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Adolescent Anterior Knee Pain
Adolescent Anterior Knee Pain Peter G. Gerbino, MD A great many physicians believe that anterior knee pain cannot be broken down into its component pathologic processes. This is incorrect. If one knows the sites that are capable of generating pain and knows how to test those sites, localizing the involved sites is not difficult. It is more work to learn which pathologic processes occur in clusters and why each process evolves. Treatment begins to make sense and, perhaps even more important, the failure of certain treatments begins to make sense. A stepwise approach to obtaining the right history followed by an examination that identifies the sites of pain leads to appropriate diagnoses. Usually, adolescent anterior knee pain turns out to be Sinding-Larsen-Johansson, Osgood-Schlatter, patellofemoral, fat pad, or plica syndrome or a combination of these syndromes. Other syndromes are less common. Treatment frequently requires reducing or redistributing patellofemoral joint reactive forces by one or more of several techniques. Oper Tech Sports Med 14:203-211 © 2006 Elsevier Inc. All rights reserved. KEYWORDS anterior knee pain, patellofemoral syndrome, chondromalacia patella, SindingLarsen-Johansson, Osgood-Schlatter, patellar tendinosis, plica, fat pad, lateral release, patella compression, patella grind
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nterior knee pain in the adolescent continues to be one of the more difficult to treat problems in musculoskeletal medicine for 2 main reasons. The first is that the patient can experience pain, patellofemoral instability, or both. Patients and clinicians frequently have a difficult time discriminating between pain and instability, especially when instability leads to pain. The second reason is that the sources of pain are poorly understood and that frequently there are multiple painful sites. This kind of confusion leads to imprecise diagnoses and generic, “one size fits all” treatment interventions. The inevitable result is failed interventions, unhappy patients, frustrated physicians and therapists and wasted time. Success rests on understanding the pathophysiology of all possible sources of pain, accurate diagnosis, and selection of appropriate interventions for each pathologic process.
Pathophysiology Anatomy With the notable exception of articular cartilage, every structure in the knee contains noceceptive nerve endings.1,2 Those that have been found to correlate to painful knee syndromes Monterey Joint Replacement and Sports Medicine, Monterey, CA. Address reprint requests to Peter G. Gerbino, MD, Monterey Joint Replacement and Sports Medicine, 900 Cass Street, Suite 200, Monterey, CA 93940. E-mail: [email protected]
1060-1872/06/$-see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1053/j.otsm.2006.04.003
include nerves in patella subchondral bone, fat pad, synovium, retinaculae and joint capsule, plicae, patella tendon, patella tendon apophysis, iliotibial band, and femoral condyle bone.3-6 After trauma, pain fibers in the menisci and ligaments may be activated and cause pain as well. Other sources of pain generation include the infrapatellar branch of the saphanous nerve and other more remote peripheral or central nerves referring pain to the knee. Certain anatomic relationships are critical for normal knee homeostasis. Quadriceps strength, patella tracking, patella tendon length, size of medial plica, size of lateral and medial fat pads, and tightness in various structures around the knee all play roles in the various causes of anterior knee pain. A concept that frequently is overlooked with respect to anatomic variations and anterior knee pain is that of accommodation. Very few knees have perfect alignment or muscle and soft-tissue balance. Despite this, most knees accommodate to their anatomy and have no pain. Finding a lateral tracking patella, tight hamstrings, or weak quadriceps does not mean that that finding was necessarily the cause of the knee pain.
Mechanics The mechanics of the knee refers to the mechanical functioning of the 3 chondral compartments of the joint and to the dynamic forces in the compartments and in the soft tissues around the knee. Excessively tight tendinous structures, such as the iliotibial band, can rub prominent bony areas, leading 203
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204 Table 1 Conditions Leading to Pain in the Anterior Knee Condition
Anatomic site
Pathology
Sinding-Larsen-Johansson Osgood-Schlatter Patellar tendinosis Patellofemoral syndrome Fat pad syndrome Plica syndrome Retinacular pain Iliotibial band friction Juvenile rheumatoid arthritis Infection Neoplasm Osteochondritis dissecans Meniscus tear Neurogenic pain Complex regional pain Referred pain
Distal patella pole Tibial tubercle Patella tendon Patella bone Patella fat pad(s) Medial plica Lateral retinaculum ITB at lateral knee Synovial lining Bone or soft tissue Anywhere in knee Medial condyle Medial or lateral Infrapatellar branch Sympathetic nerves Usually hip
Apophyseal traction Apophyseal traction Microtears, degeneration Pain, compression Hypertrophy, synovitis Fibrosis, hypertrophy Neuritis, degeneration Bursitis, tendinosis Autoimmune synovitis Infection of joint Various processes Stress fracture Tear from trauma Trauma or irritation Minor trauma SCFE, Perthes, infection
to bursitis or tendon damage. A tight quadriceps mechanism can lead to traction injuries such as Osgood-Schlatter Syndrome, Sinding-Larsen-Johansson syndrome, patellar tendinosis, or to patellofemoral overload pain. A lateral tracking patella may be an incidental finding or may indicate chronic lateral patella facet subchondral overload (sometimes called excessive lateral pressure syndrome) with or without medial plica impingement. Of all the mechanical components to knee function, the most critical is patellofemoral joint reactive forces (JRFs). Patellofemoral JRFs have been measured as high as 8000 Newtons.7 These forces are absorbed by the patella and knee extensor mechanism. It is no accident that the majority of painful areas in adolescent anterior knee pain arise in the extensor mechanism. Likewise, it is appropriate that altering extensor mechanics is a basic tenet for managing many types of anterior knee pain.
Pathologic Processes Sixteen different pathologic processes can lead to complaints of knee pain in the young athlete. Of these, the first 8 listed in Table 1 are the most common. Many of these are technically not anterior, but because there is frequently pain at more than one site, they are included. Success in understanding this group of conditions requires the ability to identify all 16 processes and determine which ones are present in a given patient.
Sinding–Larsen–Johansson Syndrome (SLJ) Pathophysiology SLJ is classified as an apophysitis and an enthesitis. Unfortunately, it is not an inflammatory process and, therefore, the names are deceptive. Studies performed to determine the precise nature and etiology of the lesion have suffered from preconceptions and assumptions. What is known is that it occurs in mainly young boys aged 10 to 14 and is associated with excessive running and jumping, which is consistent
with SLJ being an extensor mechanism traction injury. Whether the traction leads to tendon microtears and subsequent calcification or causes physeal cartilage stress fracture or both remain to be proven. Some recent studies have made the case for physeal stress fracture stronger8,9 and it may well be that what tibial tubercle avulsion fracture is to OsgoodSchlatter, patella sleeve fracture is to SLJ. Diagnosis An active preadolescent boy with anterior knee pain is the typical patient, but active girls can have SLJ as well. Running, jumping, and climbing will exacerbate pain. The physical examination will show tenderness at the distal pole of the patella but not in the fat pads or with patella compression. Some boys also will have tenderness at the tibial tubercle. Frequently, the quadriceps is weak and tight and, almost always, the hamstrings are tight. Imaging studies are not mandatory, but plain films frequently are obtained. They can be normal or show ossification in the patella tendon just distal to the patella (Fig. 1). The ossification can be present in the initial radiographs or appear later as the condition matures, which has been interpreted to mean that the process is a calcific tendinitis10 but could just as likely mean that a piece of unossified apophyseal cartilage had avulsed and later became ossified. Treatment Relative rest is the mainstay of treatment. It is felt that avoiding the running and jumping that are associated with the greatest pain will allow the injury to heal. Addressing the hamstring and quadriceps tightness and weakness that is usually found will help prevent recurrence. Physical therapists frequently are used to help with the strength and flexibility. Some of the children who develop SLJ are so active that relative rest is very difficult to achieve. They will stop their organized athletic activity but continue to stress the knee by bounding around the house. In these patients, a knee immobilizer or even a cylinder cast may be necessary to achieve relative rest. Four to 10 weeks of pain-free rest typically is
Adolescent anterior knee pain
205 not resulted in healing (the tibial tubercle remains tender to palpation), operative excision of the ossicle and tubercleplasty can be considered.
Patellar Tendinosis Pathophysiology In the older adolescent, excessive running and jumping causes injury to the patella tendon, rather than to the apophyses. The most common site of injury is at the insertion on the distal pole of the patella. Once thought to be a tendinitis, this condition is now known to be progression of microtears at the bone-tendon interface. Acute exacerbations after jumping can result in transient swelling and inflammation, but the primary pathologic process is collagen degradation following fiber tears.14 Figure 1 Lateral radiograph of SLJ syndrome. The ossific changes in the patella tendon could represent calcific tendinitis or ossification of a portion of the apophysis.
required for full healing. Surgical intervention is rarely required.
