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

Introduction

The 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 may be difficult to obtain and only available in certain parts of the world and resorption and collapse of the allograft are a possibility in the first 2 years after transplantation in approximately 25%–30% of cases. For these reasons, if an osteochondral defect is well contained, my preferred treatment is for the use of autologous bone graft (ABG) or ABG plus cells, i.e., matrix-induced autologous chondrocyte implantation (MACI) sandwich technique. In parts of the world where MACI is not available, ABG alone may be highly effective but not as durable. Certainly, for small focal deep osteochondral areas of damage, a cancellous ABG is a very reasonable first-choice treatment. I reserve the 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 ACI procedure.

Osteochondritis Dissecans

Osteochondritis dissecans (OCD) has undergone many treatment strategies from surgical excision as advocated more than 150 years ago to osteochondral autogenous transplants (OATS).

The disease is rare under the age of 10 years and over the age of 50 years. The male-to-female ratio has been reported as 2:1 or 3:1 with bilateral involvement in up to 33%. The medial femoral condyle is affected approximately ¾ of the time with ¾ of the lesions affecting the lateral (intercondylar) portion of the medial femoral condyle. Kindreds with clear hereditary patterns have been documented as well as evidence to suggest no clear pattern of familial tendency.

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