Articular cartilage injuries in the athlete's knee: current concepts in diagnosis and treatment.

Degenerative arthritis is an enormous problem which affects millions of people in the United States and around the world. Once established, it is a debilitating disease that impacts our sporting and recreational activities, our ability to work, and our quality of life for the rest of our lives. The basic lesion in degenerative arthritis is damage to the articular cartilage, either through acute trauma, a "wear and tear" process, or a combination of the two. The traditional non-operative treatments of arthritic problems have included medications (ie, nonsteroidal antiinflammatory drugs [NSAIDs] and acetaminophen), activity modifications, and cortisone injections. Traditional surgical treatments have primarily been aimed at debridement of damaged tissue such as torn menisci and irregular articular surfaces. Failure of these treatments often necessitates total joint replacement. What if we could repair these articular cartilage lesions at an early stage, before they began the progression to degenerative arthritis? This is precisely the goal of evolving cartilage repair technology. Cartilage repair is a rapidly developing and exciting area of research in orthopaedic surgery, and this interest has even spawned the International Cartilage Repair Society (ICRS), which was founded in 1997. Much of the pioneering work in this area has been done in the knee, although the basic principles and surgical techniques can be applied to other joints. The remainder of this article will focus on our progress with cartilage injuries in the knee.

Basic Science of Articular Cartilage

Articular cartilage provides a smooth, low-friction surface to diarthrodial joints, which allows a smooth gliding movement and serves to transmit loads across the joint and to dissipate peak stresses on the underlying subchondral bone. It is a viscoelastic material that demonstrates a time-dependent behavior when exposed to a constant stress. In essence, it is like a slow-moving sponge that will slowly compress when squeezed, then slowly regain its shape when pressure is released.

Articular cartilage is arranged into functional layers or zones (superficial, intermediate, deep) which blend into a calcified zone, which in turn is adherent to the underlying subchondral bone (Fig. 1). There is no vascular supply via the subchondral bone, and there are no nerve endings within the cartilage.

In the knee, load-bearing and lubrication duties are shared with the menisci. The medial meniscus transmits 50% of the load in the medial compartment, and the lateral meniscus transmits 70% of the load in the lateral compartment. The menisci transmit approximately 50% of the load with the knee in extension, and about 85-90% in flexion. (1) Thus, with meniscal injury in which there is partial or complete loss of the functioning meniscus, loads transmitted to the articular surface increase dramatically, in turn making the articular cartilage vulnerable to injury and degeneration.

Incidence of Articular Surface Injuries

The true total incidence of articular cartilage injuries is unknown. It is believed that many injuries to the articular cartilage are asymptomatic. The deleterious effects to articular cartilage of a traumatic impact may take time to manifest themselves, and the ability of standard radiographs and magnetic resonance imaging (MRI) to detect early partial thickness injuries is limited. Arthroscopic visualization, which is our most sensitive evaluation tool, may initially only show minor pathologic changes in traumatized cartilage which will eventually go on to degenerate. Noyes (2) suggests that between 5 and 10% of patients presenting with acute hemarthrosis of the knee after a sports- or work-related injury in fact have a full thickness chondral injury. Curl et al (3) reviewed 31,516 knee arthroscopies and found that chondral injuries were reported in 63% of the cases. There were 2.7 articular cartilage injuries reported per knee, and among patients under 40 years of age, 5% were found to have grade IV (full thickness) unipolar lesions of the medial femoral condyle. Therefore, although we do not know the true incidence, the number of symptomatic articular cartilage injuries is significant in both the athletic and non-athletic population.

Repair Response of Articular Cartilage

The long-term effects of an injury to articular cartilage depend on the amount of damage to the extracellular matrix and to the chondrocytes. An injury which only results in injury to the matrix, with survival of all chondrocytes, has the potential to heal, as the surviving chondrocytes may be able to synthesize new matrix and repair the lesion. On the other hand, an injury with significant death of chondrocytes and matrix is met with an inadequate repair response which is unable to duplicate normal articular cartilage. If the injury penetrates into subchondral bone, which is a vascular structure, the usual tissue repair process ensues. That is, fibrin clot formation occurs, followed by cell migration from the bone marrow, followed by vascular ingrowth. This ultimately results in the formation of fibrocartilage, which is principally type I collagen, and has inferior mechanical properties and durability compared to native hyaline articular cartilage.