Osgood-Schlatter Syndrome (OS) Pathophysiology Closely related to SLJ is OS. The child with OS is slightly older (12-15 years), but it is still predominantly boys that are very active in running and jumping. The site of injury is the tibial tubercle apophysis and the mechanism of injury repetitive traction by the patellar tendon. As in SLJ, it is unknown whether the lesion is microtears of the tendon, stress fracture of the physis, or both. The only inflammation occurs with acute exacerbations of the condition when there is new swelling and possible bursitis. The bony bumps that are the hallmark of chronic OS are caused by widening of the physis between the tibial tubercle apophysis and the anterior tibia. Most authors have concluded that OS is a common risk factor for tibial tubercle avulsion fracture.11-13 Diagnosis An active, running, jumping young male is the typical patient. Symptoms will localize to the tibial tubercle. There is more likely to be an enlarged, tender tubercle if the condition has been ongoing for several months. As in SLJ, the hamstrings and quadriceps are usually tight and frequently weak as well. Radiographs are not mandatory but will show enlargement and/or fragmentation of the tibial tubercle apophysis with widening of the tibial tubercle physis (Fig. 2). Treatment OS is treated exactly the same as SLJ. Relative rest achieving the pain-free state is required. Stretching and strengthening the quadriceps and hamstrings with the physical therapist prevents recurrence. Use of a knee immobilizer or cylinder cast may be necessary in especially active children to achieve the pain-free state. Use of patella tendon straps to redirect tensile forces can bring temporary relief. These can be used to nurse the athlete through a few events, but do not constitute treatment. In rare cases where 10 weeks of pain-free rest has
Diagnosis The presenting patient typically is a male high-school basketball player. He will complain of pain with jumping (hence the lay-term, “jumper’s knee”). There is tenderness at the distal pole of the patella and if the process has been ongoing for some time, the fat pads may be tender as well. There can be an associated patellofemoral syndrome with a positive patella compression test. Despite the usual high level of development in the athletes, it is common to find tight and weak hamstrings and quadriceps muscles. Early in the process, imaging studies, including magnetic resonance imaging (MRI), are normal. Longer-term MRI can show degenerative changes at the insertion site (Fig. 3). Treatment Relative rest decreases symptoms and will allow healing in acute cases. Prevention requires hamstring stretching and quadriceps strengthening. Patella tendon straps redirect tensile forces and can give temporary relief, but do not address etiology. Chronic cases can be difficult to resolve. Deep tissue massage, ultrasound, and iontophoresis of corticosteroids have been used with some success to try to stimulate healing. Recently, use of transdermal nitroglycerin to enhance local blood flow has been successful for treating other tendinopa-
Figure 2 Lateral radiograph of OS syndrome. Ossicle fragmentation and separation from the anterior tibia increase over time if the problem goes untreated.
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Figure 3 Saggital MR image of a patella tendon with chronic patellar tendinosis. Over time, the microtears at the insertion on the patella distal pole increase. Progressive degeneration is seen as a focal area (arrow) of fluid within the tendon.
thies.15,16 Its role in patella tendinosis is yet to be determined, but the concept offers enticing possibilities. When nonoperative interventions have failed, operative excision of the necrotic tendon fibers and drilling of the patella insertion site can be successful.
Patellofemoral Syndrome (PFS) The term PFS is imprecise and has been used interchangeably with patellofemoral pain syndrome, anterior knee pain, and chondromalacia patella. Anterior knee pain refers to all pain about the anterior knee and chondromalacia patella means actual damage to the patella cartilage that may or may not be associated with specific knee pain. The International Patellofemoral Study Group has recommended using more precise terms based on site of injury, but has not proposed a new term for pain associated with patella compression.17 We will use PFS to describe pain associated with a patella compression or grind test. Pathophysiology The reason or reasons that can cause a patella to be painful remain unknown. The patella subchondral bone contains many nerve endings and pain can come from direct stimulation of substance P and calcitonin gene-related peptide fibers18 or from elevated fluid pressures in the bone.19 The case for elevated intraosseous pressure in painful patellae has been made in several papers and there is evidence of such pressure elevations in scientific studies.19-25 This has been termed “patellar hypertension syndrome.”19 The premise is that elevated venous intraosseous pressure is caused by some alteration in homeostasis and this leads to pain. An entire school of thought had evolved that drilling or otherwise decompressing the patella would lead to pain relief.19,22,26-29 Other studies found that bone decompression was not worthwhile.30,31 Not explained by this theory was why the pressure becomes elevated, why the patella only hurts under load and what happens to pressure (and pain) once the drill holes heal. A recent study has confirmed that patients with anterior
P.G. Gerbino knee pain have the majority of their pain arising in the patella.32 A follow-up study has shown that patella compression within a physiologic range of forces leads to both patella deformation and measurable intraosseous pressure elevation (Gerbino PG, Kerr H, Soto R, et al, unpublished data). It is consistent with another study showing measurable intraosseous pressure changes in vivo as the knee was flexed.22 This poses the possibility that elevated intraosseous patella pressure may arise from patella compression during loading (load-deformation). Loading the patella with high JRFs would lead to patella deformation, elevated pressure, and pain. There would not necessarily have to be subchondral stress fractures for this phenomenon to occur, although enough compression to the patella would certainly lead to stress fractures in some patients with PFS. The pain could arise from direct mechanical stimulation of nerve fibers, from the resultant intraosseous pressure elevation or from both. If increased JRF is the direct cause of PFS, then tilt, maltracking, patella alta, patella infera, weak quadriceps, excessive jumping, and poor shock absorption in a hyperpronator all cause PFS by increasing relative JRF. This theory also has the advantage of explaining why lowering JRF decreases pain. Diagnosis In contrast to understanding the etiology of patellar pain, diagnosing it is straightforward. The patient complains of anterior knee pain. It is exacerbated by anything that increases patellofemoral JRF, such as running, jumping, climbing, prolonged sitting. The physical examination specific for PFS is the patella compression or grind test. It has also been called the pain provocation test. The patient is supine with the knee extended. To avoid the possibility of entrapping suprapatellar synovium between the patella and trochlea, the knee can be flexed 30° over a bump. The patella is then loaded in an anterior-posterior direction with or without a grinding motion. If the patient experiences pain, the only site capable of generating that pain is the patellar subchondral bone. There are no imaging studies capable of confirming patellar pain or PFS. Plain films and computed tomography (CT) are very good at documenting abnormal patella tilt, but tilt is a common finding and not necessarily related to symptoms. Previous studies have shown that bone scan can detect patella changes in a subset of patients with PFS,25,33 but bone scan or SPECT bone scan would be considered excessive radiation for diagnosis or research in this population. One recent study has found evidence of subchondral stress fracture in patients with PFS by MRI analysis.34 This further supports the theory that PFS results from patella load-deformation under elevated JRF. The problem with making the diagnosis of PFS is that PFS does not usually occur as an isolated entity. It was found to typically occur with fat pad syndrome and/or plica syndrome.32 If one or both of these other syndromes are present along with PFS, failure to address them all will result in inadequate treatment.
Adolescent anterior knee pain Treatment The relationship of the patella to the trochlea was not emphasized in the diagnosis section because lateral tracking, patella tilt, patella alta, patella infera, high Q-angle, and patella hypermobility are not, in and of themselves, pathologic. Very few patellae have perfect alignment and most have no PFS. However, we can alter patellofemoral JRF by modifying tracking in these various situations. There are braces to modify lateral tracking and tilt. Taping the patella various ways can modify forces. Exercises can strengthen and stretch various muscles. The use of foot orthotics slows pronation and internal tibial rotation, changing patellofemoral dynamics. Of all the interventions to treat PFS, the single most efficacious has been quadriceps strengthening.35-39 The vastus medialus obliquus cannot really be isolated to “pull the patella medially,”40 but for some reason overall quadriceps strengthening works. Perhaps the stronger muscle group permits landing with a shorter “arc” resulting in decreased JRF on a regular basis. Bracing does seem to help,41 but taping only works for a very short time.42 Newer findings have been that people with PFS have relatively weaker hip flexors,43 abductors, and external rotators.44 Many physical therapists have long known this and incorporated hip and core strengthening in their rehabilitation protocols. A complete regimen for PFS includes straightleg and short-arc quadriceps strengthening (closed-chain seems to be a bit better than open-chain38), hamstring and iliotibial band (ITB) stretching, complete hip and core strengthening, and appropriate bracing as warranted. Relative rest from activities that generate high patellofemoral JRF is also necessary. In most cases, nonoperative treatment will be successful if all sources of pain are addressed. Occasionally, the patella pain will persist. If there is patella tilt, a lateral retinacular release will result in redistribution of patellofemoral forces and pain relief.45 If there is patella subluxation, it may be necessary to add medial retinacular imbrication to centralize the patella. These procedures can be performed open or arthroscopically. If previous damage to the patella (after fracture, for example) requires further decreasing JRF to relieve pain, tibial tubercle anteriorization can be performed once physes close. If lateral instability coexists with persistent patella pain, a Fulkerson anteromedialization of the tubercle will be effective.46
Fat Pad Syndrome (FPS) Pathophysiology Also called Hoffa’s Syndrome, FPS is a common occurrence. The pain generators are the lateral and/or medial fat pads on either side of the patella tendon. Direct trauma, or more commonly, microtrauma and synovitis lead to fat pad enlargement, eventually causing a soft tissue impingement in the patellofemoral joint. Dye has shown that this tissue is extremely sensitive47 and failure to appreciate fat pad enlargement and pain has probably led to the majority of failed treatments for anterior knee pain. Any type of inflammatory process can result in fat pad synovial hypertrophy. These
207 include trauma, infection, rheumatoid arthritis and the inflammation that occurs with cartilage degeneration. Chronic patellofemoral syndrome probably leads to microparticulate chondral debris that, in turn, leads to fat pad syndrome. Each pathological process has distinctly different pain afferents that need to be individually addressed. Diagnosis The history and presentation is identical to PFS. Careful inspection of the knee in extension will show bulging, rather than dimpling on either side of the patella tendon (Fig. 4A), which can easily be confused with an effusion and there can be an associated effusion. Hoffa’s test is diagnostic. The knee is flexed and each fad pad tested by depressing with the thumb while extending the knee (Fig. 5A and B). This forces the pad into the patellofemoral joint, exacerbating the pain. In normal patients, this test does not cause pain. It must be remembered that patients with anterior knee pain usually have 2 to 4 painful sites, so the examination needs to include all potential sites. Radiographs are unremarkable in FPS. MRI does show the enlarged fat pads on saggital views (Fig. 4B), but it is difficult to know whether the enlargement is pathologic and radiologists rarely comment on fat pad size. Treatment Because FPS typically is found with PFS, one is usually adding specific FPS interventions to a PFS protocol. Oral antiinflammatory medicines can decrease fat pad synovitis in acute cases. Correcting patellofemoral overload with exercises, bracing and rest may lead to decreased effusions and resolution of the synovitis. Bracing in the circumstance of PFS plus FPS can put pressure on the lateral fat pad, worsening the pain. It has been reported that injection of corticosteroid into the fat pad can cause shrinkage.48 These interventions will work best on relatively acute FPS. Chronic cases result in thickened, fibrotic fat pads that cannot be shrunk. These are best treated with arthroscopic debridement. At the time of surgery, concomitant pathology such as thickened medial plica and lateral patella tracking can be treated as well. Rehabilitation involves standard muscle strengthening and stretching while maintaining patella mobility.
