Articular Cartilage Injury

Articular Cartilage Injury

Aman Dhawan

Vasili Karas

Brian J. Cole

  • Articular cartilage is a complex structure lining the articulating surfaces of diarthrodial joints. It provides a smooth, low-friction surface, while minimizing peak stress on the underlying subchondral bone.

  • Injuries to the chondral surfaces occur in all joints of the human body. Articular injury of the knee has received the most attention in the literature. This chapter will focus primarily on articular injury as it pertains to the knee joint; however, many of the principles of evaluation, grading, and management hold true for chondral injury in any anatomic joint.

  • Injury to articular cartilage is very common; in one retrospective review of 31,516 knee arthroscopies, 63% of patients were found to have chondral injury (21). Cartilage injury of the knee affects approximately 900,000 Americans annually, resulting in over 200,000 surgical procedures (20). Notably, the literature analyzing the prevalence of articular cartilage pathology does not provide significant guidance or insight into the prevalence of lesions that are or become symptomatic and require treatment.

  • Although nonsurgical management of articular cartilage injury has remained largely the same over the past decade, surgical treatment of chondral injuries continues to evolve. Reparative, restorative, and reconstructive techniques continue to be refined, giving surgeons more tools and options for biologic reconstruction of articular surfaces.


  • Articular cartilage is composed of water (65%-80% of wet weight), collagen (10%-20% of wet weight), proteoglycans (10%-15% of wet weight), and chondrocytes (5% of wet weight). The collagen in native cartilage is primarily type II, with smaller quantities of types V, VI, IX, X, and XI. Chondrocytes are the cells responsible for the production of the extracellular matrix. These cells differentiate from mesenchymal stem cells during skeletal morphogenesis and are subsequently a low turnover cell type. Chondrocytes receive their nutrition and oxygen from the surrounding synovial fluid via diffusion (16). In the intact, uninjured knee, the articular cartilage shares load-bearing responsibility with the menisci (up to 70% from the lateral meniscus), making the chondral surfaces significantly vulnerable to injury and degeneration with partial or complete injury or removal of the menisci.

  • Because of the limited vascular, neural, and lymphatic access, in addition to the limited capacity of chondrocyte division and migration, the healing response of articular cartilage is poor. Partial-thickness injury that does not penetrate the tidemark, the demarcation between the deep layer and calcified layer of cartilage, will result in cellular insult with decreased matrix production by the underlying and surrounding chondrocytes and ultimately little healing. In artilage matrix and cell injuries, decreased proteoglycan concentration, increased hydration, and disorganization of the collagen network occur (16,21).

  • Injury that penetrates the tidemark into the calcified cartilage layer and the subchondral bone (an osteochondral lesion) will illicit an inflammatory response that includes an influx of marrow contents (undifferentiated mesenchymal stem cells, cytokines, and growth factors including transforming growth factor-β [TGF-β] and platelet-derived growth factor [PDGF]) triggered by hemorrhage and fibrin clot. The osteochondral injury has potential for a more robust healing response including a resultant repair that more closely resembles fibrocartilage (vs. native hyaline cartilage) composed of primarily type I collagen. This fibrocartilage-like repair is less stiff and more permeable than normal articular cartilage (16,21). Fibrocartilaginous repair tissue is far less durable than native hyaline cartilage and often begins to show evidence of depletion of proteoglycans, increased hydration, fragmentation and fibrillation, increased collagen content, and loss of chondrocytes within 1 year (15).

  • Although the natural history of chondral injuries is not completely understood, it is postulated that defects, particularly larger, full-thickness injuries, can progress via edge loading and elevated contact pressures on the adjacent articular surfaces. This progression may lead to degradation of the surrounding chondral surfaces and ultimately osteoarthrosis.

Patient Evaluation

  • Articular cartilage injury can be caused by an acute injury that results in a focal chondral or osteochondral injury or chronic/subacute injuries or conditions that result in degenerative lesions. Damage to the chondral surfaces can occur in isolation or, as is often the case, in association with other intra-articular injury. The evaluating physician should maintain a high index of suspicion for chondral injury when evaluating the knee for any causes of pain, effusion, instability, or mechanical symptoms.

  • A thorough history should include details related to the onset of symptoms (traumatic or insidious), mechanism of injury, previous injuries and surgery, and symptom-provoking activities.

  • A thorough physical examination should evaluate formal alignment, abnormal gait, swelling, effusions, instability, meniscal symptoms, range of motion, strength, and neurovascular abnormalities. Crepitus, catching, locking, or grinding can occur with focal irregularities of the articular surfaces. Diagnosis of all concomitant pathology is critical to formulate a successful, global treatment plan.

  • Radiographic workup should include posterior-anterior, weight-bearing, 45-degree plain films and patellofemoral, and non-weight-bearing lateral projections. Evaluation on plain films for joint space narrowing, subchondral sclerosis, osteophytes, and cysts should be performed. History and physical examination, along with these radiographs, are often all that is needed to make the appropriate diagnosis. Magnetic resonance imaging (MRI) can be valuable to assess the status of the knee ligaments and menisci but can underestimate the degree of cartilage abnormalities seen during arthroscopy (36). Use of 3.0-tesla magnets, cartilage imaging sequence techniques including fat-suppressed or fat-suppressed spoiled gradient-echo imaging, and balanced free precession steady-state sequences have improved detection and characterization of chondral injuries using MRI (6). Routine MRI sequences are typically sufficient to evaluate for subchondral abnormalities that may become useful findings during definitive decision making.


