Jumper's Knee

Updated: Mar 11, 2019
Author: Garrett Scott Hyman, MD, MPH; Chief Editor: Craig C Young, MD 



Blazina et al first used the term jumper's knee (patellar tendinopathy, patellar tendinosis, patellar tendinitis) in 1973 to describe an insertional tendinopathy seen in skeletally mature athletes,[1] although Sinding-Larson, Johansson, and Smillie once described this condition. Jumper's knee usually affects the attachment of the patellar tendon to the inferior patellar pole. The definition was subsequently widened to include tendinopathy of the attachment of the quadriceps tendon to the superior patellar pole or tendinopathy of the attachment of the patellar tendon to the anterior tuberosity of the tibia. The term jumper's knee implies functional stress overload due to jumping (see image below).

The proximal patellar tendon is most commonly affe The proximal patellar tendon is most commonly affected in jumper's knee.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Knee Pain Overview, Knee Injury, and Tendinitis.



United States

Jumper's knee is certainly one of the more common tendinopathies affecting skeletally mature athletes, occurring in as many as 20% of jumping athletes. With regard to bilateral tendinopathy, males and females are equally affected. With regard to unilateral tendinopathy, the male-to-female ratio is 2:1.

Functional Anatomy

The rectus femoris and 3 vasti muscles (ie, the vastus medialis, vastus lateralis, and vastus intermedius muscles) join in a common quadriceps tendon that inserts on the patella, the largest sesamoid bone in the human body. This same tendon is known as the patellar tendon from the inferior pole of the patella to its distal insertion at the tibial tuberosity.

Radiologic and histologic studies have shown that the posterior proximal fibers of the patellar tendon appear to be most commonly affected in jumper's knee.[2] Counter to these findings, however, biomechanical research has demonstrated that these posterior fibers can withstand greater tensile strains before failing, compared with the anterior fibers.[3]

Sport-Specific Biomechanics

Risk factors and biomechanics

Jumper's knee is believed to be caused by repetitive stress placed on the patellar or quadriceps tendon during jumping. It is an injury specific to athletes, particularly those participating in jumping sports such as basketball,[4, 5, 6, 7, 8] volleyball,[7, 8, 9, 10] or high or long jumping.[7, 10] Jumper's knee is occasionally found in soccer players, and in rare cases, it may be seen in athletes in nonjumping sports, such as weight lifting and cycling.

Investigators have implicated sex, greater body weight, genu varum and genu valgum, an increased Q angle, patella alta and patella baja, and limb-length inequality as intrinsic risk factors.[11] However, the only biomechanical impairment prospectively linked to jumper's knee is poor quadriceps and hamstring flexibility.

Vertical jump ability, as well as jumping and landing technique, are believed to influence tendon loading.[4, 10, 12] Volleyball players with a natural ability for jumping high are at increased risk for developing jumper's knee.[13]

In a cohort of elite young volleyball players, male sex, volume of training, and match exposure were all noted to be risk factors. One third of boys aged 16-18 years developed the condition compared with 8% of girls.[14] In a cross-sectional survey of 891 nonelite athletes in the Netherlands, the prevalence of jumper's knee varied from 14.4% and 2.5% for different sports (eg, basketball, volleyball, handball, korfball, soccer, field hockey, and track and field). Younger age, taller body stature, higher body weight, and sport-specific loading characteristics of the knee extensor apparatus were all risk factors for developing jumper's knee.[15]

Overtraining and playing on hard surfaces have been implicated as extrinsic risk factors.

Interestingly, the patellar tendon experiences greater mechanical load during landing than during jumping because of the eccentric muscle contraction of the quadriceps. Therefore, eccentric muscle action during landing, rather than concentric muscle contraction during jumping, may exert the tensile loads that lead to injury.[16, 17]




Jumper's knee (patellar tendinopathy, patellar tendinosis, patellar tendinitis) commonly occurs in athletes who are involved in jumping sports such as basketball and volleyball. Patients report anterior knee pain, often with an aching quality. The symptom onset is insidious. Rarely is a discrete injury described. Usually, involvement is infrapatellar at or near the infrapatellar pole, but it may also be suprapatellar.