Plica Syndrome Pathophysiology After PFS and FPS, the third most-common additional site of pain about the knee is the medial plica.32 The plica is a vestigial fold of tissue found in most knees. Why it becomes painful is not definitively known, but it is hypothesized to thicken after direct trauma or if it repeatedly rubs the nonarticular medial femoral condyle because of a lateral tracking patella. In theses cases, the plica is tender to palpation as is the synovial tissue it rubs on the nonarticular medial femoral condyle. The problem in all cases is felt to be a synovitis resulting from mechanical irritation. Diagnosis The history and initial presentation is indistinguishable from PFS and FPS, as the 3 frequently occur together. The plica is easily palpated as a thickened band between the medial pa-
208
P.G. Gerbino show the thickened plica on the patellofemoral axial cuts (Fig. 6), but is not required to make the diagnosis. Treatment Early in the process, interventions that medialize the patella (taping, bracing, quadriceps strengthening) will decrease plica rubbing and allow healing. Oral antiinflammatory drugs can help. Injecting the plica with corticosteroids has been reported to be useful.49 Once the plica has become fibrotic, it may not be possible to adequately relieve impingement and arthroscopic debridement becomes necessary. As previously mentioned, if a laterally tracking patella has caused the plica hypertrophy, a lateral retinacular release may be required. If there is a coexistent FPS, the fat pads should be debrided. Failure to address the lateral tracking or fat pads can result in poor outcomes.
Figure 4 (A) Photograph of a knee with fat pad syndrome. Note the bulging fat pad on the lateral side of the patella rather than dimpling of the fat pad as would occur in a normal knee. (B) Sagittal MRI demonstrating fat pad enlargement with clear demarcation between normal fat pad and hypertrophic portion (arrow). (Color version of figure is available online.)
tella and medial meniscus. A normal plica is not tender to palpation. The synovium covering the nonarticular portion of the medial femoral condyle is easily palpated and is usually more tender than is the plica, itself. A lateral tracking patella and tight lateral retinaculum is almost always found. MRI will
Figure 5 Hoffa’s test for assessing fat pad tenderness. First the knee is flexed. Next the fat pad (lateral or medial) is depressed into the patellofemoral joint with the thumb (A). Next, the knee is extended while forcing the fat pad into the patellofemoral joint (B). A normal fat pad is not tender with this test. A painful, enlarged fat pad may be exquisitely tender with this maneuver. (Color version of figure is available online.)
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209 unnamed lateral capsular arteriole 1.5 cm distal to the vastus muscle fibers. Quadriceps atrophy is rapid after lateral release and physical therapy should be started quickly. Full strength recovery is expected by 12 weeks. A patella medializing brace is worn for extended walking or athletic activities during the rehabilitation phase.
Iliotibial Band Syndrome Pathophysiology Also called ITB friction syndrome, ITB syndrome is primarily a bursitis. Because of ITB tightness, overuse or both, the bursa between the ITB and tibia becomes inflamed. Over time, there can be an ITB tendinosis as well. ITB overuse is thought to occur with specific activities such as running downhill or if the gluteus maximus is otherwise being overworked. The ITB is the distal tendinous insertion of the gluteus maximus and overuse of this structural unit leads to tendinosis similar to other tendinopathies. The gluteus maximus is forced to overwork in its role as a hip stabilizer when the other hip and core muscles are inadequate.
Figure 6 Axial MR image of patellofemoral joint showing enlarged medial plica (arrow). Normal plicae are fine, thin lines, whereas fibrotic plicae are thicker and can be irregular.
Diagnosis Lateral knee pain in the absence of a traumatic injury should make one suspicious for ITB syndrome. Although technically not a source of anterior knee pain, it can accompany PFS and other overuse problems. Palpation of the distal ITB, especially with the Ober test (Fig. 7), elicits tenderness and is diagnostic. If the ITB is tight, the lower extremity will not come to the midline. Testing the hip and core muscles will almost always confirm strength deficits for the types of activity desired. No imaging studies are used for assessing ITB syndrome.
Lateral Retinacular Pain (LRP) Pathophysiology Chronic lateral retinacular tightness results in neuromatous degeneration and pain.50,51 In one study it was found in 10% of young patients with anterior knee pain.32 The mechanism for this degeneration is not known. Diagnosis All patients with LRP will have lateral tracking patellae and tight retinaculae. There is usually lateral patella tilt and palpation of the lateral capsule elicits pain. Common associated patella pathologies include PFS, FPS, plica and patella subluxation. Radiographs, especially the Merchant view, can show patella tilt, but are not diagnostic. Treatment First-line treatment for LRP is patella medialization with quadriceps strengthening and bracing. Taping the patella in the medial direction can be used for diagnosis or for short duration activities. Associated anterior knee pain pathologies need to be diagnosed and addressed. If pain persists, a lateral retinacular release is performed.45 Care should be taken to release the retinaculum from the fibers of the vastus lateralus to the lateral portal and ensure hemostasis all along the capsule. A large hemarthrosis will result without cautery of the
Figure 7 Photograph demonstrating the prone version of the Ober test for ITB tightness. Palpation of the ITB can be performed looking for tenderness at the same time. The lower extremity is elevated off the table by the examiner and should come to the midline unless the ITB is tight. In this case the ITB is tight when the extremity is still 30° from the midline, indicating a large contracture. (Color version of figure is available online.)
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210 Treatment Relative rest, ITB stretching, and strengthening of the hip and core muscles will resolve most cases. Occasionally the bursa will require an injection of corticosteroid to alleviate pain. Rare cases require release of the posterior fibers of the ITB distally.
Other Causes of Anterior Knee Pain The 8 previously discussed pathologic processes will be responsible for most anterior knee pain complaints. Patella instability (subluxation and dislocation) is not discussed as a separate entity because, although there is certainly pain associated with an episode of subluxation, it does not necessarily cause anterior knee pain. Anterior knee pain from patella instability results from PFS, FPS, and plica. The PFS results from repetitive trauma to the patella or from overload because the quadriceps is weakened from post-traumatic atrophy (reflex-inhibition).52,53 FPS occurs from chronic PFS and from synovitis that results from particulate cartilage debris following subluxation. For patella instability, the instability is treated in addition to the anterior knee pain pathologic processes. Additional sources of anterior knee pain include any process that causes an inflammatory effusion (juvenile rheumatoid arthritis, infection, neoplasm or internal derangement). Internal derangements include osteochondritis dissecans (OCD), loose bodies, torn menisci, torn ligaments, and chondral injuries. Sources of pain that do not cause pain by inflammatory effusion include neoplasm (pain from mechanical enlargement), OCD (bone pain separate from particulate inflammation), stress fracture, neurogenic pain, and referred pain. Of these sources, neurogenic and referred pain bear special mention.
related. It is recommended that any child younger than the age of 10 with complaints of knee pain receive a thorough hip examination as well. Any athlete of any age with a knee examination that does not show a classic pathologic process should have a hip examination. Hip pathology that can present as knee pain includes developmental hip dysplasia, septic arthritis of the hip, sickle cell crisis, stress fracture of the hip and Legg-Calve-Perthes disease. An overweight 13-year-old patient with knee pain and no findings about the knee should be evaluated for possible slipped capital femoral epiphysis. Treatment for these conditions is specific, depending on the diagnosis.
Conclusion Successful diagnosis and treatment of adolescent anterior knee pain requires a history that determines location of painful site(s), inciting activities, age of patient and any prior trauma. A complete stepwise examination includes inspection and range of motion followed by palpation of patella distal pole, tibial tubercle, ITB, both fat pads, patella in compression, medial plica, nonarticular medial femoral condyle and lateral retinaculum. If there was trauma, the menisci and ligaments should be tested as well. Hamstring, quadriceps, ITB and hip muscles should be tested for tightness and strength. The most frequent finding in adolescents will be PFS and the PFS will most commonly be found in conjunction with FPS and/or plica syndrome. Each process must be addressed. PFS that is treated with a medializing brace and becomes more painful has a coexistent FPS that was not appreciated. All causes of adolescent anterior knee pain are treated initially by nonoperative means. Occasionally, nonoperative treatment is not effective or adequate. In those cases, specific operative interventions are used to address each persistent pathologic process.
Neurogenic Knee Pain About the knee, neurogenic pain occurs in 1 of 3 ways. After trauma or surgery, a neuroma in a superficial sensory nerve can develop. Palpation elicits a painful Tinel’s sign and treatment is massage or operative excision if massage fails. The second type of neurogenic pain has been called saphenous neuritis.54 It can occur after injury or surgery as well. It responds to desensitization massage and correction of other derangements. The third type of neurogenic pain is painful sympathetic nerve dysfunction now termed complex regional pain syndrome. This poorly understood entity results after relatively minor injury and can become crippling if not treated early and aggressively. Main treatment interventions include physical therapy to desensitize the region, oral nerve desensitizers such as pregabalin or gabapentin and psychological counseling.
