Patellofemoral Pain Syndrome
Introduction & Etiology
The patellofemoral joint is a common site of pain. (1) The broad term “Patellofemoral pain syndrome” (PFPS) encompasses a spectrum of signs and symptoms. The spectrum begins with asymptomatic functional malalignment of the patella and ends in severe patellofemoral arthritis. The diagnosis of “Chondromalacia patellae” (CMP) occupies the mid-portion of the PFPS continuum, beginning with visible cartilage alterations and eventually leading to patellofemoral arthritis. (2) Chondromalacia may begin at any age and is commonly found in teenagers. (3) The incidence of CMP increases with age and is more common in females. (3)
Retropatellar cartilage breakdown is the hallmark feature of chondromalacia. (4) Chondromalacia progresses in the following step-wise fashion: cartilaginous swelling and softening (stage 1), partial thickness fissuring (stage 2), full thickness fasciculations (stage 3), and cartilage destruction with exposure of subchondral bone (stage 4). (5) Stage 4 chondromalacia represents the onset of DJD and is indistinguishable from that disorder. (5)
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Patellar cartilage differs from typical joint cartilage in many ways. Patellar cartilage is incongruently thicker in certain areas, more permeable, less stiff, and more compressible. (6) The remaining etiologic factors for CMP are nearly identical to those of patellofemoral pain syndrome. Imbalanced actions of the static and dynamic knee stabilizers can alter the distribution of forces to the patellofemoral articular surface and related soft tissues. These biomechanical tracking stressors are compounded through activities of daily living, causing irritation and eventually wear to the patellofemoral cartilage.
Any factor that alters normal patellofemoral mechanics is a risk factor for chondromalacia patellae. This includes lateral tracking disorders, tightness in the lateral knee capsule, weakness of the vastus medialis or quadriceps, pes planus, hip abductor weakness, joint overloads/overuse, trauma, patellar hypermobility, and muscle imbalance, particularly quadriceps or iliotibial band hypertonicity and vasus medialis or quadriceps weakness. (7-10) Weakness in the quadriceps or hamstring muscles increases one’s risk of developing patellofemoral pain three to five-fold. (11) Weakness in the hip abductors is common in patients with knee pain and is a significant contributor to patellofemoral pain. (12,13) Some researchers question whether hip abductor weakness is a cause or effect of patellofemoral pain. (40) Additional risk factors for the development of CMP include obesity, hypermobility/instability, prior cruciate ligament injury, and prior trauma, fracture, or patellar subluxation. (3,14-16)
Clinical Presentation
Clinically, CMP patients present with complaints nearly indistinguishable from PFPS. Symptoms include dull peripatellar pain that is exacerbated by activities that load the joint, including prolonged walking, running, squatting, kneeling, jumping, arising from a seated position, or stair climbing – especially walking down stairs or downhill. (2,18). Disruption of patellofemoral cartilage may result in crepitus, intermittent locking, or giving way. (18)
Clinical evaluation of CMP should be directed toward identifying factors that create imbalanced force on the patella, i.e., PFPS. Patients suffering with patellofemoral pain often have hypertonic soleus, hamstring, iliopsoas, piriformis, and thigh adductor muscles with tightness in the iliotibial band and posterior hip capsule. (7,19,20) Weakness in the quadriceps or hamstring muscles increases one’s risk of developing the problem three to five-fold. (11) Weakness in the gluteus maximus or medius is common in patients with knee pain and contributes to PFPS. (12,13) Gluteus medius weakness may be assessed by observing for pelvic drop or knee valgus (Trendelenburg sign) when performing a single leg stand, overhead squat test, single leg squat, or single leg 6″ step down. Patients with anterior knee pain frequently have a greater prevalence of trigger points in their hip, thigh, and lumbar spine muscles. (41,42)
Palpation generally reveals peripatellar tenderness with exacerbation of symptoms upon patellar compression. Clinicians may consider alternatives to the Patellar grind test, (a/k/a “Clarke sign”), as this assessment has been shown to be unreliable, and may even generate new complaints. (21,22) Patellar mobility may be assessed with the Patellar Glide test and Patellar tilt test or by observing patellar tracking during active knee flexion/ extension (Patellar tracking assessment). (23) Static assessment of patellofemoral orientation is an unreliable measurement tool. (24,25) Historically, increased Q angles were thought to increase lateral pressures and were considered an etiologic factor. (26) Newer studies show that normal Q angles vary from 10 to 20 degrees and are similar in symptomatic and non-symptomatic patellofemoral patients. (27,28)
Differentiation of meniscal pain from patellofemoral pain may be accomplished by having the patient perform a two-legged squat. Meniscal pain is generated at the bottom of the squat, while patellofemoral pain is present during descent and ascent.
