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Chondromalacia Patella

Editor: Edward E. Griffin Updated: 4/22/2023 2:23:51 AM

Introduction

In 1906, for the first time, pathological changes in the patellar cartilage were reported by Budinger et al. Then, Kelly et al described these pathological changes as chondromalacia patellar (CMP).[1] Originally, the word "chondromalacia" stemmed from Greek words. Chondros means cartilage, and malakia means softening.[2] In general, chondromalacia (sick cartilage) is an affliction of the hyaline cartilage coating of the articular surfaces of the bone. CMP is when the posterior articular surface of the patella starts losing its density when in a healthy state and becomes softer with subsequent tearing, fissuring, and erosion of the hyaline cartilage. It is commonly recognized as involving the extensor mechanism of the knee and is accordingly 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 medication injections can lead to chondromalacia development. Chondromalacia can occur in any joint and is especially common in those with trauma and deformities.[3][4][5][6][7]

Etiology

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Etiology

Several paths can lead to the development of CMP; however, the pain generator is not clearly identified and is usually multifactorial. Multiple factors have been involved, including:

Lower Limb Malalignment and Patellar Maltracking

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° in men and 17° in women. This variance arises because, anatomically, the pelvis is normally wider in females than in 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, >20° to 25°, indicates lateral pull of the patella in the trochlear groove of the femur and a mechanism of articular cartilage wear and tear. The tibial tubercle trochlear groove distance (TT-TG) is a linear equivalent of the Q angle and a more accurate measure of assessing patellar maltracking.

Patellar maltracking results in narrow contact pressure areas, increased stress, and further pain. Additionally, patellar alignment in the vertical plane can be abnormal. Patella alta (high-riding) and patella baja (low-riding) are both conditions that have also been implicated as causes of chondromalacia. Foot and ankle anatomic variances (pes planus) that cause an increased valgus orientation of the knee cause increased lateral wear of the patellofemoral joint. For example, high-heel shoes, which create increased stress on the patellofemoral joint, can also contribute to chondromalacia. CMP can be associated with miserable malalignment syndrome, a combination of specific anatomic criteria that results in increased Q angle and patellofemoral dysplasia. These criteria include femoral anteversion, genu valgum, and external tibial torsion or pronated feet.

Muscular Weakness

Weakness of the vastus medialis obliques and general core muscles.

Patellar Lesions

Chondromalacia is also seen as a complication of injuries to the patella, immobilization (casting, rehabilitative periods), and surgical procedures that lead to quadriceps atrophy. The cause is microtrauma from decreased quadriceps pull on the patella. 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 in this positioning, an abnormal Q angle is often the cause. Contrary to congenital increased cartilage vulnerability, which is not modifiable, 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. Among the causes, patella subluxation is the most common as it is more frequently missed, as there is no frank dislocation.[8]

Epidemiology

More women than men are affected, which is attributed to increased Q angles in women. There does not appear to be a hormonal cause of variation. Young adults who participate in running sports or workers who increase stress on their patellofemoral joint through repeated stair climbing and/or kneeling have a higher incidence of chondromalacia.[9]

Pathophysiology

Normally, patellar hyaline cartilage has a bluish-white, smooth, glistening, and resilient appearance. The pathology of CMP begins with softening, swelling, and edema of the articular cartilage, resulting in a dull or slightly yellowish-white appearance.[10][11] The pathology characteristically starts in the middle of the medial patellar facet, or just distal to it, and starts small, measuring about half an inch or more in diameter.[11] This then progresses to cartilage fibrillation, fissuring, and fragmentation in the more advanced stages.[1][11] Some reports suggest that CMP may be reversible or progress to advanced patellofemoral joint osteoarthritis.[12]

Pathological Process in Chondromalacia Patellae

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 proteoglycans, which are then secreted into the extracellular matrix. Hyaline cartilage is avascular. Its nutrients diffuse into the matrix from synovial fluid. It does not heal well due to a lack of blood supply. Hyaline cartilage is also devoid of lymphatic and neural tissue. The cartilage responds to both environmental factors 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 and 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 decreases the cartilage's water content. Loss of the cartilage's elastic properties develops because of the cross-linking of collagen fibrils that also occurs with aging. The superficial zone of hyaline cartilage is the first zone to degenerate in the aging process. The anterior fat pad and the joint capsule are most commonly involved in generating pain signals, while the subchondral bone is less likely to cause pain signals. The pathology of CMP begins with softening, swelling, and edema of the articular cartilage.

