Get access to all handy features included in the IVIS website
- Get unlimited access to books, proceedings and journals.
- Get access to a global catalogue of meetings, on-site and online courses, webinars and educational videos.
- Bookmark your favorite articles in My Library for future reading.
- Save future meetings and courses in My Calendar and My e-Learning.
- Ask authors questions and read what others have to say.
Miscellaneous Orthopaedic Diseases
Get access to all handy features included in the IVIS website
- Get unlimited access to books, proceedings and journals.
- Bookmark your favorite articles in My Library for future reading.
- Save future meetings and courses in My Calendar and My e-Learning.
- Ask authors questions and read what others have to say.
Asynchronous Growth of the Radius and Ulna
Normal synchronous growth of the radius and ulna yields a straight antebrachium with normal articular surfaces at the elbow and carpus. Growth in length of the radius and ulna comes from the physes, or growth plates. The distal radial physis accounts for 60% to 70% of the radius length, while the distal ulnar physis accounts for 100% of the ulna length distal to the elbow (80% - 85% of the overall ulna length) [1,2]. Therefore, the diaphyses of the radius and ulna must slide past each other to maintain a straight antebrachium (Fig. 98-1) .
Figure 98-1. Adapted from Carrig CB, Vet Clin N Am 13,91, 1983 (Ref 2). Growth of the radius and ulna is depicted at ~2 months, ~4 months, ~ 6 months, and ~9 months of age. Following the radiographic markers (arrows) as age increases shows that the radial and ulnar cortices must slide past each other during growth. Also noteworthy: the fastest growth occurs between 4 months and 6 months of age; the vast majority of growth is complete by 6 months of age; from the level of the elbow distally (note proximal ulnar marker) virtually 100% of the ulnar length comes from the distal ulnar physis.
Asynchronous growth of the radius and ulna (AGRU) results in an antebrachium that is shortened and has angular, rotational and/or bowing deformity (Fig. 98-2) [1-5]. Less obvious, but more significant, are the articular malformations of the elbow and/or carpus [1-6]. The articular surfaces are sculpted for each individual during growth via Wolff’s law.* Forces that are normal in direction and proportion yield a congruent, healthy, and mechanically effective joint. Abnormal forces, as occur with AGRU, yield an incongruent, unhealthy, and mechanically ineffective joint that cannot be corrected and often not even significantly improved with contemporary techniques . AGRU has numerous etiologies, each with specific clinical abnormalities reflecting which part(s) of the synchronous growth is abnormally effected [1-6]. Regardless of the specific etiology, however, all forms of AGRU have the pathologies described above to some extent.
*Wolff’s law: "a bone, normal or abnormal, develops the structure most suited to resist the forces acting upon it". Dorland’s Medical Dictionary, 28th ed. Philadelphia: Saunders.
Figure 98-2. Puppy with AGRU of the right foreleg which is shortened, bowed, and externally rotated.
The most recognized form of AGRU is premature closure of the distal ulnar physis, also referred to as radius curvus (Fig. 98-2). The distal ulnar physis is cone shaped, which concentrates compressive forces. Excessive compressive forces, i.e., when a dog jumps down from a relatively high place and lands first and most forcefully on its front leg(s), can result in Salter-Harris V (compression) fractures. (Other Salter-Harris fracture types can also occur.) This inciting trauma is often not witnessed by the owner, or is soon forgotten because the duration of lameness is short. If radiographs are taken soon after the trauma, the nondisplaced Salter-Harris V fracture is not detectable. Radiographs when AGRU is present, but before normal physeal closure, show premature closure of the distal ulnar physis. The distal ulnar physis stops growing and becomes an anchoring point for the distal radius, tethered via fibrous connective tissue. The pathology is mechanically analogous to a moving boat tethered to an anchor caught on the bottom. Premature closure of the distal ulnar physis results in the radius deviating laterally with supination (remember the distal ulna is caudolateral to the distal radius). Additionally, there is cranial bowing of the distal radius (the radius is growing in length while the ulna is not), malarticulation of the radiocarpal joint with valgus deformity, humeroulnar subluxation with varus deformity, and shortening of the antebrachium (Fig. 98-3). Similar deformity occurs if the lateral part of the distal radial physis stops growing prematurely (partial closure), which is the second most commonly observed form of AGRU .
