Successful management of articular cartilage lesions starts with a thorough examination emphasizing patient history, range of motion limitations, and an understanding of underlying anatomy and biomechanics.
By Walter L. Jenkins, PT, DHS, ATC
Rehabilitation of articular cartilage lesions presents a unique challenge to the clinician. Given a limited capacity for healing and the lack of sensory input from articular cartilage, clinicians face a more complex rehabilitation model than commonly utilized with other soft tissue structures. Although symptoms provide a baseline for evaluation, a greater understanding of articular cartilage anatomy and biomechanics is necessary when designing and implementing a comprehensive rehabilitation program for these lesions.
Anatomy and biomechanics
An understanding of articular cartilage anatomy and biomechanics is helpful in developing the principles of rehabilitation. Articular cartilage has a diverse structure, allowing it to withstand considerable force. Many authors have divided articular cartilage into zones based upon the unique characteristics within each area.1-4 The matrix of each zone has varying amounts of collagen, ground substance, and water. Generally collagen provides strength, ground substance provides durability, and water gives the articular cartilage flexibility. Both collagen and ground substance are produced by chondrocytes. Since chondrocytes are not able to reproduce, the healing capacity of articular cartilage is limited. When injury occurs, and chondrocytes die, the cartilage is unable to maintain necessary levels of collagen and ground substance.
Structural changes to articular cartilage occur as we age. Generally, the overall size (depth) of articular cartilage decreases. This occurs for several reasons. First, secondary to injury, the number of chondrocytes decreases. Since chondrocytes are responsible for production of ground substance, these elements decrease as previously described.5,6 Additionally, collagen becomes weaker over time due to a decrease in the overall number of fibers. Simultaneously, however, the existing fibers become thicker and less resilient. 4 Therefore as we age there is less elasticity in articular cartilage secondary to decreased collagen resiliency, and a loss of ground substance and water. 4,5,7 The result is a less durable articular cartilage matrix as we age. 6
Articular cartilage is a viscoelastic structure. It is able to resist mechanical loads differently based upon the type of force. There are several different types of mechanical force that act on articular cartilage. These include compression, tension, shear and torsion. Collagen structures are primarily designed for tension loading,8 while compression, shear, and torsion loading are destructive to collagen.1,9 Ground substance and water improve the ability of articular cartilage to withstand all types of loading. Since collagen is weakest with compression, shear, and torsion loading, the presence of ground substance and water are critical to preservation of articular cartilage. Of particular importance is the replenishment of water. Approximately 65 to 80% of the total weight of articular cartilage is water. 10 Without water, collagen is more easily injured with any type of loading. Therefore replenishment of water is a central issue for articular cartilage health. Movement of a joint is the primary method used for water replenishment. During movement, the articulation between the opposing joint surfaces provides the compression necessary for synovial fluid to be absorbed into the articular cartilage matrix. Preservation of normal joint movement, including full range of motion, appears to be helpful to articular cartilage health.11 Injured articular cartilage is less flexible secondary to weakened collagen, and decreased amounts of ground substance and water.6
Additionally, viscoelastic structures change their ability to withstand loading or force based on the speed of loading. Generally, articular cartilage becomes stronger with faster speeds of movement. This is important when administering a rehabilitation program. Although intuitively it would seem prudent to implement rehabilitation programs at slower speeds, due to its viscoelastic nature, articular cartilage is actually stronger at faster speeds. 12
Many authors describe four zones in articular cartilage,1-4,5,8 each with varying amounts of collagen, ground substance, and water. Additionally collagen is arranged differently in each zone to optimize articular cartilage strength and provide variable ways to respond to loading. (Figure 1) Generally zone one displays the most stiffness, while zones two and three allow the articular cartilage matrix to adapt to various loads. This arrangement appears to be related to the collagen and ground substance content differences within each zone.13-15
The collagen arrangement in zone one is parallel to the joint surface. 2 Therefore at the joint surface, when joint compressive forces occur, collagen becomes attenuated. Since collagen adapts well to stretching and is able to withstand large tension loads, this arrangement is optimal for distribution of joint compressive loads. As discussed earlier, joint compressive loading is assisted by water. With joint motion, water is moved within the articular cartilage matrix.
