Anterior knee pain

European Journal of Radiology 62 (2007) 27–43 Anterior knee pain Eva LLopis a,b , Mario Padrón c,∗ a Hospital de la Ribera, Alzira, Valencia, Spain Carretera de Corbera km 1, 46600 Alzira Valencia, Spain c Clı́nica Cemtro, Ventisquero de la Condesa no. 42, 28035 Madrid, Spain b Received 15 January 2007; received in revised form 16 January 2007; accepted 17 January 2007 Abstract Anterior knee pain is a common complain in all ages athletes. It may be caused by a large variety of injuries. There is a continuum of diagnoses and most of the disorders are closely related. Repeated minor trauma and overuse play an important role for the development of lesions in Hoffa’s pad, extensor mechanism, lateral and medial restrain structures or cartilage surface, however usually an increase or change of activity is referred. Although the direct relation of cartilage lesions, especially chondral, and pain is a subject of debate these lesions may be responsible of early osteoarthrosis and can determine athlete’s prognosis. The anatomy and biomechanics of patellofemoral joint is complex and symptoms are often unspecific. Transient patellar dislocation has MR distinct features that provide evidence of prior dislocation and rules our complication. However, anterior knee pain more often is related to overuse and repeated minor trauma. Patella and quadriceps tendon have been also implicated in anterior knee pain, as well as lateral or medial restraint structures and Hoffa’s pad. US and MR are excellent tools for the diagnosis of superficial tendons, the advantage of MR is that permits to rule out other sources of intraarticular derangements. Due to the complex anatomy and biomechanic of patellofemoral joint maltracking is not fully understood; plain films and CT allow the study of malalignment, new CT and MR kinematic studies have promising results but further studies are needed. Our purpose here is to describe how imaging techniques can be helpful in precisely defining the origin of the patient’s complaint and thus improve understanding and management of these injuries. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Patellofemoral joint; Intraarticular derangements; Osteoarthrosis 1. Introduction Anterior knee pain in the athlete is a common challenging problem to evaluate, diagnose and treat. Injuries of the anterior knee can be caused by two mechanisms: acute traumatic and overuse injuries and most of the knee-structures can be injured by both mechanisms. In case of injuries that are due mainly to sport, there is a higher incidence of acute injuries in contact sports, such as football, whereas in non-contact sports, such as track and field and running there is a higher incidence of overuse related injuries [1]. The concept of anterior knee pain is shifting away from the long-held view of structural characteristics to the consideration of pathophysiological processes that include osseus and soft tissues’ increased metabolic activity as an etiologically important factor in the genesis of patellofemoral pain [6]. ∗ Corresponding author. E-mail addresses: [email protected], [email protected] (E. LLopis), [email protected] (M. Padrón). 0720-048X/$ – see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejrad.2007.01.015 Anterior knee pain can be divided in many different ways. Jackson divided it into ‘distinct’ and ‘obscure’, including under distinct those focal lesions that can be clinically and radiologically defined and under obscure dynamic problems, such as maltracking and the excessive lateral pressure syndrome [7]. Meanwhile Post, suggested a way to narrow the list of potential diagnosis, depending on whether the pain is constant, activity related, sharp or intermittent [2]. And Christian et al. adopted a more anatomical point of view, dividing it into patellar tendon causes, patella, intraarticular pathology and bursitis [8]. Although for practical reasons an anatomical division is chosen in this paper, we would emphasize that all these structures are closely related and must be seen as a single mechanism. Since it may be clear from this brief introduction, the term anterior knee pain encompasses a wide group of different but related pathological entities [2]. The study of the patellofemoral joint is even more complicated by the use of expressions that have different meanings. The use of ambiguous terms should be known and abandoned in order to improve communication between physicians [3–5]. 28 E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 2. Pathophysiology One of the primordial functions of the patella is to displace the patella tendon away from the centre of rotation of the knee and so increase its moment arm. The contact point between the patella and the trochlea is a fulcrum and in the patella the contact area sweeps up from superior to inferior as the knee flexes from extension through 90◦ of flexion. The load transmitted through the patellofemoral joint increases with flexion and dynamic movements [7]. The envelope of function defined by Dye [6] is the range of load that can be applied across an individual joint in a given period without supraphysiological overload or structural failure. When there is adequate homeostasis the load applied is successfully handled, but if the load exceeds this range, or the joint is out of homeostasis due to chronic or acute injury, then the risk of injuries is higher and pain is experienced. The ability of a joint to tolerate loads depends on multiple factors: alignment, neuromuscular control and tone, absolute loads over time, etc. [6]. However, the dynamic character of knee homeostasis is not limited to osseous components. Peripatellar soft tissues, particularly peripatellar synovial lining and fat pat structures also contribute to the development of patellofemoral pain, including load as an important factor. This alternative, biologically oriented perspective of the genesis of anterior knee pain, results in a more rational explanation and safer therapeutic approaches than traditional ones that are only structurally based. Imaging techniques must also develop towards a more physiologic view of the problem, or even with the advent of new diagnostic test will not light more on the enigma of patellofemoral pain. Any patellofemoral structure that possesses a sensory nerve supply can be a potential source of anterior knee pain. A combination of innervated tissues can be involved concurrently, making specific diagnosis more difficult. Free nerve ending are concentrated in the patellar tendon, the retinacular tissue, the pes anserinus, and especially in the synovial tissues and fat pad. Articular surfaces, menisci and ligaments are less sensitive. Articular cartilage is a-neural but subchondral underlying bone has the potential to generate pain when overloaded by serious overlying cartilage deficiency. Elevated intraarticular pressure in the patella can also be associated with pain [9]. such as SCFE and adults with varying degrees of osteoarthritis may complain of knee pain, and their knee examination is unremarkable. The absence of significant findings in the knee should provoke thorough evaluation of the hip. Limitations of motion, especially internal rotation or an abnormal gait should raise suspicion of hip pathology [10]. Torsional deformity has been suggested as a source of knee pain in young patients. Anatomic studies have demonstrated a theoretical relationship between increased femoral anteversion and femoropatellar