Figure 98-3. Radiograph showing premature closure of the distal ulnar physis causing antebrachial shortening, substantial curvature and humeroulnar subluxation.
Complete closure of the distal radial physis results in relatively minor angular deformity, decreased length of the antebrachium, and malarticulation of the carpus and elbow. Premature closure of the proximal radial physis results in a substantial widening of the radiohumeral joint, radioulnar malarticulation, and shortening of the antebrachium (Fig. 98-4). An additional but uncommon cause of AGRU is a radius and ulna fracture that heals in a single mass (synostosis), which prevents the sliding of the diaphyses (Fig. 98-5).
Figure 98-4. Radiograph showing premature closure of the proximal radial physis resulting in substantial widening of the radiohumeral joint (arrow), radioulnar malarticulation and shortening of the antebrachium.
Figure 98-5. Photo of synostosis due to prior fracture and subsequent union of the radius and ulna to each other. Note the large step deformity of the radial head and coronoid processes with accompanying degenerative joint disease.
The severity of deformity depends on the potential growth remaining at the time of physeal damage (premature closure). Potential growth is a combination of the dog’s age and adult size. Approximately 90% of bone length is obtained by 6 months of age in all but giant breed dogs, with the most active growth occurring between 3 and 4 months of age. A 3-month-old dog has more potential bone growth than a 5-month-old dog of the same adult size. Similarly, a 4-month-old Labrador retriever has more potential growth than a 4-month-old Chihuahua. The more potential bone growth, the worse the deformity will be if left untreated. The most effective treatment is removal of a section of the ulna (anchor rope) on the same side of the interosseous ligament as the pathology as soon as AGRU begins. Ulnar osteotomy is most effective if performed early and enough potential bone growth remains to correct the pathologies.
Atraumatic etiologies of AGRU also exist [4,5]. The most common cause of AGRU is selective breeding, which creates and perpetuates achondroplastic/chondrodysplastic breeds such as basset hounds, English bulldogs, and dachshunds. Although the condition is generally accepted in these breeds, the pathologies exist nevertheless. AGRU is also present in dogs with dwarfism, an inherited condition reported in the Labrador retriever, malamute, Norwegian elkhound, and Samoyed breeds.4 A mild form of AGRU also occurs with retained cartilaginous core [4,5].
Retained Cartilaginous Core
Retained cartilaginous core (RCC) is an abnormality of endochondral ossification in which conversion from physeal cartilage to bone is delayed at the distal ulnar physes. The etiology is most likely a clinical manifestation of osteochondrosis. Clinical abnormalities are usually limited to lateral deviation of the carpii, usually up to 10° (Fig. 98-6). Radiographically, the distal ulnar physis extends an excessive distance proximally. RCC predominantly affects juvenile Great Danes, although the condition may persist into adulthood and/or affect other large breeds. Treatment is typically not indicated [4,5].
Figure 98-6. (A) Retained cartilaginous core (RCC) of distal ulna causing slight carpus valgus. (B) Radiograph of distal antebrachium showing RCC, seen as excessive proximal extension of the distal ulnar physis (arrows) in shape of a flame.
Puppy Carpal Laxity Syndrome
Puppy carpal laxity syndrome is carpal hyperextension or hyperflexion in the absence of an identifiable cause (e.g., tendon rupture or fractures) (Fig. 98-7) . Puppies with this condition are not in pain and have a full range of motion of the carpus. The condition can be unilateral or bilateral, and typically occurs at 2 to 5 months of age. Multiple puppies in a litter may be affected, suggesting an etiology of nutrition, environment, husbandry, or inheritance. A breed predilection is not recognized, however, and mixed breeds are affected at least as often as pure breeds. The etiology is unknown. The pathophysiology appears to be an imbalance in muscle tone between the extensor and flexor muscles of the carpus. Correction of the condition occurs spontaneously in the vast majority of dogs in less than or up to 2 weeks, although the condition will persist into adulthood in rare cases. Encouraging exercise has been recommended. Treatment with splints prolongs correction to about 6 weeks [4-6].
