Chondromalacia (sick cartilage) is an affliction of the hyaline cartilage coating of the articular surfaces of the bone. It results in the softening and then subsequent tearing, fissuring, and erosion of hyaline cartilage. It is commonly recognized as involving the extensor mechanism of the knee and accordingly is often referred to as chondromalacia of the patella, patellofemoral syndrome, or runner's knee. The undersurface of the patella is covered with hyaline cartilage that articulates with the hyaline cartilage covered femoral groove (trochlear groove). Post-traumatic injuries, microtrauma wear and tear, and iatrogenic injections of medication can lead to chondromalacia development. Chondromalacia occurs in any joint and is especially common in joints that have had trauma and deformities.[1][2][3][4][5]
Several paths lead to the development of chondromalacia. Iatrogenic injection of chondrotoxic medication into a joint is one that patients can avoid. Intra-articular injections of bupivacaine and high doses or frequent intra-articular injections of corticosteroid lead to softening and/or articular cartilage dysfunction. Most often, chondromalacia is associated with abnormal (microtrauma) wear and tear of the patellofemoral joint's hyaline cartilage. Lateral positioning of the patella in the patella-femoral joint is a frequent cause of chondromalacia. Although a tight lateral retinaculum or a lateral synovial plica may be implicated as the cause of this positioning, an abnormal Q angle is often the cause.
The Q angle is the measurement of the pull of the quadriceps muscle relative to the pull of the patella tendon on the patella. A normal angle is 14 degrees in men and 17 degrees in women. This variance is created because anatomically, there normally is a wider pelvis in females than males. The Q angle is measured by drawing a line from the center of the anterior iliac spine to the center of the patella (quadriceps pull) and a second line from the mid-portion of the patella to the tibial tubercle (patella tendon pull). An abnormally high Q angle indicates lateral pull of the patella in the trochlear groove of the femur and a mechanism of articular cartilage wear and tear.
The alignment of the patella in the vertical plane can also be abnormal. Patella alta (high riding), and patella baja (low riding), are both conditions that have also been implicated as a cause of chondromalacia.
Chondromalacia is also seen as a complication of injuries, immobilization, and surgical procedures that lead to quadriceps atrophy. The cause is the micro-trauma created by the decreased pull of the quadriceps muscle on the patella.
Finally, foot and ankle anatomic variances (pes planus) that cause an increased valgus orientation of the knee cause increased lateral wear of the patellofemoral joint. Shoes, for example, high-heel shoes, which create increased stress on the patellofemoral joint, can also contribute to chondromalacia.
More women than men are affected, and this is attributed to increased Q angles in women. There does not appear to be a hormonal cause of variation. Active young adults who participate in running sports or workers who increase stress in their patellofemoral joint by repeated stair climbing and/or kneeling have a higher incidence of chondromalacia.
Hyaline cartilage is composed of chondrocytes that are dispersed throughout an extracellular matrix. This matrix consists of type 2 collagen, proteoglycans, and water. The chondrocytes produce the proteoglycans and which are then secreted into the extracellular matrix. Hyaline cartilage is avascular. Its nutrients diffuse into the matrix from synovial fluid. It does not repair well because of the lack of blood supply. Hyaline cartilage is also devoid of lymphatic and neural tissue.
The cartilage reacts to both the environment and physical loads. Destruction of hyaline cartilage can occur in response to chondrotoxic substances injected into a joint. It can also occur through exposure to cytokinins and proteolytic enzymes produced in response to intra-articular bacterial infections.
Hyaline cartilage degeneration also occurs in response to microtrauma wear and tear. Repeated activities that create compressive stress on the patella-femoral joint or increased loads applied to the joint can lead to chondromalacia.
Aging also affects hyaline cartilage. The number of chondrocytes in the cartilage decreases, which correlates with a reduction in the number of proteoglycans produced. This reduction leads to a decrease in the water content of the cartilage. Loss of the cartilage's elastic properties develops because of the crosslinking of collagen fibrils that also occurs with aging. The superficial zone of hyaline cartilage is the first zone to degenerate in the aging process.
Hyaline cartilage has four zones. The most superficial zone is a gliding surface that is the articular surface of hyaline cartilage. The arrangement of its collagen fibers is parallel to the articular surface to resist shear forces. Other layers include a transitional zone that resists compressive forces and a deep zone that resists shear forces. The collagen fibers in this zone are perpendicular to the articular surface. The fourth zone is the deep calcified zone. This zone contains hydroxyapatite and calcium salts. The deep calcified zone secures the hyaline cartilage to bone.
