Canine Osteochondrosis

Osteochondrosis (OC) is a disorder affecting the process of endochondral ossification in growing people and animals including dogs, horses, pigs, and chickens [1]. Although the clinical manifestations associated with OC are well described, the etiology and pathogenesis are not yet completely understood. Osteochondrosis affects the articular-epiphyseal and physeal cartilage cells and can be expressed clinically as osteochondritis dissecans lesions, fragmentation of the medial coronoid process of the ulna (FCP), ununited anconeal process (UAP), retained cartilage cores, Osgood-Schlatter syndrome (OC of the tibial tuberosity), slipped epiphysis, or incomplete ossification of the humeral condyle. All these conditions are considered to have a similar pathogenesis. Osteochondrosis is a common cause of secondary osteoarthritis in people and domestic animals [2]. Osteochondritis dissecans (OCD) is the most common clinical manifestation of osteochondrosis. Although osteochondritis is a misnomer because it implies inflammation of bone and cartilage, it has become entrenched in veterinary medical terminology. Synonyms for OCD found in the literature include osteochondrosis dissecans and dyschondroplasia. Regardless of the terminology, to the veterinarian OCD indicates a dissecting cartilaginous lesion between the bone epiphysis and articular surface. Lesions of canine OCD have been described on the cervical vertebrae, glenoid surface of the scapula, proximal humerus, distal humerus, distal radius, femoral head, distal femur, tibial tarsal bone, and most recently, the lumbosacrum.

This chapter is an overview of the normal growth and ossification of the canine appendicular skeleton, followed by an in-depth review of the pathology and pathogenesis of osteochondrosis. Pathogenic factors specific to the shoulder, elbow, stifle, tarsus, lumbosacrum, and incomplete ossification of the humeral condyle are also described.

Normal Growth and Ossification of the Canine Skeleton

The growing canine skeleton is composed of cartilage and bone. Three distinct embryonic lineages are responsible for the formation of the skeleton [3,4]. The craniofacial skeleton arises from cranial neural crest cells, the vertebral skeleton is derived from paraxial mesoderm (somites), and the limb skeleton is formed from the lateral plate mesodermal cells [3,4]. Cells from each lineage migrate to locations in the embryo where bone will eventually form and there they develop into characteristic mesenchymal condensations of high cell density [3,4]. These condensations develop into osteoblasts or chondrocytes [3,4]. The cells in the region of the craniofacial skeleton develop into osteoblasts and directly form bone by intramembranous ossification. In the remaining skeleton, chondrocytes develop first and provide a framework of cartilage models. The cartilage models are replaced by bone and bone marrow through the endochondral ossification process.

The cartilage models of future appendicular bones grow by appositional and interstitial growth and quickly resemble the future bone in shape and relative size [3,5]. As capillaries enter and supply the surrounding perichondrium, osteoblasts are formed from circulating progenitor cells and begin to lay down a thin layer of bone around the cartilage. At the same time, the chondrocytes in the center become hypertrophic. As the collar of bone and area of hypertrophy continue to enlarge, the matrix surrounding the hypertrophic chondrocytes begins to calcify by incorporating hydroxyapatite. This results in a network of trabeculae with a cartilaginous core, called primary spongy bone. Primary spongy bone is rapidly resorbed and secondary spongy bone with new trabeculae is formed. The actual process of replacing calcified cartilage (endochondral ossification) occurs in the mid-diaphysis of long bones first. The initial area of ossification is called the primary ossification center and extends in each direction toward the end of the cartilage model. As the process continues, secondary ossification centers develop in each epiphysis. A plate of cartilage remains between the ossified secondary and primary centers and is responsible for the longitudinal growth of long bones [3]. This plate is called the physeal growth plate (Fig. 100-1). The cartilage on the end of the secondary ossification center that is closest to the joint is termed the articular-epiphyseal cartilage complex (AECC). Epiphyseal cartilage of this complex is responsible for growth of the epiphysis and the development of its shape. At maturity in normal dogs, articular cartilage is all that remains on the surface of the bony epiphyses.

