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Patellofemoral Pain in Female Athletes

Tumia, Nezar M.B.Ch.B., FRCS*; Maffulli, Nicola M.D., M.S., Ph.D., FRCS(Orth)

Section Editor(s): Maffulli, Nicola M.D.

Sports Medicine and Arthroscopy Review: March 2002 - Volume 10 - Issue 1 - p 69-75
The Female Athlete

Patellofemoral pain syndrome (PFPS) is the most common complaint in female athletes. There are clear structural, biomechanical, sociological, and hormonal differences between women and men that contribute to an increased incidence of PFPS in women. Unfortunately, the etiology of PFPS is still not well understood. It may represent the end result of multiple intrinsic and extrinsic factors. Three major factors can be attributed to its etiology: quadriceps muscle imbalance and/or weakness, lower extremity and patellofemoral malalignment, and physical overload of patellofemoral joint. Exclusion of intraarticular pathology is essential to diagnose PFPS. Imaging can be helpful to diagnose any associated patellar instability. Conservative management, a mainstay in management, includes rehabilitation focusing on proprioception, strength, flexibility, endurance, and a gradual progression of the musculoskeletal load. Various training programs are in use, including isometric open kinetic chain exercises and eccentric closed kinetic chain exercises. Surgery may be required if conservative measures fail. Various procedures have been described, including lateral retinaculum release and proximal and distal realignment procedures.

From *Department of Orthopedic Surgery, University of Aberdeen Medical School, Polwarth Building, Foresterhill, Aberdeen AB25 2ZD, Scotland; and the †Department of Trauma and Orthopedic Surgery, Keele University School of Medicine, North Staffordshire Hospital, Thornburrow Drive, Hartshill, Stoke on Trent, Staffordshire, ST4 7QB, England.

Address correspondence and reprint requests to: Nicola Maffulli, M.D., Department of Trauma and Orthopedic Surgery, Keele University School of Medicine, North Staffordshire Hospital, Thornburrow Drive, Hartshill, Stoke on Trent, Staffordshire, ST4 7QB, England. E-mail:

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The term “anterior knee pain” encompasses all pain-related problems of the anterior portion of the knee, and covers terms such as chondromalacia patella, patellofemoral arthralgia, patellar pain, patellar pain syndrome, and patellofemoral pain. Therefore, excluding anterior knee pain resulting from intraarticular pathologies, patellar tendinopathy, peripatellar bursitis, the plica syndrome, Sinding Larsen and Osgood Schlatter lesions, and other rarely occurring conditions, remaining patients with a clinical presentation of anterior knee pain could be diagnosed with patellofemoral pain syndrome (PFPS). 2,30

Recently, there has been an increase in female participation in recreational and competitive sports, leading to an increased awareness of overuse knee injuries. Anterior knee pain is the most common knee complaint. It constitutes 25% of knee injuries and 5% of all injuries seen in a British sports injury clinic. 1,4 Anterior knee pain can be very frustrating for the patient and the orthopedic surgeon or sport medicine physician, and can dramatically curtail or even end the patient's participation in sports. Anterior knee pain is more common in women. 1,3,4,17–19,21,26 Female athletes demonstrate a higher incidence of knee injuries than male athletes when participating in the same sports. 17–21,26

There are clear differences between men and women that contribute to the increased risk of developing PFPS, including structural differences in pelvis width, femoral anteversion, quadriceps angle, tibial torsion, quadriceps strength, knee joint ligament laxity, and proprioception. 2–5,18–20 Sociologic differences, such as work and postural factors, including sitting with legs adducted and wearing high heels, which necessitate slight knee flexion during walking, also contribute to the risk of developing PFPS. 22,23 Hormonal differences in the form of hormonal fluctuations, and the effect of estrogen and other female sex hormones on connective tissue, may also contribute. 3,24,25

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Anatomy and biomechanics

The patellofemoral joint (PFJ) consists of the patella, the distal and anterior parts of the femur, their articular surfaces, and the surrounding structures. The function of the patella is to increase the lever arm of the quadriceps, allowing it to work more effectively to extend the knee. Three-quarters of the articular surface of the patella are covered by thick hyaline cartilage.