Referred Knee Pain Any time a child complains of knee pain, one must consider that the source of pain could actually be the hip. The younger the child, the more likely it is that a knee complaint is hip-
References 1. Biedert RM, Stauffer E, Friederich NF: Occurrence of free nerve endings in the soft tissue of the knee joint. A histologic investigation. Am J Sports Med 20:430-433, 1992 2. Witonski D, Wagrowska-Danielewicz M: Distribution of substance-P nerve fibers in the knee joint in patients with anterior knee pain syndrome. A preliminary report. Knee Surg Sports Traumatol Arthrosc 7:177-183, 1999 3. Dye SF, Vaupel GL, Dye CC: Conscious neurosensory mapping of the internal structures of the human knee without intraarticular anesthesia. Am J Sports Med 26:773-777, 1998 4. Niva MH, Kiuru MJ, Haataja R, et al: Bone stress injuries causing exercise-induced knee pain. Am J Sports Med 34:78-83, 2006 5. Fulkerson JP, Tennant R, Jaivin JS, et al: Histologic evidence of retinacular nerve injury associated with patellofemoral malalignment. Clin Orthop Relat Res 197:196-205, 1985 6. Sanchis-Alfonso V, Rosello-Sastre E, Revert F, et al: Histologic retinacular changes associated with ischemia in painful patellofemoral malalignment. Orthopedics 28:593-599, 2005 7. van Eijden TM, Weijs WA, Kouwenhoven E, et al: Forces acting on the patella during maximal voluntary contraction of the quadriceps femoris muscle at different knee flexion/extension angles. Acta Anat (Basel) 129:310-314, 1987 8. Freedman DM, Kono M, Johnson EE: Pathologic patellar fracture at the
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9.
10. 11. 12. 13.
14.
15.
16.
17.
18. 19.
20.
21. 22.
23. 24.
25.
26.
27.
28. 29. 30. 31.
site of an old Sinding-Larsen-Johansson lesion: a case report of a 33-year-old male. J Orthop Trauma 19:582-585, 2005 De Flaviis L, Nessi R, Scaglione P, et al: Ultrasonic diagnosis of OsgoodSchlatter and Sinding-Larsen-Johansson diseases of the knee. Skeletal Radiol 18:193-197, 1989 Medlar RC, Lyne ED: Sinding-Larsen-Johansson disease. Its etiology and natural history. J Bone Joint Surg Am 60:1113-1116, 1978 Nimityongskul P, Montague WL, Anderson LD: Avulsion fracture of the tibial tuberosity in late adolescence. J Trauma 28:505-509, 1988 Bang J, Broeng L: Spontaneous avulsion of the tibial tuberosity following Osgood-Schlatter disease. Ugeskr Laeger 157:3061-3062, 1995 Baltaci G, Ozer H, Tunay VB: Rehabilitation of avulsion fracture of the tibial tuberosity following Osgood-Schlatter disease. Knee Surg Sports Traumatol Arthrosc 12:115-118, 2004 Fu SC, Chan BP, Wang W, et al: Increased expression of matrix metalloproteinase 1 (MMP1) in 11 patients with patellar tendinosis. Acta Orthop Scand 73:658-662, 2002 Paoloni JA, Appleyard RC, Nelson J, et al: Topical glyceryl trinitrate treatment of chronic noninsertional achilles tendinopathy. A randomized, double-blind, placebo-controlled trial. J Bone Joint Surg Am 86A:916-922, 2004 Paoloni JA, Appleyard RC, Nelson J, et al: Topical glyceryl trinitrate application in the treatment of chronic supraspinatus tendinopathy: a randomized, double-blinded, placebo-controlled clinical trial. Am J Sports Med 33:806-813, 2005 Grelsamer RP: Patellofemoral Semantics: The Tower of Babel, in International Patellofemoral Study Group Position Papers. Available at: http://www.ipsg.org/index.html. Accessed May 2, 2006. Buma P: Innervation of the patella. An immunohistochemical study in mice. Acta Orthop Scand 65:80-86, 1994 Schneider U, Breusch SJ, Thomsen M, et al: .A new concept in the treatment of anterior knee pain: patellar hypertension syndrome. Orthopedics 23:581-586, 2000 Lemperg RK, Arnoldi CC: The significance of intraosseous pressure in normal and diseased states with special reference to the intraosseous engorgement-pain syndrome. Clin Orthop Relat Res 136:143-156, 1978 Bjorkstrom S, Goldie IF, Wetterqvist H: Intramedullary pressure of the patella in Chondromalacia. Arch Orthop Trauma Surg 97:81-85, 1980 Miltner O, Siebert CH, Schneider U, et al: Patellar hypertension syndrome in adolescence: a three-year follow up. Arch Orthop Trauma Surg 123:455-459, 2003 Arnoldi CC, Lemperg K, Linderholm H: Intraosseous hypertension and pain in the knee. J Bone Joint Surg Br 57:360-363, 1975 Hejgaard N: Intra-articular pressures and intraosseous pressure in the human knee and its implication for patello-femoral pain syndromes. An experimental study using simulated joint effusion. Acta Orthop Belg 50:791-801, 1984 Arnoldi CC, Djurhuus JC, Heerfordt J, et al: Intraosseous phlebography, intraosseous pressure measurements and 99mTC-polyphosphate scintigraphy in patients with various painful conditions in the hip and knee. Acta Orthop Scand 51:19-28, 1980 Hejgaard N, Arnoldi CC: Osteotomy of the patella in the patellofemoral pain syndrome. The significance of increased intraosseous pressure during sustained knee flexion. Int Orthop 8:189-194, 1984 Wolter D, Ratusinski C: Extra-articular, fan shaped drilling of patellar spongiosa in chrondopathia patellae. Operation method and initial results. Unfallchirurg 88:425-431, 1985 Morscher E: Osteotomy of the patella in chondromalacia. Preliminary report Arch Orthop Trauma Surg 92:139-147, 1978 Deliss L: Coronal patellar osteotomy: preliminary report of its use in chondromalacia patellae. Proc R Soc Med 70:257-259, 1977 Reid DC, Wilson J, Magee D: Intraosseous pressures in the patellofemoral pain syndrome. Am J Knee Surg 3:80-84, 1990 Simank HG, Graf J, Kerber A, et al: Long-term effects of core decom-
211
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33. 34. 35.
36.
37.
38.
39.
40. 41.
42.
43.
44.
45. 46.
47.
48. 49.
50.
51.
52.
53.
54.
pression by drilling. Demonstration of bone healing and vessel ingrowth in an animal study. Anat (Basel) 158:185-191, 1997 Gerbino PG 2nd, Griffin ED, d’Hemecourt PA, et al: Patellofemoral pain syndrome: evaluation of location and intensity of pain. Clin J Pain 22:154-159, 2006 Hejgaard N, Diemer H: Bone scan in the patellofemoral pain syndrome. Int Orthop 11:29-33, 1987 Niva MH, Kiuru MJ, Haataja R, et al: Bone stress injuries causing exercise-induced knee pain. Am J Sports Med 34:78-83, 2006 Kannus P, Niittymaki S: Which factors predict outcome in the nonoperative treatment of patellofemoral pain syndrome? A prospective follow-up study. Med Sci Sports Exerc 26:289-296, 1994 Natri A, Kannus P, Jarvinen M: Which factors predict the long-term outcome in chronic patellofemoral pain syndrome? A 7-yr prospective follow-up study. Med Sci Sports Exerc 30:1572-1577, 1998 Witvrouw E, Lysens R, Bellemans J, et al: Which factors predict outcome in the treatment program of anterior knee pain? Scand J Med Sci Sports 12:40-46, 2002 Witvrouw E, Lysens R, Bellemans J, et al: Open versus closed kinetic chain exercises for patellofemoral pain. A prospective, randomized study. Am J Sports Med 28:687-694, 2000 Crossley K, Bennell K, Green S, et al: A systematic review of physical interventions for patellofemoral pain syndrome. Clin J Sport Med 11: 103-110, 2001 Malone T, Davies G, Walsh WM: Muscular control of the patella. Clin Sports Med 21:349-362, 2002 Van Tiggelen D, Witvrouw E, Roget P, et al: Effect of bracing on the prevention of anterior knee pain—a prospective randomized study. Knee Surg Sports Traumatol Arthrosc 12:434-439, 2004 Kowall MG, Kolk G, Nuber GW, et al: Patellar taping in the treatment of patellofemoral pain. A prospective randomized study. Am J Sports Med 24:61-66, 1996 Tyler TF, Nicholas SJ, Mullaney MJ, et al: The role of hip muscle function in the treatment of patellofemoral pain syndrome. Am J Sports Med 34:630-636, 2006 Ireland ML, Willson JD, Ballantyne BT, et al: Hip strength in females with and without patellofemoral pain. J Orthop Sports Phys Ther 33: 671-676, 2003 Panni AS, Tartarone M, Patricola A, et al: Long-term results of lateral retinacular release. Arthroscopy 21:526-531, 2005 Bellemans J, Cauwenberghs F, Witvrouw E, et al: Anteromedial tibial tubercle transfer in patients with chronic anterior knee pain and a subluxation-type patellar malalignment. Am J Sports Med 25:375-381, 1997 Dye SF, Vaupel GL, Dye CC: Conscious neurosensory mapping of the internal structures of the human knee without intraarticular anesthesia. Am J Sports Med 26:773-777, 1998 Duri ZA, Aichroth PM, Dowd G: The fat pad. Clinical observations. Am J Knee Surg 9:55-66, 1996 Rovere GD, Adair DM: Medial synovial shelf plica syndrome. Treatment by intraplical steroid injection. Am J Sports Med 13:382-386, 1985 Fulkerson JP, Tennant R, Jaivin JS, et al: Histologic evidence of retinacular nerve injury associated with patellofemoral malalignment. Clin Orthop Relat Res 197:196-205, 1985 Sanchis-Alfonso V, Rosello-Sastre E, Monteagudo-Castro C, et al: Quantitative analysis of nerve changes in the lateral retinaculum in patients with isolated symptomatic patellofemoral malalignment. A preliminary study. Am J Sports Med 26:703-709, 1998 MacIntyre DL, Robertson DG: Quadriceps muscle activity in women runners with and without patellofemoral pain syndrome. Arch Phys Med Rehabil 73:10-14, 1992 Thomee R, Renstrom P, Karlsson J, et al: Patellofemoral pain syndrome in young women. II. Muscle function in patients and healthy controls. Scand J Med Sci Sports 5:245-251, 1995 Morganti CM, McFarland EG, Cosgarea AJ: Saphenous neuritis: a poorly understood cause of medial knee pain. J Am Acad Orthop Surg 10:130-137, 2002
A
nterior knee pain in the adolescent continues to be one of the more difficult to treat problems in musculoskeletal medicine for 2 main reasons. The first is that the patient can experience pain, patellofemoral instability, or both. Patients and clinicians frequently have a difficult time discriminating between pain and instability, especially when instability leads to pain. The second reason is that the sources of pain are poorly understood and that frequently there are multiple painful sites. This kind of confusion leads to imprecise diagnoses and generic, “one size fits all” treatment interventions. The inevitable result is failed interventions, unhappy patients, frustrated physicians and therapists and wasted time. Success rests on understanding the pathophysiology of all possible sources of pain, accurate diagnosis, and selection of appropriate interventions for each pathologic process.