Figure 100-1. Histologic sections that demonstrate the mechanism of longitudinal growth as seen morphologically in the growth plate and the metaphysis. (A) Undecalcified section of the proximal tibial metaphyseal growth plate with part of the epiphysis (above) and the metaphysis (below) from a 9-day-old rabbit. In the growth plate, the zone of germinal (resting) cells (A), proliferating (columnar) cells (B), transitional (hypertrophying) cells (C), and vesiculated cells (between arrows) are seen. The matrix in the longitudinal bars separating the columns of vesiculated cells is calcined (von Kossa’s stain; 50x). (B) Section of the junction between the proximal tibial metaphyseal growth plate (top) and the metaphysis (bottom) in a newborn puppy. It illustrates how the horizontal bars of the cartilage matrix are eroded by vascular sprouts (small arrows) and how chondroclasts (large arrows) resorb calcified matrix in the longitudinal bars (Hematoxylin and eosin (H&E) stain; 250x). (From Summer-Smith, G. (Ed.): Bone in Clinical Orthopedics. Philadelphia, W.B. Saunders, 1982.)

The process of ossification starts at weeks 3 to 4 in the canine fetus, but cannot be detected radiographically until 3 weeks prior to parturition. When a puppy is born, the epiphyses are still cartilaginous with no or only small secondary centers of ossification present. By 2 to 4 months of age, depending on breed, only the physeal growth plates and articular cartilages remain unossified [6].

Normal Growth of the Articular-Epiphyseal Cartilage Complex

Articular cartilage is divided into three regions: superficial, middle and deep (Fig. 100-2) [7]. The superficial region is immediately under the surface of the joint and consists of the lamina splendens (composed of filamentous proteins that bind proteinaceous material and provide lubrication for joint surfaces) and the gliding zone (cells are parallel to the surface) [8]. The middle region has cells arranged perpendicularly to the surface of the articular cartilage and is divided into the transitional zone (characterized by cell activity and interstitial growth, allowing the articular cartilage to cover the epiphysis during growth) and the radial zone (composed of cells lined up in irregular columns). The superficial and middle regions are responsible for the expansion of the articular surface during development. The deep region is composed of calcified cartilage and subchondral bone supporting the articular cartilage. Vascular invasion of calcified tissue occurs here, followed by endochondral ossification. The deep region is responsible for the development of epiphyseal bone. A thin wavy hematoxylin-stained line called the tidemark can be seen histologically separating the non-calcified tissue of the middle region from the calcified tissue of the deep region in adults [5].

Figure 100-2. Histologic section of the articular cartilage of the proximal humerus from a 9-day-old rabbit. The immature joint cartilage is the growth cartilage of the epiphysis. The germinal (resting) cells (a) are located about four or five cell layers away from the joint surface. Deeper in the cartilage is the zone of proliferating cells (b), and then the zone of hypertrophying (vesiculated) cells (c), where the cartilage is invaded by vessels paving the way for ossification (H&E stain; 50x). (From Summer-Smith, G. (Ed.): Bone in Clinical Orthopedics. Philadelphia, W.B. Saunders, 1982).

Normal Growth of the Physeal Growth Plate

The physeal growth plate and the epiphyseal component of the AECC differentiate into four morphologically and chemically distinct zones during development (Fig. 100-3). From the epiphysis toward the metaphysis, they are the resting (reserve or germinal), proliferative, hypertrophic, and calcifying zones; orderly maturation of cells in these zones is required for proper endochondral ossification [1,3]. The cells of the resting zone are small and relatively inactive. The proliferative adjacent zone has both local and systemic growth factors that stimulate chondrocyte proliferation. In this zone clonal expansion of proliferated cells takes place toward the metaphysis (cartilage-bone junction) where the cells enlarge, arrange in columns and eventually hypertrophy [3]. The cells of the hypertrophic zone are highly metabolically active, but do not divide. The matrix surrounding the hypertrophic cells continues to calcify, and the lowermost cells undergo apoptosis (regulated cell death) [3]. Osteoclasts and osteoblasts, which have developed from progenitor cells brought in by invading blood vessels, remove the calcified cartilage and deposit bone, respectively. When maturity is reached, the metaphyses and diaphysis are united and the cartilaginous portion is completely replaced by bone. With few exceptions, in mature animals the only remaining cartilage is the hyaline cartilage of the joint surfaces.

