Chondromalacia (ICD code: M94.2) refers to the breakdown and softening or fibrous degeneration of articular cartilage. “Chondro” stands for cartilage and “malacia” for softening. According to the definition, the condition is classified as a so-called chondropathy, or cartilage disease.
Articular cartilage plays a crucial role in joint function; it covers the articular surfaces of all synovial joints. On the one hand, the cartilage ensures a smooth surface on the joint surfaces, thereby enabling low-friction movement. On the other hand, it acts as a shock absorber and cushions joint movements.
The thickness of the cartilage varies depending on the joint, ranging from 0.5 mm in the small joints of the fingers to 5 mm in the knee joint. However, excessive stress on the joints as well as acute injuries can damage the cartilage. This impairs joint function, leading to limited mobility and pain.
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In chondromalacia, the layer of cartilage covering the bone is softer than normal. This softening can occur to varying degrees of severity and progress to the complete loss of cartilage tissue.
What are the different grades of cartilage damage?
Cartilage damage (chondropathy) is classified into grades based on its extent. This classification, established by Outerbridge—who first described the condition—ranges from Grade 0 to Grade 4. The key criterion is the depth of the cartilage damage.
- In Grade 0 chondropathy, the cartilage tissue is completely intact and healthy. There is no damage and, therefore, no impairment of joint function.
- Grade 1 chondropathy is characterized by localized softening of the cartilage. The cartilage substance is still fully intact and smooth. Softened areas are found particularly in regions subjected to intense compressive stress.
- In contrast, Grade 2 chondropathy is characterized by roughened cartilage with small cracks.
- In Grade 3, the cracks extend all the way to the bone, leaving the bone partially exposed.
- In Grade 4 chondropathy, the cartilage layer is completely destroyed, and the bone is fully exposed. Normal joint function is thus no longer possible, leading to corresponding symptoms.
There is also a more recent classification based on ICRS criteria. ICRS stands for the International Cartilage Research Society, an organization specializing in cartilage diseases. In many respects, this classification corresponds to the Outerbridge classification; however, the extent and depth of the lesion are described in even greater detail.
- ICRS Grade 0: No detectable defects
- ICRS Grade 1
- 1A: intact surface, slight softening
- 1B: Additional superficial cracks
- ICRS Grade 2: Lesion depth < 50% of the cartilage thickness
- ICRS Grade 3: Lesion depth > 50% of cartilage thickness, bone not yet exposed
- ICRS Grade 4: Lesion extends down to the bone
Chondromalacia is usually caused by overuse of the affected joint. Sports or occupational activities can place stress on the joint and damage the cartilage. In particular, sports that place a high and unilateral load on the joint, as well as sports that require extreme ranges of motion in the joints, are considered risk factors for chondromalacia. These include, for example, tennis and soccer. Runners also frequently suffer cartilage damage in the hip or knee joints. In the case of lesions in the hip joint, microlesions—that is, tiny tears and damage caused by the constantly repetitive motion of the hip during running—are frequently observed.
However, genetic factors also appear to play a role in the development of chondromalacia. Depending on one’s genetic predisposition, cartilage tissue may be more or less resilient.
Traumatic events—such as an accident or a fall—are also among the causes of cartilage softening. Sudden and forceful impact or twisting movements of the joint can lead to tears in the cartilage tissue. In the case of bone fractures, direct damage to the cartilage—known as a cartilage contusion—is also possible. However, these are always severe Grade 4 injuries. Finally, inflammation and chronic joint effusions can also lead to softening of the cartilage tissue and make it more susceptible to injury.
The symptoms depend primarily on the severity and exact location of the cartilage damage. Articular cartilage has neither blood vessels nor nerve fibers. Therefore, the cartilage damage itself does not cause pain. The pain results from irritation of the bone and bone marrow.
In the early stages, chondromalacia usually goes unnoticed. Some patients merely experience an unpleasant sensation of pressure in the affected joints. As the damage progresses, however, the pain increases, especially during movement. Later on, patients experience pain not only during movement but also at rest. Pressure on the affected joint—or, in the case of the knee, on the kneecap—also triggers pain; in some cases, joint effusion may develop, causing noticeable swelling.
If chondromalacia is suspected based on the present symptoms, the affected joint is examined first. Even a visual examination of the joint (inspection) can reveal initial signs of cartilage disease, such as joint effusion, redness, or swelling of the skin over the joint. Furthermore, carefully palpating the joint while it is at rest is one of the first diagnostic steps.
This is followed by an examination under load, during which the joint is passively moved and slowly rotated. Passive means that the patient does not move the joint themselves; instead, all movements are performed by the examining physicians. This is the only way to detect the typical pain associated with chondromalacia. Depending on the extent of the cartilage damage, so-called crepitus may also be perceived during joint movements. This is a crackling sound caused by direct bone-on-bone friction in grade 4 chondromalacia.
Following the visual inspection and physical examination, an ultrasound examination of the joint is usually performed. This can reveal both joint effusion and the joint surfaces. In some cases, an X-ray examination will also be necessary. This is particularly important following an accident to confirm or rule out a bone fracture. Additionally, chondromalacia is often accompanied by densification of the bone tissue beneath the articular cartilage.