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Clinical Evaluation of Articular Cartilage Lesions

Evaluation of an injured joint should include a pertinent history, a careful physical examination, and appropriate radiographic or diagnostic studies. Traditionally, our focus in the knee has been on fractures and ligamentous and meniscal injuries, with less emphasis on articular cartilage injuries. This was possibly due to the fact that there was little to offer the patient with an acute articular cartilage injury. As quoted previously, the incidence of articular surface injury is significant, and it must be included in the differential diagnosis. Symptoms include swelling, pain with weight-bearing, catching, locking, and even giving way. On exam, the presence of joint line pain, joint line tenderness, and effusion may be present and should increase the index of suspicion. Ligamentous and meniscal injuries should be ruled out by appropriate exam (ie, negative McMurray test, negative Lachman and posterior drawer, no collateral ligament laxity) and MRI if necessary. Significant degenerative arthritis is usually evident on plain radiographs with visible osteophytes and joint-space narrowing. Fractures can also usually be found on plain radiographs. Aspiration of a large effusion in an acutely injured joint often helps confirm a traumatic origin (bloody effusion), rule out infection or other unusual causes, and decompress the joint to give some symptomatic relief. Standard radiographs, preferably weight bearing, should always precede MRI or other more complex studies.

If the diagnosis is still in question after physical exam and plain radiographs, MRI is usually the diagnostic test of choice. MRI technology continues to improve and modern units are able to visualize articular cartilage. Full thickness lesions are usually visible on MRI, but shallow lesions are more difficult to detect. The initial results associated with the use of standard spin-echo pulse sequences for the detection of articular cartilage lesions were disappointing, but the use of newer MRI imaging techniques have proven to have sensitivities of more than 95% for the detection of focal abnormalities. However, studies of the agreement between MRI and arthroscopy on the grade or severity of the lesion have varied between 47% and 96%. (4) For the practicing clinician utilizing MRI, this suggests that articular cartilage lesions can be missed, and the severity can be under- or overrepresented, especially if the MRI has not been recently upgraded. For specifics on newer imaging protocols, the reader is referred to a recent article by Brittberg and Winalski (4) who have outlined the recommended protocols by the ICRS for imaging articular cartilage. For the primary care physician, orthopaedic referral is indicated for patients with a positive MRI or persistent symptoms, despite a negative MRI and a course of non-operative treatment. Figure 2 shows plain radiographs of a patient with a recent injury and patellofemoral pain. These radiographs show no significant abnormalities. Figure 3 is an axial MRI image of the same patient. The MRI shows a significant abnormality of the patellar articular cartilage with bone bruising, or subchondral edema, which suggests abnormally high stresses transferred, and injured bone.

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The gold standard for evaluation of articular cartilage lesions is arthroscopic assessment. Various classification schemes have been devised for grading cartilage damage or chondromalacia based on their appearance at arthroscopy or open surgery. (2) The reader should note that chondromalacia is synonymous with articular cartilage injury, and is frequently used interchangeably. These classification systems usually grade lesions based on their size and depth. The Outerbridge classification system is the most commonly used system for grading cartilage lesions. Figure 4 diagrams the Outerbridge system. Figure 5 shows an arthroscopic photo of a full thickness, or grade IV, lesion of the patella.

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Treatment of Articular Cartilage Injuries

Nonoperative treatment options. The vast majority of articular cartilage lesions do not cause symptoms or any significant disability. However, some patients present with complaints of pain, swelling, giving way, locking, catching, or crepitus. The pain and swelling are believed to be related to cartilage breakdown products and the release of enzymes and cytokines. This, in turn, can cause painful synovitis and swelling, with further painful distension of the joint capsule. Another source of pain lies in the subchondral bone, where periarterial nerve fibers are often stimulated by increased force transmission, or possibly vascular congestion.