Figure 100-3. Schematic drawing of the development of a long bone. A, Early in fetal life, the long bone consists only of cartilage. B, When the fetus is about 30 days old, it has some cortical and trabecular bone at midshaft. The cortical bone is formed by periosteal apposition, whereas the trabecular bone is formed by endochondral ossification. C, In the newborn puppy, the entire diaphysis (which includes the two metaphyses) is made of cortical and trabecular bone including bone marrow, while the epiphyses have just begun to ossify. D, When the puppy is a few months old, the only cartilage left in the long bone is the one in the growth plates and in the immature joint.

Vascular Supply and Nutrition of Epiphyseal Cartilage

The epiphyseal cartilage of both the physeal growth plate and the AECC have a well-developed blood supply through a network of cartilage canals [1,9,10]. The cartilage canals regress as the animal ages and the growth cartilage becomes thinner. The physiologic process of this regression is termed chondrification [10]. Chondrification causes the vessels, nerve fibers, and stromal cells within the canals to be substituted with cartilage without pathologic effects on the surrounding tissue [10]. Nutrition is supplied to the AECC by these blood vessels, in addition to synovial fluid.1 The contribution of each source depends on age, species, and anatomic location [1]. In the adult, articular cartilage receives a minor contribution from vessels of the subchondral bone, obtaining most of its nutrients from the synovial fluid.

Pathophysiology

Pathology and Morphology

Osteochondrosis is characterized by failure of normal differentiation of cartilage to bone during endochondral ossification; neither matrix calcification nor vascular penetration occurs in focal areas of the growing epiphyseal/articular cartilage, resulting in retention of cartilage rather than conversion to bone.1 Although abnormal focal regions of retained cartilage are avascular, they receive nutrients from diffusion of synovial fluid and continue to grow. This results in focal abnormally thickened cartilage, which is less resistant (more compliant) to mechanical stresses. The increased thickness eventually prevents adequate diffusion of nutrients and results in a disturbance of the metabolism of the basal layer. Degeneration and necrosis of the chondrocytes at the base of the OC lesion are the ultimate outcome, which can lead to the separation of the retained cartilage from the underlying calcified tissue. This phenomenon occurs along the tidemark and rarely involves subchondral bone.11 The resulting fragments are characteristic of OCD lesions when they develop in the AECC.

In the AECC the earliest identifiable histologic lesion is termed osteochondrosis latens and is identified as focal necrosis of the cartilage canal vessels and the surrounding cartilage of the resting zone of the epiphyseal cartilage [10]. If the necrotic cartilage resists resorption and persists as a cone of dead tissue surrounded by bone it is termed osteochondrosis manifesta and appears grossly as an area of delayed endochondral ossification [10]. Because this necrotic cartilage is soft and friable, it does not provide a suitable foundation for the over-laying AECC; thus, even minimal trauma can lead to fissure and fracture formation. When these fissures and fractures extend from the necrotic tissue to the articular surface it is termed osteochondritis dissecans [10]. In pigs and horses, early lesions of OC of the AECC have been associated with abnormalities in cartilage canal blood vessels [10,12-15]. These abnormalities have been hypothesized to cause local ischemia and chondronecrosis.

Spontaneous repair attempts of the OCD lesions usually occur beneath the cleft with granulation tissue production, fibrogenesis, and osteoblastic and osteoclastic activity. Subchondral bone formation occurs at the base of the granulation tissue, but does not extend past the tidemark. The granulation tissue undergoes chondrification and may even develop some hyaline cartilage. Continuous passive motion during healing may encourage hyalinization of the fibrocartilage [5]. The success of the reparative process is related to the size and extent of the defect as well as time from development. Small defects can completely heal through matrix flow and intrinsic repair (chondrocytes, proliferation and increased extracellular matrix production). In large defects, however, fibrocartilage degenerates within one year, which leads to secondary osteoarthritis from release of breakdown products [5,16].

Osteochondrosis of the AECC can lead to OCD lesions in the shoulder, elbow, stifle, hock, and vertebral articular facets, and FCP [17]. Two types of OCD lesions of the AECC exist. Type I OCD lesions are the classic form and occur when the lesion is in or near the center of a convex joint surface. In these cases, the cartilage flap does not have contact with any vascular tissue, such as the joint capsule. As a result, the flap eventually becomes detached and floats in the joint. This flap may be resorbed or may increase in size as a result of nourishment from synovial fluid. When the flap is free in the joint and becomes ossified it is termed a loose body or "joint mouse". These lesions typically occur in the humeral head, medial condyle of the humerus, and the lateral and medial femoral condyles.