arthritis. The combination of increased lower 3. Extrarticular origin Because the perception of pain is a function of complex central nervous system factors other than direct nociceptive output of innervated patellofemoral structures, knee pain can also be perceived from a hip injury. Also because hip extensor muscles play an important role in lower extremity function and contribute up to 25% of energy absorption during landing. When the hip musculature does not absorb its share of the load, other parts must compensate. Therefore, deficits in hip strength increase the load on the knee irrespective of the rotational changes that may occur in the presence of hip weakness. Patients complaining of knee pain should have a clinical examination of the hip. For instance, children with hip pathology Fig. 1. Sagital SE PDWi and coronal fat saturation SE T2Wi shows a chronic anterior cruciate ligament rupture with thinning, increased signal intensity and irregularity on anterior femoral condyle and patellar cartilage. E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 29 extremity internal rotation, knee valgus, and pes planus has been described as miserable malalignment. Physical examination focusses on the entire body starting with observation of gait. Malalignment of the lower extremity should be noted, including increased femoral anteversion, inward orientation of the patella, external tibial torsion, or foot pronation. When patients are asked to localize their pain, most will grab the anterior aspect of the knee. 4. Knee instability and ligament injuries Anterior knee pain can be caused by an injury of intraarticular structures: the natural history of ACL and PCL rupture is still not fully understood, and both surgical and conservative treatment may result in cartilage degeneration. This is secondary to instability due to changes in normal knee axis after ligament rupture. ACL deficiency leads to rotational instability overloading the medial compartment. The most common cartilage lesion in ACL deficiency is located in the articular surface of the medial femoral condyle (Fig. 1). Although PCL rupture used to be considered a benign injury, partially due to its ability to heal spontaneously, new studies demonstrate it frequently can develop degenerative changes. PCL deficiencies lead to posterior tibial translation and increase pressure over the anteromedial compartment (Fig. 2). Multiple intraarticular injuries increase the risk of instability and therefore the development of degenerative changes and anterior knee pain. Anterior knee pain with decrease range of motion after anterior cruciate reconstructions may be caused by arthrofibrosis, cyclops lesion or infrapatellar contraction syndrome. Arthrofibrosis is a contracture of retropatellar fat pad and patellar tendon. The cyclops lesion is bone and/or fibrous tissue lying ante- Fig. 3. Patient with decrease knee motions after ACL hamstring type reconstruction. MR shows intermediate signal intensity mass in axial SE PDWi and low signal intensity mass on sagittal SE T1Wi (black arrows). This fibrous nodule impinges the intercondylar notch with knee flexion and extension movements. rior to the anterior cruciate ligament graft in the tibial tunnel (Fig. 3). Finally infrapatellar contraction syndrome is a fibrous hyperplasia in the peripatellar tissues [11]. 5. Patella 5.1. Bipartite patella Fig. 2. Thirty-year-old football player with a chronic PCL complete mid rupture, chronic instability leads to chondral surface lesions in the anterior lateral femoral condyle (arrow head) and subchondral bone edema is noted (arrow). The patella ossifies between the ages of 3 and 5 years with gradual coalescence of multiple centers of ossification. 30 E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 In 1–2% of the population the patella is not completely fused and develops as two unfused ossification centers. It is often bilateral and considered a normal asymptomatic variant. Occasionally it may become painful due to overuse or acute injury. Symptoms will vary depending on the location of the bipartite patellar and the soft tissue attachments. The distal pole of the patella has attachment of the patellar tendon and may be difficult to distinguish from the endstage of Sinding–Larsen–Johanson syndrome, and from sleeve fracture of the patella. When located in the lateral margin a stress phenomenon may be related to the lateral retinaculum. The most common location of bipartite patella is in the superolateral corner at the insertion of the vastus lateralis, and is the commonest site of symptoms. On radiographs corticated margins help to differentiate it from patellar fracture. Although diagnosis can usually be made with radiography and clinical correlation, MRI may aid diagnosis by showing increased signal intensity on fat-suppressed T2W images or STIR images in the soft tissues, or bone marrow edema. Stress fracture must be ruled out in patients with marked bone marrow edema [7,8,10]. 5.2. Fractures A direct traumatic blow to the patella may cause a patellar fracture, or contusion. A direct blow with a lesser force, such as that sustained in a dashboard injury without an overt significant identifiable pain may cause the sudden onset of pain that may persist for a long time. It is essential to rule out associated intraarticular ligament injuries in order to plan adequate treatment (Fig. 4). In children the patellar sleeve avulsion fracture is a rare but important lesion in which the unossified inferior pole plus a small amount of bone is avulsed along with a sleeve of retropatellar articular cartilage and periosteum. Another rare injury is avulsion of the unfused tibial tubercle. 5.3. Acute patellar dislocation Acute lateral patellar dislocation can be seen as a result of acute trauma or torsional stress on the extensor mechanism with or without underlying patellar malalignment. When patellar dislocation results from a blow to the outside of the knee there Fig. 4. Volume rendering reconstruction of multidetector CT presurgical (a), and after post-surgical fixation (c), and MPR reconstruction presurgical (b) and postsurgical (d). Multiple fragments displaced are seen after a direct blow patellar fracture, after fixation patella shows an anatomic “ad integrum” restoration. E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 31 Fig. 5. Acute patella dislocation, axial fat saturation SE T2Wi shows medial retinacular rupture (white arrow), medial anterior capsule tear with joint effusion extending to surrounded soft tissues (stars), and lateral femoral condyle bone contusion (arrow head). may be associated medial ligamentous injuries. It is most often seen in young athletes [8]. The dislocation often reduces spontaneously without treatment and the patient may not be aware that it has occurred. Clinical examination and radiographs are nonspecific. MR is very useful and some findings strongly suggest prior dislocation. Patellar dislocation results in distinct soft-tissue and bone injuries (Fig. 5 and Table 1). Effusion or hemarthrosis is frequent although it may escape to the soft tissues. Medial retinacular injury and medial joint capsule tear with hematoma, edema and tearing of its fibers. Vastus medialis rupture must be ruled out. Lateral femoral condyle contusion and medial patellar facet bone contusion representing trabecular microfractures occur as the patella relocates. Articular cartilage injury is common along the medial patellar facet end the lateral femoral condyle, and can have associated osteochondral lesions or loose bodies [12]. 