Depending on the duration of symptoms, jumper's knee can be classified into 1 of 4 stages, as follows:

  • Stage 1 – Pain only after activity, without functional impairment

  • Stage 2 – Pain during and after activity, although the patient is still able to perform satisfactorily in his or her sport

  • Stage 3 – Prolonged pain during and after activity, with increasing difficulty in performing at a satisfactory level

  • Stage 4 – Complete tendon tear requiring surgical repair


Physical examination may reveal the following findings:

  • Point tenderness at the inferior patellar pole, superior patellar pole, or tibial tuberosity

  • Hamstring and quadriceps tightness

  • Normal ligamentous stability of the knee during testing

  • Normal knee range of motion

  • Normal neurovascular examination

  • Normal hip and ankle examination

  • Intra-articular effusion of the knee (rare)


The cause of jumper's knee remains unclear.

Histologic specimens are devoid of inflammatory cells; therefore, the disease process probably rarely involves a true tendinitis. Histologic studies have found increased numbers of mast cells associated with vascular hyperplasia, as well as an increased number of apoptotic cells.[18]

Biomechanical research has shown that a greater tensile load is borne by the anterior fibers.[3] This observation contradicts the theory that jumper's knee is caused by repetitive tensile loading, given that the proximal posterior patellar tendon is routinely affected.

The degenerative "tendinosis" rather than inflammatory "tendinitis" model has prevailed since the 1970s. Hamilton and Purdam have proposed an adaptive model, whereby compressive rather than tensile loads occur at the proximal posterior aspect of the tendon, resulting in structural changes from altered biomechanical forces.[19] This model is said to account for the presence of the routinely found asymptomatic lesions, and perhaps the absence of inflammatory cells in histologic specimens.

Almekinders et al suggested that stress shielding by the anterior fibers may lead to degenerative change or tendon wear of the posterior ones due to compressive forces.[2] They also proposed that such stress shielding and/or compressive forces, rather than repetitive tensile loads, may be more important etiologic factors in insertional tendinopathy.





Laboratory Studies

See the list below:

  • The diagnosis of jumper's knee is based on the history and clinical findings. Laboratory and imaging tests are rarely necessary.

  • Laboratory studies are not indicated unless other potential causes, such as systemic, inflammatory, or metabolic disease, must be ruled out.

Imaging Studies

See the list below:

  • Radiographic imaging is not necessary to make the diagnosis of jumper's knee. Such imaging may be helpful for excluding other potential maladies.

  • Certain imaging findings do support the diagnosis. For instance, ultrasonography may show thickening and hypoechogenicity of tendon fibers.[19] Signs of hypervascularity may be seen with color Doppler ultrasonography. Plain x-ray may show a radiolucency at, or elongation of, the involved pole.

  • Ultrasonography and magnetic resonance imaging (MRI) are both highly sensitive for detecting tendon abnormalities in both symptomatic and asymptomatic athletes.[20, 21, 22, 23, 24] Therefore, a significant number of false-positive results makes routine testing impractical. The advent of less expensive, portable, musculoskeletal ultrasonography units, may allow for more liberal screening in some organizations.

  • Ultrasonography combined with color or power Doppler may demonstrate peritendinous neovascularization.[21, 22] Some investigators advocate sclerosing injections that target this neovascularization as a treatment for jumper's knee.[21, 25]

Other Tests

See the list below:

  • None are required.


See the list below:

  • None are required.



Acute Phase

Rehabilitation Program

Physical Therapy

Most patients with jumper's knee (patellar tendinopathy, patellar tendinosis, patellar tendinitis) respond to a conservative management program, such as the one suggested below.

