Stephen C. Jones1 and Caleb Hudson2 1 Bark City Veterinary Specialists, Park City, UT, USA 2 Nexus Veterinary Specialists, Victoria, TX, USA Osteochondrosis (OC) is a developmental orthopedic disease that affects the differentiation of physeal chondrocytes leading to the development of a focal necrotic articular cartilage lesion.1 Physiologic loading of the OC lesion can result in cracks, fissures, and the formation of a cartilaginous flap. Once a flap has developed, the condition becomes known as osteochondritis dissecans (OCD). OCD usually affects young, rapidly‐growing large and giant breed dogs with affected dogs often exhibiting clinical signs in the first 6–12 months of life.1,2 Great Danes, Newfoundlands, German Shepherds, Mastiffs, Rottweilers, Irish Wolfhounds, Labrador Retrievers, and Golden Retrievers are known to be at‐risk breeds for the development of OCD.1–3 OCD can affect many joints in dogs and cats. OCD has been reported in the caudal humeral head,3 elbow joint,3 stifle joint,4 tibio‐tarsal joint,5 glenoid cavity,6 vertebra,7–10 patella,11 tibial tuberosity,12 distal radius,13 acetabulum,13 and femoral head.1 OCD of the caudal humeral head accounts for the majority of cases in dogs (76%), followed by the stifle joint (16%), the tarsus (4.5%), and the distal humerus (3.5%).3 This book chapter will discuss only these four most common locations. OCD in other locations is very rare and accounts for a very small percentage of the overall number of OCD cases seen in dogs. The exact etiology and underlying pathogenesis of OC is still not fully understood. Even the name of the condition itself lends itself to confusion. The word “osteochondritis” suggests an inflammatory etiology, but histological studies of bone removed during surgical OC lesion debridement fail to show any signs of osteonecrosis. In fact, histological findings strongly support a pathogenesis characterized by failure of endochondral ossification secondary to localized avascular necrosis of the epiphyseal cartilage.14 A range of environmental and genetic risk factors have been proposed. Historically, trauma was considered a primary causative factor for OC in people. In most cases, however, no single traumatic event is reported. Repetitive cartilage stress may play a more important role as a precipitating factor for the onset of clinical signs and lameness. Dietary factors, such as copper deficiency, excess phosphorus, and excess dietary energy, have also been implicated in the development of OC.14 Genetics seem to play an important role in the development of OC. In horses, for example, offspring from affected sires are more than twice as likely to develop OC as those from normal sires.15 Despite well‐documented evidence suggesting that genetics play an important role in the etiopathogenesis of OC in multiple species, specific genes and alleles related to OC have not yet been identified. Ultimately, the development and clinical expression of OC are likely the result of a combination of etiological risk factors, both genetic and nongenetic in nature. Dogs with OCD most commonly present with signs of thoracic or pelvic limb lameness anywhere between 5 and 10 months of age.13 The magnitude of lameness can vary from dog to dog, but it often starts insidiously and eventually becomes an obvious toe‐touching lameness with non‐weight‐bearing lameness occasionally seen. Some dogs can present much later in life, and in some patients, OCD may be found incidentally on radiographic examination.3 As the OCD disease process progresses, joint inflammation causes effusion, decreased range of motion, and pain on joint manipulation. Crepitus is occasionally palpable in more chronic cases. Radiographs performed in the early stages of stifle OCD often demonstrate a faint radiolucent defect beneath the articular margin. The surgeon should closely scrutinize the radiographs, as this finding can be subtle and easy to miss (Figure 51.1). Soft tissue opacity in the joint space secondary to joint effusion is usually appreciated in stifle and tarsal joints with OCD. Given the summation of other bones and/or dense overlying soft tissue, joint effusion is more difficult to see in the elbow and shoulder joints. If clinical suspicion of OCD exists and regular orthogonal radiographs are not confirmatory, oblique projection radiographs should be acquired (Figure 51.2). As the disease progresses, a more distinct round‐to‐oval‐shaped radiolucent defect at the articular surface is seen. Typically, a ring of sclerotic bone surrounds this radiolucent defect (Figure 51.1). In some instances, the cartilaginous flap mineralizes and can be seen overlying the radiolucent defect, or it can become detached and is seen as a mineralized joint mouse elsewhere in the joint (Figure 51.1). Computed tomography (CT) can