5.4. Patella stress fractures disease has been implicated as a predisposing factor for developing a stress fracture [13]. 6. Cartilage lesions Many terms have used to describe cartilage lesions and articular surface injuries increasing confusion among the medical community. The Greek term chondromalacia means soft cartilage, a pathological entity and therefore should used in radiological reports. Moreover many different classifications have been used by different authors and societies. The one described by Bohndorf [14] combines arthroscopic and MRI findings with emphases on the distinction between cartilage injuries with intact and disrupted cartilage (Tables 2 and 3). Common causes include trauma, overuse and instability and it can be seen isolated or associated with other structural injuries of the patellar tendon, Hoffa’s fat pad, malalignment. Early diagnosis is important because when mild it may be reversible but when severe or advanced it can lead to osteoarthritis [3,7,8]. Stress fractures of the patella are rare. They occur predominately at the junction of the middle and distal one third of the patella; at this transitional site, the most distal fibers of the quadriceps and the most proximal fibers of the patellar tendon insert on the anterior patella. The most common orientation of stress fractures is transverse (Fig. 6). The mechanism of patellar stress fractures can be attributed to the mechanical stresses placed on the patella by the extensor mechanism and the cellular response to physical stress. Initial radiographs can be normal, whereas more advanced cases show sclerotic edges, without significant comminution. Early diagnosis is important to provide conservative treatment before separation of the fragments occurs [13]. Although infrequent, the tibial tubercle has also been identified as an area affected by stress fracture. Osgood Schlater Table 1 Acute patella dislocation, imaging findings 1. Medial retinaculum and medial capsule injury 2. Lateral femoral condyle contusion 3. Medial patella facet contusion, with or without cartilage lesion associated Fig. 6. Twenty-eight-year-old weekend running without direct trauma and anterior knee pain, sagittal PDWi reveals a lineal hipointense incomplete stress fracture extending from the anterior cortex. 32 E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 Table 2 Arthroscopic cartilage classification, outerbridge classification Chondromalacia patella (outerbridge) Grade 1 Grade 2 Grade 3 Grade 4 Closed disease 1A. The surface looks normal but the probe reveals a soft spongy feel or pitting edema 1B. A blister or raised portion of the cartilage surface is seen but examination with a probe shows this to be boggy. The surface is still intact Open disease: the probe will now reveal fissures Severe exuberant, fibrillation and crabmeat appearance The fibrillation is full-thickness and the erosive changes extend down to bone which may be exposed. This is in effect osteoarthritis. The size of the lesion needs to be recorded MR imaging provides excellent soft tissue differentiation and allows internal cartilage structure to be shown; surface defects or thinning are easily shown using fast spin echo proton density (FSEPD) weighted sequences. The use of fat suppression may allow increasing accuracy and emphasizes underlying bone marrow edema. New 3D gradient echo sequences are being used to improve spatial resolution, but its accuracy is disputed and some authors find multidetector CT arthrography or MR arthrography to be more sensitive. Promising areas of physiological imaging have been reported, including T2 mapping, diffusion-weighted imaging and dGEMRIC (delayed gadolinium enhanced imaging) [15]. Lesions can be divided into subchondral injuries, osteochondral fractures and pure chondral injuries. Subchondral injuries have intact cartilage surface (Fig. 7). Osteochondral fractures have disrupted cartilage surface with cortical bone (Fig. 8). The underlying subchondral bone is intact in pure chondral injuries. Chondral surface flap can be detached and the fragment may be displaced or not (Fig. 9). The most common sign of an unstable fragment is a high signal intensity line between the fragment and the underlying bone. However, cartilage lesions also include thinning compared to normal, fissures (Fig. 10) or cracks and circumscribed signal irregularities of the cartilage. The term “osteochondrosis or osteochondritis dissecans” was commonly used for osteochondral lesions in young athletes. Sometimes the lesion is associated with maltracking. More often osteochondritis dissecans occurs in the femoral sulcus (Fig. 11), Fig. 7. Sagittal SE PDWi shows a lineal fracture in the femoral condyle with intact cartilage surface. Fig. 8. Coronal fat saturation SE T2Wi shows a large osteochondral fragment partially detached with bone marrow edema associated. Table 3 Bohndorf classification of acute articular surface lesions (14) A. Acute injury of the articular surface with intact cartilage (subchondral injury) a. Subchondral microfracture (bone bruise) b. Subchondral impactation (geographic, crescentic, lineal type) B. Acute injury of the articular surface with disrupted cartilage (chondral, osteochondral lesion) a. Softening of cartilage with or without fissuring or fibrillation b. Chondral flap or overt chondral fracture (“flake”) c. Depression of cartilage into bone (condensing of cartilage and immediate subchondral bone) d. Osteochondral indentation e. Osteochondral flake fracture (partially or totally detached) Fig. 9. Axial SE PDWi reveals chondral delamination or flap (arrow) with detachment of the fragment, located into the lateral recess (arrow heads). E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 33 Fig. 10. Axial BFFE reveals a chondral acute injury with a central fissure (arrow). especially the inner aspect of the medial trochlea, although they can also appear in the patella (Fig. 12). Its origin has been associated with many factors, although traumatic and mechanical stress are thought to be the most likely causes. MR permits the cartilage lesion to be diagnosed and the stability of the fragment to be defined, making possible to grade lesions (Table 4) [16–19]. 7. Injuries of the extensor mechanism of the knee 7.1. Anatomic and functional review Extensor mechanism injuries are a major cause of anterior knee pain in the elite athlete. Patellar tendinopathy as pathology Fig. 12. Axial SE PDWi, osteochondral defect in a 15-year-old tennis player with partially detached osteochondral fragment. has increased over the past few years, probably because athletes undergo more strenuous and prolonged periods of training and competitions [20]. Variations from relative inactivity to active training may explain why white collar professionals who take part in occasional sporting pursuits are typically at particular risk. The direct injection of steroid, systemic corticosteroids, fluoroquinolones are associated with an increased risk of tendon rupture [21]. The quadriceps tendon connects the rectus femoris, the vastus intermedius, the vastus mediales and the vastus lateralis to the patella. The tendon inserts on the proximal pole and continues distally as a tendinous expansion over the anterior patella to merge with the patella tendon, most of the fibers anterior to the patella are a continuation of the rectus femoris tendon. The patellar tendon is the distal