Type II OCD lesions occur at the periphery of the joint surface providing contact between the cartilage flap and the joint capsule or ligament. Eventually the flap will undergo endochondral ossification and not produce a joint mouse. Osteochondritis dissecans lesions of the medial or lateral ridge of the talus and sacrum, as well as fragmented coronoid process and ununited anconeal process, are typically type II lesions [6].

Clinically, OC lesions can be divided into four grades, with grade I the most mild and grade IV the most severe. Grade I classification is given in cases with grossly normal articular cartilage and a small defect in the subchondral bone, whereas grade IV is given when a cartilage flap is separated from the bone. Grades II and III are given subjectively to cases that fall between mild and severe. Because animals are not in pain until the fissure reaches the articular cartilage, grade IV (OCD lesion) is the most common form diagnosed by veterinarians.

In the physeal growth plate, early lesions of OC are much less obvious than in the AECC until after failure of endochondral ossification has occurred. In the growth pate, retained cartilage is composed of viable hypertrophic chondrocytes. Retention of cartilage in the growth plate usually does not lead to necrosis, probably owing to the presence of vessels in the cartilage. The majority of these lesions heal uneventfully. Clinical signs may manifest if a pathologic fracture occurs within the thickened cartilage or, more importantly, if it occurs at the distal end of the ulna. Incongruity of the radius and ulna can occur owing to slowed growth of the ulna relative to the radius. Occasionally, incongruity can be seen as a result of OC of the distal radial growth plate. Osteochondrosis of the physeal growth plate can result in UAP, retained cartilaginous cores of the distal ulna, and genu valgum (knock-knee) [17].

Pathogenesis

The underlying lesions of osteochondrosis occur in the growing animal, although they may not show clinical signs until adulthood [1]. The primary lesion of OCD is a dissecting cartilaginous separation between calcified and noncalcified tissues [5]. The necrotic base of the OC lesion is the starting point for fissures. If the necrotic cartilage is large enough and/or there is sufficient trauma has occurred, a cleft will form from the articular cartilage to the subchondral bone. This results in synovitis from release of inflammatory mediators, joint effusion, and clinical evidence of lameness. It has been suggested that premature disruption of the nutritional function of the vasculature of the cartilage canals results in cartilage necrosis (osteochondrosis latens) [18]. Recently it has been shown that there is premature cessation of blood supply to the epiphyseal growth cartilage caused by focal interruption of the vessels leading from the bone marrow into the cartilage canals [10]. This study proposed that OC occurs secondary to ischemic necrosis caused by microtrauma to the vessels of the cartilage canals in the transition zone between bone and cartilage [10]. It has also been suggested, based on the finding of an increased amount of lipid in OCD cartilage flaps, that delayed calcification may be a result of a lipid metabolism defect [19].

The effects on the subchondral bone adjacent to the OCD lesion are typically myelofibrosis and trabecular remodeling. It can be quite extensive, but necrosis of the bone is not a prominent feature of OCD. Subchondral bone cyst formation is a possible, but uncommon, sequela to OCD.

Suggested contributing factors for OC development are trauma, familial/hereditary predisposition, ischemia, rapid growth, and dietary factors [1]. The etiology is likely multifactorial, with no single factor accounting for all aspects of the disease. Our current understanding of the contributions of trauma and genetic factors is discussed below.

