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). Focal chondral defects have long been implicated in the subsequent development of OA. Focal chondral defects result from various causative factors that may genetically predispose to early breakdown and wear.

Genetics may predispose to early cartilage wear and OA. In addition, metabolic, inflammatory, and developmental diseases may lead to articular cartilage damage. These may include Gaucher disease, hemophilia, hemachromatosis, 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 chondral lesions.¹ Traumatic events and developmental causative agents such as osteochondritis dissecans 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 (up to 65 years).¹^–³ The most common locations for these defects are the medial femoral condyle (up to 32%) and the patella.^2,³ Most are detected incidentally during meniscectomy or anterior cruciate ligament reconstruction.^1,⁴ Notably, despite the relatively high incidence, many of these defects are incidental in nature and asymptomatic. Articular cartilage lesions have no spontaneous repair potential and have a propensity to worsen with time. Even though the natural history is not completely understood, those involved in cartilage repair agree on the importance of looking for background factors that predispose to the formation of these defects—malalignment and compartment overload of the tibiofemoral or patellofemoral compartment, joint laxity, contracture, meniscal insufficiency, and, of course, genetic predisposition to OA— for which clinical, biologic, or genetic markers currently are lacking.

Effect of running and other sports on OA

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 progression of knee OA.⁵^–⁸ 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.⁹ 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.¹⁰^–¹² These activities include sports involving torsion and impact, such as soccer, weight lifting, and sprinting.^13,¹⁴ 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 development of large areas of delamination.¹⁵ Other studies have demonstrated that known articular injury greater than 1 cm² has progressed to OA, with greater than 14-year follow-up in more than half of patients allowed to participate in sports.¹⁶ Even when known cartilage injuries are treated with articular cartilage repair by use of microfracture or autologous chondrocyte implantation, OA may develop in as many as one third of patients¹⁷ as early as 5 years after treatment. This may be due to missed axial alignment versus the severity of the instigating initial injury in producing articular cartilage injury because this has not been found with autologous chondrocyte implantation alone when alignment was carefully assessed and treated.^18,¹⁹

Anterior cruciate ligament injury

Another consideration that often directly relates to participation in athletics is injury to the anterior cruciate ligament (ACL) and subsequent development of knee OA. This severe trauma is generally associated with bone bruising at the time of subluxation of the tibiofemoral joint with tear of the ACL.^20,²¹ Biopsies of the overlying articular cartilage to the bone bruise have demonstrated that the superficial and middle zones of articular cartilage have greater than 50% cartilage apoptosis in addition to loss of proteoglycans, indicating severe injury to the overlying cartilage surface with a propensity for late articular cartilage loss and delamination and the possibility of progression to OA.²² Bone bruises in the study have been shown to occur in greater than 80% of ACL-injured knees.²²

The untreated chronic ACL deficient knee has an increased risk of articular cartilage injury, especially as the time from initial injury increases.^23,²⁴

Long-term follow-up of ACL-injured patients has consistently demonstrated an association between ACL injury and the development of knee OA. It has been postulated that disruption of the normal mechanics of the knee and continued instability with resultant shear forces to the articular surfaces also predispose to injury to the meniscus, which is the secondary stabilizer of the knee. Loss of the meniscus as a shock absorber is a significant contributor to subsequent OA development. Surgical repair of the ACL aims to restore normal biomechanics to the knee. However, ACL repair has not been shown to reduce the incidence of knee OA compared with nonoperative management.²⁵ This finding may support the theory that it is the initial trauma and bone bruising with overlying cartilage injury and subsequent ligament failure that eventually lead to OA, which is my belief.

Neuman et al ²⁶ reported that the primary risk factor for development of knee OA after ACL injury was whether a meniscectomy had been performed. This finding seems to support the view that maintenance of knee loading and chondroprotection from the meniscus are important considerations in this issue. More investigation is needed to determine the causative factors responsible for early OA development in this population.