Description and Treatment of an OCD Lesion of the Proximal Groove and Medial Ridge of the Femoral Trochlea in a Dog

Abstract

This report describes a hitherto unreported site of stifle osteochondritis dissecans, its surgical treatment and functional outcome. A 7-year-old male Belgian Shepherd with a history of grade 2 left hindlimb lameness of 4 months duration, presented with moderate left hindlimb lameness associated with mild muscle atrophy, stifle effusion and discomfort at stifle manipulation, without any associated instability. Radiographs showed an irregular defect on the proximal part of the femoral trochlea associated with subchondral sclerosis. Arthroscopic findings were consistent with an osteochondritis dissecans lesion of the groove and axial side of the medial ridge of the femoral trochlea and confirmed by histopathological analysis of the removed fragment. Treatment included removal of the osteochondral fragment, debridement and picking of the lesion bed. Four months of follow-up revealed improvement of the lameness despite a persistent slight discomfort in full stifle extension with associated joint effusion. Concurrent magnetic resonance imaging and arthroscopic recheck showed thin fibrocartilage partially covering the treated lesion without any sign of synovitis, with no other stifle injury. Eight months postoperatively, the owners reported satisfactory limb function. This is the first report of stifle osteochondritis dissecans localized in the proximal groove and axial side of the femoral trochlea, successfully treated surgically.

Keywords

osteochondritis dissecans - femoral trochlea - dog - arthroscopy

Introduction

Osteochondritis dissecans (OCD) is a well-known orthopedic disease that mostly affects dogs under 1 year of age, especially in large breeds.[1] It corresponds to an abnormal endochondral ossification in which the cartilage of the epiphysis fails to produce subchondral bone, resulting in a focal area of thickened cartilage, which then may crack and lead to the formation of a cartilage flap. The etiology and pathogenesis of OCD are still not fully understood, but repeated trauma, hormonal and nutritional factors, genetics and local ischemia have been suggested.[2] [3] Although OCD may affect various joints, some locations are more frequently reported, such as the caudal humeral head, the medial portion of the humeral condyle, the lateral condyle of the femur and the plantar aspect of the medial trochlear ridge of the talus.[2] These lesions have also been sporadically reported in other sites such as the glenoid rim of the scapula, the distal or proximal radius, the patella and the sacrum.[2] [4] [5] [6]

Although stifle OCD is not uncommon, it usually affects the articular surface of the lateral femoral condyle in more than 90% of cases, and has been described as a unilateral and bilateral lesion.[7] [8] Other reported sites of stifle OCD include the medial femoral condyle, both lateral and medial femoral condyles and the intercondylar fossa of the femur.[2] [7] [9] [10] In addition, OCD localized in the femoral trochlear ridge has been reported only once.[10] Two cases of canine OCD of the abaxial side of the medial femoral trochlear ridge have been reported and were treated with open approach, flap removal, and recession wedge sulcoplasty.[10] However, to the authors' knowledge, there are no reports of OCD of the trochlear groove extending into the axial side of the medial trochlear ridge. In addition, the arthroscopic description of femoral trochlear OCD and its surgical treatment have not been reported to date.

Therefore, the objectives of this report were to describe an unusual site of stifle OCD, the surgical treatment and the functional outcome.

Case Description

Case History

A 7-year-old, neutered, pure-breed, male Groenendael Belgian Shepherd weighing 36 kg was referred to the hospital for investigation of grade 2 left hindlimb lameness with approximately 4 months duration. The lameness became worse after exercise, and no improvement was reported after conservative management combining cimicoxib (2 mg/kg, once a day) and strict rest. No traumatic episode was reported by owners prior to the onset of the lameness. The referring veterinarian's radiographs demonstrated only moderate stifle joint effusion associated with mild osteoarthritis on the distal patella, the femoral trochlea and the femoral sesamoid bones.

On presentation, the dog had grade 2 lameness of the left hindlimb. There was also mild left gluteal and quadriceps muscle atrophy, mild stifle effusion and moderate discomfort with cracking on manipulation. No stifle instability was observed. The remaining orthopedic and physical examinations were unremarkable.

Radiographs of the left stifle, obtained under sedation, revealed a focal irregular defect in the proximal femoral trochlea, accompanied by mild subchondral sclerosis and focal bone lysis of the cranial metaphyseal cortex at the level of the lesion. Additionally, moderate joint effusion and mild osteoarthritic changes were observed in the distal patella, femoral trochlea and femoral sesamoid bones ([Fig. 1]). Based on these findings, exploratory arthroscopy was performed.