More precise assessments can be made using cross-sectional imaging, particularly computed tomography (CT) or magnetic resonance imaging (MRI). These tests allow for the evaluation of both the bone and the joint surfaces.
What happens during arthroscopy?
However, direct visualization of the articular cartilage is only possible through arthroscopy. For this procedure, an optical probe with a video camera at its tip is inserted into the joint through a small incision. This small camera allows for a detailed examination of the joint and the cartilage. Using additional instruments inserted during the procedure, arthroscopy also allows for the simultaneous removal of dead cartilage and smoothing of the joint surface. Furthermore, the depth of the cartilage damage can be precisely determined.
Arthroscopy is an invasive diagnostic procedure that can only be performed under anesthesia (usually general anesthesia, less commonly spinal anesthesia). It should therefore only be performed when medically indicated. One possible indication, for example, would be planning for an artificial joint replacement, which is often indicated by a preliminary arthroscopy, and the patient is informed of the prospects for success.
In some cases, however, arthroscopy can also be used to clean and smooth the bone or cartilage to such an extent that a joint replacement is no longer—or not yet—necessary. Among other things, medications can also be injected into the joint to help rebuild the cartilage tissue or prevent further deterioration.
Arthroscopy is therefore both a diagnostic procedure and a form of treatment.
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Conservative acute treatment should be started immediately after diagnosis. Stress on the affected joint should be reduced, which is absolutely essential for protecting the cartilage. Cold or heat therapy, as well as local application of anti-inflammatory and pain-relieving creams or ointments, can further alleviate symptoms.
Once the symptoms have subsided, physical therapy can help patients return to an active and pain-free life. In most cases, this can be done on an outpatient basis close to home; however, in some cases, this treatment is also performed on an inpatient basis at a rehabilitation clinic specializing in this condition.
In cases of bone fractures, a cast or surgical intervention is often necessary. Surgery may also be advisable even in the absence of a bone injury. This is particularly true when symptoms do not improve despite consistent conservative therapy and the pain does not significantly subside or disappear. In these cases where conservative therapy has failed, there is usually significant cartilage damage. This can only be effectively treated through surgery. Various options for cartilage therapy are available for this purpose. For example, drilling (microfracturing) can improve the cartilage’s ability to regenerate, allowing healthy cartilage tissue to grow into these drill channels.
Larger cartilage defects with exposed bone, on the other hand, often require a procedure known as abrasion arthroplasty. In this procedure, the damaged cartilage is exposed and abraded using arthroscopy. This allows stem cells from the bone marrow to enter the wound, where, in the best-case scenario, they form new cartilage.
Subsequently, as part of a procedure known as joint debridement, the joint is cleaned of the removed cartilage and bone material using an irrigation fluid. However, it usually takes several weeks—and in some cases, several months—for new cartilage tissue to form. For this reason, patients should take the weight off the affected joint in the initial period after surgery, for example by using crutches.
In most cases, gradual, pain-adapted weight-bearing on the joint can begin after 2 weeks. Prolonged immobilization of the joint should be avoided, as this can lead to shrinkage of the joint capsule and subsequently increase the risk of joint stiffness. This is especially true for the shoulder joint, which is at risk of stiffness after just a few days of immobilization. Appropriate physical therapy is therefore particularly important after surgery and helps ensure that the joint functions properly again.
What is chondromalacia?
Chondromalacia describes a softening of the cartilage, specifically the articular cartilage. This leads to changes in the cartilage layer and damage to the cartilage tissue. Chondromalacia of the kneecap is particularly common and is also referred to as chondromalacia patellae or chondropathy.
What symptoms does chondromalacia cause?
A typical symptom is pain in the front of the knee, as well as discomfort when weight is placed on the affected joint. Crepitus, swelling, and tenderness over the affected joint area are common. Limited mobility and reduced weight-bearing capacity of the affected joint are also possible.
How is the diagnosis made?
The diagnosis is made through a physical examination and assessment of the knee. Additional diagnostic tools may include MRI, other imaging techniques, or arthroscopy. The diagnosis and treatment depend on the extent and location of the cartilage damage.
What can cause chondromalacia?
There are various possible causes of chondromalacia. These include overuse, patellar misalignment, musculoskeletal misalignments, obesity, or a mechanically induced imbalance between load and load-bearing capacity. Osteochondrosis dissecans and other cartilage defects may also play a role.
How is chondromalacia treated?
Treatment for chondromalacia usually begins with conservative therapy and measures such as physical therapy, adjusting the type of sport, and reducing stress on the knee joint. In cases of advanced cartilage damage or Grade 4 chondropathy, surgical treatment, microfracturing, or other procedures may be necessary. In select cases, hyaluronic acid, autologous procedures, or stem cells from the bone marrow are used to treat cartilage damage. The Outerbridge classification ranges from Grade 0 and Grade 1 to Grade 3 and Grade 4 and aids in treatment planning.
