conditions affecting the coxofemoral and sti e joints.
Clinical signs usually reported in dogs with FCP include stiffness or a stilted forelimb gait, most obvious when
 rst rising or after prolonged rest or vigorous exercise. Bilateral involvement is common in which case lameness may be dif cult to detect. These dogs often stand with the elbow adducted and the antebrachium externally rotated (supinated) in a presumed attempt to shift weight away from the affected medial compartment to the lateral compartment of the elbow joint. Joint effusion may be present on physical examination. Pain is often elicited during maximal  exion,  rm supination in moderate  exion, deep digital pressure over the insertion of biceps brachii tendon on the ulna and extension of the elbow joint. These limb manipulations may increase the degree of lameness transiently after the examination. Disease of the medial coronoid process and changes associated with the articulating medial aspect of the distal humeral condyle (trochlea) are the most common pathologic changes noted surgically. Lesions noted on the medial coronoid process at surgery include cartilage malacia,  brillation,  ssuring and erosion and on histopathology subchondral bone micro ssuring and erosion are noted.
Erosive cartilage lesions, often referred to as ‘kissing lesions’, frequently develop on the articulating surface of the trochlea of the humeral condyle, in association with medial coronoid pathology.
Treatment of FCP by either conservative management, surgical removal of fragments by either arthrotomy or arthroscopy or corrective osteotomies has yielded similar outcomes. Irrespective of the method of treatment elected, osteoarthritis of the elbow progresses and the prognosis for a return to normal function is guarded. A total elbow replacement procedure may be required in severe cases of elbow osteoarthritis.5
While the etiopathogenesis of UAP and OCD are understood, there is no uniform agreement regarding the etiopathogenesis of FCP. FCP is an inherited
trait, although the genes responsible have yet to be identi ed. Abnormal endochondral ossi cation of the coronoid process, abnormal bone structure or abnormal biomechanics of the elbow joint have been proposed
as potential mechanisms. Histopathological studies
of elbows affected by FCP have demonstrated that these lesions are non-healing fractures, likely a result of repetitive excessive loading.
Fragmented coronoid process (FCP) was  rst identi ed in dogs by Olsson in 1974. It was initially believed that FCP, like OCD of the humeral condyle, was a manifestation
of osteochondrosis or a disturbance in endochondral ossi cation. However it has since been substantiated that FCP is not a manifestation of osteochondrosis,
but instead is a result of supraphysiologic loading, cumulating in fatigue failure and microfracture formation in the trabecular subchondral bone of the craniodistal
tip or the radial incisure of the medial coronoid process. Despite extensive research over the past three decades, the exact etiopathogenesis of FCP has yet to be elucidated and remains controversial, although abnormal biomechanics of the elbow resulting in this supra- physiologic loading of the medial coronoid process are considered the most likely cause.
Elbow incongruity refers to a malalignment of the articulating surfaces of the bones composing the elbow joint. There are two main types of joint incongruity; physiologic and pathologic. Physiologic incongruity
in the elbow joint occurs where the trochlear notch
of the elbow has a small concave incongruence that allows more equal stress distribution under high load and ensures better nutrition of the articular cartilage. Such incongruence is not thought to be involved
in the development of FCP. Pathologic incongruity refers to humero-ulnar con ict resulting in increased load concentrated in the area of the medial coronoid process. The main current biomechanical theories

   574   575   576   577   578