help better delineate the osseous anatomy at the level of the articular surface and results in increased detection of OCD lesions as compared to radiographs.16 Furthermore, it has been shown that radiographs consistently underestimated the size of OCD lesions in the caudal humeral head when compared with CT.17 CT, therefore, is considered the preferred diagnostic modality when articular defect reconstruction is to be attempted. In addition to improving the accuracy of lesion size determination, CT permits the surgeon to develop a better understanding of the exact location and topography of the lesion. Some surgeons find it helpful to create a 3D surface rendering (digital and/or printed) of the affected joint, to better appreciate the lesion location and size. It is important, however, to realize that surface reconstructions do not account for cartilaginous defects and/or subchondral bone pathology and, thus, may underestimate the true size of the articular cartilage lesion. Early in the formation of a cartilaginous OCD flap and prior to the development of trabecular bone sclerosis, an OCD lesion may not be radiographically identifiable. In the shoulder joint, the use of positive contrast arthrography was found to be 88% accurate in the detection of discontinuity of the cartilage associated with nonmineralized flaps.18 However, in the same study, CT accuracy at detecting thickened cartilage covering a subchondral defect where no surface cartilage defect existed was only 55%.18 Ultrasonography (US) has been shown to be a useful imaging modality for detecting nonmineralized cartilage flaps in the canine shoulder joint. In one study of 29 joints with OC/OCD lesions, 21 joints were fully visualized and 8 were partially visualized using US.19 Magnetic resonance imaging (MRI) has also been shown to be a valuable diagnostic modality in the detection of canine shoulder OC/OCD lesions (Figure 51.3).20 A recent study found that the odds of detecting an OC lesion were 3.2 times higher with MRI than US.21 Interestingly, in that same study, diagnostic accuracy of OC/OCD was highest for MRI (94.4%), followed by radiography (88.9%), with US having the lowest accuracy of the modalities compared (82.6%).21 While MRI is a theoretically appealing imaging modality in cases of OC/OCD, limited availability, the necessity of general anesthesia, and high procedural costs along with a lack of comparative studies assessing the diagnostic accuracy of MRI for OCD in joints other than the shoulder are limitations to the widespread use of MRI as a diagnostic imaging modality for OC/OCD in dogs. Figure 51.1 Lateral (a,c) and craniocaudal (b,d) radiographs of a 4‐month‐old Labrador (a,b) and an 18‐month‐old German Shepherd (c,d). Note how discernible the radiolucent defect and the surrounding trabecular sclerosis are in the older (dotted white lines) versus the younger (solid white line) dog. The surgeon should pay close attention to the joint contour and opacities in the younger patients where the OCD lesion can easily be missed. Note also the mineralized body in the cranial joint pouch of the older dog (orange arrow, c). This presumably represents a detached mineralized OCD flap. Source: © Stephen C. Jones. OC is commonly found in the affected joint bilaterally, even if the dog or cat is not displaying clinical signs in the contralateral limb. OCD is reported to be present bilaterally in 16%, 41%, 75%, and 40% of humeral head, distal humerus, stifle, and tarsus cases, respectively.4,5,22,23 The veterinarian is advised to perform diagnostic imaging on the affected and the contralateral joints, even if clinical signs are only present unilaterally. The presence of a radiographically identifiable lesion, in the absence of clinical signs, however, presents a conundrum. While radiographically identifiable OC lesions in younger patients (<6 months) may be clinically silent, these lesions often progress to a flap (OCD) over time and ultimately result in clinical lameness. Conversely, some patients with clinically asymptomatic OC lesions go on to heal by bone infilling of the subchondral OC defect and do not progress to flap formation with the associated pain and lameness. The decision of whether to perform surgery on the clinically unaffected side is, therefore, challenging with no clearly correct answer. Ultimately, the decision to operate unilaterally or bilaterally should be made in concert with the owner. Ideally, it is best to adopt a wait‐and‐see approach on the nonclinical side. The owner, however, must be aware of the potential necessity for second‐side surgery at a later date. The joint affected should be considered in the decision‐making process for unilateral versus bilateral surgery. Debridement of a nonclinical OC lesion in the shoulder, where OC/OCD lesion debridement