Fig. 1 (A) Caudocranial and (B) mediolateral radiographs of the left stifle. Note the irregular defect of the proximal part of the femoral trochlea (red arrow) associated with mild subchondral sclerosis and focal bone lysis of the cranial metaphyseal cortex, along with moderate joint effusion and mild osteoarthritis on the distal patella, the femoral trochlea and the femoral sesamoid bones.

Surgical Technique

Premedication was performed with medetomidine (4 μg/kg, intravenous) and methadone (0.2 mg/kg, intravenous). Induction was performed with propofol (2 mg/kg, intravenous) and ketamine (1 mg/kg, intravenous), and volatile anesthesia was maintained with isoflurane in dioxygen. Intraoperative analgesia was provided by a femoral and sciatic nerve block with bupivacaine (2 mg/kg). Antibiotic medication prophylaxis was provided by cefazolin (22 mg/kg, intravenous) 30 minutes prior to surgery.

The dog was placed in dorsal recumbency. Routine lateral parapatellar arthroscopy was performed and revealed a large ovoid cartilaginous flap mimicking an OCD-like lesion on the proximal part of the groove and axial side (inside the trochlear groove) of the medial ridge of the femoral trochlea ([Fig. 2]). The cartilage flap was proximodistally oriented and remained partially attached to the subchondral bone. In addition, the distal and caudal aspects of the patella showed Modified Outerbridge Score grade 2 (MOS-2) cartilage lesions (superficial cartilage damage).[11] The remaining examination of the medial and lateral intra-articular compartments revealed severe synovitis.

Fig. 2 Arthroscopic appearance of the osteochondritis dissecans flap located on the proximal groove and medial ridge of the femoral trochlea (black arrow).

Mobilization of the OCD-like lesion was attempted arthroscopically; however, due to the large size of the flap and its firm attachment, conversion to an open medial arthrotomy was necessary. Following lateral luxation of the patella, the lesion was identified ([Fig. 3]) and the flap was easily removed using a probe and DeBakey forceps. The bed of the lesion was debrided with curettes, and subchondral bone picking was performed using a 1.2-mm Kirschner wire (Synthes, West Chester, MA) on a power drill (De Soutter, Aston Clinton, United Kingdom) to access the vasculature of the subchondral bone and thereby promote fibrocartilage production. The joint was flushed before routine closure.

Fig. 3 (A) Intraoperative photograph of the osteochondritis dissecans lesion located on the proximal groove and axial portion of the medial ridge of the femoral trochlea (black arrow). Note the longitudinally oriented cartilage flap mildly attached to the proximal third of the femoral trochlear groove and medial ridge. (B) The cartilage flap is being raised off the femoral trochlear groove and medial ridge with a probe (black arrow). (C) Intraoperative photograph after flap removal, curettage and picking of the underlying subchondral bone. Note the irregular contour of the defect, the microdrill holes and the bleeding subchondral bone (black ellipse). (D) Flap removed from the proximal groove and medial ridge of the femoral trochlea.

Postoperative analgesia was provided with morphine (0.2 mg/kg, intravenous, every 4 hours for 24 hours), firocoxib (5 mg/kg, per os, once a day for 3 weeks), gabapentin (10 mg/kg, per os, three times a day for 2 weeks) and tramadol (2 mg/kg, per os, two times a day for 5 days).

The flap was submitted for pathological analysis. The fragment removed from the femoral trochlea was fixed in 10% neutral buffered formalin and routinely processed for histopathological analysis. The fragment of epiphyseal cartilage showed degenerative and necrotic chondroid changes characterized by articular cartilage cleft, fissures and mineralization and chondrocyte rarefaction and clustering with hypereosinophilia of the cartilaginous matrix ([Fig. 4]). These findings were consistent with our arthroscopic diagnosis and confirmed the diagnosis of OCD.

Fig. 4 Biopsy of the cartilage flap. Fragment of epiphyseal cartilage showing degenerative and necrotic chondroid changes characterized by articular cartilage cleft, fissures and mineralization and chondrocyte rarefaction and clustering with hypereosinophilia of the cartilaginous matrix (hematoxylin and eosin saffron stain, bar = 500 μm).