extension of the tendon of the quadriceps, extending from the inferior pole of the patella to the tibial tuberosity, 25–30% thinner than the quadriceps tendon, therefore more often the target of overuse trauma in sports [20]. The extensor mechanism has two important functions, the accelerating function, with concentric contraction as in jumping or kicking a ball, and the decelerating function, with eccentric contraction as in landing after jumping or running down stairs. The decelerating mechanism loads the patellar tendon beyond its inherent tensile strength. The extensor mechanism also plays Table 4 Osteochondritis dissecans classification International cartilage repair society [19] Stage 1 Fig. 11. Sagittal SE PDWi, shows an instable osteochondral fragment in the medial femoral condyle, hiperintensity fluid signal outlines completely the underlying fragment (arrow). Stage 2 Stage 3 Stage 4 Stable lesion in continuity with the host bone, covered by intact cartilage Partial discontinuity of the lesion, stable on probing Complete discontinuity of the lesion but fragment is not dislocated Dislocated fragment 34 E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 Fig. 13. Patella alta, sagittal T1Wi and fat saturation PDWi, patellar tendon length ratio with patellar diameter is greater than 1.2 indicative of patella alta. Associated findings are patellar tendinopathy with increased signal intensity and Hoffa’s pad edema. an important role in controlling internal and external tibial rotation [20]. Due to the unique mechanical properties and internal structure of tendons, forces generated by movement are rarely enough to rupture patellar tendon on their own and injuries are believed to result from repeatedly loading the extensor mechanism. Degenerative changes rather than inflammation are found in most ruptured tendons, suggesting that there is a pre-rupture phase and even predisposition to rupture. Pathogenesis of patellar tendinopathy is complex and how extrinsic and intrinsic factors combine to trigger the degeneration of patellar tendon has not been established. Extrinsic factors are the most commonly indicated: repetitive mechanical overload. It is more difficult to demonstrate the contribution of intrinsic factors. Intrinsic factors include malalignment, patella alta (Fig. 13), impingement of the inferior pole of the patella onto the tendon, patellar laxity and muscular tightness [22]. Until recently an athlete with exercise-related pain and tenderness at the patellar tendon was diagnosed as having a tendonitis or an inflammatory condition. After Puddu’s and recent new pathology-proven studies, especially of the Achilles and patellar tendon, which demonstrated that there were no inflammatory cells, the histological myth of tendonitis has now changed [23,24]. Macroscopically there is loss of the normal organized fibrilar appearance with microscopically proven clefts in collagen and necrotic fibers, as well as mucoid degeneration with variable fibrosis and neovascularization. Patellar tendinopathy was first related to jumping and was commonly referred as “jumper’s knee”. Alternative terms such as tendinitis or tendinosis should only be applied following histological studies. The term ‘tendinopathy’ has been accepted by the majority of orthopaedic and sports related physicians, and can be used to describe both acute and overuse conditions. Other terms are reserved for pathological labels [22,22]. 7.2. Patellar tendinopathy imaging findings Imaging assessment can be performed with plain films, US and MRI. Plain films depict dystrophic calcifications within the tendon and fragmentation of the tendon’s insertion secondary to repetitive traction (Table 5), Sinding–Larsen–Johansson disease, at the inferior patellar pole or at the proximal tibial tubercle in Osgood Schlatter’s disease. Both US and MR are excellent tools for assessing morphological internal information about this superficial tendon (Figs. 14 and 15). We must keep in mind that sometimes morphological changes do not run parallel to clinical complaints, and imaging findings can be detected in asymptomatic athletes. However, patients with asymptomatic imaging findings are at greater risk of developing them, therefore the relevance of these findings has yet to be determined. Table 5 Blazina clinical classification for patellar tendinopathy Blazina stage 1 2 3 3b 4 Clinical findings Pain only present after athletic participation with no undue functional impairment Pain during and after activity, but still able to perform at satisfactory level Pain present during and after activity but more prolonged, with progressive difficulty in performing at satisfactory level Partial rupture (not included by all clinicians) The patellar tendon is ruptured E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 35 On MR the tendon shows increased signal intensity on T1W images relative to the tendon and markedly increased signal intensity on T2W GRE images, T2 FSE images and STIR (Figs. 13–15). An increased signal intensity on T2W GRE images relative to that seen on T2 W FSE images has been postulated as histologically important, although complete correlation with the clinical complaint or long term studies has not been established. Radiologists must be aware of possible associated magic angle phenomena that can artificially increase signal intensity, resulting in false positive. Lost of the normal tendon Fig. 14. Proximal third patellar tendinopathy, extend US (13a) and sagittal fat saturation SE PDWi MRI correlation showing marked thickening of patellar tendon (1) with increased hyperechogenicity (1), partial rupture is seen as a lineal fluid signal on MR and hypoechogenicity on US (arrow heads), associated Hoffa’s pad edema (stars) and entesopathy (arrow) was found. On ultrasound the tendon must be evaluated with a high resolution high frequency lineal transducer with the knee semi-flexed in both transverse and longitudinal planes [25,26]. Characteristic monographic features include focal or diffuse hypoechogenicity, tendon thickening, irregularity of the tendon envelop, swelling of the surrounding tendon and structures and increased vascularity on color Doppler (Figs. 14 and 15). Hyperechogenic areas may be seen and they represent dystrophic ossification. Irregularities on patellar insertion to the patella or at the tibial insertion are also frequently encountered. Color Doppler US examination frequently reveals neovascularization in chronic painful tendinopathy and can be used as an adjunct to grey scale US, offering greater confidence in the diagnosis of tendinosis [22,27]. New research in US contrast media and tendons is taking place, and perhaps this will help us understand pathological intratendon changes and could also be used as an early diagnosis technique in those patients with clinically suspected tendinopathy and negative imaging findings that could benefit from early physical therapy. In patellar tendon ruptures hypoechogenicity is noted over the entire thickness of the tendon. Rupture produces an acoustic vacuum with irregular edges [21]. Fig. 15. Diffuse tendinopathy, extend US (14a), power Doppler (14b) and sagittal fat saturation SE PDWi (14c). Imaging findings show marked thickening of the tendon, with increase echogenicicy and signal intensity, as well as peritendinous edema with liquid (arrow). Doppler signal within the tendon and peritendinous tissues indicates neovasculatization. 