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The goals of initial treatment are to reduce pain and limit disability related to the cartilage lesion. These would include patient education, weight reduction, and activity modification. For the athlete, the exercise routine should be modified to include more low-impact exercise. Cross-training with cycling or swimming is usually well-tolerated, both mentally and physically by the athlete, especially in the early phases of recovery after an injury. As symptoms improve, gradually increase the high-impact phases of athletic training to the athlete's tolerance. For the non-athlete, weight control and non-aggravating exercise programs can be helpful. Other non-pharmacologic modalities would include heat and ice application, selective bracing, and physical therapy programs.

Pharmacologic treatment usually includes mild analgesics and NSAIDs. Other potentially useful agents include injectable local corticosteroids, chondroprotective agents such as oral glucosamine and chondroitin sulfate, and injectable hyaluronic acid for viscosupplementation. Although NSAIDs are widely prescribed and useful for treatment of the symptoms of degenerative arthritis, there is currently no evidence that these drugs will alter the natural history of cartilage degeneration. (5) Also, gastrointestinal bleeding is a significant side effect of NSAIDs, although the newer COX-2 NSAIDs are reported to have a lower incidence of gastrointestinal bleeding side effects.

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Viscosupplementation, by means of hyaluronic acid (HA) injections, has been available in the United States since 1997, but was available first in Europe, then in Canada, prior to 1997. In osteoarthritis, there is a decrease in the viscosity and elasticity of synovial fluid, and the hyaluronic acid has a lower molecular weight than that found in normal knees. This observation led to the use of injectable HA to replenish the normal properties of synovial fluid. In vitro studies of human synoviocytes have shown that exogenous HA stimulates production of endogenous HA, and potentially positively stimulates other biochemical processes. (5)

Operative treatment options. Numerous surgical treatment options have been tried and are available for the symptomatic articular cartilage lesion. These options are outlined in Table 3. All of these options are currently in use, but the majority of lesions are treated by either debridement and lavage or a repair stimulation technique. A small percentage of articular surface lesions are treated with cell and tissue transplantation techniques. These techniques show promise in recreating a new articular surface with similar properties to native articular cartilage. Very limited experience has been reported with biologic and synthetic polymers used to fill in articular surface defects. Various success rates have been reported for each of these options, and results vary with the age of the patient and size of the lesion, as well as other variables.

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Repair stimulation techniques. Repair stimulation techniques (Fig. 6) try to take advantage of the normal tissue repair processes to create a new joint surface. Vascular channels are created by puncturing the subchondral bone. Inflow of blood and marrow products creates a healing response which typically forms fibrocartilage. As stated previously, fibrocartilage has inferior mechanical and wear properties compared to native hyaline cartilage. Varying clinical results have been reported, with most studies showing initial improvement followed by deterioration of results with time. (6,7)

Cell and tissue transplantation. Other techniques have been devised to repair articular cartilage, since repair stimulation techniques do not allow the recreation of normal or near-normal articular cartilage. Cell and tissue transplantation techniques rely on implantation of "normal" tissue into the area of cartilage loss. The donor sites for the "normal" tissue can be another site in the knee, a cadaver, or a cell culture of normal tissue.

The osteochondral autograft technique utilizes normal tissue from another area of the knee and implants it into the defect. Cartilage, along with a plug of underlying bone, is moved from an area of low stress to an area of high stress where the lesion exists. This is analogous to moving hair plugs from one part of the scalp to another to treat baldness. Figure 7 diagrams the technique. Hangody (8) and other authors have reported promising results with this technique. This is probably best-indicated for small- to medium-sized lesions, as there is not enough donor material available for large lesions.

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Osteochondral allograft techniques are used in which the donor site is from a cadaver. These must be done with fresh grafts if cell viability is to be expected, and this significantly limits its use. The technique is very similar to the osteochondral autograft technique shown in Figure 7, except that the graft source is a cadaver instead of another area of the knee.