  • Although MRI is being used with more frequency to evaluate chondral injuries, arthroscopic evaluation remains the most accurate way to assess the location, depth, size, shape, and stability of a chondral or osteochondral defect of the articular surface. The Outerbridge classification is most widely used to grade these injuries (Table 6.1) (48). More recently, the International Cartilage Repair Society has modified this to a more comprehensive description and grading system (see Table 6.1) (13). The International Cartilage Repair Society grading system can be used to describe lesions both arthroscopically and using advanced radiologic imaging techniques.


  • As with most joint pathology, initial treatment of articular cartilage injuries is typically conservative with recommendations that include activity modification, judicious use of nonsteroidal anti-inflammatory drugs (NSAIDs), glucosamine and chondroitin sulfate, corticosteroid injections, and consideration for viscosupplementation (22). Patients with mechanical symptoms (including catching, locking, sensation of loose body, or giving way), acute motion loss, or failed nonsurgical management with pain and loss of function should be considered for surgical intervention.

Table 6.1 Modified International Cartilage Repair Society (ICRS) Classification System for Chondral Injury (40)

Grade of Injury

Modified ICRS System

Grade 0

Normal cartilage

Grade I

Superficial fissuring

Grade II

< 1/2 cartilage depth

Grade III

> 1/2 cartilage depth up to subchondral plate

Grade IV

Through subchondral plate, exposing subchondral bone


Arthroscopic Debridement and Lavage

  • Arthroscopic debridement and lavage is a consideration for a first-line surgical intervention in a patient with a symptomatic articular cartilage injury. This treatment modality allows the surgeon to perform diagnostic arthroscopy to assess the chondral injury and the remainder of the joint. Patient expectations must be managed in that the results of this procedure can range from diagnostic to therapeutic due to the removal of degenerative debris, loose nonviable chondral fragments, and lavage of the associated inflammatory cytokines such as interleukin-1 and tumor necrosis factor-α (1). Care is taken to preserve intact, healthy articular cartilage. Arthroscopic lavage alone has been proven to provide at least short-term benefits in 50%-70% of patients (1,24). In a select group of highly active individuals, especially in season when return-to-sport time lines are critical, arthroscopic debridement may prove to be beneficial in the short term. In general, however, the results of arthroscopic debridement and lavage are often not durable and deteriorate over time, and the primary benefit that remains is the diagnostic information obtained to help guide future treatment decisions (Table 6.2) (10,32,33,54,58).

Fragment Fixation

  • Fixation of a chondral lesion is predicated on the condition, size, shape, defect location, and adequacy of subchondral bone attached to the osteochondral fragment. Radiographic and MRI evaluation can help with the determination of many of these factors and appropriateness of this surgical option. Prior to fixation of the osteochondral fragment, both the fragment and defect must be prepared to create an adequate
    healing milieu. The fragment must be reduced anatomically into its bed, and fixation may then be completed using either absorbable or nonabsorbable implants. Occasionally, bone graft augmentation is required for deeper cavitating lesions. Treating osteochondral lesions with the same considerations as a fracture nonunion will lead to more predictable healing. These factors include debriding fibrocartilage at the base of the lesion, microfracture augmentation of the base to promote bleeding, and rigid fixation with compression. Resorbable fixation placed without the intention to remove the implant should be buried to or beneath the level of the subchondral bone because these lesions can subside over time. Metallic implants removed at 6 to 8 weeks allow the opportunity to verify fragment healing and prevent the untoward effects of prominent hardware that can develop over time. Successful healing of the osteochondral fragment with the use of headless metallic cannulated screws has been reported in up to 90% of patients (1).

Table 6.2 Results of Arthroscopic Debridement and Lavage


No. of Patients

Mean Follow-Up


Kirkley et al., 2008 (37)


2 years

Randomized controlled trial: Arthroscopy and PT vs. PT alone showed no difference in WOMAC, or SF-36 between groups (P = 0.22).

Jackson and Dieterichs, 2003 (34)


4-6 years

Retrospective case series:

Stage I: 100% excellent/good

Stage II: 90.6% excellent/good

Stage III: 48.7% excellent/good

Stage IV: 11.9% excellent/good

Moseley et al., 2002 (47)


2 years

Randomized controlled trial: Debridement, lavage, and placebo showed no difference in KSPS, AIMS2-P, and SF-36 scores.

Steadman et al., 2001 (55)


11.3 years

Retrospective case series:

Lysholm 58.8→89

Tegner 3.1→5.8

Work 4.9→7.6

Sports 4.2→7.1

Timoney et al., 1990 (58)


48 months

Retrospective case series:

63% good

37% fair/poor

Jackson, 1989 (33)


3.5 years (2-9 years)

Retrospective case series:

68% remained improved

Sprague, 1981 (54)


14 months

Retrospective case series:

74% good

26% fair/poor

AIMS2-P, Arthritis Impact Measurement Scales; KSPS, Knee-Specific Pain Scale; PT, physical therapy; WOMAC, Western Ontario and McMaster Universities Arthritis Index; SF-36, Short Form-36.

Marrow-Stimulating Techniques

  • The goal of marrow stimulation techniques is the delivery of mesenchymal stem cell progenitors to the defect bed and the subsequent formation of a fibrocartilage-like repair tissue from these cells. This technique can be performed in a number of ways to include drilling, abrasion, and microfracture and always involves penetration of the calcified cartilage layer into the subchondral bone to allow the migration of progenitor cells to the articular surface. Because of the limited fill that may occur in some lesions, particularly larger ones greater than 2 cm2, and the different structural and biomechanical properties of this fibrocartilage-like repair tissue (see earlier Basic Science section), the best results are typically achieved with relatively small defects in a low-demand patient population (1). Results of microfracture technique are summarized in Table 6.3.

May 22, 2016 | Posted by in SPORT MEDICINE | Comments Off on Articular Cartilage Injury
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