Pathophysiology Anatomy With the notable exception of articular cartilage, every structure in the knee contains noceceptive nerve endings.1,2 Those that have been found to correlate to painful knee syndromes Monterey Joint Replacement and Sports Medicine, Monterey, CA. Address reprint requests to Peter G. Gerbino, MD, Monterey Joint Replacement and Sports Medicine, 900 Cass Street, Suite 200, Monterey, CA 93940. E-mail: [email protected]
1060-1872/06/$-see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1053/j.otsm.2006.04.003
include nerves in patella subchondral bone, fat pad, synovium, retinaculae and joint capsule, plicae, patella tendon, patella tendon apophysis, iliotibial band, and femoral condyle bone.3-6 After trauma, pain fibers in the menisci and ligaments may be activated and cause pain as well. Other sources of pain generation include the infrapatellar branch of the saphanous nerve and other more remote peripheral or central nerves referring pain to the knee. Certain anatomic relationships are critical for normal knee homeostasis. Quadriceps strength, patella tracking, patella tendon length, size of medial plica, size of lateral and medial fat pads, and tightness in various structures around the knee all play roles in the various causes of anterior knee pain. A concept that frequently is overlooked with respect to anatomic variations and anterior knee pain is that of accommodation. Very few knees have perfect alignment or muscle and soft-tissue balance. Despite this, most knees accommodate to their anatomy and have no pain. Finding a lateral tracking patella, tight hamstrings, or weak quadriceps does not mean that that finding was necessarily the cause of the knee pain.
Mechanics The mechanics of the knee refers to the mechanical functioning of the 3 chondral compartments of the joint and to the dynamic forces in the compartments and in the soft tissues around the knee. Excessively tight tendinous structures, such as the iliotibial band, can rub prominent bony areas, leading 203
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204 Table 1 Conditions Leading to Pain in the Anterior Knee Condition
Anatomic site
Pathology
Sinding-Larsen-Johansson Osgood-Schlatter Patellar tendinosis Patellofemoral syndrome Fat pad syndrome Plica syndrome Retinacular pain Iliotibial band friction Juvenile rheumatoid arthritis Infection Neoplasm Osteochondritis dissecans Meniscus tear Neurogenic pain Complex regional pain Referred pain
Distal patella pole Tibial tubercle Patella tendon Patella bone Patella fat pad(s) Medial plica Lateral retinaculum ITB at lateral knee Synovial lining Bone or soft tissue Anywhere in knee Medial condyle Medial or lateral Infrapatellar branch Sympathetic nerves Usually hip
Apophyseal traction Apophyseal traction Microtears, degeneration Pain, compression Hypertrophy, synovitis Fibrosis, hypertrophy Neuritis, degeneration Bursitis, tendinosis Autoimmune synovitis Infection of joint Various processes Stress fracture Tear from trauma Trauma or irritation Minor trauma SCFE, Perthes, infection
to bursitis or tendon damage. A tight quadriceps mechanism can lead to traction injuries such as Osgood-Schlatter Syndrome, Sinding-Larsen-Johansson syndrome, patellar tendinosis, or to patellofemoral overload pain. A lateral tracking patella may be an incidental finding or may indicate chronic lateral patella facet subchondral overload (sometimes called excessive lateral pressure syndrome) with or without medial plica impingement. Of all the mechanical components to knee function, the most critical is patellofemoral joint reactive forces (JRFs). Patellofemoral JRFs have been measured as high as 8000 Newtons.7 These forces are absorbed by the patella and knee extensor mechanism. It is no accident that the majority of painful areas in adolescent anterior knee pain arise in the extensor mechanism. Likewise, it is appropriate that altering extensor mechanics is a basic tenet for managing many types of anterior knee pain.
Pathologic Processes Sixteen different pathologic processes can lead to complaints of knee pain in the young athlete. Of these, the first 8 listed in Table 1 are the most common. Many of these are technically not anterior, but because there is frequently pain at more than one site, they are included. Success in understanding this group of conditions requires the ability to identify all 16 processes and determine which ones are present in a given patient.
Sinding–Larsen–Johansson Syndrome (SLJ) Pathophysiology SLJ is classified as an apophysitis and an enthesitis. Unfortunately, it is not an inflammatory process and, therefore, the names are deceptive. Studies performed to determine the precise nature and etiology of the lesion have suffered from preconceptions and assumptions. What is known is that it occurs in mainly young boys aged 10 to 14 and is associated with excessive running and jumping, which is consistent
with SLJ being an extensor mechanism traction injury. Whether the traction leads to tendon microtears and subsequent calcification or causes physeal cartilage stress fracture or both remain to be proven. Some recent studies have made the case for physeal stress fracture stronger8,9 and it may well be that what tibial tubercle avulsion fracture is to OsgoodSchlatter, patella sleeve fracture is to SLJ. Diagnosis An active preadolescent boy with anterior knee pain is the typical patient, but active girls can have SLJ as well. Running, jumping, and climbing will exacerbate pain. The physical examination will show tenderness at the distal pole of the patella but not in the fat pads or with patella compression. Some boys also will have tenderness at the tibial tubercle. Frequently, the quadriceps is weak and tight and, almost always, the hamstrings are tight. Imaging studies are not mandatory, but plain films frequently are obtained. They can be normal or show ossification in the patella tendon just distal to the patella (Fig. 1). The ossification can be present in the initial radiographs or appear later as the condition matures, which has been interpreted to mean that the process is a calcific tendinitis10 but could just as likely mean that a piece of unossified apophyseal cartilage had avulsed and later became ossified. Treatment Relative rest is the mainstay of treatment. It is felt that avoiding the running and jumping that are associated with the greatest pain will allow the injury to heal. Addressing the hamstring and quadriceps tightness and weakness that is usually found will help prevent recurrence. Physical therapists frequently are used to help with the strength and flexibility. Some of the children who develop SLJ are so active that relative rest is very difficult to achieve. They will stop their organized athletic activity but continue to stress the knee by bounding around the house. In these patients, a knee immobilizer or even a cylinder cast may be necessary to achieve relative rest. Four to 10 weeks of pain-free rest typically is
Adolescent anterior knee pain
205 not resulted in healing (the tibial tubercle remains tender to palpation), operative excision of the ossicle and tubercleplasty can be considered.
Patellar Tendinosis Pathophysiology In the older adolescent, excessive running and jumping causes injury to the patella tendon, rather than to the apophyses. The most common site of injury is at the insertion on the distal pole of the patella. Once thought to be a tendinitis, this condition is now known to be progression of microtears at the bone-tendon interface. Acute exacerbations after jumping can result in transient swelling and inflammation, but the primary pathologic process is collagen degradation following fiber tears.14 Figure 1 Lateral radiograph of SLJ syndrome. The ossific changes in the patella tendon could represent calcific tendinitis or ossification of a portion of the apophysis.
required for full healing. Surgical intervention is rarely required.
Osgood-Schlatter Syndrome (OS) Pathophysiology Closely related to SLJ is OS. The child with OS is slightly older (12-15 years), but it is still predominantly boys that are very active in running and jumping. The site of injury is the tibial tubercle apophysis and the mechanism of injury repetitive traction by the patellar tendon. As in SLJ, it is unknown whether the lesion is microtears of the tendon, stress fracture of the physis, or both. The only inflammation occurs with acute exacerbations of the condition when there is new swelling and possible bursitis. The bony bumps that are the hallmark of chronic OS are caused by widening of the physis between the tibial tubercle apophysis and the anterior tibia. Most authors have concluded that OS is a common risk factor for tibial tubercle avulsion fracture.11-13 Diagnosis An active, running, jumping young male is the typical patient. Symptoms will localize to the tibial tubercle. There is more likely to be an enlarged, tender tubercle if the condition has been ongoing for several months. As in SLJ, the hamstrings and quadriceps are usually tight and frequently weak as well. Radiographs are not mandatory but will show enlargement and/or fragmentation of the tibial tubercle apophysis with widening of the tibial tubercle physis (Fig. 2). Treatment OS is treated exactly the same as SLJ. Relative rest achieving the pain-free state is required. Stretching and strengthening the quadriceps and hamstrings with the physical therapist prevents recurrence. Use of a knee immobilizer or cylinder cast may be necessary in especially active children to achieve the pain-free state. Use of patella tendon straps to redirect tensile forces can bring temporary relief. These can be used to nurse the athlete through a few events, but do not constitute treatment. In rare cases where 10 weeks of pain-free rest has
Diagnosis The presenting patient typically is a male high-school basketball player. He will complain of pain with jumping (hence the lay-term, “jumper’s knee”). There is tenderness at the distal pole of the patella and if the process has been ongoing for some time, the fat pads may be tender as well. There can be an associated patellofemoral syndrome with a positive patella compression test. Despite the usual high level of development in the athletes, it is common to find tight and weak hamstrings and quadriceps muscles. Early in the process, imaging studies, including magnetic resonance imaging (MRI), are normal. Longer-term MRI can show degenerative changes at the insertion site (Fig. 3). Treatment Relative rest decreases symptoms and will allow healing in acute cases. Prevention requires hamstring stretching and quadriceps strengthening. Patella tendon straps redirect tensile forces and can give temporary relief, but do not address etiology. Chronic cases can be difficult to resolve. Deep tissue massage, ultrasound, and iontophoresis of corticosteroids have been used with some success to try to stimulate healing. Recently, use of transdermal nitroglycerin to enhance local blood flow has been successful for treating other tendinopa-
Figure 2 Lateral radiograph of OS syndrome. Ossicle fragmentation and separation from the anterior tibia increase over time if the problem goes untreated.