36 E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 Fig. 16. Focal tendinopathy, SE T1Wi with microcoil reveals focal increase signal intensity in the posterior lateral aspect of patellar tendon (star), with loss of the normal sharp margin of the tendon (short black arrows), abnormal signal intensity of surrounding fat (long black arrow), and subtle irregularity in the lateral femoral condyle cartilage surface (white arrow). contour especially in its deeper portion, with or without signal intensity represent an early tendinopathy stage (Fig. 16). Tendon thickening is also a classic finding although exact measures show considerable overlap. Thickening can be focal or fusiform. Discontinuity with fluid signal intensity focal areas have been associated with partial tears. The classical distribution of injury affects the osteotendinous junction. Typically findings occur in the deep posterior portion of the patellar tendon, adjacent to the lower pole of the patella. Several theories have been proposed, a relatively vascular area, loading exposes this region to more strain. However, other locations are not infrequently encountered with inferomedial distribution, resulting from traction from the rectus femoris and vastus intermedius or distally at the tibial tuberosity. There is a high prevalence of associated findings that it might be important to correlate with clinical symptoms. Pathological enthesial conditions may show: bone or chondral avulsion, bone marrow edema or chronic enthesopathic changes, cortical remodelling, cortical defects or subcortical cysts. Peritendinous findings are frequent, peritendinous irregularity or edema, edema within the pre-patellar or Hoffa fat. Other associated findings such as retinacular tears and chondromalacia can be seen. MR imaging permits an accurate evaluation of associated intraarticular injuries [28]. Local injections of steroid have been associated with many dogmas and controversy. Usually injections are given blindly. Different imaging-guided percutaneous techniques for an accurate patellar tendinosis treatment, especially using US-guided techniques, have been described. Peritendinous injection of steroid combined with aggressive rehabilitation may reduce symptoms and the possible harmful effects of steroid inside the tendon [29]. Alfredson and Ohberg’s group has largely proved the utility of sclerosing the area of vascular ingrowth using polydocanol has produced promising clinical results in patients with Achilles tendinopathy. They have recently demonstrated good results in patients with patellar tendinopathy, improving knee function and reducing pain. Polydocanol is used as the sclerosing agent and also has a local anaesthetic effect. The injection is performed under Doppler US guidance to ensure injection into or near to the neovessels and to monitor injection until the circulation had stopped [30–33]. Growth factors and blood clots have also been injected into the tendon to increase tendon healing. Although they all seem very promising treatment tools, further controlled trials and long-term studies are essential to test these new treatments. Imaging techniques still have some limitations in the evaluation of tendinopathy, so further research is needed. This would include the long-term relevance of findings in asymptomatic patients, an earlier diagnostic tool for those patients with clinically suspected tendinopathy and negative imaging or how to follow up after treatment. 7.3. Quadriceps tendinopathy The superior strength, mechanical advantage and better vascularity of the quadriceps tendon make quadriceps tendinopathy much less frequent than patellar. Imaging findings are similar to those of patellar tendinopathy. In adolescent avulsion injuries of the proximal patella, apophysis is more common than tendinopathy (Fig. 17). Special attention should be given to femoral anteversion and tibial torsion. In older individuals degenerative changes such as calcification in the tendon or spur formation at the superior pole of the patella may be present. Partial ruptures are rare. If the vastus intermedius tendon is injured, there may be no detectable deformity. Fig. 17. US and Doppler of quadriceps tendinopathy of a 33-year-old professional cycling demonstrating fusiform distal quadriceps tendon thickening, hyperechogenic areas of dystrophic ossification (white arrow) and increased Doppler colour signal within the tendon (white arrow heads). E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 7.4. Patellar and quadriceps tendon acute injury Direct trauma to the patellar tendon provides an obvious means of disruption, although in the healthy knee extensor musculotendinous unit tensile overload usually results in transverse fracture at the patella. Sudden pain associated with a popping or tearing sensation is usually experienced, hemarthosis usually follows and causes the knee joint to swell [21]. MRI is useful to distinguish between partial and complete rupture. Complete discontinuity with proximal tendon fragment retraction is better seen on fluid sensitive sequences, such as STIR or fat saturation T2W. Hematoma extending to subcutaneous fat is frequently associated (Fig. 18). 7.5. Osgood Schlatter disease and Sinding–Larsen–Johanson disease The adult patellar tendon is firmly anchored to the bone by Sharpey fibers, but in the growing child the attachment is more tenuous. A repeated microavulsion injuries accompanied by incomplete fibro-osseous repair result in prominence of the tubercle, and this is called Osgood Schlatter disease. Repetitive traction of the proximal patellar tendon on the distal pole of the patella leads to Sinding–Larsen–Johanson syndrome. This condition occurs at a time when increasing demands are made on a still immature skeleton. It primarily affects athletically active adolescents and is most commonly seen in boys aged between 10 and 14 years. Diagnosis is clinical pain over the distal pole of the patellar or tibial tubercle with tenderness and painful kneeling. Imaging is not usually needed; however radiographies will show varying calcification or fragmentation due to partial separation of 37 chondro-osseous fragments. Ultrasound and MRI show calcifications, widening tendon and peritendinous oedema, when symptomatic bone marrow edema and marked peritendinous edema is present (Fig. 19) [7,8]. 8. Hoffa’s fat pad syndrome Hoffa’s fat pad is an intraarticular, but extrasynovial structure, that is richly vascularized and innervated. Infrapatellar fat pad pathology may be a cause of anterior knee pain. This condition is frequently associated with other knee problems, patellar tendinopathy, ligament reconstruction, meniscus tear or malalignment. Direct trauma has also been attributed as a cause. Changes in the fat pad have been noted as an indirect sign of occult traumatic patella. The different subsets of fat pad oedema patterns appear to be distinct entities since they are associated with different abnormalities, and take two main forms: posterior, Hoffa’s infrapatellar impingement syndrome, and impingement of the supero lateral aspect of the Hoffa pad. Hoffa’s fat pad syndrome was first described by Hoffa in 1904. It is thought to represent hypertrophy and inflammation of the infrapatellar fat pad secondary to impingement between the femoral condyles and tibial plateau during knee extension. Symptoms include anterior knee pain inferior to the pole of the patella. Pain is exacerbated by knee extension [11]. MR imaging show increased signal intensity on T2W and small effusion (Fig. 20). In subacute and chronic phases due to hemosiderin and fibrin deposits low signal can be seen on T1W and T2W. Bowing of the patellar tendon from mass effect is seen frequently. Fibrous tissue may be transformed into fibrocartilaginous tissue, and can rarely ossify [34]. Isolated Hoffa’s fat pad oedema is significantly associated with trochlear abnormalities. Fig. 18. Coronal fat saturation SE T2Wi, sagittal gradient echo T2Wi showed retraction of quadriceps tendon and a large fluid collection consistent with complete quadriceps tendon rupture. 