Patellar motion during knee flexion and extension is not only proximal and distal translation. In addition, the patella also slightly tilts and rotates, so that the whole of its articular surface articulates with the femoral trochlea. Patellofemoral compression forces increase with increasing knee flexion up to 90°, reaching up to eight times the body's weight. 2,4,27,34

The shape of the patella, the femoral trochlea, and the patellar retinaculum act as passive stabilizers of the patella. The dynamic stabilizers include all the periarticular muscles of the knee. The force vector of the quadriceps muscle is lateral to the longitudinal axis of the knee joint, forming an angle called the “Q angle.” There is a wide individual variation in the Q angle of asymptomatic individuals, but generally it is wider in females because of a wider pelvis, increased femoral anteversion, and excessive tibial torsion. The Q angle in an individual can be bilaterally asymmetric. 28 The vastus medialis obliquus (VMO) muscle, which has its own nerve supply, pulls the patella medially when the knee is at an angle of 65°. 2–4,26–29 Generally, women inherently have more excessive knee joint laxity than men. This appears to contribute to diminished joint proprioception, which predisposes to connective tissue and ligament injury. 17,31

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Etiology of PFPS

Despite the high incidence of PFPS, its causes have remained enigmatic. There is no single factor causing PFPS, but it may represent the end result of numerous pathophysiologic processes. Various authors have cited both extrinsic and intrinsic parameters as etiologic factors. 1–3,6,11,32,33 Extrinsic factors include excessive exercise, overtraining, training errors, poor equipment, and ignorance of the condition. Intrinsic factors include lower limb malalignment, leg length discrepancy, muscle imbalance, and joint laxity.

Malalignment of the lower extremity found in women with PFPS includes femoral neck anteversion, genu valgum, genu recurvatum, increased Q angle, tibia vara, hyperpronation of the forefoot, and leg length discrepancy (Fig. 1). 3–6,32,34–38 A high Q angle creates a greater valgus vector and increases the lateral pull of the patella, which, in its turn, causes increased pressure on the lateral facet of the patella. This can lead to patellar subluxation, cartilage softening, and retinacular stress, and may contribute to perpetuate PFPS. However, clinical studies have shown that the Q angle does not vary significantly between patients with PFPS and healthy individuals. 39–41 Foot pronation is an important predisposing factor to develop PFPS in females. Excessive foot pronation, which is functional rather than structural (as in pes planus), leads to an increase in the Q angle and anterior displacement of the proximal tibia that causes knee flexion, thereby overloading the PFJ. 42,43

FIG. 1

FIG. 1

Patellofemoral malalignment has been described as a major cause of anterior knee pain in young adults. 44–46 Three different patterns of patellar malalignment are described: subluxation without tilting, subluxation with tilting, and tilting without subluxation. Chronic lateral subluxation of the patella leads to shortening of the lateral retinaculum. With knee flexion, the patella migrates medially into the femoral trochlea, and the lateral retinaculum sustains excessive stretching, which may cause nerve damage and lead to PFPS. 7,32,47–49 Various limits of normality of patellar tracking have been reported, but none have been shown unequivocally to be a significant factor in the etiology of PFPS. 2,10,12,50 Patella alta has been described as a possible contributing factor in patellar instability, 46 and therefore predisposes to PFPS.

Quadriceps muscle imbalance or hypotrophy have been frequently cited as etiologic factors of PFPS. 3,4,16–19,32,35,40,41,51–53 Various patterns of imbalance have been described. The abnormal relationship in the activation pattern of the VMO and vastus lateralis (VL) can alter the dynamics of the PFJ. The electrical activity of the VMO fibers is twice that of the rest of the quadriceps muscle group. 54 The imbalance in this 2:1 ratio may lead to lateral tracking of the patella by the action of the VL during knee extension. 32 Thomee et al. 41 reported reduced strength and lower EMG activity of VMO in patients with PFPS. Bennett et al. 8 reported the differences in VMO orientation in females, which make the patella more prone to instability.