is expected to have a very good prognosis for functional outcome post‐operatively, is more justifiable than debridement of a nonclinical lesion in other joints, where the prognosis after surgery is less favorable. Another option is to visually assess the nonclinical side at the time of the initial surgery. This is especially appealing when using arthroscopy, which is minimally invasive and, therefore, is expected to result in minimal patient morbidity on the nonclinical side. When deciding on whether to make an open surgical approach on a clinically silent side, the veterinarian should take into account the size of the lesion radiographically, the presence of other radiographic factors that may indicate ongoing joint pathology (joint effusion, for example), and owner factors (economics, logistics, etc.). If diagnostic arthroscopy/arthrotomy is performed, the presence of a visible cartilage defect and/or visible evidence of joint synovitis would warrant cartilage lesion debridement. Figure 51.2 Lateral stifle radiographs of a dog with OCD of the lateral femoral condyle. Note that the lesion is not easily appreciated on the straight lateral (a) view (white arrow) but becomes more obvious when an oblique (b) view is acquired (orange arrow). Source: © Stephen C. Jones. Figure 51.3 T2‐weighted 3‐Tesla sagittal MRI images of the left (a) and right (b) shoulder joints in a 12‐month‐old Dutch Shepherd with a left‐sided OCD lesion. The hyperintense (bright) joint fluid can be seen surrounding the hypointense (dark) flap (red arrow). Source: © Stephen C. Jones. If the surgeon is planning to perform a joint resurfacing procedure, careful scrutiny of the patient’s skin for evidence of dermatitis or pyoderma should be performed. Any pre‐existing skin disease should be treated aggressively until completely resolved before attempting a joint resurfacing procedure, where a surgical site infection would be likely to result in a catastrophic outcome. In some patients with large OCD lesions affecting the medial aspect of the humeral condyle, the femoral condyle, or the trochlea of the talus, or in patients with advanced degenerative joint disease (DJD) present at the time of OCD diagnosis, the prognosis associated with surgical debridement or partial joint resurfacing procedures may be guarded. In this group of patients, joint replacement surgery may be considered as a first‐line treatment option for OCD. Even if OCD lesion debridement is ultimately selected over joint replacement surgery, it is important to educate owners prior to OCD debridement surgery on the expected outcome for the affected joint to ensure that reasonable expectations exist. The goals of any OCD treatment are to reestablish a congruent joint surface, to provide an improved long‐term functional outcome, and to minimize OA progression. OCD treatment options consist of conservative management, open/arthroscopic removal of the cartilage fragment with debridement/stimulation of the subchondral bed, osteochondral autograft transplantation, osteochondral allograft transplantation, synthetic osteochondral resurfacing, and total joint replacement. Treatment decisions should be based on patient considerations such as the joint affected, patient age, degree of lameness, underlying OA, patient temperament, and comorbidities, OCD lesion type (location and topography), and owner factors such as economic considerations, compliance, and post‐operative management/outcome expectations. While this chapter will focus primarily on the treatment of OCD lesions with an arthrotomy approach, it should be noted that arthroscopy presents a much less invasive option for the treatment of most cases of OCD and, where possible, is the preferred treatment approach over arthrotomy. OCD flap removal and subchondral bone debridement are facilitated with the use of specialized instrumentation due to the limited working space available inside most joints and the need to treat the OCD lesion while minimizing iatrogenic damage to the surrounding articular cartilage. The optimal instrumentation for OCD debridement is arthroscopic hand instruments, which were designed for use during arthroscopic surgery but which can be utilized just as effectively during open surgery. Arthroscopic hand instruments have small tips and a long, thin shaft designed to fit into a small joint space. The most common arthroscopic hand instruments utilized for OCD lesion debridement include graspers, blunt probes (meniscal probes), and curettes. Graspers are used to grasp and remove the flap from the joint (Figure 51.4a). Blunt probes are used to manipulate the flap and assess the depth of the OCD defect (Figure 51.4b). A curette is used to conservatively debride the subchondral bone bed in the OCD defect until healthy, bleeding bone is observed (Figure 51.4c). An arthroscopic power shaver can also be utilized through an arthrotomy approach to debride the subchondral bone bed of the OCD lesion after flap removal. A micropick is also sometimes utilized to create focal microfractures in the subchondral bone bed and promote vascular ingrowth (Figure 51.4d). If an arthroscopic grasper is not available, a small mosquito hemostat can be used in most patients to grasp and remove the OCD flap. General principles of surgical technique utilized for OCD lesion treatment are similar between joints, regardless of the surgical treatment technique being utilized. General principles of each surgical treatment technique will be covered in this section, while variations from the standard technique that may be applicable to specific joints will be mentioned further in the sections pertaining to each individual joint. After an arthrotomy (or arthroscopy) has been performed, the joint should be thoroughly evaluated by visual inspection and probing. The OCD lesion should be identified and thoroughly inspected. The cartilage flap should be grasped and gently pulled and manipulated to remove it from the joint surface. Careful probing around the lesion often reveals additional cartilage that is not appropriately adhered to the subchondral bone; this cartilage should also be removed using a grasper or curette. Following flap removal, the subchondral bed is debrided down to a bleeding surface. This can be performed using a curette, high‐speed burr, arthroscopic shaver, or some other instrument capable of removing the often‐dense sclerotic subchondral bone of the OCD bed. The premise behind curettage of the subchondral bone is to create hemorrhage, which promotes infiltration of pluripotent mesenchymal stem cells from the subjacent metaphyseal bone into the lesion bed, thereby initiating repair and lining of the defect with fibrocartilage.1,2 To encourage bleeding and blood vessel ingrowth in OCD lesions where the underlying bone bed is very sclerotic, a technique referred to as microfracture can be utilized. Microfracture consists of the creation of multiple small holes in the sclerotic surface of the subchondral bone so that the underlying, more normally vascularized bone can communicate with the bone surface. Microfracture is performed by impacting the tip of a micropick into the subchondral bone surface of the OCD defect. Typically, numerous small holes are created, separated from each other by approximately 1–2 mm. When performed correctly, hemorrhage should be observed from the defects created in the sclerotic subchondral bone.24 Figure 51.4 (a) Arthroscopic graspers are used to grasp and remove the flap from the joint. (b) Shown here is a meniscal probe. Blunt probes, such as the meniscal probe, are used to manipulate the flap and assess the depth of the OCD defect. (c) A curette is used to conservatively debride the subchondral bone bed in the OCD defect until healthy, bleeding bone is observed. (d) A micropick is occasionally utilized to create focal microfractures in the subchondral bone bed and promote vascular ingrowth from the subchondral metaphysis. Source: © Caleb Hudson. As an alternative to flap extirpation and curettage of the subchondral bed, the surgeon may opt to resurface the OCD lesion. A detailed description of the surgical techniques available for joint resurfacing is beyond the scope of this chapter but can be found in the pertinent literature cited herein. The OCD lesion can be resurfaced using an osteochondral autograft, harvested from the dog’s own stifle joint.25 While this technique offers the ability to resurface the lesion using the patient’s own hyaline cartilage, thereby minimizing the chances of graft rejection, it does result in donor‐site morbidity and the inability to match recipient site cartilage thickness or surface topography. Osteochondral allograft transplantation (graft obtained from a donor dog cadaver) negates the issues with donor site morbidity, but these grafts are more susceptible to graft rejection and, in theory, have the potential for disease transmission.26 One significant advantage of an allograft over an autograft, however, is the ability to match the cartilage thickness and topography of the OCD site. More recently, synthetic resurfacing has become another available treatment option for dogs with OCD (Figure 51.5).27,28
51
Osteochondrosis
Introduction
Etiology
Indications and Pre‐op Considerations
History and Physical Examination
Diagnostics
Plain Radiography
Computed Tomography
Additional Diagnostics
Considerations
Treatment Options
Specialized Surgical Instrumentation
Surgical Treatment of OCD
Cartilage Fragment Removal with Debridement/Stimulation of the Subchondral Bed
Joint Resurfacing Techniques
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