Figure 98-7. (A) "Bucked" carpii or carpal hyperflexion in a juvenile. (B) "Dropped" carpii or carpal hyperextension in a juvenile.
Ectrodactyly is a true congenital deformity (present at birth) wherein the paw’s shape is that of two large toes rather than four normal sized toes (Fig. 98-8), giving rise to the synonyms of "lobster claw" and "split-hand deformity" [4,5,8]. Typically only one front paw is affected. Subluxation of the ipsilateral elbow occurs in slightly less than half the cases of ectrodactyly. Radiographs of the foot reveal various bizarre combinations of fused and absent metatarsal and phalanges bones. Ectrodactyly has been proven to be of an inherited etiology in humans and cats, and is probably inherited in dogs as well. Medium and large breed dogs (especially mixed breed dogs) have been reported with ectrodactyly thus far in the literature. Treatment is usually not necessary, as most dogs with ectrodactyly have few if any clinical signs other than the anatomic deformity.
Figure 98-8. (A) Ectrodactyly (a.k.a. "Lobster Claw", or "split hand" deformity) shown from the ventral perspective. (B) Radiograph of ectrodactyly showing bizarre combination of fusion and absence of bones.
The most common form of "dwarfism" in dogs is intentional selection of the autosomal dominant trait to create and perpetuate "toy" and "miniature" breeds, as well as breeds such as the basset hound. The term "dwarf" is not conventionally used to describe intentional dwarfism, and the condition is not generally considered pathologic. However, clinical problems do occur that are attributable to the selective breeding owing to conformation (especially joint malarticulation). Dwarfism will refer to unintentional.
Dwarfism has been reported in the beagle, cocker spaniel, English pointer, French bulldog, Great Pyrenees, Labrador retriever, malamute, Norwegian elkhound, miniature poodle, Samoyed, Scottish deerhound, and Scottish terrier [4,5]. The author has observed dwarfism most often in the Labrador retriever, almost certainly influenced by the breed’s current popularity (i.e., number of Labrador retrievers and ill-advised breeding practices). Dwarfism can occur owing to a variety of anomalies and modes of inheritance, each yielding a characteristic phenotype and associated pathologies. Achondroplastic dwarfism is the term used for humans. It results in a phenotype of short limbs and a normal trunk, which is the most common form of dwarfism in dogs (Fig. 98-9). Autosomal recessive inheritance is the etiology in breeds in which the mode has been studied.4 Dogs with dwarfism appear normal at birth, but the condition becomes obvious in a few months. Individual bones can be affected equally or unequally, resulting in straight or curved legs, and/or the front legs versus rear legs being equal or unequal in length. Associated pathologies include retinal dysplasia (Labrador retriever), retinal detachment and cataracts (Labrador retriever and Samoyed), and hemophilia (malamute). Owners are often unaware the conformation is abnormal (if the dog is pure breed) and should be informed. In addition, owners should be advised to have the dog evaluated for associated pathologies and the reasons that neutering the dog is important.
Figure 98-9. Achondroplastic dwarfism in German Shepherd dog at (A) 3 months old and (B) 9 months old. Note the normal appearance of the trunk and abnormally short legs. Photographs courtesy of Mr. Fred Lanting, AKC Judge, Willow Wood Consulting.
Pituitary dwarfism (also called hypophyseal infantilism) is caused by under secretion of growth hormone and gonadotropin deficiency, resulting in a proportional dwarfism with retention of infantile characteristics (Fig. 98-10). The most obvious infantile characteristic is the failure of an adult hair coat (primary hairs) to develop, and easy epilation of the puppy (secondary) hair, resulting in alopecia in areas of high friction such as the caudal thighs, caudal forearms, and around the collar .
Figure 98-10. Pituitary dwarfism in a 1 year old dog-wolf hybrid (right), with a normal dog (left). Photograph courtesy of Mr. Fred Lanting, AKC Judge, Willow Wood Consulting.