A large number of chondrocytes and a small amount of ground substance is contained in zone one.6,7 Since chondrocytes are responsible for collagen production, repair of injury is optimal in this zone. Prolonged static loading appears to result in higher strain being placed on zone one. 16
Health in the intermediate layers of articular cartilage is more dependent on the structures in zones one and four. The collagen in zone two and three is not arranged parallel to the joint surface.6 Therefore, when joint loading occurs, the collagen is loaded in a non-linear fashion (zone two) or results in a compressive load (zone three). Neither of these types of loads is optimal for collagen. Increased load must be absorbed by the ground substance in both of these zones. Fortunately, zones two and three have large amounts of ground substance.5,9 Zone three is primarily designed to resist compressive loads.9
Zone four is a transition from the articular cartilage matrix in the superficial and intermediate zones to subchondral bone. The primary purpose of this layer is to attach the articular cartilage matrix to the underlying subchondral bone and provide a barrier for movement of fluids from the subchondral bone into the superficial layers of articular cartilage.17,18 As we age, there is a less distinct barrier between zone four and the subchondral bone.4 Zone four is commonly a primary site of articular cartilage pathology.19-22 Bone bruises in subchondral bone have been observed with knee injuries and are thought to progress to articular cartilage injury. 23-29
History. Evaluation of articular cartilage lesions requires the clinician to be alert to signs and symptoms of joint pathology. Of particular importance are joint symptoms, including swelling and effusion, temperature change, and mechanical symptoms such as crepitus, “giving way,” and “catching.”30,31 Patient complaints of joint pain or periarticular pain are valuable to the clinician, and should be focused upon. Commonly patients will complain of aching in joints after static loading (standing), or during/after periods of inactivity. Stiffness, particularly after periods of rest, is also quite common.32 Previous history of joint injury, including surgery, should be probed carefully. Normally a younger person does not complain of joint symptoms without a history of trauma or surgery. Likewise, it is easier to make a determination of articular cartilage injury in older athletes if a relationship has been established with a previous joint injury.
Articular cartilage lesions commonly result in functional limitations such as problems with walking for long distances or difficulty with prolonged standing. Disabilities related to activities of daily living, competitive athletics, and recreational activities commonly occur secondary to functional loss. Knee osteoarthritis is one of the leading diseases associated with significant morbidity. It is predicted to rise as the population ages. 32-35
A thorough history should include questioning about symptoms in multiple joints. When patients complain of symptoms in multiple joints, other pathologies such as gout, pseudogout, hemochromatosis, or Reiter’s syndrome may be the source of the joint symptoms. 32,36-38
Active and passive range of motion. Normal joints have normal range of motion (ROM). In patients with articular cartilage lesions, ROM loss is quite common. Movement in all planes of motion, and in each direction within a given plane, should be observed and measured. In joints like the hip, limitation of joint motion commonly occurs during multiple movements. Typically in hinge joints both extension (hyperextension) and flexion ROM are limited. Range of motion symmetry between bilateral extremity joints is normal and should be a treatment goal whenever possible.11 To this end, precise measurement of ROM bilaterally is the first step in a successful treatment program. Although there are no established “norms” for ROM, at least one study has shown that restoration to within the guidelines provided by the International Knee Documentation Committee (IKDC) is predictive of improved function and decreased symptoms.12 The IKDC guidelines for knee ROM are within 2° of extension (hyperextension) and within 5° of flexion, relative to the contralateral (uninjured) limb. In patients with knee pathology, restoration of full ROM is helpful when attempting to optimize the outcome.39-41
Resisted range of motion. Strength deficits are common in injured joints. Following a joint injury, muscle atrophy occurs secondary to a reflex inhibition of the muscles surrounding the injured joint.42-44 Other factors including pain, disability, and the amount of time since the injury can influence the amount of muscle atrophy. Some joints appear to be more susceptible to muscle atrophy than others. For instance, knee joint osteoarthritis has been associated with quadriceps atrophy.45