Decreased quadriceps muscle flexibility creates high patellofemoral stresses during sporting or daily life activities, and therefore predisposes to PFPS. 9

Many rehabilitation regimens concentrate on the VMO because of its medializing action on the patella. However, neither exercises proposed to selectively activate the VMO muscle, nor patellar taping, improve the VMO–VL ratio. 10 The significance of muscle activity in closed vs. open kinetic chain exercises has not been extensively studied, and the results of the available studies are inconclusive. 8,9 Further investigations should study the significance of muscular imbalances and clarify whether they are a cause or effect (or both) of PFPS.

Physical overload of the PFJ is regarded as a risk factor for developing PFPS in athletes. 2,51–55,57 Classically, patients with anterior knee pain are more likely to be involved in competitive sports than their age-matched controls, and pain is associated with increased physical activity. 4,18,26 The biomechanics of the PFJ may induce a higher risk of overuse in some individuals, and a combination of malalignment and diminished muscle function may increase this risk. Excessive body load, change in training habits (including increased training, and poor equipment and training technique can lead to PFPS, by overloading the PFJ and exceeding functional adaptive structural responses. 54,55 After running, the concentration of proteoglycan fragments increases in the knee joint, possibly a result of mechanical overloading or a high turnover rate of the cartilage matrix. 56 In athletes, PFPS has been considered an overuse injury, but the athletic activity is not always a predictor of symptoms. 10,50–53,57

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The most common symptoms in patients with PFPS are pain, crepitus, giving way, and catching, with occasional stiffness and swelling.

Pain is reported as peripatellar and/or retropatellar pain, ranges from mild to severe, and is often aggravated by physical activity, especially downhill and speed running. The source of patellofemoral pain in patients with PFPS is unclear, as there are no nerve endings in the articular cartilage, although the subchondral bone is innervated. Reactive synovitis is a possible source of pain, and the patellar retinacula are potential sources of patellofemoral pain. 7 Increased physical activities could result in peripatellar soft tissue irritation, and pain may then originate from retinacular nerve endings, with malalignment and overuse as magnifying factors.

Crepitus is not always present in patients with PFPS, and can be present without pain or other symptoms.

Giving way of the limb in patients with PFPS results from a sudden relaxation due to pain inhibition of the quadriceps during loading of the PFJ while standing, and should be distinguished from giving way because of ligamentous instability or from a meniscal lesion. Transient catching is often reported, but it is not due to intraarticular pathology.

Weakness of the quadriceps is common in patients with PFPS. The decreased torque and reduction in EMG activity in patients with PFPS, especially with eccentric knee extension, may result from quadriceps inhibition at heavy patellofemoral loads, such as in eccentric knee extensions and single leg vertical jumps. This inhibition and the ability to develop high force torque in different situations should be considered when developing treatment programs for patients with PFPS. 7,9,12,13 Swelling is mild, intermittent, and rare.

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Plain radiographs should be obtained in patients with patellar maltracking, or when symptoms continue despite appropriate management, to exclude pathology such as osteochondritis dissecans, bipartite patella, and neoplasm. Standard radiographs should include a standing antero-posterior view, which show varus and valgus deviations, patellar height, condylar width, and tibial tubercle location. True lateral view allows measuring the vertical height of the patella 44,45 (Fig. 2) and the shape of the femoral trochlea. 8,58 Skyline view of the patella at 30° of knee flexion shows the morphology of the PFJ, including femoral trochlea (the trochlear angle normally >124° and <145°) (Fig. 3A) and patellar subluxation and dysplasia (congruence angle). 8

FIG. 2

FIG. 2

FIG. 3

FIG. 3

Computed tomography gives more details of lower limb alignment, such as femoral anteversion, external tibial rotation, trochlear angle, external trochlear inclination angle, normally 30° (Fig. 3B), and patellar inclination angle (Fig. 3C). 8,59

Magnetic resonance imaging can be useful to evaluate patellar tracking abnormalities, the articular cartilage, quadriceps muscle, and lateral retinacula, 60 but its role in the management of PFPS is unclear.