Diagnostics & Differential
Knee radiographs may be necessary to rule out fracture in those with a history of trauma or osteoarthritis and in patients older than 50. Radiographs may also be appropriate in patients with significant swelling, a recent history of knee surgery and in those whose pain does not improve with a trial of treatment. (29) Radiographic assessment of CMP would include a lateral, AP, tunnel, and patellofemoral (merchant or sunrise) view.
Chondral lesions are often difficult to diagnose by plain x-ray. The presence of osteophytes, cysts, subchondral sclerosis, and articular space narrowing is indicative of cartilaginous injury. (30) MRI is the modality best suited to identify cartilage lesions. (31) Clinicians should recognize that cartilage lesions are exceptionally prevalent in symptomatic populations. (43) Like so many other degenerative conditions, there appears to be little correlation between the radiographic severity of CMP and the patient’s subjective complaints. (32)
The differential diagnosis for anterior knee pain includes: fracture, infection, neoplasm, patellar or quadriceps tendinopathy, bursitis and cartilaginous irritation including osteochondritis dissecans, and patellofemoral arthritis. Additional considerations would include Sinding-Larsen-Johansson syndrome, plica, iliotibial band syndrome, symptomatic bipartite patella and referred pain from the spine or hip. (33)
Management
If left untreated, CMP may result in premature degenerative joint disease. (31) Management of CMP should progress from minimization of aggravating factors and anti-inflammatory measures to long-term correction of functional deficits. Decreasing fear-avoidance behavior may lead to improved outcomes. (10) Lifestyle modification may be necessary to reduce pain-provoking activities, especially running, jumping and activities that induce a valgus stress. Athletes should avoid allowing their knee to cross in front of their toes while squatting. Electrotherapy and ice may be useful initially for reduction of pain and inflammation. NSAIDS or anti-inflammatory medication may provide short-term benefit for relief of pain and inflammation.
Myofascial release and stretching should be directed at hypertonic muscles, including the TFL, gastrocnemius, soleus, hamstring, piriformis, hip rotators and psoas. Myofascial release or IASTM may be appropriate for tightness in the iliotibial band, posterior hip capsule and lateral knee retinaculum.
Since gluteus medius and VMO weakness are key factors in the development of PFPS and knee pain, strengthening exercises are generally necessary for those muscles. (34) Stabilization exercises may include: pillow push (push the back of your knee into a pillow for 5-6 seconds), supine heel slide, terminal knee (short-arc) extension, clam, glute bridge, semi-stiff dead lift and posterior lunge. Eccentric quadriceps strengthening is more effective than concentric exercise in the treatment of PFPS. (36)
Manipulation may be necessary for restrictions in the lumbosacral and lower extremity joints. Hypermobility is common in the ipsilateral SI joint, with restrictions present contralaterally. Patellofemoral problems are part of a complex biomechanical chain, and corrective taping, including “McConnell taping” is generally ineffective. (37,38) Kinesiotape for PFPS has anecdotal support. Glucosamine sulfate may provide benefit.
Arch supports or custom orthotics may be necessary to correct hyperpronation. Research has shown that runners with anterior knee pain benefit from a combination of exercise and foot orthotics. (39) Runners should change shoes every 250 to 500 miles. Mesenchymal stem cells have demonstrated utility for managing isolated osteochondral defects in the knee. (44) A surgical “lateral release” of the lateral retinaculum is a last resort when conservative measures have failed.
References
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Clinical Pearls
* The spectrum of PFPS begins with asymptomatic functional malalignment of the patella and ends in severe patellofemoral arthritis. The diagnosis of “Chondromalacia patellae” (CMP) occupies the mid-portion of the PFPS continuum- beginning with visible cartilage alterations and eventually leading to patellofemoral arthritis.
*Weakness in the quadriceps or hamstring muscles increases one’s risk of developing patellofemoral pain three to five fold.
* Differentiation of meniscal pain from patellofemoral pain may be accomplished by having the patient perform a two-legged squat- meniscal pain is generated at the bottom of the squat, while patellofemoral pain is present during descent and ascent.