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Figure 3 Saggital MR image of a patella tendon with chronic patellar tendinosis. Over time, the microtears at the insertion on the patella distal pole increase. Progressive degeneration is seen as a focal area (arrow) of fluid within the tendon.
thies.15,16 Its role in patella tendinosis is yet to be determined, but the concept offers enticing possibilities. When nonoperative interventions have failed, operative excision of the necrotic tendon fibers and drilling of the patella insertion site can be successful.
Patellofemoral Syndrome (PFS) The term PFS is imprecise and has been used interchangeably with patellofemoral pain syndrome, anterior knee pain, and chondromalacia patella. Anterior knee pain refers to all pain about the anterior knee and chondromalacia patella means actual damage to the patella cartilage that may or may not be associated with specific knee pain. The International Patellofemoral Study Group has recommended using more precise terms based on site of injury, but has not proposed a new term for pain associated with patella compression.17 We will use PFS to describe pain associated with a patella compression or grind test. Pathophysiology The reason or reasons that can cause a patella to be painful remain unknown. The patella subchondral bone contains many nerve endings and pain can come from direct stimulation of substance P and calcitonin gene-related peptide fibers18 or from elevated fluid pressures in the bone.19 The case for elevated intraosseous pressure in painful patellae has been made in several papers and there is evidence of such pressure elevations in scientific studies.19-25 This has been termed “patellar hypertension syndrome.”19 The premise is that elevated venous intraosseous pressure is caused by some alteration in homeostasis and this leads to pain. An entire school of thought had evolved that drilling or otherwise decompressing the patella would lead to pain relief.19,22,26-29 Other studies found that bone decompression was not worthwhile.30,31 Not explained by this theory was why the pressure becomes elevated, why the patella only hurts under load and what happens to pressure (and pain) once the drill holes heal. A recent study has confirmed that patients with anterior
P.G. Gerbino knee pain have the majority of their pain arising in the patella.32 A follow-up study has shown that patella compression within a physiologic range of forces leads to both patella deformation and measurable intraosseous pressure elevation (Gerbino PG, Kerr H, Soto R, et al, unpublished data). It is consistent with another study showing measurable intraosseous pressure changes in vivo as the knee was flexed.22 This poses the possibility that elevated intraosseous patella pressure may arise from patella compression during loading (load-deformation). Loading the patella with high JRFs would lead to patella deformation, elevated pressure, and pain. There would not necessarily have to be subchondral stress fractures for this phenomenon to occur, although enough compression to the patella would certainly lead to stress fractures in some patients with PFS. The pain could arise from direct mechanical stimulation of nerve fibers, from the resultant intraosseous pressure elevation or from both. If increased JRF is the direct cause of PFS, then tilt, maltracking, patella alta, patella infera, weak quadriceps, excessive jumping, and poor shock absorption in a hyperpronator all cause PFS by increasing relative JRF. This theory also has the advantage of explaining why lowering JRF decreases pain. Diagnosis In contrast to understanding the etiology of patellar pain, diagnosing it is straightforward. The patient complains of anterior knee pain. It is exacerbated by anything that increases patellofemoral JRF, such as running, jumping, climbing, prolonged sitting. The physical examination specific for PFS is the patella compression or grind test. It has also been called the pain provocation test. The patient is supine with the knee extended. To avoid the possibility of entrapping suprapatellar synovium between the patella and trochlea, the knee can be flexed 30° over a bump. The patella is then loaded in an anterior-posterior direction with or without a grinding motion. If the patient experiences pain, the only site capable of generating that pain is the patellar subchondral bone. There are no imaging studies capable of confirming patellar pain or PFS. Plain films and computed tomography (CT) are very good at documenting abnormal patella tilt, but tilt is a common finding and not necessarily related to symptoms. Previous studies have shown that bone scan can detect patella changes in a subset of patients with PFS,25,33 but bone scan or SPECT bone scan would be considered excessive radiation for diagnosis or research in this population. One recent study has found evidence of subchondral stress fracture in patients with PFS by MRI analysis.34 This further supports the theory that PFS results from patella load-deformation under elevated JRF. The problem with making the diagnosis of PFS is that PFS does not usually occur as an isolated entity. It was found to typically occur with fat pad syndrome and/or plica syndrome.32 If one or both of these other syndromes are present along with PFS, failure to address them all will result in inadequate treatment.
Adolescent anterior knee pain Treatment The relationship of the patella to the trochlea was not emphasized in the diagnosis section because lateral tracking, patella tilt, patella alta, patella infera, high Q-angle, and patella hypermobility are not, in and of themselves, pathologic. Very few patellae have perfect alignment and most have no PFS. However, we can alter patellofemoral JRF by modifying tracking in these various situations. There are braces to modify lateral tracking and tilt. Taping the patella various ways can modify forces. Exercises can strengthen and stretch various muscles. The use of foot orthotics slows pronation and internal tibial rotation, changing patellofemoral dynamics. Of all the interventions to treat PFS, the single most efficacious has been quadriceps strengthening.35-39 The vastus medialus obliquus cannot really be isolated to “pull the patella medially,”40 but for some reason overall quadriceps strengthening works. Perhaps the stronger muscle group permits landing with a shorter “arc” resulting in decreased JRF on a regular basis. Bracing does seem to help,41 but taping only works for a very short time.42 Newer findings have been that people with PFS have relatively weaker hip flexors,43 abductors, and external rotators.44 Many physical therapists have long known this and incorporated hip and core strengthening in their rehabilitation protocols. A complete regimen for PFS includes straightleg and short-arc quadriceps strengthening (closed-chain seems to be a bit better than open-chain38), hamstring and iliotibial band (ITB) stretching, complete hip and core strengthening, and appropriate bracing as warranted. Relative rest from activities that generate high patellofemoral JRF is also necessary. In most cases, nonoperative treatment will be successful if all sources of pain are addressed. Occasionally, the patella pain will persist. If there is patella tilt, a lateral retinacular release will result in redistribution of patellofemoral forces and pain relief.45 If there is patella subluxation, it may be necessary to add medial retinacular imbrication to centralize the patella. These procedures can be performed open or arthroscopically. If previous damage to the patella (after fracture, for example) requires further decreasing JRF to relieve pain, tibial tubercle anteriorization can be performed once physes close. If lateral instability coexists with persistent patella pain, a Fulkerson anteromedialization of the tubercle will be effective.46
Fat Pad Syndrome (FPS) Pathophysiology Also called Hoffa’s Syndrome, FPS is a common occurrence. The pain generators are the lateral and/or medial fat pads on either side of the patella tendon. Direct trauma, or more commonly, microtrauma and synovitis lead to fat pad enlargement, eventually causing a soft tissue impingement in the patellofemoral joint. Dye has shown that this tissue is extremely sensitive47 and failure to appreciate fat pad enlargement and pain has probably led to the majority of failed treatments for anterior knee pain. Any type of inflammatory process can result in fat pad synovial hypertrophy. These
207 include trauma, infection, rheumatoid arthritis and the inflammation that occurs with cartilage degeneration. Chronic patellofemoral syndrome probably leads to microparticulate chondral debris that, in turn, leads to fat pad syndrome. Each pathological process has distinctly different pain afferents that need to be individually addressed. Diagnosis The history and presentation is identical to PFS. Careful inspection of the knee in extension will show bulging, rather than dimpling on either side of the patella tendon (Fig. 4A), which can easily be confused with an effusion and there can be an associated effusion. Hoffa’s test is diagnostic. The knee is flexed and each fad pad tested by depressing with the thumb while extending the knee (Fig. 5A and B). This forces the pad into the patellofemoral joint, exacerbating the pain. In normal patients, this test does not cause pain. It must be remembered that patients with anterior knee pain usually have 2 to 4 painful sites, so the examination needs to include all potential sites. Radiographs are unremarkable in FPS. MRI does show the enlarged fat pads on saggital views (Fig. 4B), but it is difficult to know whether the enlargement is pathologic and radiologists rarely comment on fat pad size. Treatment Because FPS typically is found with PFS, one is usually adding specific FPS interventions to a PFS protocol. Oral antiinflammatory medicines can decrease fat pad synovitis in acute cases. Correcting patellofemoral overload with exercises, bracing and rest may lead to decreased effusions and resolution of the synovitis. Bracing in the circumstance of PFS plus FPS can put pressure on the lateral fat pad, worsening the pain. It has been reported that injection of corticosteroid into the fat pad can cause shrinkage.48 These interventions will work best on relatively acute FPS. Chronic cases result in thickened, fibrotic fat pads that cannot be shrunk. These are best treated with arthroscopic debridement. At the time of surgery, concomitant pathology such as thickened medial plica and lateral patella tracking can be treated as well. Rehabilitation involves standard muscle strengthening and stretching while maintaining patella mobility.