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It is not surprising that so many treatment regimens are in use, as basic scientific knowledge is lacking, and no strong evidence-based protocols based on the nature and etiology of PFPS are available. Unfortunately, there is little scientific evidence on which to base management of the condition. Initially, PFPS should be managed nonoperatively, and the most frequently recommended management regimen is rehabilitation. 2–4,9,10,12–16,50–53 Surgery is rarely indicated. Key factors in a rehabilitation program include strength, flexibility, proprioception, endurance, functional training, and a gradual progression of the musculoskeletal load without increasing the symptoms. 9,13 However, the effects of an exercise program for PFPS have not been scientifically and systematically documented. Variable success rates are reported, with great variability among studies in diagnosis, physical activity level, gender, and age of the patients. 50–53 Compliance is important, and even in well-supervised exercise programs, compliance is poor.

In general, a rehabilitation program should include (1) education; (2) symptomatic control; (3) a progressive resistance program of isometric quadriceps and iso-inertial hamstrings exercises; (4) a graduated running program; and (5) a maintenance program.

Isometric training (open kinetic chain exercises) for patients with moderate PFPS, and a soft brace for those with symptoms that are more serious, is recommended. 11 Eccentric isokinetic (closed kinetic chain exercises) exercises are currently in fashion, but closed kinetic chain exercises are only a little more effective than open kinetic chain exercises in reducing pain and increasing function. 9,62 However, both closed and open kinetic chain exercise programs show similar significant functional improvements over a control group with no treatment. 13,14,61 Better muscle activation with increased motor unit recruitment and better physiologic activation of the vastus medialis muscle may thus be achieved.

Some authors propose a comprehensive approach, based on standardized information, pain monitoring, and an individually designed progressive exercise program. 9,11,13,61 Significant pain reduction and strength and physical activity level improvements are seen after 12 weeks of treatment. 8,14,61 Improvements may be a result of time, the standardized information, the pain monitoring system, the gradually progressive training program, and the reduced physical activity.

The exercises may modify the influx of afferent signals with reduced reflex inhibition and possible increase in endorphins. 61 Training might also induce increased diffusion of nutrients to the articular cartilage through cyclical loading and unloading of the PFJ, and improved nutrition to surrounding joint structures and muscles with increased vascularity. 8,11,61 Thus, the training program may produce beneficial effects on the PFJ, as adaptive changes can be seen in muscles, tendons, ligaments, and the cartilage after regularly repeated, slowly progressing, nonstrenuous rehabilitation. However, this is only speculative, with limited scientific support. Strenuous exercises may cause a gradual breakdown of the musculoskeletal tissue, with deleterious effects and increased pain. The increased physical activity after treatment may contribute to the further improvements in symptoms and muscle function seen in the longer term.

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Patellar taping

Patellar taping was originally developed to create a mechanic medial shift to the patella, thus centralizing it and thereby improving patellar tracking. 63 However, patellar taping does not improve the EMG activity ratio between the VMO and the VL muscles. Studies on patellar taping have shown variable results. 14,15,61–65 Some authors reported no advantages in adding taping to a well-planned rehabilitation program. 14,61,63 In the appropriate hands, and with the right technique, patellar taping has been successful. 15 However, more basic and clinical research, with longitudinal andrandomized controlled trials, should be performed to clarify its role in PFPS.

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More than 100 surgical procedures have been described for the treatment of patients with PFPS when nonoperative management has failed. Most of these operations have not been evaluated with randomized controlled trials. Surgery is aimed at correcting malalignment (realignment procedures), or other abnormalities of the knee extensor mechanism or the injured cartilage. 4,16

Lateral release: This procedure aims to release the pressure between the lateral patellar facet and trochlea resulting from tight lateral retinaculum. The lateral retinaculum is sectioned longitudinally, 2 cm from the patellar edge. It can be performed arthroscopically, and can be combined with other realignment procedures. 4,66 Its main indications are (1) abnormally high lateral patellar compression with tenderness and tightness of the lateral retinaculum, and lateral patellar tilt; (2) degenerative disease of the patellofemoral joint with lateral patellar tilt; and (3) persistent patellofemoral pain associated with a lateral traction osteophyte at the insertion of the lateral retinaculum into the patella. The procedure is not recommended for prepubertal patients, or in cases of severe patellofemoral osteoarthrosis with normal patellar tracking. Results have often been unpredictable, with a reported rate of satisfactory results between 20% and 92% of patients. Its biomechanical effects are unclear. 4,67,68