In dogs and cats, congenital agenesis of the diaphysis of the radius is the most common form of this rare condition [4,5]. Conventional nomenclature indicates the affected bone first (i.e., radius, ulna, tibia, fibula), followed by amelia (complete agenesis) or hemimelia (complete agenesis of the diaphysis). In addition to dogs and cats, humans, goats, rats, and chickens have been reported to have hemimelia.
The pathogenesis of hemimelia is failure of the radius to develop in utero. The etiology is unconfirmed, although inheritance is generally postulated. One breeding pair of cats reproduced kittens with amelia over multiple litters (three of eight kittens affected). Other proposed etiologies include accidents in utero, irradiation, drug toxicities, vaccines, and dietary deficiencies (especially minerals, e.g., zinc, copper, manganese). Unilateral occurrence being more common than bilateral obscures the proposed etiologies.
Cats are reported to have radial hemimelia more often than dogs. No size or breed predilection exists. History indicates that the owners noticed the deformity (Fig. 98-11) (shortened antebrachium with varus deformity and/or carpus valgus) at or soon after birth. In older dogs, the appearance of the deformity could be confused with one form of AGRU (distal radius closure), although palpation reveals the lack of a radius diaphysis. Radiographs confirm the diagnosis. Limb function is commensurate with the deformity, ranging from not weight-bearing to good (albeit abnormal). Effective treatment has not been devised, nor is heroic surgery indicated as the condition is ostensibly not painful. Amputation can be performed for cosmesis or treatment of chronic decubital ulcers. Neutering affected animals is recommended, and arguably others in the genetic lineage as well.
Figure 98-11. Hemimelia/ Amelia. (A) Cat with hemimelia showing carpal subluxation and gross deformity of foreleg (thumb is on shoulder and other hand is behind the elbow). (B) Radiograph showing absence of the radius with malarticulation of the carpus and elbow.
Rickets and Osteomalacia
Osseous deformity and hypomineralization owing to abnormal metabolism of vitamin D, calcium, and phosphorus from various etiologies is referred to as "rickets". Osteomalacia is the adult onset form, although conventional use often substitutes the term rickets. "Renal rickets" is probably the form seen most often clinically in dogs. Inappropriate all-meat diets in "big cats" (tigers, lions, etc.), especially juveniles, causes severe hypomineralization. A group of related juvenile Vizslas (Fig. 98-12) was studied at Auburn University’s College of Veterinary Medicine over a period of several months. Affected dogs had pronounced curvature and shortening of the long bones, which also affected range of motion of adjacent joints. Nutritional and concurrent renal failure were effectively eliminated as causes, and rickets was tentatively diagnosed.
Figure 98-12. Vizsla with rickets. (A) Note the curvature of the front legs and shortened stature. (B) In these radiographs of the distal radius and ulna at approximately 8 weeks of age, there is the characteristic marked widening of the physis in the distal radius and ulna. (C) Several months later there continues to be abnormal appearing metaphysis though the physis have a more normal appearing physeal width.
Bone cysts in dogs are rare and include subchondral, simple (cystic), and aneurysmal forms [4,5]. Subchondral bone cysts are relatively small and identified radiographically. Simple and aneurysmal bone cysts are relatively large and often readily palpable. Differential diagnosis between neoplasia and simple bone cyst or aneurysmal bone cyst can be difficult. Therefore, confirming a diagnosis and case management should be performed with due diligence.
Subchondral bone cysts are an osteochondrosis lesion most commonly identified in horses. Subchondral bone cysts are lined with synovial membrane and contain serosanguinous fluid, myxoid, or fibrous tissue. Forage obliterates the cyst and establishes a new blood supply to initiate healing. It is performed if the cyst is large enough or causing a clinical problem and prior to development of significant degenerative joint disease.
Simple bone cysts contain serosanguinous fluid and are lined with fibrous tissue. They can occur in the metaphysis of any long bone or multiple long bones (polyostotic). The most common presentation is a single simple bone cyst (monostotic) located in the distal radius or distal ulna of a juvenile or young adult, large breed dog. Doberman pinchers and German shepherd dogs appear to be over-represented. The etiology of simple bone cysts is uncertain, although the typical signalment of juvenile or young adult dogs suggests an aberration of, or insult during, bone growth. A hereditary predisposition has been suggested for Doberman pinschers. Clinical signs include lameness and painful swelling of the affected metaphysis (with or without pathologic fracture of the bone cyst). Radiographs image a large, expansile mass, absence of osteolysis and/or osteogenesis, variable amounts of cortical thinning, and a fluid density center (Fig. 98-13).