Follow-up

Postoperatively, strict rest was implemented for 8 weeks with only 10-minute leash walks allowed three to four times daily. This was followed by a gradual increase in exercise. At the hospital, the lameness could not be detected 4 months postoperatively. However, slight discomfort was elicited at the limit of stifle extension, and mild left stifle effusion was still evident. Thus, magnetic resonance imaging (MRI) followed by an arthroscopic reexamination of the left stifle joint was performed. The MRI revealed the persistence of the osteochondral defect localized to the proximal part of the groove of the femoral trochlea with only partial restoration of cartilage in the distal part of the lesion, without any damage to the cruciate ligaments or menisci ([Fig. 5]). The arthroscopy revealed thin fibrocartilage covering the treated area of the femoral trochlea which failed to completely fill the osteochondral defect ([Fig. 6]). The distal and caudal aspect of the patella still showed MOS-2 cartilage lesions, without any progression. No sign of synovitis was observed during the arthroscopy. Finally, no lameness was reported by the owners 8 months postoperatively.

Fig. 5 Magnetic resonance imaging examination of the left stifle 4 months postoperatively. (A) T2 3D TSE and (B) T1 3D VIBE images showing a persistent osteochondral defect located in the proximal part of the groove and axial part of the medial ridge of the femoral trochlea (yellow ellipses), with only partial cartilage restoration in the distal and axial part of the lesion (red arrows), without any subchondral inflammation, nor damage to the cruciate ligaments or menisci, nor synovitis. T2, transverse relaxation time; 3D, 3 dimension; TSE, turbo-spin-echo; VIBE, volumetric interpolated breath-hold examination.

Fig. 6 Arthroscopic appearance of the healed lesion located on the proximal groove and medial ridge of the femoral trochlea 4 months postoperatively. The treated lesion is covered by thin fibrocartilage (black arrow). T2, transverse relaxation time; 3D, 3 dimension; TSE, turbo-spin-echo; VIBE, volumetric interpolated breath-hold examination.

Discussion

This report presents the first case of an aged dog diagnosed with OCD at the proximal groove and axial side of the medial ridge of the femoral trochlea. Although the knee is the most common joint affected by OCD in humans, the trochlea is an infrequently reported site of knee OCD, accounting for only 3.8% of knee OCD.[12] In contrast, canine stifle OCD is much less frequent, with more than 90% of lesions involving the articular surface of the lateral condyle.[7] [8] Only two cases of canine OCD of the abaxial side (outside the trochlear groove) of the medial femoral trochlear ridge have been reported. These were treated with a recession wedge sulcoplasty through an open approach.[10] In the present case, no other stifle lesions were observed during the two arthroscopic examinations and the MRI, despite the fact that additional stifle lesions are reported in up to 65% of cases of stifle OCD, primarily involving cranial cruciate ligament rupture.

The advanced age of the dog at the onset of clinical signs is also uncommon. Osteochondritis dissecans is known to be a juvenile condition that most commonly affects young, rapidly growing, large and giant breed dogs.[2] [3] Concerning the particular localization of stifle OCD in the femoral trochlea, a previous report described two 7-month-old English Bulldog siblings presenting with chronic left pelvic limb lameness, which is consistent with the usual presentation in dogs.[10] However, a recent study on the epidemiology of canine OCD found that stifle OCD is diagnosed later than OCD in other joint locations.[1] The median age at first diagnosis of stifle OCD was 2.62 years, compared to 0.74 years for all OCD locations and 0.73 years for tarsal joint OCD. Additionally, in that study, the age at first diagnosis ranged from 0.45 to 8.82 years, which is consistent with the age of our case. The late diagnosis of stifle OCD may be attributed to early clinical signs being mistaken for other causes of hindlimb lameness, or to the absence of signs suggestive of OCD, with OCD being discovered as an incidental finding during radiography or arthroscopy for other stifle conditions. In our particular case, the late clinical presentation may be explained by the very limited osteoarthritis lesions, but also by the proximal non-weight-bearing localization of the lesion. Indeed, the stifle flexion angle is in the range of 35 to 93 degrees during walking and trotting, and it has been shown that the distal pole of the patella first contacts the trochlea at a flexion angle of 45 degrees.[13] [14] At this flexion angle, the patellofemoral contact area and patellofemoral contact pressure are the lowest in an intact stifle, and significantly lower than at 60 and 90 degrees.[14] These findings mean that the patellofemoral contact area increases with increasing stifle flexion angles, while the patella moves distally on the femoral trochlea, which confirms that the proximal part of the femoral trochlea is less exposed to contact pressure. The late clinical expression may also be explained by excessive physical activity or previous trauma, although not reported by the owners. This has been described in femoral trochlear OCD in humans, where the condition can be associated with squatting or jumping activities.[15] [16] [17]