Histopathology

Hyaline cartilage has 4 zones. The most superficial zone is a gliding surface, ie, the articular surface of hyaline cartilage. The arrangement of its collagen fibers is parallel to the articular surface, resisting 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 the bone.

History and Physical

Anterior knee pain is the most common chief complaint of patients with CMP; however, a high proportion of patients present with insidious onset of vaguely diffuse retropatellar or prepatellar pain. This pain is usually made worse by activities that increase stress on the patellofemoral joint, such as ascending or descending stairs, squatting, kneeling, running, or prolonged sitting; it is also known as theatre pain. In addition to the anterior knee pain, effusion, wasting of the quadriceps, and retropatellar crepitus have all been reported in patients with CMP, despite none being specific.[13] Hence, reliable diagnosis depends on excluding other differential diagnoses presenting with anterior knee pain.

The varied etiological factors of chondromalacia mandate a thorough history and physical evaluation to 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 evaluate the appearance of the quadriceps and the presence of atrophy, the orientation of the foot and ankle, and a specific evaluation of the patellofemoral joint.

Specific evaluation of the patellofemoral joint should include assessment of pain, effusion, quadriceps strength, patella mobility, and crepitus. Particular attention to signs of patella maltracking, which includes increased femoral anteversion, increased external tibial torsion, lateral patella subluxation, loss of medial patellar mobility, and a positive patellar apprehension test. The physical examination test that specifically evaluates the knee for CMP is the Clark test. This test evaluates patellofemoral grinding and pain by compressing the patella against the femoral trochlea and having the patient contract their quadriceps, which pulls the patella through the groove.

Evaluation

Evaluation of condromalacia patella may include:

  • Conventional radiographs: Anteroposterior, lateral, and notch views. Radiographs have lower sensitivity and specificity in early grades of CMP. In advanced stages, it may show chondrosis, cystic changes, advanced cartilage loss, or joint-space loss. In general, radiographs can provide guidance on the underlying etiology, such as in cases of trochlear dysplasia, patella alta, patella baja, or lateral patellar tilt. 
  • Computed tomography scan: provides more information regarding patellofemoral alignment by delineating trochlear geometry. The TT-TG distance can be measured on the computed tomography scan. In addition, torsional deformities of the lower limb can be detected and measured.
  • Arthrography with plain radiographs or computed tomography arthrography: Despite low sensitivity, it may demonstrate inhibited contrast in areas of chondromalacia. Also, my sport successfully focuses on areas of cartilage or irregular cartilage or lost cartilage, but again in advanced stages.[14]
  • MRI scan: is the modality of choice for articular cartilage assessment, with the best appearances on the T2 sequences, where abnormal cartilage shows high signal intensity. Non-invasive, more reliable, and with a higher detection rate than arthroscopy.[15][16] Radiologically, patellofemoral congruency can be assessed using multiple variables: sulcus angle, trochlear depth, patellar angle, and lateral patellar tilt angle. In an MRI study of patients with CMP, both the lateral patellar tilt angle and trochlear depth were significantly decreased, while the sulcus angle was significantly higher. And no correlation was reported between patellar angle and CMP.[17] Another MRI study reported that patients with CMP had a lower lateral patellar tilt angle, a lower trochlear depth, and a higher sulcus angle. The ratio of the trochlear sulcus angle to trochlear depth was also suggested as a powerful predictor for early cases of CMP.[18] Additionally, tibial slope and patellar height were important predictors of CMP.[5] Another MRI study evaluated the correlation between obesity and CMP and reported that subcutaneous knee fat thickness was significantly higher in CMP patients than in normal populations. Additionally, a significant correlation was reported between subcutaneous knee fat thickness and the grade of CMP. Female patients were found to have thicker subcutaneous knee fat and more serious CMP than male patients.[19]
  • Arthroscopy: This is the most efficient modality in diagnosing chondromalacia and determining the location and size of cartilage lesions, as well as patella position. However, because of its invasiveness, non-invasive methods are essential for diagnosis.[13][20]