Figure 98-13. Bone cyst in the distal ulna demonstrating an expansile, multi-trabeculated appearance with thin cortices.
Simple bone cysts do not usually cross the physis or involve the epiphysis. A bone cyst may also be asymptomatic and identified as an incidental finding. Asymptomatic cases of simple bone cyst may not require surgery, especially if the ulna is involved as it is not a major weight bearing bone. Surgery is indicated if biopsy is desired to confirm the diagnosis, the simple bone cyst is causing clinical problems (e.g., lameness), and/or if preemptive intervention to avoid a pathologic fracture is desirable (especially a bone bearing significant weight such as the radius). Surgical correction can be via forage of the cyst and into the adjacent medullary cavity, or curettage and bone grafting. With either technique, fracture stabilization devices such as bone plates or external fixators minimize the risk of pathologic fracture. In humans, injection of simple bone cyst with corticosteroid has been reported as a successful treatment.
Aneurysmal bone cysts contain large vascular sinusoids, are expansile, osteolytic and locally invasive of adjacent bone and soft tissue. Aneurysmal bone cysts have been classified as probably intraosseous arteriovenous shunts, but have also been classified as neoplastic. Aneurysmal bone cysts have been diagnosed in young adults to geriatric dogs. Clinical signs are localized pain and swelling, usually of several months’ duration. A predilection exists for the axial skeleton, although any bone can be affected. Treatments are intended to decrease vascularity while maintaining structural strength, and include debridement with bone grafting, radiation therapy, and cryotherapy. Aneurysmal bone cysts have been reported in dogs, cats, horses, and people.
Congenital Shoulder Luxation
Congenital shoulder luxation is a disease of small and toy breed dogs that, in the author’s opinion, is in many ways analogous to congenital medial patella luxation, albeit much less common. Clinical signs are first observed when the puppy begins to walk, or in young adults, depending on severity. Clinical signs range from non-weight-bearing and constant luxation, to the more common intermittent luxation and associated intermittent lameness (Fig. 98-14). Palpation may reveal a medial luxation. Applying medial pressure on the proximal humerus and abducting the elbow with one hand while palpating the relative position of the acromion process with the other hand should diagnose medial shoulder luxation or subluxation. Radiographs are indicated to access the changes to the glenoid cavity and humeral head, with craniocaudal stress radiographs if used for the purpose of diagnosis or documentation.
Figure 98-14. Congenital shoulder luxation (left) in a puppy. (A) Note the Abduction of the arm, with lateral position of elbow, prominent acromial process (solid arrow) and medial placement of humeral head (dashed arrow). (B) Radiograph showing congenital medial shoulder luxation. Note the flat to convex shape of the affected glenoid cavity.
The condition is presumed not to be of traumatic etiology, and by convention is called congenital, but may be developmental. Medial luxation or subluxation of the shoulder dictates coexisting insufficiency of the medial collateral ligament and joint capsule, with possible involvement of the subscapularis muscle/tendon. Because congenital shoulder luxation involves abnormal forces in a juvenile, Wolff’s law dictates that the glenoid cavity and humeral head develop an abnormal shape. The glenoid cavity may be more shallow, flat, or even convex, with or without identifiable erosion of the medial brim; the humeral head is flattened to varying extents.
Treatment should be proportional to the severity. Various surgical techniques have been described to stabilize the luxation, with relatively low success rates. A flat or convex glenoid cavity would logically predict poorer results of medial stabilization, as would complete luxation and the presence of osteoarthritis. Shoulder arthrodesis is a reasonable option in dogs owing to the high mobility of the scapula. However, the presence of the infraspinatus nerve and the sparse amount of scapular bone (i.e., decreased ability of implants to hold) makes arthrodesis problematic in these small and toy breed dogs. Dogs with infrequent intermittent lameness that appears to the owner to be non-painful may be harmed more by surgery than helped [4,5].