  • Activity modification: Decrease activities that increase patellofemoral pressure (eg, jumping, squatting). Possibly initiate gentle eccentric loading activities.[16, 26, 27]

  • Cryotherapy: Apply ice for 20-30 minutes, 4-6 times per day, especially after activity.

  • Joint motion and kinematics assessment: Evaluate hip, knee, and ankle joint ranges of motion.

  • Stretching: Stretch (1) flexors of the hip and knee (hamstrings, gastrocnemius, iliopsoas, rectus femoris, adductors), (2) extensors of the hip and knee (quadriceps, gluteals), (3) the iliotibial band, and (4) the patellar retinaculum.

  • Strengthening: Strengthen muscles using closed kinetic chain and eccentric exercise (ie, single-leg squat descents). Jonsson and Alfredson found eccentric quadriceps strengthening on a decline board superior to concentric strengthening in terms of pain, treatment satisfaction, and return to play.[16] Kongsgaard et al demonstrated that eccentric squats on a decline board of 25º increases patellar tendon loading versus standard eccentric squats on a level surface.[26]

  • Sport-specific proprioceptive training and plyometrics

Ultrasonography or phonophoresis may decrease pain symptoms. A patellofemoral brace with a patellar cutout and lateral stabilizer or McConnell taping may improve patellar tracking and provide stability through augmentation of proprioception. Provide arch supports or orthotics to correct foot malalignments.

Stage I

The treatment of jumper's knee is often specific to the degree of involvement. Stage I, which is characterized by pain only after activity and no undue functional impairment, is often treated with cryotherapy. The patient should use ice packs or ice massage after terminating the activity that exacerbates the pain and later again that evening. If aching persists, a course of regularly prescribed anti-inflammatory medications should be administered for 10-14 days.

Often, cryotherapy and anti-inflammatories suffice in the first stage, although some cases relapse once the course of anti-inflammatories is completed. Long-term use of anti-inflammatories should be avoided in the young athlete. Local corticosteroid injections are not advised in stage I treatment. In addition, most competitive athletes do not agree to rest and immobilization, given that the condition does not affect their performance at this point. For this reason, use of a counterforce strap has been suggested to relieve some of the tension on the affected area and thereby ameliorate the symptoms.

A comprehensive physical therapy program should include aggressive quadriceps and hip flexor stretching along with progressive strengthening. Begin with closed kinetic strengthening exercises, such as lunges, leg presses, and squats. Focus is given to the eccentric phase with each activity. Strict attention to proper technique is important to reduce stress on the patellofemoral joint and patellar tendon and to allow for progressive strengthening.

The strengthening program should progress to proprioceptive and plyometric exercises. Plyometrics include activities, such as jump roping, within the patient's pain tolerance. A good warm-up activity before stretching and strengthening is important to increase blood flow and tissue compliance. An exercise bicycle can be used to perform aerobic warm-up exercises. If significant anterior knee pain occurs, the seat should be adjusted slightly higher to eliminate excessive and repetitive knee flexion loading.

Stage II

In stage II, the patient has pain both during and after activity but is still able to participate in the sport satisfactorily. The pain may interfere with sleep. At this point, activities that cause increased loading of the patellar tendon (eg, running, jumping) should be avoided.

A comprehensive physical therapy program, as discussed above in Stage I, should be implemented. For pain relief, the knee should be protected by avoiding high loads to the patellar tendon, and cryotherapy should continue. The athlete should be instructed in alternative conditioning.

Once the pain improves, therapy should focus on knee, ankle, and hip joint ranges of motion; flexibility; and strengthening. Eccentric strengthening (perhaps on a decline board) should be emphasized because eccentric contractions allow for a greater generation of force and simulate landing in many sports. Advanced therapy should include plyometrics and sport-specific training, as tolerated.

If the pain becomes increasingly intense and if the athlete becomes more concerned about his or her performance, a local corticosteroid injection may be considered. The physician should explain that the steroid could cause further tendon degeneration, and perhaps even rupture, if the athlete begins loading the tendon too quickly once the symptoms improve.