Proximal realignment: Several different techniques for proximal soft tissue realignment have been described, and are indicated in patients who (1) are skeletally immature and have a history of recurrent dislocations; (2) have an increased congruence angle with patellofemoral pain; and (3) have dysplastic femoral trochlea and poor medial patellar support of the VMO muscle, with recurrent patellar subluxations or dislocations. Satisfaction is normally high, but these procedures are now rarely used in isolation. 69–71

Distal realignment: These procedures are most often used in patients with recurrent patellar subluxation or dislocation, and less for patellofemoral pain. They consist of transfer of the tibial tubercle. The indications are (1) persistent patellofemoral pain combined with excessive patellar tilt or subluxation or increased congruence angle; (2) lateral patellar degenerative joint disease with increased Q angle; and (3) failed lateral release procedure, especially in patients with significant lateral tilt or subluxation. Transfer of the tibial tubercle is contraindicated in skeletally immature patients, given the high risk of development of genu recurvatum in this age group. Satisfaction is high, but long-term results are unclear.

Anteromedial tibial tubercle transfer and elevation: The procedure is indicated in patients with malalignment, increased Q angle, and mild-to-moderate PFJ osteoarthrosis. 72,73

Elevation of the tibial tubercle: Marked decrease of patellofemoral compression forces is produced by elevation of the tibial tubercle of 1.2 cm to 2.5 cm. The main indication for this procedure is with moderate degeneration joint disease of the PFJ that is unresponsive to conservative management. Results have been unpredictable, and the long-term results unsatisfactory; this procedure is now rarely used for the treatment of PFPS.

Articular cartilage procedures: These procedures include open or arthroscopic patellar shaving, local excision of defects with drilling of the subchondral bone, facetectomy, and transplantation of autologous chondrocytes. The major benefit of arthroscopic interventions might well be the dilution effect with washout of the debris from the knee joint.

No comparative studies on these procedures are available, and the results are often satisfactory in the short term, but less is known about the long-term outcomes. 4,16

Patellectomy: Excision of the patella should be considered the last resort to treat patellofemoral diseases, as it may result in a considerable decrease in functional ability. The main indication is severe patellofemoral pain after a failed realignment in patients younger than 40 years. Contraindications are tibial–femoral disorders and patellofemoral pain of unknown origin.

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In general, patellofemoral pain syndrome is more common in women, due to the clear differences in the biomechanics of the lower extremities to men. Risk factors for development of PFPS include knee joint malalignment, selective disturbances within the quadriceps muscle, and increased physical overload. Patellofemoral pain syndrome is a therapeutic challenge. Standardized information and reduced and modified physical activity levels will suffice in most PFPS patients with mild symptoms. Avoidance of excessive physical exercise and prolonged sitting with knees flexed seem to be most effective. However, patients with PFPS should not completely abstain from physical activities, although they should modify them.

Women with PFPS need to be patient. Improvements occur slowly, especially at the beginning, and the positive effects of rehabilitation take time. Rehabilitation should progress gradually, and the success of a management regime depends on adjusting the exercises of the rehabilitation program to the patient's symptoms and needs.