Congenital Elbow Luxation
Congenital elbow luxation occurs predominantly in English bulldogs, basset hounds, Yorkshire terriers, Pekingese, and other small and toy dogs [4,5]. A hereditary etiology has been suggested, but not confirmed. The pathogenesis has been speculated to be an in utero insufficiency of the elbow’s medial collateral ligament and perhaps annular ligament. The luxation is lateral in all but one documented case , and can be unilateral or bilateral. The critical pathologies with congenital elbow luxation are the lateral location of the triceps muscle insertion (hence, contraction does not extend the elbow), and malarticulation in a young dog, causing gross osseous deformities of the joint (see Wolff’s law). Congenital elbow luxation causes an obvious deformity (Fig. 98-15) consisting of lateral luxation, flexion of the elbow, and pronation of the antebrachium. Appearance of affected dogs has been compared to the praying mantis insect. Gait is likewise overtly abnormal, since inability to extend the elbow(s) causes the dog to crawl (Fig. 98-16). A craniocaudal radiograph of the affected leg yields a Cr-Cd image of the humerus and a lateromedial image of the radius and ulna (Fig. 98-17), as opposed to adult dogs with traumatic elbow luxation in which the radius and ulna are not typically rotated.
Figure 98-15. Congenital elbow luxation. Note that in the craniocaudal radiograph of the elbow there is a lateromedial view of the radius and ulna. (B) In mediolateral radiograph of the elbow there is a craniocaudal view of the radius and ulna.
Figure 98-16. Congenital elbow luxation is a juvenile. Note the "Praying Mantis" appearance of the front legs due to inability to extend the elbows. There is also internal rotation of the antebrachii and abnormal topographic anatomy of the elbows.
Figure 98-17. Radiographs of dog with congenital elbow luxation. (A) Pin placement for modified external correction. (B) Placement of rubber band on the pin tips (external to the skin) of appropriate tension reduces the luxation while allowing flexion and extension of the elbow joint necessary for juvenile joint health.
Satisfactory treatment of congenital elbow luxation depends on age at the time of surgery and adult weight of the dog. If treated when only a few weeks old, a modified external fixator (Fig. 98-18) typically results in a functional joint (although radiographically abnormal). A small K-wire (e.g., 0.062”) is placed mediolaterally through the olecranon near the triceps insertion; a second K-wire is likewise placed transcutaneously across the distal humeral epicondyles, and a rubber band of appropriate tension is placed externally from the lateral tip of the olecranon pin to the medial tip of the transepicondylar pin, which rotates the olecranon to the correct functional position caudally. The dog is encouraged to walk on the leg normally (i.e., not splinted) until reduction is maintained without the rubber band present (typically a couple of weeks) [9,10]. Success of this technique is fairly reliably predicted based on the ease of manually reducing the luxation. For older dogs, in which the luxation is not readily reduced, transposition of the olecranon can yield reasonable function in some cases. Heavier dogs (e.g., English bulldogs), especially if not treated early, have a poor prognosis for a functional joint; arthrodesis is an option for unilateral cases.
Figure 98-18. Multiple cartilaginous exostosis occurred in multiple other locations in this dog. Cartilage covering the exostosis (arrow) was visible on histopathology.