38 E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 Fig. 20. Sagittal fat saturation SE T2Wi shows marked increase signal intensity and effusion in infrapatellar fat pad representing Hoffa pad syndrome, slightly anterior patellar tendon bowing is noted. Synovial plica is a common redundant fold in the synovial lining of the knee, which is present up to 60–80% of the population. The most commonly encountered are infrapatellar plica (ligamentum mucosum), suprapatellar plica and mediopatellar plica. Infrequently plica becomes symptomatic secondary to direct trauma or overuse. An injury to the plica leads to inflammation and fibrosis tissue proliferation and tensile changes in the plica. This process can alter joint mechanics and lead to further knee pathology. On MR, plicas appear as lineal low signal intensity structures surrounded by joint fluid [36]. Fig. 19. Symptomatic Osgood Schlatter disease, plain lateral knee film (a) and sagittal SE PDWi (b). Fragmentation of tibial tubercule (white arrow), patellar distal tendon widening and peritendinous edema (arrow heads) are characteristic features of symptomatic Osgood Schlatter disease. Superolateral Hoffa/prefemoral fat pad oedema is significantly associated with chondromalacia patella, femoral trochlear abnormality, patellar malalignment, patellar tendon abnormality and patella alta. MRI shows oedema in the superior aspect of the infrapatellar fat pad, with loss of normal fat plane between the patellar tendon and the lateral femoral condyle. Oedema may extend into the central superior aspect of the fat pad (Fig. 21). This variant is frequently overlooked [35]. The clinical importance of these entities needs to be established by further long-term pathological, clinical, biomechanical and radiological studies. 9. Plica Synovial plica may be a rare source of anterior knee pain in adolescents, although the relationship between plica and anterior knee pain is controversial. Many authors caution that this diagnosis is overrated, in particular medial plica syndrome, and unnecessary plicas have been removed. Fig. 21. Sagittal fat saturation SE PDWi demonstrates superior aspect of infrapatellar fat pad edema. E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 39 Fig. 22. Axial SE PDWi reveals a thick medial hypointense plica (black arrow) with an associated medial femoral condyle cartilage lesion (white arrow) causing anterior pain in a professional basket 22-year-old player. Medial plica syndrome is a combination of clinical symptoms associated with a pathological plica. Usually found in a young athletic patient involved in repetitive flexion-extension movements, such as rowing, swimming, cycling or basketball. The medial plica is a band of tissue originating at the undersurface of the quadriceps tendon and courses medially and obliquely to the medial border of the patella and attaches distally to the synovium. Sakakibara classified the medial plica into four types on the basis of size. Large plica that covers the medial femoral condyle can be trapped between the medial condyle and the patella and cause internal damage (Fig. 22). Due to repetitive contact this condition may develop into a cartilage injury [10,36,37]. Boles et al could not find any MR characteristics to be predictive of subsequent resection at arthroscopy. However, larger series could demonstrate a significant relationship of the plica width to the trochlear cartilage or oedema within the suprapatellar fat [37]. The suprapatellar plica is located at the border between the suprapatellar bursa and the knee joint cavity. Recently it has been suggested that the suprapatellar plica may be a cause of anterior knee pain, especially when a complete septum is found, which separates the suprapatellar pouch from the joint proper. Repetitive mechanical stimuli on the patellar articular surface with impingement of the membrane between the condyle and the patella have been speculated as possible etiological factors. MRI has shown an effusion in the upper compartment which does not communicate with the joint below, better seen in sagittal plane (Fig. 23). When marked synovial thickening or haemorrhage mass is associated a similar effect can be seen [36,38,39]. Infrapatellar plica is the most common plica in the knee. On MR imaging it is seen as linear low signal intensity anterior and parallel to the ACL on sagittal images. Traditionally the infrapatellar plica has been thought to be incidental and not a source of symptoms. However, some studies describe this as an Fig. 23. Surgically proven complete suprapatellar plica in a 13-year-old school soccer player, patient presented with soft tissue mass. Sagittal gradient echo T2Wi (a) and sagittal fat saturation SE T1Wi (b) after intravenous gadolium reveal a complete septum with heterogeneous content (black arrow head) and thickening enhancing synovial layer (arrow). 40 E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 Fig. 24. Sagittal fat saturation SE PDWi demonstrates an inferior plica (black arrow head) with a subtle Hoffa pad edema, however careful relation with patient’s symptoms must be establish before surgical treatment is planned. infrequent cause of anterior knee pain that only is thought of when no other evidence of internal derangement is found and acute rupture can mimic ACL rupture (Fig. 24) [40,41]. 10. Iliotibial band syndrome Iliotibial band friction syndrome (aka runner’s knee) results from constant friction between the iliotibial band and the lateral femoral epicondyle. Iliotibial tract originates proximally from the confluence of the fascia from the tensor fascia lata, gluteus maximus and the gluteus medius. Distally there is an anterior expansion of the iliotibial band, which attaches to the patella acting as a stabilizer and crossing the knee to insert on the Gerdy’s tubercule. The posterior expansion reaches the biceps tendon. It appears more frequently in distance runners, cyclists and military recruits, although the condition can occur with any activity requiring repetitive knee flexion and extension. A biomechanical study in runners noted that the posterior edge of the band impinges against the lateral epicondyle just after footstrike in the gait cycle. The friction occurs at, or slightly below, 30◦ of flexion, as a consequence of tibial internal rotation, and the band moves laterally with knee extension. Genu varum, excessive pronation with internal rotation of the tibia, lateral condylar spur or leg length discrepancy can increase the tension of the iliotibial band or create friction to the epicondyle. Other potential risk factors for the development of iliotibial band syndrome are high weekly mileage, time spent running on a track and muscular weakness of knee extensors, knee flexors and hip abductors. Hip abduction weakness is prone to increase thigh adduction and increase tension over the iliotibial band [20,42]. Fig. 25. Axial fat saturation SE T2Wi show soft tissue edema surrounding iliotibial band (white arrow heads) and bone marrow edema (arrow) in its patellar insertion. Repetitive microstrains and friction to the epicondyle may lead to degenerative changes or chronic bursitis [20]. The MRI task is to confirm the diagnosis and exclude other diagnoses, such as lateral meniscus tear. MRI shows significant thickening of the iliotibial band over the lateral femoral epicondyle, a small bursa deep to the iliotibial band in the region of the lateral epicondyle and oedema in the surrounding structures. Signal changes in the fat region deep to the iliotibial band, which is a richly innervated and vascularized fat layer, have been associated with an anatomically based theory of fat compression beneath the tract as the origin of iliotibial band syndrome (Fig. 25) [20]. 