Plica Syndrome Pathophysiology After PFS and FPS, the third most-common additional site of pain about the knee is the medial plica.32 The plica is a vestigial fold of tissue found in most knees. Why it becomes painful is not definitively known, but it is hypothesized to thicken after direct trauma or if it repeatedly rubs the nonarticular medial femoral condyle because of a lateral tracking patella. In theses cases, the plica is tender to palpation as is the synovial tissue it rubs on the nonarticular medial femoral condyle. The problem in all cases is felt to be a synovitis resulting from mechanical irritation. Diagnosis The history and initial presentation is indistinguishable from PFS and FPS, as the 3 frequently occur together. The plica is easily palpated as a thickened band between the medial pa-
208
P.G. Gerbino show the thickened plica on the patellofemoral axial cuts (Fig. 6), but is not required to make the diagnosis. Treatment Early in the process, interventions that medialize the patella (taping, bracing, quadriceps strengthening) will decrease plica rubbing and allow healing. Oral antiinflammatory drugs can help. Injecting the plica with corticosteroids has been reported to be useful.49 Once the plica has become fibrotic, it may not be possible to adequately relieve impingement and arthroscopic debridement becomes necessary. As previously mentioned, if a laterally tracking patella has caused the plica hypertrophy, a lateral retinacular release may be required. If there is a coexistent FPS, the fat pads should be debrided. Failure to address the lateral tracking or fat pads can result in poor outcomes.
Figure 4 (A) Photograph of a knee with fat pad syndrome. Note the bulging fat pad on the lateral side of the patella rather than dimpling of the fat pad as would occur in a normal knee. (B) Sagittal MRI demonstrating fat pad enlargement with clear demarcation between normal fat pad and hypertrophic portion (arrow). (Color version of figure is available online.)
tella and medial meniscus. A normal plica is not tender to palpation. The synovium covering the nonarticular portion of the medial femoral condyle is easily palpated and is usually more tender than is the plica, itself. A lateral tracking patella and tight lateral retinaculum is almost always found. MRI will
Figure 5 Hoffa’s test for assessing fat pad tenderness. First the knee is flexed. Next the fat pad (lateral or medial) is depressed into the patellofemoral joint with the thumb (A). Next, the knee is extended while forcing the fat pad into the patellofemoral joint (B). A normal fat pad is not tender with this test. A painful, enlarged fat pad may be exquisitely tender with this maneuver. (Color version of figure is available online.)
Adolescent anterior knee pain
209 unnamed lateral capsular arteriole 1.5 cm distal to the vastus muscle fibers. Quadriceps atrophy is rapid after lateral release and physical therapy should be started quickly. Full strength recovery is expected by 12 weeks. A patella medializing brace is worn for extended walking or athletic activities during the rehabilitation phase.
Iliotibial Band Syndrome Pathophysiology Also called ITB friction syndrome, ITB syndrome is primarily a bursitis. Because of ITB tightness, overuse or both, the bursa between the ITB and tibia becomes inflamed. Over time, there can be an ITB tendinosis as well. ITB overuse is thought to occur with specific activities such as running downhill or if the gluteus maximus is otherwise being overworked. The ITB is the distal tendinous insertion of the gluteus maximus and overuse of this structural unit leads to tendinosis similar to other tendinopathies. The gluteus maximus is forced to overwork in its role as a hip stabilizer when the other hip and core muscles are inadequate.
Figure 6 Axial MR image of patellofemoral joint showing enlarged medial plica (arrow). Normal plicae are fine, thin lines, whereas fibrotic plicae are thicker and can be irregular.
Diagnosis Lateral knee pain in the absence of a traumatic injury should make one suspicious for ITB syndrome. Although technically not a source of anterior knee pain, it can accompany PFS and other overuse problems. Palpation of the distal ITB, especially with the Ober test (Fig. 7), elicits tenderness and is diagnostic. If the ITB is tight, the lower extremity will not come to the midline. Testing the hip and core muscles will almost always confirm strength deficits for the types of activity desired. No imaging studies are used for assessing ITB syndrome.
Lateral Retinacular Pain (LRP) Pathophysiology Chronic lateral retinacular tightness results in neuromatous degeneration and pain.50,51 In one study it was found in 10% of young patients with anterior knee pain.32 The mechanism for this degeneration is not known. Diagnosis All patients with LRP will have lateral tracking patellae and tight retinaculae. There is usually lateral patella tilt and palpation of the lateral capsule elicits pain. Common associated patella pathologies include PFS, FPS, plica and patella subluxation. Radiographs, especially the Merchant view, can show patella tilt, but are not diagnostic. Treatment First-line treatment for LRP is patella medialization with quadriceps strengthening and bracing. Taping the patella in the medial direction can be used for diagnosis or for short duration activities. Associated anterior knee pain pathologies need to be diagnosed and addressed. If pain persists, a lateral retinacular release is performed.45 Care should be taken to release the retinaculum from the fibers of the vastus lateralus to the lateral portal and ensure hemostasis all along the capsule. A large hemarthrosis will result without cautery of the
Figure 7 Photograph demonstrating the prone version of the Ober test for ITB tightness. Palpation of the ITB can be performed looking for tenderness at the same time. The lower extremity is elevated off the table by the examiner and should come to the midline unless the ITB is tight. In this case the ITB is tight when the extremity is still 30° from the midline, indicating a large contracture. (Color version of figure is available online.)
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210 Treatment Relative rest, ITB stretching, and strengthening of the hip and core muscles will resolve most cases. Occasionally the bursa will require an injection of corticosteroid to alleviate pain. Rare cases require release of the posterior fibers of the ITB distally.
Other Causes of Anterior Knee Pain The 8 previously discussed pathologic processes will be responsible for most anterior knee pain complaints. Patella instability (subluxation and dislocation) is not discussed as a separate entity because, although there is certainly pain associated with an episode of subluxation, it does not necessarily cause anterior knee pain. Anterior knee pain from patella instability results from PFS, FPS, and plica. The PFS results from repetitive trauma to the patella or from overload because the quadriceps is weakened from post-traumatic atrophy (reflex-inhibition).52,53 FPS occurs from chronic PFS and from synovitis that results from particulate cartilage debris following subluxation. For patella instability, the instability is treated in addition to the anterior knee pain pathologic processes. Additional sources of anterior knee pain include any process that causes an inflammatory effusion (juvenile rheumatoid arthritis, infection, neoplasm or internal derangement). Internal derangements include osteochondritis dissecans (OCD), loose bodies, torn menisci, torn ligaments, and chondral injuries. Sources of pain that do not cause pain by inflammatory effusion include neoplasm (pain from mechanical enlargement), OCD (bone pain separate from particulate inflammation), stress fracture, neurogenic pain, and referred pain. Of these sources, neurogenic and referred pain bear special mention.
related. It is recommended that any child younger than the age of 10 with complaints of knee pain receive a thorough hip examination as well. Any athlete of any age with a knee examination that does not show a classic pathologic process should have a hip examination. Hip pathology that can present as knee pain includes developmental hip dysplasia, septic arthritis of the hip, sickle cell crisis, stress fracture of the hip and Legg-Calve-Perthes disease. An overweight 13-year-old patient with knee pain and no findings about the knee should be evaluated for possible slipped capital femoral epiphysis. Treatment for these conditions is specific, depending on the diagnosis.
Conclusion Successful diagnosis and treatment of adolescent anterior knee pain requires a history that determines location of painful site(s), inciting activities, age of patient and any prior trauma. A complete stepwise examination includes inspection and range of motion followed by palpation of patella distal pole, tibial tubercle, ITB, both fat pads, patella in compression, medial plica, nonarticular medial femoral condyle and lateral retinaculum. If there was trauma, the menisci and ligaments should be tested as well. Hamstring, quadriceps, ITB and hip muscles should be tested for tightness and strength. The most frequent finding in adolescents will be PFS and the PFS will most commonly be found in conjunction with FPS and/or plica syndrome. Each process must be addressed. PFS that is treated with a medializing brace and becomes more painful has a coexistent FPS that was not appreciated. All causes of adolescent anterior knee pain are treated initially by nonoperative means. Occasionally, nonoperative treatment is not effective or adequate. In those cases, specific operative interventions are used to address each persistent pathologic process.
Neurogenic Knee Pain About the knee, neurogenic pain occurs in 1 of 3 ways. After trauma or surgery, a neuroma in a superficial sensory nerve can develop. Palpation elicits a painful Tinel’s sign and treatment is massage or operative excision if massage fails. The second type of neurogenic pain has been called saphenous neuritis.54 It can occur after injury or surgery as well. It responds to desensitization massage and correction of other derangements. The third type of neurogenic pain is painful sympathetic nerve dysfunction now termed complex regional pain syndrome. This poorly understood entity results after relatively minor injury and can become crippling if not treated early and aggressively. Main treatment interventions include physical therapy to desensitize the region, oral nerve desensitizers such as pregabalin or gabapentin and psychological counseling.
Referred Knee Pain Any time a child complains of knee pain, one must consider that the source of pain could actually be the hip. The younger the child, the more likely it is that a knee complaint is hip-
References 1. Biedert RM, Stauffer E, Friederich NF: Occurrence of free nerve endings in the soft tissue of the knee joint. A histologic investigation. Am J Sports Med 20:430-433, 1992 2. Witonski D, Wagrowska-Danielewicz M: Distribution of substance-P nerve fibers in the knee joint in patients with anterior knee pain syndrome. A preliminary report. Knee Surg Sports Traumatol Arthrosc 7:177-183, 1999 3. Dye SF, Vaupel GL, Dye CC: Conscious neurosensory mapping of the internal structures of the human knee without intraarticular anesthesia. Am J Sports Med 26:773-777, 1998 4. Niva MH, Kiuru MJ, Haataja R, et al: Bone stress injuries causing exercise-induced knee pain. Am J Sports Med 34:78-83, 2006 5. Fulkerson JP, Tennant R, Jaivin JS, et al: Histologic evidence of retinacular nerve injury associated with patellofemoral malalignment. Clin Orthop Relat Res 197:196-205, 1985 6. Sanchis-Alfonso V, Rosello-Sastre E, Revert F, et al: Histologic retinacular changes associated with ischemia in painful patellofemoral malalignment. Orthopedics 28:593-599, 2005 7. van Eijden TM, Weijs WA, Kouwenhoven E, et al: Forces acting on the patella during maximal voluntary contraction of the quadriceps femoris muscle at different knee flexion/extension angles. Acta Anat (Basel) 129:310-314, 1987 8. Freedman DM, Kono M, Johnson EE: Pathologic patellar fracture at the
Adolescent anterior knee pain
9.