Given the age, medical history, orthopedic examination and radiographic findings, arthroscopy was the procedure of choice to evaluate the articular surfaces of the stifle joint, as well as the cruciate ligaments and meniscus, to rule out a partial cruciate ligament rupture or a meniscal lesion. In our institution, arthroscopy is the preferred choice over non-invasive imaging techniques as arthroscopy offers both comprehensive visualization and treatment of intra-articular lesions.[18] [19] In our case, the arthroscopy was converted to an open arthrotomy due to the size of the cartilage flap, which was too large to be detached and removed through the arthroscopic portal. Removal of the flap, debridement of the OCD bed and subsequent subchondral bone picking were performed, as reported in both human and veterinary medicine.[9] [10] [16] Fragment removal of an OCD-like lesion, located in the intercondylar fossa of the femur, was described in a dog with an excellent outcome.[9] Another report described a similar technique of fragment removal associated with a recession wedge sulcoplasty in two dogs presented with OCD of the abaxial side of the medial femoral trochlear ridge, with a concurrent shallow trochlear groove.[10] The authors also reported an excellent long-term outcome. The recession wedge sulcoplasty technique could have been an option, but we considered a more conservative approach.

Due to persistent left stifle effusion and mild discomfort during full stifle extension, an MRI and arthroscopic follow-up were performed 4 months postoperatively to document the healing of the lesion and to rule out any additional lesions. In our case, the MRI and arthroscopic findings were consistent with a persistent osteochondral defect located on the proximal part of the groove of the femoral trochlea, with only partial cartilage restoration in the distal part of the lesion. There was no damage to the cruciate ligaments or menisci. The partial coverage of the lesion by thin fibrocartilage 4 months postoperatively may be related to the unusual location of the lesion, but also to the reduced healing capacity of an aging dog. No comparison to similar cases can be made as this is the first report of the debridement of an OCD lesion located at the femoral trochlear groove, and the healing characteristics of debrided OCD in this rare site remain unknown. Failure of complete fibrocartilage healing may occur in other locations of OCD.[18] Other surgical options have been reported as first-line treatments or as revision surgery after failure of conventional flap removal and debridement of the lesion. Autogenous osteochondral grafting and synthetic osteochondral resurfacing implants have been reported to fill the residual osteochondral defect in dogs diagnosed with stifle OCD.[20] [21] Other surgical treatment options include the replacement of the femoral trochlea with a trochlear prosthesis, as has been previously described for patellar luxation in dogs, and also more anecdotally, in a dog with a severe bone defect in the femoral trochlea caused by hematogenous osteomyelitis.[22] [23] Given the improvement in limb function, decreased pain and the MRI and arthroscopic findings, it was decided, after discussion with the owners, not to pursue any additional surgical procedures.

In conclusion, this is the first case of OCD located on the trochlear groove in an older dog, arthroscopically diagnosed and successfully treated by fragment removal and debridement picking, through an open stifle arthrotomy. This procedure resulted in substantially improved limb function 8 months postoperatively.

Conflict of Interest

None declared.

Acknowledgements

The authors would like to thank Dr. (Vet.) Marion Fusellier for the MRI analysis and images, and Dr. (vet.) Jérôme Abadie for the histopathological analysis and image presented in this report.

Authors' Contributions

J.M.: Surgeon in charge of the case, collected data, drafted the manuscript, assisted with revision of the manuscript, checked the final manuscript and approved the final manuscript for submission.

G.J.: Second surgeon during the reported surgery, collected data, assisted with revision of the manuscript, checked the final manuscript and approved the final manuscript for submission.

R.T.: Surgeon in charge of the case, performed the reported surgery, assisted with revision of the manuscript, checked the final manuscript and approved the final manuscript for submission.

G.O.: Participated in writing the final manuscript and approved the final manuscript for submission.

M.P.: Surgeon in charge of the case, performed the reported surgery, assisted with a draft of the manuscript and revisions, checked the final manuscript and approved the final manuscript for submission.

Ethical Approval

The authors confirm that the ethical policies of the journal have been adhered to as noted on the journal's author guidelines page. No ethical approval was required as this is a case report with no original research.

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Publication History

Received: 31 January 2025

Accepted: 09 April 2025

Article published online:
27 May 2025