Stage III

In stage III, the patient's pain is sustained, and performance and sport participation are adversely affected. Although discomfort increases, therapeutic measures similar to those described above should be continued, along with abstinence from the inciting activity. Relative rest for an extended period (eg, 3-6 wk) may be necessary in stage III. The athlete should avoid only those activities that incite the pain to prevent deconditioning, and he or she should be encouraged to continue an aggressive alternative cardiovascular and strength-training program.

If the pain is refractory to these measures, the options are limited. One can either abandon participation in jumping sports and/or consider surgery. In a randomized controlled trial, Bahr et al demonstrated no difference in outcome between surgical and nonsurgical treatment for patients with grade III tendinopathy.[28] The authors advocated 12 weeks of eccentric quadriceps strengthening before considering tenotomy. Only approximately half of athletes in both the surgical and nonsurgical treatment groups were well enough to return to sport within 1 year.[28]

Stage IV

Stage IV involves tendon rupture that requires surgical repair.

Medical Issues/Complications

Knee immobilization is contraindicated because it results in stiffness and may lead to muscle or joint contracture, further prolonging an athlete's return to play.

Surgical Intervention

There is likely a limited role for surgical treatment of jumper's knee with some recent low level evidence studies demonstrating potential benefit from arthroscopic patellar release.[29, 30]

Three principal surgical procedures include drilling of the involved pole, tendon excision, and resection of the involved pole.

Drilling of the involved pole

The goal of drilling is to increase the vascular supply to the affected area. This should allow for healing of the affected tendon and improve pain and tenderness. However, this procedure has yielded disappointing results.

Tendon excision

The second procedure involves longitudinal excision of the involved tendon, with subsequent restructuring of the residual tendon. Excision need not be limited to the tendon, as the inferior pole of the patella may be removed as well. The advantage of this procedure is that it does not disrupt the continuity of the quadriceps mechanism and allows for a relatively rapid return to play. On the other hand, visualization of the area is rather poor, and the clinician may overlook degradation of the patellar or peripatellar area or at the intercondylar portion of the femur, or they may even overlook degenerative changes in the tendon itself. Results have been mixed; some patients improve whereas others have been unable to return to their previous level of performance despite prolonged rest.

Resection of the involved pole

The third procedure calls for resection of the involved pole of the patella after inspection of the undersurface of the patella, the corresponding patellar face of the femur, and the involved tendon. Reattachment of the involved tendon and reinforcement of the medial patellar retinaculum are also parts of this procedure.

As reported by Blazina et al, the principal benefit is that this resection allows complete assessment of the extensor mechanism and provides the most suitable bed for favorable reattachment of the involved tendon into a raw, bony surface.[1] In addition, a tendon with degradation in multiple locations is best treated with such a procedure, as it enhances visualization of the affected area. Although this is the most involved procedure, it is effective in select patients. Complete overhaul of the entire extensor mechanism, however, is not required in many cases.

Open tenotomy was compared with an eccentric strengthening regimen in a randomized, controlled trial.[28] The authors found both surgery and the eccentric strengthening provided equivalent benefit in terms of pain reduction and functional improvement and return to sport at 1 year.


Consultation with a physical medicine and rehabilitation specialist or an orthopedic specialist is recommended.

Other Treatment

Injection therapy for patellar tendinopathy

  • Consider injection therapies for patients with tendinopathy in whom conservative therapy has failed.  Injectate options include corticosteroids, platelet-rich plasma (PRP), high volume injection with saline, and dextrose-based prolotherapy.

  • PRP injections are placed into or adjacent to the diseased tendon region under image-guidance.  Most investigators perform a series of at least 2 injections, approximately 2 weeks apart.[31, 32]

  • High volume injections with saline often use ~30-40 ml at the interface between the tendon and the paratenon, in the region of neovascularization as seen on color Doppler with musculoskeletal ultrasound.

