Hereditary musculoskeletal disorders include several diseases, such as elbow dysplasia, osteochondrosis, hip dysplasia, medial patellarluxation 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 first 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 reflection of differential rate of growth. Resultant elbow osteoarthritis is the third most common orthopedic condition affecting adult dogs, after conditions affecting the coxofemoral and stifle joints.

Clinical signs usually reported in dogs with FCP include stiffness or a stilted forelimb gait, most obvious when first rising or after prolonged rest or vigorous exercise. Bilateral involvement is common in which case lameness may be difficult 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 flexion, firm supination in moderate flexion, 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, fibrillation, fissuring and erosion and on histopathology subchondral bone microfissuring 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 identified. Abnormal endochondral ossification 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 first identified 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 ossification. 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 conflict resulting in increased load concentrated in the area of the medial coronoid process. The main current biomechanical theories proposed to cause humero-ulnar conflict and resultant supraphysiologic loading of the medial coronoid process include static elbow incongruity (radio-ulnar length disparity), dynamic elbow incongruity (radio­ ulnar longitudinal incongruence),ulnar trochlear notch geometric incongruity, primary rotational instability of the radius and ulna relative to the distal humerus and musculo-tendinous mismatch. Whether pathologic incongruity itself is the cause of forelimb pain and lameness is difficult to determine as it is usually associated with FCP.

Radio-ulnar step incongruity occurs due to disparate growth of the paired radius and ulna during skeletal development. In the case of a short radius, increased contact pressure has been reported in the area of the tip of the medial coronoid process in cadaveric studies of radii shortened experimentally18 and FCP has been induced by premature closure of the distal radial physis and resultant radial shortening. Radio-ulnar incongruity may be a dynamic state, only occurring at certain joint positions or during elbow loading. Diagnosis of radio­ ulnar incongruity during arthroscopy has been reported to have a higher diagnostic value than radiography and computed tomography (C1), as dynamic incongruity may be observed. Dynamic elbow incongruity may be present transiently during the development of elbow dysplasia but resolved by the time of diagnosis, making identification difficult.

Geometric incongruity, resulting in an elliptical ulnar trochlear notch that is too constrained to accommodate the humeral condyle, is another proposed etiology. Theoretically, this anomaly would cause increased pressure to occur on both the anconeal process and the medial coronoid process and both FCP and UAP could occur in the same joint. However, the incidence of UAP and FCP occurring in the same elbow is low and following three-dimensional digitizing studies and those examining the radius of curvature of the ulnar trochlear notch in breeds typically affected compared with those unaffected with FCP, it is considered unlikely that the conformation of the ulnar trochlear notch alone is responsible for clinical disease.

Commonly recognised lesions associate d with medial coronoid disease are typified by cartilage malacia, fibrillation, fissuring and erosion in addition to subchondral bone micro-cracks and fragmentation. Frictional erosion of the medial humeral condyle (‘kissing lesion’) is frequently associated with coronoid disease whilst osteochondrosis of the medial aspect of the humeral condyle may give rise to lesions of osteochondritis dissecans. This plethora of pathology and ensuing full thickness cartilage erosion with subchondral bone exposure in the region defined by the medial coronoid process and medial aspect of the humeral condyle has been referred to as medial compartment disease (MCD). Elbow incongruity such as radio-ulnar step defects, humero-ulnar incongruence/conflict, varus deformity of the humerus or imbalance between skeletal and muscular mechanics may contribute to medial compartment syndrome of the elbow joint in dogs. Pathology of the lateral aspect of the elbow joint is far less commonly observed.

Non-surgical treatment of elbow osteoarthritis should always be considered as the first treatment option. Conservative treatment of osteoarthritis is based on 4 major components: 1) weight loss/control, 2) controlled low-impact activity, 3) NSAIDS, 4) chondroprotection. More recent additions to these treatments include physical therapy (a type of controlled low-impact activity), acupuncture, and intra-articular injection of hyaluronic acid, steroids, platelets enriched plasma or autologous conditioned plasma or stem cells. While medical treatment of osteoarthritis is well accepted and has been evaluated in several clinical studies, very few data are available for the most recent treatment modalities. Surgical treatments may include radial or ulnar osteotomies to address perceived incongruity, removal of free fragments and cartilage debris, debridement of lesions and subchondral micro-picking. Osteochondral Autograft Transfer System (OATS™, Arthrex, Naples, FL) allows resurfacing of lesions associated with OCD. Osteotomy of the ulna may lead to varus deformity of the limb and subsequent increased load on the medial compartment. Novel osteotomies have been recently described and are under investigation. The aim of these osteotomies is to achieve similar results to the sliding humeral osteotomy (shift in compartmental pressure) but with a less invasive procedure. A proximal ulnar ostotomy has been developed by lngo Pfeil and Slobodan Tepic with the goal of causing a valgus tilt of the distal ulna and therefore of the limb. Another options for end stage elbow osteoarthritis include uni- or bi-compartmental arthroplasty. The data available for elbow arthroplasty is still scarce compared to total hip replacement. Total elbow replacement such as the Iowa total elbow or the TATE elbow replacement (both from Biomedtrix) offer semi-constrained implants with cemented or cementless fixation. The early results of the TATE are promising, but further long-term studies are needed. The main limitation of the elbow arthroplasty is that if revision surgery following catastrophic failure is needed, arthrodesis or amputation may be the only options. A more recent surgical option for medial compartment disease consists of a resurfacing prosthesis which aims at eliminating the medial compartment collapse and bone-to-bone contact caused by advanced medial OA. This procedure is called CUE (from Arthrex Vet System). Although few cases have been performed, the initial results are promising with good to excellent return to activity and minimal morbidity.