11. Bursitis: medial collateral bursitis and prepatellar bursitis Medial collateral bursitis is inflammation of the bursae deep to the medial collateral ligament. Patients describe pain along the medial joint line, especially under valgus stress. MRI may show inflammation of the bursa [11]. Prepatellar bursitis results whether from direct trauma or chronic friction from frequent kneeling. It occurs more frequently in sports like wrestlers, who get it from their knees E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 Fig. 26. Sagittal fat saturation SE PDWi of a 40-year-old demonstrate a thick prepatellar bursa with effusion. rubbing on the mats or volleyball players from diving onto their knees for the ball. Imaging is not usually needed; its role is to rule other internal derangement or complications. US or MR demonstrate prepatellar bursa thickening with effusion (Fig. 26). 12. Patellar malalignment, patellar maltracking Patellar malalignment is the abnormal positioning of the patella in any plane, and refers to the static relationship between the patella and the trochlea at a given degree of flexion, and the relationship between femur, patella and tibia. Tracking refers to dynamic patellofemoral alignment during knee motion. The result of patellofemoral malalignment and maltracking is unfavourable stresses and shearing forces that exceed the physiological threshold of tissue and result in cartilage, tendon, ligament or bone injuries. The fact that abnormal measurements are found on asymptomatic knees and differences depending on knee flexion makes it more difficult to define patellar malalignment [3,43,44]. The most common form is rotational malalignment, whereby the patella is tilted, lateral side down. Patella alta or baja, and abnormal position of the tibial tuberosity are other forms of patellar malalignment. Several measurements are obtained from the axial or sunrise view on radiographs, from the axial CT plane and from the lateral radiographs of the knee. The Q angle is the angle between a line joining the anterior superior iliac spine and the centre of the patella, and a line joining the centre of the patella and the tibial tuberosity. This is a clinical measurement and reflects the degree of valgus transitional force upon the patella. The normal value is 15◦ . The tibial tubercle-trochlea groove (TT-TG) distance can substitute the Q angle. This compares the position of the trochlea groove with the tibial tubercle: two axial CT slices are superimposed, one at the level of the trochlear groove and the other at 41 Fig. 27. TT-TG compares the distance between the tibial tubercle and the trochlea groove must be determined from superimposed CT images, one at the level of the trochlear groove and the other at patellar tendon tibial attachment. Two sagittal lines are drawn, one through the tibial tubercle and the other through the deepest point of the trochlear groove. The distance between the two is the TT-TG distance. Distance greater than 1.8–2 cm is considered to be abnormal. patellar tendon tibial attachment. Two sagittal lines are drawn, one through the tibial tubercle and the other through the deepest point of the trochlear groove. The distance between the two is the TT-TG distance. Distance greater than 1.8–2 cm has high specificity for maltracking (Fig. 27) [8,43]. Standard axial view or axial 20–30◦ CT scanner provides several measurements and anatomic views of different patellar shapes. Subtle subluxation is reduced by 30◦ of flexion [45]. More frequently used are sulcus angle, congruence angle, the lateral patellofemoral angle and the lateral patellar displacement. Sulcus angle measures trochlear depth, the angle formed between the two femoral condyles facets. The congruence angle is usually measured from a 45◦ flexion axial view. The measurement is made by bisecting the sulcus angle to create a zero reference line. Then a line is drawn from the lowest point on the patella to the sulcus angle point. The angle created is then measured. The normal value is between −6 ± 11 (Fig. 28). The lateral patellofemoral angle is calculated by measuring the angle of the lateral patellar facet compared with a line drawn across the femoral condyles, the normal patella is normally open laterally. Lateral patella displacement is measured by comparing the lateral margin of the patella to the lateral femoral condyle apex. In the normal knee the lateral patellar margin should lie no more than 1 mm lateral to the perpendicular (Fig. 29) [8,43]. Lateral view of the knee allows assessment of the vertical position of the patella and has been demonstrated as an effective tool for the evaluation of the alignment of the patellofemoral joint. The ability to easily obtain images at full extension and different degrees of flexion demonstrates how the patella is engaged in the trochlea with flexion. The most frequently used method is the Insall-Salvati method, which measures the ratio between the patellar tendon length and the maximal diagonal length of the patella (Fig. 30). The normal ratio is approximately 1, a ratio lower than 0.8 is considered to show patella baja, while a ratio greater than 1.2 is indicative of patella alta. Patella alta 42 E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 Fig. 28. Axial 30◦ patellofemoral CT Merchant technique for congruence angle defines the relationship between apex of the patella and the femoral trochlea. Sulcus angle (1) measures the trochlear depth formed between the two femoral condyles, normal 135◦ ± 10◦ . Sulcus angles establishes a zero reference (2), a second line is projected to the lowest point of the patella (3), normal value is −6◦ ± 11◦ . is associated with lateral patellar dislocation and subluxation, chondromalacia and patellar tendinopathy (Fig. 13). MR can also be used to obtain accurate traditional patellofemoral indices, and the advantage is its ability to characterize the status of soft tissues of the knee [8,43]. Dynamic MR and CT have been advocated to improve accuracy of imaging modalities mimicking physiological conditions, however further studies must be developed in order to increase our understanding of this process. Fig. 30. Patella position must be evaluated on the basis of the ratio of the patellar length to the greatest diagonal length, normal value 0.8 to 1.2, lower than 0.8 is related as “patella baja” and greater than 1.2 is indicative of “patella alta”. 