Idiopathic Chondromalacia Patellae

The term. Chondromalacia patellae is softening of the articular cartilage on the posterior (articular) surface of the patella, from the Greek chondros, cartilage, and malakia, softening. The softening may progress to fibrillation, fissuring and erosion. It is one of the commonest causes of knee pain in young people, classically young adults and often women.

A finding, not a disease. The term describes the cartilage; it is not a single pathophysiological diagnosis. It overlaps with patellofemoral pain without being the same thing, because many patients with anterior knee pain have normal cartilage and chondromalacic change can be found without symptoms. The diagnosis should therefore not be assumed from pain alone. Idiopathic chondromalacia is the form that arises without a clear anatomical cause.

Outerbridge grading. Cartilage change is graded arthroscopically by the Outerbridge classification. Grades II and III are separated by the size of the fissured area, and the cutoff is Outerbridge's original half an inch, about 1.3 cm.

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The mechanism. Softening is the morphological expression of cartilage that is mechanically overloaded or intrinsically vulnerable. Early matrix breakdown, with proteoglycan loss, collagen-network disruption and increased water content, progresses to fibrillation, fissuring and erosion. This is the same early-degeneration cascade described in Articular Cartilage Structure.

Idiopathic or secondary. Idiopathic chondromalacia has no clear anatomical cause. It is typical of young adults and women and is attributed to subtle overload or patellofemoral mechanics. Secondary chondromalacia has a definable driver:

• Patellar maltracking or lateral overload
• Patellar instability, with recurrent subluxation or dislocation shearing the cartilage
• Direct trauma, such as a dashboard injury or a fall on the flexed knee
• Prolonged immobilisation
• Malalignment, including the Q-angle and weak hip abductors

Symptoms. The patient has anterior or retropatellar knee pain, sometimes with crepitus. It is typically worse on climbing and descending stairs, squatting, kneeling and prolonged sitting.

The loads behind the pattern. The patella carries the thickest articular cartilage in the body, which is a clue to the forces it handles. The patellofemoral joint reaction force rises steeply with knee flexion under load, because the quadriceps tension and the angle of the extensor mechanism both increase. It is modest in level walking, several times body weight on stairs, and higher still in a deep squat.

How the loads shape the symptoms. Descending stairs loads the quadriceps eccentrically in flexion, so it hurts where walking on the flat does not, and squatting and kneeling hurt for the same reason. The theatre sign is discomfort after prolonged sitting with the knee flexed, when the patella is held loaded against the trochlea without the relief of movement. The same mechanics explain why rehabilitation is prescribed in a pain-free arc, and why closed-chain exercise near extension is tolerated when deep flexion loading is not.

Examination. There may be patellofemoral tenderness and a positive Clarke's sign, the patellar grind test: pain on patellar compression during quadriceps contraction. Contributing factors such as maltracking should be sought.

Clarke's sign is poorly specific. Pressing the patella into the trochlea while the patient contracts the quadriceps is uncomfortable in a substantial proportion of normal knees. A positive test in isolation confirms very little, and a negative one does not exclude the diagnosis. Use it as one part of a pattern, with the site of tenderness, the loading history and the assessment of tracking and proximal control, rather than as the diagnostic test.

Imaging. Imaging is usually for exclusion and grading. Radiographs, including a skyline (Merchant) view, assess patellofemoral alignment and exclude other causes, and MRI can show cartilage signal change and grade the lesion. Arthroscopy provides the definitive Outerbridge grade but is not required to make the clinical diagnosis.

Anterior knee pain is a syndrome, not a diagnosis. The patellar cartilage is only one possible source in a young adult, so the pain should be localised before it is attributed to the cartilage.

Conservative first. Management is predominantly conservative: activity modification and load management, analgesia or NSAIDs, and a structured rehabilitation programme. The programme emphasises quadriceps (VMO) and hip and core strengthening, with stretching and patellar taping or bracing. It also addresses the contributors: patellar maltracking, weak hip abductors and external rotators, tight lateral structures and other biomechanical factors.

Injections. Intra-articular hyaluronic acid and platelet-rich plasma are options for selected refractory cases. PRP has shown benefit over physiotherapy alone in some studies, particularly in younger patients. The study cited below let patients choose their own treatment, so its result is a signal and not grounds for offering injection ahead of a proper trial of physiotherapy.

Surgery. Arthroscopic chondroplasty or debridement and cartilage-restoration procedures are reserved for genuinely refractory, high-grade lesions, and realignment for a demonstrated maltracking cause. The restraint is deliberate, because the pain often does not correlate well with the cartilage grade.

Pain correlates poorly with the cartilage grade, and the reason is basic science.

Articular cartilage is aneural. It contains no nerve endings, so a fibrillated or fissured surface cannot itself generate pain, and whatever hurts is not the lesion the arthroscope is looking at. The nociceptive sources around the patellofemoral joint are:

• Subchondral bone, richly innervated and loaded increasingly as the overlying cartilage thins and loses its load-distributing function. It is the likeliest source in high-grade disease, and the reason bone marrow oedema on MRI tracks symptoms better than the cartilage signal does.
• The lateral retinaculum, which contains free nerve endings and shows neural changes in chronic anterior knee pain, particularly where it is tight
• The synovium and the infrapatellar (Hoffa) fat pad, both densely innervated and readily irritated
• The subchondral plate and peripatellar soft tissues more generally, plus central sensitisation in long-standing cases

What follows. Three practical consequences come out of this:

1. A patient can have Outerbridge III change and no pain, because the cartilage lesion is silent until it changes the loading of something innervated.
2. A patient can have severe pain with pristine cartilage. That is patellofemoral pain, and it is why arthroscopy for anterior knee pain alone so often finds nothing to explain the symptoms.
3. Chondroplasty treats the lesion, not the pain generator, which is why debriding a chondromalacic patella for pain gives such unreliable results. Modifying the loading of the subchondral bone and the tension in the retinaculum is what changes symptoms, and that is a rehabilitation problem far more often than a surgical one.