Chapter 11 Treatment of Deep Osteochondritis Dissecans Lesions, Avascular Necrosis, and Osteochondral Defects of the Knee Using Autologous Bone Grafting

INTRODUCTION

CLASSIFICATION AND MANAGEMENT

AVASCULAR NECROSIS

CLINICAL RESULTS—CASE SERIES—TECHNIQUE FOR TREATMENT OF DEEP CONTAINED OSTEOCHONDRAL DEFECTS

RESULTS

CONCLUSION

Introduction

Management of an osteochondral defect in the knee is one of the most difficult conditions for the orthopedist. Although a fresh osteochondral allograft seems to be the treatment of choice for this condition, allografts are not without their own problems. A size match is difficult to obtain, availability is uncertain, and resorption and collapse of the allograft are possible. For these reasons, if an osteochondral defect is well contained, my preferred treatment is autologous bone graft. I reserve use of a fresh osteochondral allograft for a defect that is peripherally uncontained and not suitable for autologous bone grafting or a failed cartilage surgery, such as a failed second-stage autologous chondrocyte implantation (ACI) procedure after bone graft or a failed ACI sandwich technique.

Osteochondritis dissecans

Osteochondritis dissecans (OCD) has undergone many treatment strategies, ranging from surgical excision as advocated more than 150 years ago ¹ to osteochondral autogenous grafting.²^–⁴

The disease is rare in individuals younger than 10 years and in those older than 50 years.⁵ The male-to-female ratio has been reported as 2:1⁶ or 3:1,⁷ with bilateral involvement in up to 33%.⁸ The medial femoral condyle is affected approximately 75% of the time (Linden, 1976 incidence study),⁵ with three fourths of the lesions affecting the lateral (intercondylar) portion of the medial femoral condyle. Kindreds with clear hereditary patterns have been documented,⁹ as has evidence suggesting no clear pattern of familial tendency.¹⁰

Many etiologies have been proposed, including repetitive microtrauma and impingement of the tibial spine,¹¹ stress fractures with no identifying trauma,¹² and vascular insult.¹³ However, vascular studies of the end the femur have demonstrated a rich vascular plexus to intramedullary cancellous bone, making this etiology unlikely.¹⁴ Histologic evaluation of specimens removed at surgery have demonstrated viable bone and cartilage and not empty lacunae.¹⁵

Classification and management

Categorization of the disease process into a juvenile or adult form is important at the time of diagnosis because the treatment and prognosis may be managed by different treatment algorithms depending on the stage of disease.¹⁶^–¹⁸

However, there is consistent agreement that knees treated by removal of OCD fragments that are detached from the weight-bearing femoral condyles do poorly.¹⁹^–²² Linden²³ noted that at average 33-year clinical and radiographic follow-up, 38 of 48 patients who had the initial manifestation after closure of the physes (i.e., adult form) had symptomatic and radiographic gonarthrosis. Linden²³ stated that “Symptoms and roentgenographic gonarthrosis become more frequent and approach 100 per cent with time” (Figure 11–1).

Figure 11–1 A 44-year-old man with typical appearance of an osteochondritis dissecans lesion after the fragment had been removed. Universal progression to osteoarthritis was noted by Linden.²³

Cystic degeneration deep to the lesion in situ may occur, which makes bony healing especially difficult, even in the juvenile form (Figure 11–2).

Figure 11–2 A, Anteroposterior x-ray film in an 18-year-old woman with lateral femoral condyle osteochondritis dissecans that has not been surgically treated. A degenerative cystic form of the condition is apparent by x-ray film and by magnetic resonance imaging (B).

Treatment by removal of the fragment and drilling to promote fibrocartilage repair is not recommended because the repair tissue is not durable and will break down.²⁴^–²⁶

Optimal treatment is aimed at assessing the stability of the OCD fragment and obtaining union by casting immobilization in a stable juvenile fragment, or in situ flap, to fixation with or without autogenous bone grafting by open or arthroscopic technique. This is the treatment of choice for the adult form (Figure 11–3). An unstable OCD lesion is assessed for the underlying bony attachment by computed tomographic scan. Fixation to the underlying bony bed by standard AO principles of delayed union with curettage, autologous bone grafting, vascularization of the defect by drilling, and rigid internal fixation gives the best results.

Figure 11–3 A 21-year-old male college hockey player with an unstable painful medial femoral condyle osteochondritis dissecans (OCD) lesion that has failed arthroscopic stabilization with absorbable tack fixation. Persistent catching, swelling, pain, and limp are presenting symptoms. The treatment plan includes open surgical open reduction internal fixation, removal of fibrous tissue at the base of the defect and undersurface of the fragment, drilling of the subchondral bone to promote vascularization of the fragment, and autologous bone grafting with stable internal fixation per classic principles of treatment of a nonunion. Later removal of the internal fixation is performed. A, Anteroposterior x-ray film demonstrates classic medial OCD lesion with a large bony fragment. B, Lateral x-ray film. C, Long alignment x-ray films demonstrate a varus knee with mechanical axis in the medial compartment. D, Open appearance of un-united fragment in situ with cracked articular cartilage surface. E, The fragment is hinged on its vascular attachment to the posterior cruciate ligament synovium toward the intercondylar notch. This maintains stability of the fragment so that it does not fall out of the wound. Note the chronic appearance of the defect base. The fragment is covered with fibrous tissue and has underlying sclerotic bone. F, The underlying fibrous tissue and sclerotic bone are removed, autogenous bone graft from the upper tibia is placed to restore the proper anatomic location of the fragment because they tend to subside, and cannulated screw guidewires are used to check the reduction before screw fixation is performed. G, Cannulated screw fixation with anatomic reduction after curettage and bone grafting. The screw heads are buried below the articular surface so as not to damage the tibial surface. H, Postoperative anteroposterior x-ray film showing anatomic reduction. I, Postoperative lateral x-ray film. J, Eight weeks postoperatively, the hardware is removed arthroscopically before weight bearing is permitted. K, The cannulated screw guidewires simplify screw removal. L, The fragment is probed carefully to assess congruency and stability. Full weight bearing is allowed postoperatively, but sports are restricted for another 4 months to allow solid healing and bone remodeling. Anteroposterior (M) and lateral (N) x-ray films 1 year after treatment show solid healing of the OCD fragment. The patient returned the following season to varsity-level hockey. He remains asymptomatic after 7 years of follow-up.

In cases of failed treatment of OCD with an empty defect or fragmented lesion, treatment options are ACI, autologous osteochondral grafting, or osteochondral allografting. ACI has the advantage of being autologous tissue in a young patient, with the potential to resurface large areas without donor site morbidity, as in osteochondral autograft transfers. Most defects can be managed by ACI alone when bone deficiency centrally is less than 6 to 8 mm deep (see Chapter 7).²⁷

When cystic changes occur under the defect (see Figure 11–2), the defect has near-vertical walls and is greater than 8 to 10 mm deep, or the defect is very sclerotic due to a chronic lesion that may have undergone drilling, abrasion, or microfracture, it is safer to remove the unhealthy bed and bone graft the defect. The bone grafting technique is much like the preparation of a dental amalgam and is described in detail in Figure 11–4.