13. Conclusions Many factors may cause anterior knee pain and can simultaneously affect several structures. It is important to remember that they act as a unique biomechanical unit. A combination of imaging findings with patient’s clinical symptoms permits an accurate diagnosis. However, a new understanding of pathophysiology and the dynamics of the patellofemoral joints is necessary to improve treatment options. Advances in cartilage imaging and dynamic MR will help radiologists and orthopaedic surgeons with the management of these complex clinical entities. References Fig. 29. Axial 30◦ patellofemoral CT, lateral patellofemoral subluxation (1) is measured by comparing the lateral margin of the patellar compared to a line perperdicular to posterior femoral condyles (1) across the lateral aspect of the lateral femoral condyle (3). More than 1 mm of displacement is considered abnormal. [1] Armsey TD, Hosey RG. Medical aspects of sports: epidemiology of injuries, preparticipation physical examination, and drugs in sports. Clin Sports Med 2004;23(2):255–79, vii. [2] Post WR. Anterior knee pain: diagnosis and treatment. J Am Acad Orthop Surg 2005;13(8):534–43. [3] Grelsamer RP. Patellar nomenclature: the Tower of Babel revisited. Clin Orthop Relat Res 2005;436:60–5. [4] Eriksson E. Tendinosis of the patellar and achilles tendon. Knee Surg Sports Traumatol Arthrosc 2002;10(1):1. [5] Kaufmann P, Bose P, Prescher A. New insights into the soft-tissue anatomy anterior to the patella. Lancet 2004;363(9409):586. [6] Dye SF. The pathophysiology of patellofemoral pain: a tissue homeostasis perspective. Clin Orthop Relat Res 2005;436:100–10. [7] Jackson AM. Anterior knee pain. J Bone Joint Surg Br 2001;83(7):937–48. [8] Christian SR, Anderson MB, Workman R, et al. Imaging of anterior knee pain. Clin Sports Med 2006;25(4):681–702. [9] Gerbino 2nd PG, Griffin ED, d’Hemecourt PA, et al. Patellofemoral pain syndrome: evaluation of location and intensity of pain. Clin J Pain 2006;22(2):154–9. [10] Shea KG, Pfeiffer R, Curtin M. Idiopathic anterior knee pain in adolescents. Orthop Clin North Am 2003;34(3):377–83, vi. E. LLopis, M. Padrón / European Journal of Radiology 62 (2007) 27–43 [11] Ellen MI, Jackson HB, DiBiase SJ. Uncommon causes of anterior knee pain: a case report of infrapatellar contracture syndrome. Am J Phys Med Rehabil 1999;78(4):376–80. [12] Lance E, Deutsch AL, Mink JH. Prior lateral patellar dislocation: MR imaging findings. Radiology 1993;189(3):905–7. [13] Drabicki RR, Greer WJ, DeMeo PJ. Stress fractures around the knee. Clin Sports Med 2006;25(1):105–15, ix. [14] Bohndorf K. Imaging of acute injuries of the articular surfaces (chondral, osteochondral and subchondral fractures). Skeletal Radiol 1999;28(10):545–60. [15] Manaster BJ, Johnson T, Narahari U. Imaging of cartilage in the athlete. Clin Sports Med 2005;24(1):13–37. [16] De Smet AA, Fisher DR, Graf BK, Lange RH. Osteochondritis dissecans of the knee: value of MR imaging in determining lesion stability and the presence of articular cartilage defects. AJR Am J Roentgenol 1990;155(3):549–53. [17] Boutin RD, Januario JA, Newberg AH, et al. MR imaging features of osteochondritis dissecans of the femoral sulcus. AJR Am J Roentgenol 2003;180(3):641–5. [18] International Cartilage Repair Society (ICRS) and Osteoarthritis Research Society International (OARSI) list of corporate members. Osteoarthritis Cartilage 2002; 10 Suppl A:xv–xxxvi. [19] International Cartilage Repair Society. ICRS cartilage injury evaluation package. Available ar: http://www.cartilage.org/evaluation package/ ICRS evaluation.pdf. Accessed December 23, 2002. [20] Panni AS, Biedert RM, Maffulli N, et al. Overuse injuries of the extensor mechanism in athletes. Clin Sports Med 2002;21(3):483–98, ix. [21] Maffulli N, Wong J. Rupture of the achilles and patellar tendons. Clin Sports Med 2003;22(4):761–76. [22] Warden SJ, Brukner P. Patellar tendinopathy. Clin Sports Med 2003; 22(4):743–59. [23] Khan K, Cook J. The painful nonruptured tendon: clinical aspects. Clin Sports Med 2003;22(4):711–25. [24] Khan KM, Bonar F, Desmond PM, et al. Patellar tendinosis (jumper’s knee): findings at histopathologic examination, US, and MR imaging. Victorian institute of sport tendon study group. Radiology 1996;200(3):821–7. [25] De Maeseneer M, Vanderdood K, Marcelis S, et al. Sonography of the medial and lateral tendons and ligaments of the knee: the use of bony landmarks as an easy method for identification. AJR Am J Roentgenol 2002;178(6):1437–44. [26] Friedman L, Finlay K, Jurriaans E. Ultrasound of the knee. Skeletal Radiol 2001;30(7):361–77. [27] Weinberg EP, Adams MJ, Hollenberg GM. Color Doppler sonography of patellar tendinosis. AJR Am J Roentgenol 1998;171(3):743–4. [28] McLoughlin RF, Raber EL, Vellet AD, et al. Patellar tendinitis: MR imaging features, with suggested pathogenesis and proposed classification. Radiology 1995;197(3):843–8. 43 [29] Fredberg U, Bolvig L, Pfeiffer-Jensen M, et al. Ultrasonography as a tool for diagnosis, guidance of local steroid injection and, together with pressure algometry, monitoring of the treatment of athletes with chronic jumper’s knee and Achilles tendinitis: a randomized, double-blind, placebo-controlled study. Scand J Rheumatol 2004;33(2):94–101. [30] Ohberg L, Alfredson H. Ultrasound guided sclerosis of neovessels in painful chronic Achilles tendinosis: pilot study of a new treatment. Br J Sports Med 2002;36(3):173–7. [31] Ohberg L, Alfredson H. Sclerosing therapy in chronic achilles tendon insertional pain-results of a pilot study. Knee Surg Sports Traumatol Arthrosc 2003;11(5):339–43. [32] Hoksrud A, Ohberg L, Alfredson H, Bahr R. Ultrasound-guided sclerosis of neovessels in painful chronic patellar tendinopathy: a randomized controlled trial. Am J Sports Med 2006. [33] Alfredson H, Ohberg L. Neovascularisation in chronic painful patellar tendinosis–promising results after sclerosing neovessels outside the tendon challenge the need for surgery. Knee Surg Sports Traumatol Arthrosc 2005;13(2):74–80. [34] Jacobson JA, Lenchik L, Ruhoy MK, et al. MR imaging of the infrapatellar fat pad of Hoffa. Radiographics 1997;17(3):675–91. [35] Saddik D, McNally EG, Richardson M. MRI of Hoffa’s fat pad. Skeletal Radiol 2004;33(8):433–44. [36] Garcia-Valtuille R, Abascal F, Cerezal L, et al. Anatomy and MR imaging appearances of synovial plicae of the knee. Radiographics 2002;22(4):775–84. [37] Boles CA, Butler J, Lee JA, et al. Magnetic resonance characteristics of medial plica of the knee: correlation with arthroscopic resection. J Comput Assist Tomogr 2004;28(3):397–401. [38] Bae DK, Nam GU, Sun SD, Kim YH. The clinical significance of the complete type of suprapatellar membrane. Arthroscopy 1998;14(8):830–5. [39] Adachi N, Ochi M, Uchio Y, et al. The complete type of suprapatellar plica in a professional baseball pitcher: consideration of a cause of anterior knee pain. Arthroscopy 2004;20(9):987–91. [40] Cothran RL, McGuire PM, Helms CA, et al. MR imaging of infrapatellar plica injury. AJR Am J Roentgenol 2003;180(5):1443–7. [41] Boyd CR, Eakin C, Matheson GO. Infrapatellar plica as a cause of anterior knee pain. Clin J Sport Med 2005;15(2):98–103. [42] Fredericson M, Cookingham CL, Chaudhari AM, et al. Hip abductor weakness in distance runners with iliotibial band syndrome. Clin J Sport Med 2000;10(3):169–75. [43] Elias DA, White LM. Imaging of patellofemoral disorders. Clin Radiol 2004;59(7):543–57. [44] Fulkerson JP. Patellofemoral pain disorders: evaluation and management. J Am Acad Orthop Surg 1994;2(2):124–32. [45] Wittstein JR, Bartlett EC, Easterbrook J, Byrd JC. Magnetic resonance imaging evaluation of patellofemoral malalignment. Arthroscopy 2006;22(6):643–9.