Trauma is the most widely considered factor in all species regarding the etiology of OC [1] and is important in the progression of OC to OCD. Trauma does not have to be severe to cause separation of cartilage and bone in the abnormal cartilage of OC. The gross and histologic appearances of the chronic lesions (lesions with a cartilaginous flap) support this theory. The usual locations are in areas with increased biomechanical stresses [1]. It has been hypothesized that epiphyseal cartilage is inherently weaker and thus more vulnerable to trauma than articular cartilage [20], however, no research currently supports this concept. Research in swine has shown that, although both the medial and lateral condyle can be affected with OC, the most clinically relevant lesions occur on the medial condyle [21]. Indeed, the medial condyle receives most of the weight-bearing forces. Most cases of OC have an insidious onset and although purely traumatic osteochondral fractures can occur, particularly in people following severe automobile accidents, they are not considered to be OC. Olsson hypothesized that local traumatic factors within joints, which vary with location, was a principal cause of canine OC [6]. He theorized that repeated microtrauma in predilection sites was crucial to the development of OC [22]. Examples of local microtrauma include impingement of the dorsolateral area of the humeral head in the shoulder joint or forced contact between the medial aspect of the lateral femoral condyle and lateral part of the intercondylar eminence in the stifle joint of animals with genu valgum. Olsson also hypothesized that transient incongruence in growth rates between the radius and ulna was a factor in ununited coronoid and ununited anconeal process as well as distal humeral OC. Further support for local microtrauma comes from studies performed in calves, which found that when they were housed on hard surfaces the prevalence and severity of OC was increased [23]. Another study compared pigs that were loaded into crates by dropping them from varying heights under 1 meter to pigs that were not loaded [24]. This study found that OC lesions were more severe and prevalent in pigs that were loaded. Unfortunately these theories have only been evaluated in the chronic stages of the disease and not in the early stages, thus the true pathogenesis remains unknown. However, because most early lesions heal, it is possible that, if joints are protected from trauma during the vulnerable development stage, clinically relevant disease could be reduced [1]. Trauma may be influenced by heritable factors, such as anatomic conformation and/or quality of the surrounding bone and cartilage, and facilitated and/or aggravated by mechanical stress to the area in the limited time period that important blood vessels exist [10].

Familial cases of OC have been reported in people, including cases in identical twins [1]. Domestic pigs, which have been genetically selected for certain traits, have a high prevalence of OC, regardless of breed, whereas wild and miniature pigs do not [25]. A polygenetic mode of inheritance of elbow joint OCD in Labrador retrievers has been shown [26]. Dog breeds that reach a mature weight of more than 20 kg tend to be more commonly affected with OC [1]. This prevalence appears to be increased in animals in which rapid growth is emphasized. There also tends to be a greater male incidence, possibly owing to a more rapid growth rate when compared with females. It has been proposed that low serum concentrations of the main metabolites of vitamin D3 found in growing large-breed dogs fed standard dog food may play a role in disturbances in endochondral ossification [27,28]. Thus, other contributing factors result in OC, not just overall growth rate and feeding regimen. It is unlikely that nutrition, hormonal influences, and trauma alone could account for the development of OC.

In general, the larger the defect the more likely a dog is to have a persistent lameness. In addition, the larger the lesion the more likely the opposite joint surface is to develop a "kissing lesion". The kissing lesion occurs as a result of lack of normal physiologic compression on the opposite articular surface, which is necessary for maintenance of healthy cartilage. If motion is present between the bone and cartilage flap, synovitis and pain will ensue. Healing will not take place owing to the motion and the presence of synovial fluid between the flap and bone. Healing will only occur if the flap is stabilized or removed.

Specific Osteochondritis Dissecans Lesions

In most cases, diagnosis is based on signalment, history, clinical signs, and physical and orthopedic examination, and confirmed with bilateral radiographs of the affected joint. Not uncommonly, advanced imaging such as computed tomography or exploratory arthroscopy or arthrotomy is required to make a definitive diagnosis. Contrast arthrography is rarely necessary.

Although most cases are presented as young dogs, any aged dog can be seen. Lameness ranges from sudden to insidious onset, from barely appreciable to non-weight bearing. Dogs can present with any degree of joint effusion, reduced range of motion, muscle atrophy, and pain associated with the OCD lesion. In most cases, regardless of treatment, development of secondary osteoarthritis is inevitable.

Shoulder Joint

Osteochondritis dissecans of the scapulohumeral joint is a common cause of lameness and is the most commonly seen form of OC in dogs in the United States [17]. Surgical removal of the cartilage flap is the preferred method of treatment in dogs with clinical signs. Long-term prognosis following surgery is good to excellent.