Isokinetic strength testing is the “gold standard” for isolated strength assessment.46,47 When testing for strength, the clinician should be aware of the principle of viscoelasticity by testing at intermediate and fast speeds initially (180° and 300° per second). Due to its viscoelastic nature, articular cartilage is stronger when loaded at a faster speed. Therefore, during the initial stages of rehabilitation when the articular cartilage is weaker, high loads with slow speed resisted motion should be avoided. Late-stage rehabilitation may require slower speed testing (120° and 60° per second) to obtain a more complete understanding of the actual strength in individual muscle groups surrounding a joint. Normative tables for isokinetic testing are published for a variety of joints.46,47 A commonly used goal for return to full function with extremity joints is for the injured limb to demonstrate a strength deficit of less than 10% to 20% compared to the contralateral extremity.46,47 Strength deficits for the quadriceps muscles have been observed in patients with osteoarthritis.48,49 Additionally, restoration of agonist and antagonist strength ratios for extremity joints is necessary for normal joint function.46,47 A loss of the normal agonist and antagonist ratio (quadriceps-to-hamstrings) has been observed in patients with knee joint osteoarthritis.50 Functional strength loss following joint injuries may last for several years.51
Joint instability and accessory motion testing. Patients with articular cartilage lesions commonly have increased joint mobility and accessory motions secondary to a previous ligament injury.35,52,53 While this portion of the examination is less “objective” than ROM (active, passive, or resisted ROM) testing, authors have reported differences when comparing uninvolved and involved paired extremity joints with unilateral pathology. Commonly there is increased joint mobility (less joint stability and/or increased accessory motion testing) on the injured side when compared to the contralateral uninjured joint. Although there is an increase in motion with joint stability testing, the “end point” remains firm and similar to the contralateral side. 53
Mechanisms of failure
A first step in understanding treatment is knowledge of what may cause pathology. There are multiple factors that cause articular cartilage injury. Joint trauma, weight, age, gender, occupational activity, nonoccupational activity, bone mineral density, postmenopausal replacement therapy, congenital abnormalities, and genetic factors have been identified as possible risk factors for articular cartilage injury.19,21,22,32,33,38 A review of other primary risk factors for articular cartilage lesions follows.
Joints with irregularly shaped articular surfaces appear to be more likely to become injured.12 Incongruent joints are loaded asymmetrically, resulting in an uneven wearing pattern. A good example of this is the patellofemoral joint. The opposing joint surfaces in the patellofemoral joint do not match leading to portions of the joint surface receiving higher loads. Joint surfaces that receive higher loads are more likely to have surface wear leading to injury. Therefore secondary to poor joint congruency the patellofemoral joint is more likely to sustain surface wear, and osteoarthritis. At least one author has identified the patellofemoral joint to be at higher risk for osteoarthritis.54 Although joint surface irregularity is not modifiable, an understanding of this risk factor can assist the rehabilitation clinician. A reduction in repetitive motion activities is warranted when a patient has irregular joint surfaces.
Movement of a joint is required for articular cartilage to receive nutrition from the synovial fluid. If a joint is deprived of movement, the articular cartilage is weakened.1,12 Therefore any treatment that reduces ROM can result in stress deprivation for articular cartilage. These include immobilization for treatment of fractures and ligament injuries, or simply activity avoidance; commonly patients suffering from joint pain attempt to decrease use of the involved extremity in order to reduce the pain. If prolonged disuse occurs then articular cartilage health may be at risk. For example, patients with osteoarthritis commonly self-limit their motion as a form of treatment. The self immobilization leads to passive ROM loss and stress deprivation for the articular cartilage. The areas where joint surface contact has been restricted appear to be more likely to develop degenerative changes.55
Additionally, chondrocytes need the increased compression provided by active motion and weight bearing to maintain articular cartilage.4 Active ROM loss for as little as one week can result in articular cartilage atrophy. The intermittent compression provided by active ROM and weight bearing is helpful in maintaining articular cartilage health.4
There is evidence that obesity is a factor in the development of osteoarthritis.56 Although the exact mechanism for this risk factor to articular cartilage health is unknown, an increase in osteoarthritis has been observed in subjects with obesity. Perhaps this is secondary to static loading rather than intermittent loading. Athletes who are involved in repetitive motion with high loading, like distance running, are no more susceptible to osteoarthritis than the general population.57 However; occupations associated with static loading, such as farming, appear to be more likely to also be associated with osteoarthritis.58,59 It is also interesting to note that weight reduction has been observed to decrease the progression of osteoarthritis.59
Examination of joints with articular cartilage lesions is more complex than examination of other soft tissue structures. An understanding of the anatomy, biomechanics, and mechanisms of failure assists the clinician in determining how to approach these lesions. Examination involves the same procedures as other soft tissues, but the clinician must learn to rely on history and range of motion impairments when these lesions are present.
Walter L. Jenkins PT, DHS, ATC, is associate professor and interim chair of the department of physical therapy at East Carolina University in Greenville, NC.
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