Anterior knee pain is the most common chief complaint of patients with chondromalacia. This pain is usually made worse with activities that increase the stress on the patellofemoral joint, for example, stair climbing, squatting, and running. Differential diagnoses for anterior knee pain include Hoffa disease, osteochondritis dessicans of the patellofemoral joint, patellar tendonitis, patella alta, patella baja, patella instability, plica, and bi-partite patella.
The varied etiological factors of chondromalacia mandate a thorough history and physical evaluation to correctly diagnose this condition and avoid mismanagement due to misdiagnosis. The history should include evaluating previous trauma, comorbid conditions, unstable joints, foot and ankle pain or dysfunction, and activity. Likewise, the physical exam should appraise quadriceps appearance, the orientation of foot and ankle, as well as a specific evaluation of the patellofemoral joint.
Specific evaluation of the patellofemoral joint should include assessment of pain, effusion, quadriceps strength, patella mobility, and crepitance. The physical examination test, which specifically evaluates the knee for chondromalacia, is Clark's test. This test evaluates patellofemoral grinding and pain by compressing the patella into the femoral trochlea and having the patient contract their quadriceps muscle-pulling the patella through the groove.
X-ray examination of the knee allows for assessment of patella anatomy and positioning in the knee, and MRI allows for additional assessment of articular cartilage water content and wear.
The Outerbridge Classification of chondromalacia is the most commonly used way of describing the severity of the degenerative process. This classification refers to four different progressive levels of degeneration. It is not uncommon to find several different levels of severity of the degenerative process in the same knee. Level 1 is a simple softening of the cartilage. Level 2 is a more advanced form of degeneration and is classified by fibrillation of the hyaline cartilage. Level 3 represents the fissuring of the articular cartilage to the level of subchondral bone. Level 4 is the most severe form and refers to an eburnated bone devoid of articular cartilage covering. Commonly, these levels are assessed with an arthroscopic evaluation of the knee. MRI radiography can also classify the degree of articular cartilage wear, but it is not as accurate as the visual assessment done at arthroscopy.[6][7][8][5][9]
Management of the patient with chondromalacia is difficult, and there is no one specific form of treatment that is universally accepted as a standard of care. Medical management should be based on the physical exam findings and can include patella stabilizing braces, physical therapy for quadriceps strengthening, orthotics which decrease pronation of the foot, and nonsteroidal anti-inflammatory medication. The use of platelet-rich plasma (PRP) is sometimes advocated, but it is not the standard of care. PRP has not been shown to improve patient outcomes consistently. Likewise, prolotherapy has been recommended by some authors, but it is not the standard of care and has not been shown to improve patient outcomes consistently.
Surgical management is indicated when there is a failure to respond to medical management. Arthroscopic evaluation and subsequent debridement of diseased cartilage (chondral abrasion), plica releases, or lateral retinacular releases are frequently the first-line of surgical management. Sometimes, open re-alignment procedures are used to improve patellofemoral tracking. The option for patellofemoral replacement arthroplasty is available but rarely used.
Patients with knee pain resulting from chondromalacia patella often achieve full recovery. Recovery can occur in as little as a month or take years, depending on the case. Teenagers often achieve long-term recovery because their bones are still growing, and their symptoms generally ameliorate after reaching adulthood.[10]
Complications in patients with chondromalacia patella may result secondary to the effects of NSAIDs (e.g., GI symptoms) use or bracing, where occasional dermatologic reactions result from the skin's reaction to the brace material. Therapeutic exercises rarely result in symptomatic aggravation. If a specific activity correlates with aggravation of symptoms, then the patient and clinician or therapist should work together to modify the activity ( r.g., alter the frequency, duration, or intensity of the activity, or cease the activity temporarily if necessary.)
Patient education revolves around compliance with medication, therapeutic exercises, post-surgical rehabilitation, and elimination of any aggravating movements or activities when possible.
The diagnosis and management of chondromalacia patella are complex and best done with an interprofessional team that includes an orthopedic surgeon, emergency department physician, sports physician, nurse practitioner, and a rheumatologist. Once diagnosed, the management is difficult because no one treatment works consistently in all patients. Nonsurgical therapy is usually the first step. If that fails, PRP and prolotherapy may be other options. Surgery is undertaken when conservative measures fail. However, the surgery does not always result in adequate outcomes, and a significant number of patients continue to complain of pain.[11][12]
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