The most common site for OC lesion development in the shoulder is the caudal central or caudal-central-medial region of the humeral head (Fig. 100-4). Lesions of the glenoid occur rarely [29]. Although the particular susceptibility of the caudal central aspect of the humeral head is not fully understood, it has been suggested that it is due to the increased thickness of cartilage normally present in that area in dogs [30,31]. It has been suggested that trauma from contact between the humeral head and the glenoid cavity of the scapula predisposes any abnormally developed cartilage to vertical fractures [30,31]. In 1965, it was proposed that the particular location of the OC lesion of the shoulder was caused by the repeated impingement of the caudal part of the humeral head by the scapula during full extension [6,32]. Olsson later suggested that this could be supported by the finding in dogs with shoulder osteoarthritis that osteophytes on the caudal region of the humeral head are often attached to the scapula by fibrous tissue, indicating a dynamic component to their development [6,32].

Figure 100-4. A series of images illustrating OCD of the caudal humeral head. (A) Lateral radiographic view of the affected side. Note the flattened area of subchondral bone (white arrows). (B) Lateral radiographic view of the normal side. Note the curved, smooth surface of the caudal humeral head. (C) An arthroscopic view of a cartilage flap (asterisk) involving the caudal humeral head. (D) An intra-operative view of the caudal humeral head showing the subchondral bone (black arrows) after flap removal.

Many cases of shoulder OCD heal spontaneously [6]. The pedicle of the cartilage flap may rupture, thereby dislodging the flap and allowing fibrocartilage to grow from the floor of the defect. The dislodged flap may develop into a joint mouse, become resorbed, or continue to grow. It is possible that the flap(s) can become a large calcified body/bodies in the caudal pouch of the joint. If the calcified body remains in the caudal pouch it may not give rise to clinical signs; however, if it becomes entrapped between the scapula and humerus it can cause sudden pain and locking of the shoulder joint. If the calcified piece migrates to the sheath of the biceps tendon it can cause persistent lameness.

Humeral head OCD most commonly affects large and giant breed dogs with 56 different breeds being identified in a study of 626 affected dogs [33]. While some large breeds such as the Swiss Mountain Dog, Great Dane, German Shepherd, Newfoundland, Rottweiler, Labrador Retriever, Golden Retriever, and Bernese Mountain Dog, are at a high risk of developing OCD of the humeral head [34,35], some large breeds such as the Doberman Pinscher, Collie and Siberian Husky are considered to be at low risk [33]. Small and medium-sized breeds can also be affected [33,36-39].

Although most dogs present for unilateral lameness, approximately 50% (range 20% to 85%) have radiographically detectable lesions bilaterally [5,31,33]. In one study, only 24% of dogs diagnosed with bilateral lesions on radiographs had clinically bilateral disease.

Elbow Joint

Several lesions of the elbow joint can be classified as manifestations of OC including fragmented coronoid process (FCP), OCD, and ununited anconeal process (UAP) (See Chapter on elbow dysplasia). Of all these, the most common cause of elbow arthrosis is some abnormality of the coronoid process (fragmented or fissured) and, less commonly, OCD of the humeral condyle [17]. The most common site for OCD in the elbow is along the medial aspect of the humeral condyle (Fig. 100-5). Careful examination must be performed to definitively diagnosis OC or OCD. Long-term prognosis following surgical treatment for OC of the elbow is guarded. Early treatment may decrease lameness, but will not prevent progression of secondary osteoarthritis.

Figure 100-5. A radiographic and intra-operative image illustrating OCD of the medial humeral condyle. (A) Lateral radiographic view of an elbow joint. Note the flattened area of the medial humeral condyle (white arrows) that has resulted in a widened joint space. (B) An intra-operative view, via a medial approach, showing the elevation of a cartilage flap (black arrow) from the medial humeral condyle.

Osteochondrosis of the elbow occurs less commonly than shoulder OC, however, the signalment is similar. Large- and giant-breed dogs are most commonly affected, with the highest prevalence in Bernese Mountain Dogs, Golden Retrievers, Labrador Retrievers and Rottweilers. In a study on 1247 Labrador Retriever puppies in an Australian breeding colony producing guide dogs, 15% had OC of the elbow [40]. The Newfoundland, Flat-coated Retriever, Chow Chow, Great Dane, and German Shepherd have also been found to be over-resented breeds with elbow OC [6,34,35]. Most dogs are presented when they are less than 1 year of age, however ages ranging from 4 months to 12 years have been reported [41-43]. Males are affected more often than females (2:1). Right and left elbows are affected equally, with bilateral disease in 20 to 50% of patients [41,44].