Autologous chondrocyte implantation (ACI) utilizes cultured chondrocytes to fill the defect in the articular surface. A potential advantage of this technique over osteochondral autografting is that there is theoretically no upper limit to the size of the lesion. The technique involves taking a biopsy of normal articular cartilage which is removed at an initial arthroscopy. The cells are stored frozen until implantation is desired. When implantation is desired, the cells are placed in tissue culture, and a large population is grown. These cells are transported as a suspension and then reimplanted into the knee at a second surgery. A patch of periosteum is used to cover the defect in order to contain the cell suspension while it matures into hyaline-like cartilage. Peterson (9) recently reported 5 to 11 year follow-up data for this procedure with 51 of 61 patients achieving good to excellent results. The technique for ACI is diagrammed in Figure 8. Figure 9 shows an arthroscopic view taken 6 months after ACI of the patella. This is from a second-look arthroscopy of the same patient shown in Figure 5. Note the smooth contour of the joint surface and the well-integrated borders.

Conclusion

Articular cartilage disease and injury are common problems facing the patient and physician today. Over the last few decades, joint replacement has become the gold standard for treatment of end-stage degenerative arthritis. However, great strides are being made in the understanding of the basic science, diagnosis, and treatment of articular cartilage disease at earlier stages. Early success has been reported in the repair of cartilage lesions using techniques such as microfracture, osteochondral autografting and allografting, and autologous chondrocyte implantation. More study is needed to refine techniques and determine more specific indications for these procedures, but the future certainly looks bright for technological development in this area.

Table 1. Composition of Mature Adult Hyaline Articular Cartilage

Extracellular matrix -- occupies 98% of cartilage volume
  Type II collagen fibers -- 50% dry weight
  Water -- 65 to 80% of total weight
  Proteoglycans -- 12% of total weight
Chondrocytes -- occupy approximately 2% of cartilage volume
  Synthesize all extracellular matrix macromolecules
  Limited ability to repair articular cartilage defects
  Ability to synthesize extracellular matrix and divide decreases with
    age (ie, programmed senescence)

Table 2. Symptoms of articular surface injury

Swelling
Pain with weight-bearing
Catching
Locking
Giving way

Table 3. Treatment options

Non-operative
  Patient education
  Weight reduction
  Activity modification
  Heat and ice application
  Selective bracing
  Physical therapy programs
  Pharmacologic treatment
Operative
  Arthroscopic debridement and lavage
  Repair stimulation
    Drilling
    Microfracture
    Abrasion arthroplasty
  Cell and tissue transplantation
    Osteochondral autografting
    Osteochondral allografting
    Autologous chondrocyte implantation
  Biologic and synthetic replacement materials

Accepted May 21, 2004.

References

1. Cole BJ, Carter TR, Rodeo SA. Allograft meniscal transplantation. Background, techniques, and results. J Bone Joint Surg Am 2002;84:1236-1250

2. Noyes FR, Bassett RW, Grood ES, et al. Arthroscopy in acute hemarthrosis of the knee: incidence of anterior cruciate ligament tears and other injuries. J Bone Joint Surg Am 1980;62:687-695.

3. Curl WW, Krome J, Gordon ES, et al. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 1997;13:456-460.

4. Brittberg M, Winalski CS. J Bone Joint Surg Am 2003;85, Supp 2:58-69.

5. Jackson DW, Scheer MJ, Simon TM. J Am Acad Orth Surg 2001;9(1):37-52.

6. Nehrer S Spector M, Minas T. Histologic analysis of tissue after failed cartilage repair procedures. Clin Orthop 1999;365:149-162.

7. Ogilvie-Harris DJ, Fitsialos DP. Arthroscopic management of the degenerative knee. Arthroscopy 1991;7:1151-1157.

8. Hangody L, Kish G, Karpati Z, et al. Mosaicplasty for the treatment of articular cartilage defects: application in clinical practice. Orthopedics 1998;21:751-756.

9. Peterson L, Brittberg M, Kiviranta I, et al. Autologous chondrocyte transplantation, biomechanics and long term durability. AJSM 2002;30(1):2-12.

S. Wendell Holmes Jr, MD

From Moore Orthopaedic Clinic and the Department of Orthopaedic Surgery, University of South Carolina School of Medicine, Columbia, SC.

Reprint requests to S. Wendell Holmes Jr, MD, Moore Orthopaedic Clinic, 14 Medical Park, Columbia, SC 29203. Email: [e-mail]