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1. Devereaux MD, Lachmann SM. Athletes attending a sports injury clinic: a review. Br J Sports Med 1983; 17:137–142.
2. Thomee R, Augustsson J, Karlsson J. Patellofemoral pain syndrome: a review of current issues. Sports Med 1999; 28:245–262.
3. Fulkerson JP, Arendt EA. Anterior knee pain in females. Clin Orthop 2000; 372:69–73.
4. Baker MM, Juhn MS. Patellofemoral pain syndrome in the female athlete. Clin Sports Med 2000; 19:315–329.
5. Hvid I, Andersen LI. The quadriceps angle and its relation to femoral torsion. Acta Orthop Scand 1982; 53:577–579.
6. Bennett W, Dougherty N, Hallisey M, Fulferson J. Insertion orientation of terminal vastus lateralis obliquus and vastus medialis obliquus muscle fibers in human knees. Clin Anat 1993; 6:129–134.
7. Sanchis-Alfonso V, Rosello-Sastre E. Immunohistochemical analysis for neural markers of the lateral retinaculum in patients with isolated symptomatic patellofemoral malalignment. Am J Sports Med 2000; 28:725–731.
8. Beaconsfield T, Pintore E, Maffulli N, Petri GJ. Radiological measurements in patellofemoral disorders: a review. Clin Orthop 1994; 308:18–28.
9. Witvrouw E, Lysens R, Bellemans J, Peers K, Vandersteraeten J. Open versus closed kinetic chain exercises for patellofemoral pain. Am J Sports Med 2000; 28:687–694.
10. 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 1998; 30:1572–1577.
11. Witrouw E, Lysens R, Bellemans J, Cambier D, Vandersteraeten J. Intrinsic risk factors for the development of anterior knee pain in an athletic population. Am J Sports Med 2000; 28:480–488.
12. Powers CM. Rehabilitation of patellofemoral joint disorders: a critical review. J Orthop Sports Phys Ther 1998; 28:345–354.
13. Brody LT, Thein JM. Nonoperative treatment for patellofemoral pain. J Orthop Sports Phys Ther 1998; 28:336–44.
14. Clark DI, Downing N, Mitchell J, Coulson L, Syzpryt EP, Doherty M. Physiotherapy for anterior knee pain: a randomized controlled trial. Ann Rheum Dis 2000; 59:700–704.
15. Ernst GP, Kawaguchi J, Saliba E. Effect of patellar taping on knee kinetics of patients with patellofemoral pain syndrome. J Orthop Sports Phys Ther 1999; 29:661–67.
16. Juhn MS. Patellofemoral pain syndrome: a review and guidelines for treatment. Am Fam Physician 1999; 60:2012–22.
17. Rozzi LS, Lephart SM, Gear WS, Fu FH. Knee joint laxity and neuromuscular characteristics of male and female soccer and basketball players. Am J Sports Med 1999; 27 (3):312–19.
18. Hewett TE, Lindenfeld TN, Riccobene JV, Noyes FR. The effect of neuromuscular training on the incidence of knee injury in female athletes. Am J Sports Med 1999; 27 (6):699–705.
19. Hewett TE. Neuromuscular and hormonal factors associated with knee injuries in female athletes: strategies for intervention. Sports Med 2000; 29 (5):313–27.
20. Arendt E, Dick R. Knee injury patterns among men and women in collegiate basketball and soccer: NCAA data and review of literature. Am J Sports Med 1995; 23:694–701.
21. Neely FG. Intrinsic risk factors for exercise-related lower limb injuries. Sports Med 1998; 26 (4):253–63.
22. Bergenudd H, Nilsson B, Lindgrade F. Knee pain in middle age and its relationship to occupational work load in psychosocial factors. Clin Orthop 1989; 245:210–15.
23. Cooper C, McAlindon T, Coggon D, Egger P, Dieppe P. Occupational activity and osteoarthritis of the knee. Ann Rheum Dis 1994; 53:90–3.
24. Hassager C, Jensen LT, Johanson JS, Riis BJ, Melkko J, Podenphant J, Risteli L, Christiansen C, Risteli J. The carboxy-terminal propeptide of type I procollagen in serum as a marker of bone formation: the effect of nandrolone decanoate and female sex hormones. Metabolism 1991; 40 (2):205–8.