Treatment / Management

A trial of long-standing conservative management for at least 1 year should be the first-line treatment. This includes rest, activity restriction, and nonsteroidal anti-inflammatory medication, which is proven to be more effective than steroids. Rehabilitation with physiotherapy should focus on closed-chain short arc quadriceps exercises and specific strengthening of vastus medialis obliquus, core muscle strengthening, and strengthening of hip external rotators. Quadriceps muscle strengthening with different exercises significantly reduces anterior knee pain in early cases of CMP.[21][22](A1)

Management of the patient with CMP is difficult, and no single treatment is universally accepted as the standard of care. Medical management should be based on the physical exam findings. It can include patellar-stabilizing braces, quadriceps-strengthening physical therapy, orthotics to reduce foot pronation, 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 consistently improve patient outcomes. Likewise, prolotherapy has been recommended by some authors, but it is not the standard of care and has not consistently been shown to improve patient outcomes.

Operative Management

Failure of conservative management prompts exploration of alternative surgical options. Even though multiple effective options are available, care should be taken when recommending the best procedure, considering the patient's age and the severity of CMP. Each procedure has its own merits, indications, and limitations. Available options include patellar cartilage excision, shaving, drilling, proximal soft tissue, and distal bony patellar realignment surgery. The most effective and straightforward surgery, avoiding quadriceps fibrosis and dysfunction, is a medial patellar tendon realignment with lateral release and reefing of the medial quadriceps expansion.[23]

Arthroscopic Evaluation and Debridement

Indicated for diseased cartilage or chondral abrasion, fibrillation, or traumatized cartilage areas (Outerbridge grade II, III, and IV chondromalacia patellofemoral joint).[24] Debridement is either mechanical or radiofrequency.[25]

Arthroscopic or open lateral retinacular release

Indicated for lateral patellar tilt and the presence of a tight lateral retinacular capsule and a loose medial capsule.

Patellar realignment surgery

Patellar realignment procedures aim to restore the biomechanical force axis of the patellofemoral joint, thereby improving function; however, some degree of patellofemoral joint degeneration may still occur.[26] These procedures are typically indicated for severe symptoms that are refractory to conservative management, including physiotherapy.

A variety of techniques have been described, primarily involving modification of the tibial tuberosity, including osteotomy, anteriorization, or elevation:

  • Maquet procedure (anterior tibial tubercle elevation): Elevation should not exceed 1 cm to minimize the risk of skin necrosis.
  • Fulkerson osteotomy (anteromedialization): Indicated in cases of patellar instability, particularly with an increased Q angle.
  • Elmslie–Trillat osteotomy: A medialization procedure used to improve patellar tracking.
  • Medial patellofemoral ligament (MPFL) reconstruction: Addresses instability by restoring medial soft tissue restraint.

These procedures are contraindicated in patients with skeletal immaturity and in the presence of superomedial patellofemoral arthrosis. Arthroscopic evaluation is recommended prior to surgery.

Patellectomy: either partial or total patellectomy. However, this procedure would be indicated only if a patient has excellent quadriceps function preoperatively and is compliant with regular postoperative exercise. Total patellectomy is considered a radical procedure for managing CMP. It is associated with greater damage to the surrounding ligaments and quadriceps femoris. Additionally, it changes the leverage effect of the extensor muscles. Several other complications have been reported in later stages after total patellectomy, such as instability of the extensor tendon and acute rupture of the patellar tendon. Hence, partial rather than total patellectomy was usually performed in managing CMP.[27][28][29](A1)

Salvage procedures (Historical)