Osteochondrosis is not only found under the umbrella term “elbow dysplasia”, but can also affect other joints such as shoulder, stifle, tarsus and sacro-iliac joint. Osteochondrosis is thought to have a multifactorial etiology. Genetic factors that affect weight gain and growth, behavior, sexual development and conformation undoubtedly are involved in the etiology of osteochondrosis. Osteochondrosis occurs primarily in medium to large and giant breed dogs. Rapidly growing representatives of these breeds seem to be predisposed. The genetic capacity for rapid growth and overfeeding may be influential during the dog’s period of rapid growth. This is an important aspect in athletic dogs as often it is the largest, most rapidly growing dog that is desired. In addition the selective breeding of performance animals may be based on performance data, conformation, and other desired qualities without knowledge of the presence of articular disease that may be subclinical in nature or affected littermates.

Biomechanical forces are another important etiologic factor in the development of osteochondrosis. Osteochondrosis lesions develop in areas of articular cartilage that are subject to increased loads. Normal joint stresses and focal trauma likely are inciting perpetuating factors involved in the pathogenesis of this condition. The strenuous activity often imposed on performance dogs at very young ages may partially account for the high incidence of osteochondrosis in many breeds of working and racing dogs.

Overnutrition in the form of excessive amounts of food and/or nutritional supplements has been incriminated as another important etiologic factor. This is evidenced by higher caloric intake in rapidly growing animals resulting in greater incidence of osteochondrosis. Excessive calcium supplementation has been definitively established to increase the development of osteochondrosis. Large and giant breed dogs are predisposed to develop osteochondrosis with elevated dietary calcium intake. Hormonal disturbances have also been incriminated through experimental production of osteochondrotic lesions following the administration of thyrotropin, growth hormone, estrogens and androgens.

Osteochondrosis is usually seen in medium, large and giant breed dogs. The clinical manifestation of the disease typically occur between 4 to 9 months of age; however, it is interesting to note that in a recent review of 626 dogs with osteochondrosis of the humeral head, 36% of the dogs presented for treatment were greater than a year of age. Osteochondrosis is usually seen more frequently in males than females. The exception to this trend is osteochondrosis of the hock, which has been reported slightly more frequent in female dogs. In dogs, osteochondrosis most commonly develops on the articular surfaces of the humeral head, humeral condyle, femoral condyles, and the trochlear ridges of the talus. Less frequently reported sites of osteochondrosis include the femoral head, patella, distal end of the radius, articular facets of the spine, and glenoid surface of the scapula. Multiple joint involvement is not uncommon. A thorough physical and radiographic examination is necessary for early detection of this disease and to avoid giving an overly optimistic prognosis for return to athletic performance.

Treatment of osteochondrosis involves excision of the cartilage flap and curettage of the subjacent subchondral bed. Osteochondritis dessicans lesions of the humeral condyle may not be as obvious as osteochondritis dissecans lesions of the humeral head. If a lesion is suspected based on the pre-operative radiographs and is not readily apparent at arthrotomy, the articular surface of the trochlea of the humeral condyle should be probed with a Freer periosteal elevator. In these instances, the malacic cartilage will readily separate from the adjacent unaffected cartilage. All diseased cartilage should be excised and the subchondral bed curettaged. Osteochondritis dissecans lesions of the humeral condyle should be differentiated from erosive or kissing lesions of the trochlea of the humeral condyle, which frequently occur in response to fragmented coronoid process.

Arthroscopy can be used to diagnose and treat lesions of the humeral condyle. Routine evaluation of the joint is performed. The coronoid processes should be carefully evaluated for the presence of a fragmented coronoid process and the OCD lesion should be differentiated from a kissing lesion. Routine arthroscopy debridement of OCD lesions including removal of the flap, curettage and micropicking as needed is performed. Novel treatment are osteochondral transfer as previously discussed in the notes.