25. Liu SH, Al-Shaikh RA, Panossian V, Finerman GA, Lane JM. Estrogen affects the cellular metabolism of the anterior cruciate ligament: a potential explanation for female athletic injury. Am J Sports Med 1997; 25 (5):704–9.
26. Hutchinson MR, Ireland ML. Knee injuries in female athletes. Sports Med 1995; 19 (4):288–302.
27. Koh J, Grabiner MD, De-Swart RJ. In vivo tracking of human patella. J Biomech 1992; 25:637–43.
28. Livingston LA, Mandigo JL. Bilateral Q angle asymmetry and anterior knee pain syndrome. Clin Biomech 1999; 14 (1):7–13.
29. Holmes SW, Clancy WG. Clinical classification of patellofemoral pain and dysfunction. J Orthop Sports Phys Ther 1998; 28 (5):299–306.
30. Johnson RP. Anterior knee pain in adolescents and young adults. Curr Opin Rheumatol 1997; 9 (2):159–64.
31. Huston LJ, Wojtys EM. Neuromuscular performance characteristics in elite female athletes. Am J Sports Med 1996; 24:427–36.
32. Sanchis-Alfonso V, Rosello-Sastre E, Martinez-Sanjaun V. Pathogenesis of anterior knee pain syndrome and functional patellofemoral instability in the active young. Am J Knee Surg 1999 Winter;12(1):29–40.
33. Clement D, Taunton J, Smart G, McNicol K. A survey of overuse running injuries. Physician Sports Med 1981; 9:47–58.
34. Amis AA, Farahmand F. Biomechanics of the extensor mechanism. The Knee 1996; 3:73–81.
35. Boucher JP, King MA, Lefebvre R, Pepin A. Quadriceps femoris muscle activity in patellofemoral pain syndrome. Am J Sports Med 1992; 20 (5):527–32.
36. Huberti HH, Hayes WC. Patellofemoral contact pressures. J Bone Joint Surg Am 1984; 66:715–724.
37. Messier SP, Davis SE, Curl WW, Lowery RB, Pack RJ. Etiologic factors associated with patellofemoral pain in runners. Med Sci Sports Exerc 1991; 23 (9):1008–15.
38. Staheli LT. Rotational problems in the lower extremities. Orthop Clin North (Am) 1987; 18:503–12.
39. Caylor D, Fites R, Worrell TW. The relationship between quadriceps angle and anterior knee pain syndrome. J Orthop Sports Phys Ther 1993; 17:11–16.
40. Fairbank JCT, Pynsent PB, Van Poortvliet JA, Phillips H. Mechanical factors in the incidence of knee pain in adolescents and young adults. J Bone Joint Surg (Br) 1984; 66 (5):685–93.
41. Thomee R, Renstrom P, Karlsson J. Patellofemoral pain syndrome in young women. II. Muscle function in patients and healthy controls. Scand J Med Sci Sports 1995; 5 (4):245–51.
42. Wallace LA, Sullivan MF. Foot alignment and knee pathology. In: Mangine RE, ed. Clinics in Physical Therapy: Physical Therapy of the Knee. 2nd ed. New York, NY: Churchill Livingstone, 1995:87–110.
43. Walsh WM. Patellofemoral joint. In: De Lee JC, Drez Jr, D eds. Orthopaedic Sports Medicine: Principles and Practice. Philadelphia: W.B. Saunders Company, 1994:1163–1248.
44. Insall J, Bullough PG, Burstein AH. Proximal `tube` realignment of the patella for chondromalacia patellae. Clin Orthop 1979; 144:63–9.
45. Insall J. `Chondromalacia patellae`: patellar malalignment syndrome. Orthop Clin North Am 1979; 10 (1):117–27.
46. Insall J, Aglietti P, Tria Jr. AJ Patellar pain and incongruence. II: Clinical application. Clin Orthop 1983; 176:225–32.
47. Fulkerson JP, Tenant R, Jaivin JS, Grunnet M. Histologic evidence of retinacular nerve injury associated with patellofemoral malalignment. Clin Orthop 1985; 197:196–205.
48. Mori Y, Fujimoto A, Okumo H, Kuroki Y. Lateral retinaculum release in adolescent patellofemoral disorders: its relationship to peripheral nerve injury in lateral retinaculum. Bull Hosp Jt Dis 1991; 51:218–29.
49. Sanchis-Alfonso V, Rosello-Sastre E, Monteagudo-Castro C, Esquerdo J. Quantitative analysis of nerve changes in the lateral retinaculum in patients with isolated symptomatic patellofemoral malalignment. Preliminary study. Am J Sports Med 1998; 26:703–709.