Patellar resurfacing: the McKeever prosthesis initially showed beneficial long-term outcomes in cases of severe CMP with advanced patellofemoral osteoarthritis; however, this procedure was abandoned due to complications such as patellar tendon lesions, secondary patellar fractures, avascular necrosis, patellofemoral joint instability, and prosthetic loosening.[30][24]

Other Treatment Modalities

Cell therapy

Autologous chondrocyte implantation was first reported in 1994 for treating cartilage defects in knee osteoarthritis.[31] Over the last 2 decades, cell therapy for osteoarthritis has emerged as a treatment option. Multiple reviewers consider CMP a mesenchymal disease; therefore, cell therapy is expected to have a positive therapeutic effect. Emerging modalities include autologous chondrocyte transplantation and mesenchymal stem cell injection.[32][33](B3)

Mesenchymal stem cells (MSCs)

Intraarticular injections of MSCs from different sources were proven safe and clinically effective in treating CMP. It has the advantages of being less invasive, providing symptomatic relief, and reducing inflammatory changes. The mechanism of MSC injection remains an area of research, but it shows promising results.[23]

Differential Diagnosis

The differential diagnosis when CMP is suspected includes:

  • CMP/osteochondral defect
  • Osteochondritis dessicans of the patellofemoral joint
  • Patellofemoral osteoarthritis
  • Patellofemoral pain syndrome
  • Lateral patellar compression syndrome
  • Plica syndrome
  • Quadriceps tendonitis/tendinopathy
  • Patellar tendonitis/ tendinopathy
  • Saphenous neuroma
  • Postoperative neuroma
  • Patellar fat pad inflammation
  • Hoffa disease
  • Patella alta
  • Patella baja
  • Patella instability
  • Bipartite patella

Staging

Outerbridge classification of CMP (5 grades from 0 to IV):

  • Grade 0: Normal cartilage
  • Grade I: Intact articular surface but soft, swollen, and oedematous. Some fibrillation and heterogeneity of the cartilage may be noted, which is translated on the MRI as high signal intensity
  • Grade II: Fissures and fragmentation of the articular surface ( an area half an inch or less in diameter)
  • Grade III: Focal, partial thickness cartilaginous defect. (an area more than half an inch in diameter)
  • Grade IV: Full-thickness defect down to the subchondral bone [11]

Commonly, these grades 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.[7][34][35][36][37] In the Asian population, Ye et al further classified CMP into an early stage (grade 1–2 Outerbridge) and an advanced stage (grade 3–4), and they assumed that with the early stage, patella cartilage can self-repair in comparison to an advanced stage when it progresses to patellofemoral joint osteoarthritis.[38]

Prognosis

CMP may be reversible or progress to patellofemoral osteoarthritis. Patients with knee pain resulting from CMP often achieve full recovery. Depending on the case, recovery can occur in as little as a month or take years. Teenagers often achieve long-term recovery because their bones are still growing, and their symptoms generally ameliorate after reaching adulthood.[39]

Complications

Complications in patients with CMP may result from NSAID use (eg, gastrointestinal symptoms) or from bracing, with occasional dermatologic reactions due to 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 (eg, alter the frequency, duration, or intensity of the activity or cease the activity temporarily if necessary)

Consultations

Consultations relevant to the treatment of CMP include:

  • Orthopedist
  • Radiologist
  • Rheumatologist
  • Physical therapist

Deterrence and Patient Education

Patient education focuses on adherence to medication, therapeutic exercises, post-surgical rehabilitation, and, when possible, eliminating aggravating movements or activities.

Enhancing Healthcare Team Outcomes

The diagnosis and management of CMP are complex and best done with an interprofessional team that includes an orthopedic surgeon, emergency department physician, sports physician, physical therapist, nurse practitioners/PAs, rheumatologist, and nursing staff. Once diagnosed, management is difficult because no single treatment consistently works for 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 positive outcomes, and a significant number of patients continue to complain of pain.[22][40] This is why interprofessional communication, record-keeping, and activity coordination are necessary to achieve optimal outcomes.

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