Stifle Joint

Osteochondrosis of the femorotibial joint is uncommon in dogs [42,45]. It occurs most commonly along the lateral femoral condyle, but can also occur on the medial femoral condyle (Fig. 100-6). Surgical treatment of stifle OCD is required, and although prognosis depends on the size of the lesion, it is generally only fair.

Figure 100-6. A series of images illustrating OCD of the femoral condyle. (A) A lateral radiographic view showing flattening of the lateral femoral condyle (white arrows) and a mineralized joint mouse in the cranial aspect of the fat pad. (B) A caudocranial radiographic view showing a flattened area of the medial femoral condyle (white arrow). (C) A CT scan three-dimensional reconstruction showing the extent of a medial femoral condyle OCD lesion (black arrow). (D) An intra-operative photo showing an OCD flap (hemostat is pointing to the flap) involving the medial femoral condyle.

Young, large-breed dogs usually present between 4 and 9 months. Breeds at risk include: boxers, Great Danes, German shepherds, Labrador retrievers, Rottweilers, bullmastiffs, bulldogs, Irish wolfhounds, golden retrievers, and Newfoundlands [34,35]. Approximately 66% of cases occur in male dogs and approximately 72% of cases are bilateral [45].

Tibiotarsal Joint

Osteochondritis dissecans of the tibiotarsal joint is well known, but uncommon. It occurs along the medial or lateral talar ridge in a cranial to caudal direction (Fig. 100-7). The medial ridge is more commonly affected. Prognosis is guarded and lameness is likely to persist even without strenuous exercise. Prognosis is improved in cases with small lesions that are treated early. Moderate to severe osteoarthritic changes are expected.

Figure 100-7. Radiographic and intra-operative images illustrating OCD of the trochlear ridge of the talus. (A) A caudocranial radiographic view of the tarsus showing the OCD lesion (black arrow) of medial trochlear ridge and secondary osteoarthritis. (B) An intra-operative view showing a nondisplaced OCD lesion (black arrow) of the lateral trochlear ridge of the talus.

A histologic study of 38 OCD flaps removed surgically from the hock joint concluded that OCD of the talus follows the same sequence of events as OCD of other joints. The one difference is that the cartilage flaps do not only undergo calcification, but also ossify and attach to the synovial membrane and/or the collateral ligament (Type II). This is likely owing to the relatively rich vascular supply from the surrounding synovial membrane and collateral ligament. Olssen suggested that the reason for the increased incidence on the medial trochlear ridge is local pressure by the tendon of the flexor hallucis longus muscle and pull by the short branch of the medial collateral ligament [6].

Most dogs present when they are less than 1 year of age, although a range of 4 months to 4 years has been reported [46]. The incidence in males and females is almost equivalent [44]. Large-breed dogs, particularly the Labrador retriever, Rottweiler, and bullmastiff are over represented [34,35,44,46]. Tarsal OCD is bilateral in approximately 60% of cases (range 54% to 69%) [45,46]. Most tarsal OCD lesions (79%) occur on the medial trochlear ridge of the talus [44,47]. Of these lesions, 80% occur on the plantar aspect of the ridge. Conversely most lesions that occur on the lateral trochlear ridge are present on the dorsal aspect of the ridge [44]. It has been reported that lesions of the lateral trochlear ridge occur more often in Rottweilers than in other breeds [48,49].

Lumbosacrum

Lumbosacral OCD is a form of cauda equina syndrome.50 Lesions of vertebral OCD vary from cartilaginous overgrowth to flaps of cartilage that separate from the underlying bone and cavitation of the vertebral epiphysis [51]. Sacral OCD is a developmental disturbance of the sacral end plate, with subsequent separation of hyaline cartilage with a bone center from the dorsal corner [52,53]. Lesions are usually on the craniodorsal corner of the sacral body, or less commonly, on the caudal endplate of the seventh lumbar vertebra (91% and 9%, respectively) [51]. Of dogs presenting with cauda equina neuropathy, 15 to 30% have been reported to have lumbosacral OCD [51,54].