50. 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 1994; 26:289–296.
51. James S. Chondromalacia in the adolescent. In Kennedy J, ed. The Injured Adolescent Knee. Baltimore: William & Wilkins, 1977:205–251.
52. Bentley G, Dowd G. Current concepts of etiology and treatment of chondromalacia patellae. Clin Orthop 1984; 189:209–28.
53. Kujala UM, Kvist M, Osterman K. Knee injuries in athletes – review of exertion injuries and retrospective study of outpatient sports material. Sports Med 1986; 3:447–60.
54. Johansson C. Injuries in elite orienteers. Am J Sports Med 1986; 14:410–15.
55. Clement D, Taunton J, Smart G, McNicol K. A survey of overuse running injuries. Physician Sports Med 1981; 9:47–58.
56. Roos H, Dahlberg L, Lohmander L. Proteoglycan fragments in knee joint fluid after exercise. Scand J Med Sci Sports 1993; 2:127–30.
57. Rolf C. Overuse injuries of the lower extremity in runners. Scand J Med Sci Sports 1995; 5:181–90.
58. Brattstrom H. Shape of the intercondylar groove normally and in recurrent dislocation of patella: a clinical and X ray anatomic investigation. Acta Orthop Scand 1964; 68(suppl):1–32.
59. Schutzer SF, Ramsby GR, Fulkerson JP. The evaluation of patellofemoral pain using computerized tomography: a preliminary study. Clin Orthop 1984; 204:286–93.
60. Shellock FG, Mink JH, Deutsch AL. Patellar tracking abnormalities: clinical experience with kinematic MRI imaging in 130 patients. Radiology 1989; 172:799–804.
61. Thomee R. A comprehensive treatment approach for patellofemoral pain syndrome in young women. Phys Ther 1997; 77:1690–1703.
62. Crossley K, Bennell K, Green S, McConnell J. A systematic review of physical interventions for patellofemoral pain syndrome. Clin J Sports Med 2001; 11:103–110.
63. McConnell J. The management of chondromalacia patellae: a long term solution. Aust J Physiother 1986; 32:215–23.
64. Bockrath K, Wooden C, Worrell T, Ingersoll CD, Farr J. Effect of patellar taping on patellar position and perceived pain. Med Sci Sports Exerc 1993; 25:989–92.
65. Gilleard W, Mc Connell J, Parsons D. The effect of patellar taping on the onset of vastus medialis obliquus and vastus lateralis muscle activity in persons with patellofemoral pain. Phys Ther 1998; 78:25–32.
66. Fu FH, Maday MG. Arthroscopic lateral release and the lateral patellar compression syndrome. Orthop Clin North Am 1992; 23:601–612.
67. Fulkerson JP, Hungerford DS, eds. Disorders of the patellofemoral joint. 2nd ed. Baltimore: Williams & Wilkins, 1990;117–119.
68. Hallisey MJ, Doherty N, Bennett WF, Fulkerson JP. Anatomy of the junction of the vastus lateralis tendon and the patella. J Bone Joint Surg (Am) 1987; 69:545–549.
69. Beals RK, Buehler K. Treatment of patellofemoral instability in childhood with creation of a femoral sulcus. J Pediatr Orthop 1997; 17:516–519.
70. Scuderi G, Cuomo F, Scott WN. Lateral release and proximal realignment for patellar subluxation and dislocation. J Bone Joint Surg 1988; 70:856–861.
71. Vahasarja V, Kinnunen P, Lanning P, Serlo W. Operative realignment of patellar malalignment in children. J Pediatr Orthop 1995; 15:281–285.
72. Fulkerson JP. Anteromedialization of the tibial tuberosity for patellofemoral malalignment. Clin Orthop 1983; 177:176–81.
73. Fulkerson JP, Becker GJ, Meaney JA, Miranda M, Folck MA. Anteromedial tibial tubercle transfer without bone graft. Am J Sports Med 1990; 18:490–96.

Section Description

Nicola Maffulli, M.D., Guest Editor


Knee pain; Rehabilitation; Patellofemoral joint; Overuse injury

© 2002 Lippincott Williams & Wilkins, Inc.