Multiple Cartilaginous Exostosis
Multiple cartilaginous exostosis (MCE) is a rare disease with the interesting pathogenesis of extra physes or articular-epiphyseal complexes* that are aberrantly located on, and usually perpendicular to, cortical bone (Fig. 98-19) [5,11,12]. The pathogenesis most widely accepted is that the MCE originated from the physis before separating. Any bone of the axial or appendicular skeleton formed by endochondral osteogenesis may have MCE, with the involvement of multiple bones being typical. As the juvenile dog grows, so do the cartilaginous exostoses. MCEs are mushroom shaped, with the stalk consisting of bone formed by endochondral osteogenesis, and the top being cartilage covered and comparable histologically to an A-E complex. Growth continues until osseous maturity, when the MCEs, the normal physes, and A-E complexes cease growth and ossify. Onset of clinical signs is predictable while the dog (and exostoses) is undergoing rapid growth (2 to 5 months of age). Clinical signs associated with MCE depend on their location and what damage (primarily via pressure) the exostoses cause to adjacent tissue. Clinical signs range from a palpable mass, to lameness (pressure on muscle, nerve and/or vessels) to paralysis (compression of the spinal cord). Diagnosis is confirmed via radiographs of multiple bones with characteristic bone lesions. The bone lesions show bone of variable shape and size extending perpendicular to the metaphysis with radiolucent areas (hyaline cartilage) capping the end. Biopsy results indicate a typical physis consistent with the age of the animal. The marrow portion of the MCE (stalk) contains adipose or hematopoietic marrow. Most cases of MCE have good outcomes unless the MCE has caused irreparable damage (e.g., to the spinal cord), because the MCE ceases growth when the normal physes cease growth. Multiple cases of MCE metamorphosis into chondrosarcomas or osteosarcomas have been reported in the literature; hence, monitoring or removal would be judicious.
Figure 98-19. Osgood-Schlatter disease in a hunting dog. There is an increased width of the physis of the tibial crest.
Osgood-Schlatter’s disease is a physitis of the tibial crest [5,13]. It has been observed in juvenile dogs, specifically active hunting breeds (e.g., pointers). Osgood-Schlatter’s disease is a condition in juvenile boys (~8-15 years old) also called "football knee". It most commonly occurs in larger, athletically active boys. The physes of the tibial crests become inflamed, painful, and radiographically abnormal (i.e., widened and irregular) (Fig. 98-20) . Adjacent soft tissues are also inflamed in the acute phase. Osteochondrosis has been a proposed etiology. The more likely and more widely accepted etiology is repetitive trauma. Tension from the patellar tendon, especially strong and repetitive forces, can overload the adjacent physis, resulting in physitis. Rest is the preferred treatment for most cases, followed by avoiding the causative activity until skeletal maturity. Fixation is required only for a displaced tibial crest (determined by flexing the stifle and palpating a lax patellar tendon and unstable tibial crest).
Figure 98-20. Hypertrophic osteopathy in an adult dog with lung tumors. (A) Periosteal reaction is present along the metacarpi and distal radius and ulna. Note that the joints are unaffected. (B) Close up of the unique “Palisades” periosteal reaction associated with HO.
Hypertrophic osteopathy (HO) is the only disease reviewed in this chapter that occurs typically in mature dogs. The most common cause of HO is a mass within the thorax. The likely pathogenesis is stimulation of the vagus nerve, which subsequently alters vascularity to the periosteum of the distal limbs, which promotes periosteal proliferation.14 This proposed pathogenesis is supported by research in which transection of the vagus nerve resulted in reversal of the periosteal lesions of the distal limbs. HO was originally called hypertrophic pulmonary osteoarthropathy (HPOA). Rhabdomyosarcomas of the urinary bladder have also been reported to cause HO, and the joint is not directly affected [15-17].
Dogs with HO are typically presented for a firm, non-painful swelling of the metacarpus, metatarsus, and phalanges. The swelling may progress more proximally in some cases. Radiographs show a characteristic, if not pathognomonic, periosteal proliferation characterized as "palisades" (columns, similar to numerous tall buildings) (Fig. 98-20B). HO is not treated per se. Rather, treatment is directed toward the underlying cause. Although neoplasia (metastatic or primary) in the thorax is the most common inciting cause of HO, other diseases have been reported to result in HO (e.g., Spirocerca lupi parasitism, emphysema, etc) .
1. Newton CD. Radial and ulnar osteotomy. In: Textbook of Small Animal Orthopaedics. Newton CD, Nunamaker DM (eds). Philadelphia: JB Lippincott, 1985, p. 533.
2. Carrig CB. Growth abnormalities of the canine radius and ulna. Vet Clin North Am 13:91, 1983.
3. Fox SM. Premature closure of the distal radial and ulnar physes in the dog. Parts I & II. Comp Cont Educ 6:128, 212, 1984....
How to reference this publication (Harvard system)?
Affiliation of the authors at the time of publication
Veterinary Teaching Hospital, Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn, AL, USA.