10. 11. 12. 13.
14.
15.
16.
17.
18. 19.
20.
21. 22.
23. 24.
25.
26.
27.
28. 29. 30. 31.
site of an old Sinding-Larsen-Johansson lesion: a case report of a 33-year-old male. J Orthop Trauma 19:582-585, 2005 De Flaviis L, Nessi R, Scaglione P, et al: Ultrasonic diagnosis of OsgoodSchlatter and Sinding-Larsen-Johansson diseases of the knee. Skeletal Radiol 18:193-197, 1989 Medlar RC, Lyne ED: Sinding-Larsen-Johansson disease. Its etiology and natural history. J Bone Joint Surg Am 60:1113-1116, 1978 Nimityongskul P, Montague WL, Anderson LD: Avulsion fracture of the tibial tuberosity in late adolescence. J Trauma 28:505-509, 1988 Bang J, Broeng L: Spontaneous avulsion of the tibial tuberosity following Osgood-Schlatter disease. Ugeskr Laeger 157:3061-3062, 1995 Baltaci G, Ozer H, Tunay VB: Rehabilitation of avulsion fracture of the tibial tuberosity following Osgood-Schlatter disease. Knee Surg Sports Traumatol Arthrosc 12:115-118, 2004 Fu SC, Chan BP, Wang W, et al: Increased expression of matrix metalloproteinase 1 (MMP1) in 11 patients with patellar tendinosis. Acta Orthop Scand 73:658-662, 2002 Paoloni JA, Appleyard RC, Nelson J, et al: Topical glyceryl trinitrate treatment of chronic noninsertional achilles tendinopathy. A randomized, double-blind, placebo-controlled trial. J Bone Joint Surg Am 86A:916-922, 2004 Paoloni JA, Appleyard RC, Nelson J, et al: Topical glyceryl trinitrate application in the treatment of chronic supraspinatus tendinopathy: a randomized, double-blinded, placebo-controlled clinical trial. Am J Sports Med 33:806-813, 2005 Grelsamer RP: Patellofemoral Semantics: The Tower of Babel, in International Patellofemoral Study Group Position Papers. Available at: http://www.ipsg.org/index.html. Accessed May 2, 2006. Buma P: Innervation of the patella. An immunohistochemical study in mice. Acta Orthop Scand 65:80-86, 1994 Schneider U, Breusch SJ, Thomsen M, et al: .A new concept in the treatment of anterior knee pain: patellar hypertension syndrome. Orthopedics 23:581-586, 2000 Lemperg RK, Arnoldi CC: The significance of intraosseous pressure in normal and diseased states with special reference to the intraosseous engorgement-pain syndrome. Clin Orthop Relat Res 136:143-156, 1978 Bjorkstrom S, Goldie IF, Wetterqvist H: Intramedullary pressure of the patella in Chondromalacia. Arch Orthop Trauma Surg 97:81-85, 1980 Miltner O, Siebert CH, Schneider U, et al: Patellar hypertension syndrome in adolescence: a three-year follow up. Arch Orthop Trauma Surg 123:455-459, 2003 Arnoldi CC, Lemperg K, Linderholm H: Intraosseous hypertension and pain in the knee. J Bone Joint Surg Br 57:360-363, 1975 Hejgaard N: Intra-articular pressures and intraosseous pressure in the human knee and its implication for patello-femoral pain syndromes. An experimental study using simulated joint effusion. Acta Orthop Belg 50:791-801, 1984 Arnoldi CC, Djurhuus JC, Heerfordt J, et al: Intraosseous phlebography, intraosseous pressure measurements and 99mTC-polyphosphate scintigraphy in patients with various painful conditions in the hip and knee. Acta Orthop Scand 51:19-28, 1980 Hejgaard N, Arnoldi CC: Osteotomy of the patella in the patellofemoral pain syndrome. The significance of increased intraosseous pressure during sustained knee flexion. Int Orthop 8:189-194, 1984 Wolter D, Ratusinski C: Extra-articular, fan shaped drilling of patellar spongiosa in chrondopathia patellae. Operation method and initial results. Unfallchirurg 88:425-431, 1985 Morscher E: Osteotomy of the patella in chondromalacia. Preliminary report Arch Orthop Trauma Surg 92:139-147, 1978 Deliss L: Coronal patellar osteotomy: preliminary report of its use in chondromalacia patellae. Proc R Soc Med 70:257-259, 1977 Reid DC, Wilson J, Magee D: Intraosseous pressures in the patellofemoral pain syndrome. Am J Knee Surg 3:80-84, 1990 Simank HG, Graf J, Kerber A, et al: Long-term effects of core decom-
211
32.
33. 34. 35.
36.
37.
38.
39.
40. 41.
42.
43.
44.
45. 46.
47.
48. 49.
50.
51.
52.
53.
54.
pression by drilling. Demonstration of bone healing and vessel ingrowth in an animal study. Anat (Basel) 158:185-191, 1997 Gerbino PG 2nd, Griffin ED, d’Hemecourt PA, et al: Patellofemoral pain syndrome: evaluation of location and intensity of pain. Clin J Pain 22:154-159, 2006 Hejgaard N, Diemer H: Bone scan in the patellofemoral pain syndrome. Int Orthop 11:29-33, 1987 Niva MH, Kiuru MJ, Haataja R, et al: Bone stress injuries causing exercise-induced knee pain. Am J Sports Med 34:78-83, 2006 Kannus P, Niittymaki S: Which factors predict outcome in the nonoperative treatment of patellofemoral pain syndrome? A prospective follow-up study. Med Sci Sports Exerc 26:289-296, 1994 Natri A, Kannus P, Jarvinen M: Which factors predict the long-term outcome in chronic patellofemoral pain syndrome? A 7-yr prospective follow-up study. Med Sci Sports Exerc 30:1572-1577, 1998 Witvrouw E, Lysens R, Bellemans J, et al: Which factors predict outcome in the treatment program of anterior knee pain? Scand J Med Sci Sports 12:40-46, 2002 Witvrouw E, Lysens R, Bellemans J, et al: Open versus closed kinetic chain exercises for patellofemoral pain. A prospective, randomized study. Am J Sports Med 28:687-694, 2000 Crossley K, Bennell K, Green S, et al: A systematic review of physical interventions for patellofemoral pain syndrome. Clin J Sport Med 11: 103-110, 2001 Malone T, Davies G, Walsh WM: Muscular control of the patella. Clin Sports Med 21:349-362, 2002 Van Tiggelen D, Witvrouw E, Roget P, et al: Effect of bracing on the prevention of anterior knee pain—a prospective randomized study. Knee Surg Sports Traumatol Arthrosc 12:434-439, 2004 Kowall MG, Kolk G, Nuber GW, et al: Patellar taping in the treatment of patellofemoral pain. A prospective randomized study. Am J Sports Med 24:61-66, 1996 Tyler TF, Nicholas SJ, Mullaney MJ, et al: The role of hip muscle function in the treatment of patellofemoral pain syndrome. Am J Sports Med 34:630-636, 2006 Ireland ML, Willson JD, Ballantyne BT, et al: Hip strength in females with and without patellofemoral pain. J Orthop Sports Phys Ther 33: 671-676, 2003 Panni AS, Tartarone M, Patricola A, et al: Long-term results of lateral retinacular release. Arthroscopy 21:526-531, 2005 Bellemans J, Cauwenberghs F, Witvrouw E, et al: Anteromedial tibial tubercle transfer in patients with chronic anterior knee pain and a subluxation-type patellar malalignment. Am J Sports Med 25:375-381, 1997 Dye SF, Vaupel GL, Dye CC: Conscious neurosensory mapping of the internal structures of the human knee without intraarticular anesthesia. Am J Sports Med 26:773-777, 1998 Duri ZA, Aichroth PM, Dowd G: The fat pad. Clinical observations. Am J Knee Surg 9:55-66, 1996 Rovere GD, Adair DM: Medial synovial shelf plica syndrome. Treatment by intraplical steroid injection. Am J Sports Med 13:382-386, 1985 Fulkerson JP, Tennant R, Jaivin JS, et al: Histologic evidence of retinacular nerve injury associated with patellofemoral malalignment. Clin Orthop Relat Res 197:196-205, 1985 Sanchis-Alfonso V, Rosello-Sastre E, Monteagudo-Castro C, et al: Quantitative analysis of nerve changes in the lateral retinaculum in patients with isolated symptomatic patellofemoral malalignment. A preliminary study. Am J Sports Med 26:703-709, 1998 MacIntyre DL, Robertson DG: Quadriceps muscle activity in women runners with and without patellofemoral pain syndrome. Arch Phys Med Rehabil 73:10-14, 1992 Thomee R, Renstrom P, Karlsson J, et al: Patellofemoral pain syndrome in young women. II. Muscle function in patients and healthy controls. Scand J Med Sci Sports 5:245-251, 1995 Morganti CM, McFarland EG, Cosgarea AJ: Saphenous neuritis: a poorly understood cause of medial knee pain. J Am Acad Orthop Surg 10:130-137, 2002