Lumbosacral OCD lesions most commonly affect German shepherds, with male dogs being over represented (4:1, male:female) [51]. Dogs are usually diagnosed when they are older than 14 months (range 14 months to 13 years; mean 6.3 years) [51]. It has been suggested that despite radiographic evidence, clinical signs do not appear until dogs are over 18 months of age.

Incomplete Ossification of the Humeral Condyle

Forelimb lameness caused by a radiographically visible radiolucent line in the center of the humeral condyle was first described by Meutstege in 1989 [55]. It subsequently became known as incomplete ossification of the humeral condyle (IOHC) and is an uncommon cause of forelimb lameness in dogs [56].

The pathogenesis of incomplete ossification of the distal intercondylar humerus epiphyseal plate (IOHC) is unknown. In normal dogs, two separate centers of ossification appear in the humeral condyle at 14 +/- 8 days after birth [57]. One ossification center includes the capitulum and the lateral aspect of the humeral condyle and one ossification center develops into the trochlea and the medial aspect of the condyle. The two centers of ossification normally unite at 70 +/- 14 days after birth [56]. The fissure line seen in IOHC of adult dogs coincides precisely with the cartilaginous remnant between the lateral and medial centers of ossification of the humeral condyle present in immature dogs (Fig. 100-8) [56]. For this reason it is thought that the source of the problem is failure of complete ossification of the humeral condyle [56]. Another possible cause is a form of stress fracture, in which the condylar fissure develops after ossification of the condyle is complete [58]. It has been proposed that incongruency in the elbow joint creates stress within the humeral condyle that either prevents ossification or promotes a stress fracture [58]. If an incongruency is the underlying factor, then IOHC may be a manifestation of elbow dysplasia. Fragmented coronoid process and OCD lesions have been found to co-exist in some cases of non-fractured condyles, suggesting that the pathogenesis is linked [56,59]. It is suspected that IOHC has a genetic basis with a recessive mode of inheritance in spaniels [56]. It has also been suggested that chondrodystrophic dogs are at greater risk [58]; however, normotrophic dogs can also be affected [59,60]. Biopsies taken from the intercondylar area during surgery usually reveal fibrous tissue, with high osteoclastic activity and plasma cell numbers suggesting chronic inflammation [56,59]. Regardless of the etiology, dogs with IOHC are predisposed to humeral condylar fractures, particularly following minor trauma. Most dogs present with a humeral condylar fracture following major or minor trauma, or following normal activity such as jumping from a height of 1 meter or less, climbing stairs, or running [56]. A radiolucent line between the condyles of the contralateral humerus is reported to be present in 44% to 86% percent of dogs [56,59], indicating that bilateral disease is common.

Figure 100-8. A series of images illustrating incomplete ossification of the humeral condyle. (A) An arthroscopic view showing the incomplete disruption in the articular surface between the medial humeral condyle (M) and the lateral humeral condyle (L). A portion of the ulnar notch (U) can be seen. (B) A postmortem specimen showing the retained cartilage (white arrow) between the medial and lateral humeral condyles. (C) A postmortem specimen showing complete disruption of the articular surface (black arrow) of the humeral trochlea. (D) A faxitron radiograph showing the retained cartilage (white arrow) between the medial and lateral humeral condyles.

Spaniel breeds are at highest risk of developing IOHC, however it has been described in several other breeds. It has been reported in Cocker Spaniels, Brittany Spaniels, Springer Spaniels, Cavalier King Charles Spaniels, Clumber Spaniels, and a Pug, a Yorkshire Terrier, a Tibetan Mastiff, a Rottweiler and several Labrador Retrievers [56,58,60-62]. A recent study from Germany also reported the German Wachtell, German Shepherd, and mixed breed dog as being at high risk [59]. Interestingly, although spaniels were well represented at the practice in this study, none were presented for IOHC [59]. Regardless of breed, males have been found to be at higher risk than females[56,59

Age of animals that present for associated non-fracture lameness range from 4 months to 5 years, with 54% presented when they are younger than 1 year [59]. Duration between first clinical signs and presentation in dogs with non-fracture lameness was 4 weeks to 12 months, with an average of 4 months [59].