Chondral Injury and Osteoarthritis: The Impact of Articular Cartilage Lesions

Introduction

Damage to the articular cartilage comprises a spectrum of disease entities ranging from single, focal chondral defects to more advanced degenerative disease and end stage osteoarthritis (OA). Long implicated in the subsequent development of osteoarthritis, focal chondral defects result from various causative factors and those factors that may genetically predispose to early breakdown and wear.

Genetics may predispose to early cartilage wear and OA in addition to metabolic, inflammatory, and developmental diseases, which may lead to articular cartilage damage. These may include Gaucher disease, hemophilia, hemochromatosis, ochronosis, Ehlers-Danlos syndrome, Paget disease, acromegaly, avascular necrosis, neuropathic arthropathy, and joint dysplasia.

Patients are approximately evenly split in reporting a traumatic versus an insidious onset of symptoms; athletic activities are the most common inciting event associated with the diagnosis of a chondral lesion. Traumatic events and developmental causative agents such as OCD predominate in younger age groups. Several large studies have found high-grade chondral lesions (Outerbridge grades III and IV) in 5% to 11% of younger patients (<40 years) and up to 60% of older patients. The most common locations for these defects are the medial femoral condyle (up to 32%) and the patella, and most are detected incidentally during meniscectomy or anterior cruciate ligament reconstruction. Notably, despite this relatively high incidence, many of these defects are incidental in nature and asymptomatic. It is agreed that articular cartilage lesions have no spontaneous repair potential and a propensity to worsen with time. Even though the natural history is still not completely understood, those involved in cartilage repair agree that one must look for background factors that predispose to the formation of these defects—malalignment and compartment overload of the tibiofemoral or patellofemoral compartments, joint laxity, contracture, meniscal insufficiency, and of course, genetic predisposition to OA—for which we are just beginning to scratch the surface through advancements in genetic, genomic, and epigenetic research.

Effect of Running and Other Sports on Osteoarthritis

Long distance running and its relationship to the development of OA is an issue of great interest. Several studies have suggested that recreational long distance running is not associated with the progression of knee OA. However, the presence of risk factors such as obesity, muscle weakness, or previous joint injury can make the knee more susceptible to the demands associated with participation in sports or athletics. In contrast to recreational involvement, participation in several athletic and sporting activities at the elite level has been associated with an increased risk of lower extremity OA. These activities include those involving torsion and impact such as soccer, weightlifters, and sprinters. Ignoring a known cartilage injury and continuing to participate in torsional impact sports such as soccer has been shown to cause progression of articular cartilage injuries with large areas of delamination developing. Other studies have demonstrated that known articular injury greater than 1 cm ² have progressed to OA with greater than 14 years follow-up in greater than half the patients observed when allowed to participate in sports. Even when known cartilage injuries are treated with articular cartilage repair by the use of microfracture or autologous chondrocyte implantation (ACI), OA may develop in as much as one-third of the patients as early as 5 years later. This may be a result of missed axial alignment versus the severity of the instigating initial injury to produce the articular cartilage injury because this has not been found with ACI alone when alignment has been carefully assessed and treated.