  • Never inject corticosteroid directly into the patellar tendon because of the potential for patellar tendon rupture.  When used, the usual corticosteroid dose is triamcinolone 40 mg/1 mL (Kenalog, Bristol-Myers Squibb Co, Princeton, NJ; Aristospan, Lek Pharmaceuticals Inc, Princeton, NJ). Inject 0.5-1 mL, with or without 0.5-1 mL of a local anesthetic agent.

  • Use aseptic technique; prepare the area with alcohol or povidone-iodine solution (Betadine, Alcon Laboratories, Inc. Fort Worth, Tex).

  • Direct the injection into the most symptomatic peritendinous area (usually at or near the infrapatellar pole).

  • Fredberg and colleagues demonstrated efficacy of ultrasound-guided peritendinous steroid injections.[33]

  • Avoid repetitive corticosteroid injections in any site, as well as injection directly into a tendon, because of the risk of tendon rupture.

  • Following the injection, the patient should ice the injection site 3 times per day, 20 minutes at a time, for 48 hours after the injection.

  • The patient should avoid any running or jumping activities for 10-14 days after the injection.

Zayni et al compared a single versus 2 injections of PRP in a randomized prospective series of elite and non-elite competitive athletes with chronic patellar tendinopathy and found that 2 injections provided superior results with 86% of athletes returning to prior level of sport participation.[32]

In a systematic review by Coombes et al, the effects of corticosteroid injections were noted to provide only short-term benefit in studies pertaining to patella tendinopathy.[34]

James and colleagues evaluated ultrasound-guided dry needling and autologous blood injections, with promising results, in persons symptomatic longer than 12 months.[35] Interestingly, neovascularity did not reduce, and even increased, in some tendons.

Ultrasonographic-guided sclerosing injections into the neovascularized patellar tendon have shown promise in reducing pain and improving function in elite Norwegian basketball, volleyball, and handball players.[25] However, few patients treated with sclerosing injections are cured, and most recreational and elite athletes persist with functional limitations beyond 2 years of follow-up.[36, 37]

Extracorporeal shock wave therapy (ESWT) provides comparable functional outcomes compared with surgery, according to Peers and colleagues.[38] ESWT was found to have no benefit over placebo in a randomized trial involving actively competing jumping athletes with symptoms for 3-12 months.[39]   Furia and colleagues found that a single application of low-energy ESWT was effective in a series of chronic patellar tendinopathy patients.[40]

Platelet-rich plasma injections (series of 2 over 2 weeks, ultrasound-guided, 2 mL volume) led to better results (outcome measures were VISA-P questionnaire and modified Blazina scale) at 6 and 12 months compared with ESWT (series of 3 treatments) in one randomized controlled trial. The two treatments were comparable in the short term (at 2 mo). Notably, no control group was included, and study participants could not be blinded.[41, 42, 43, 44, 45]

A study by Pestka et al that included 54 amateur and professional athletes with chronic patellar tendinopathy reported that arthroscopic patellar release resulted in complete recovery and return to preinjury exercise levels in 74.1% of the patients and that full return to sports was achieved after a median of 3.0 (range 0.5-12.0) months.[29] Another study reported superior outcomes for arthroscopic patellar release in patients younger than 30 years of age.[30]

Ultrasound-guided needle placement with application of a galvanic electrolytic current in and around a diseased patellar tendon was shown to provide superior functional outcomes over eccentric exercise and standard physiotherapy techniques alone.[46]   

Limited evidence also supports the use of sonographically-guided percutaneous ultrasonic tenotomy combined with PRP injection.[47]

Recovery Phase

Rehabilitation Program

Physical Therapy

An in-depth, stage-specific description of a conservative therapy program is described above (see Acute Phase). In brief, in the recovery phase, the athlete and therapist should work to restore pain-free joint range of motion and muscle flexibility, symmetric strength in the lower extremities, and joint proprioception. Sport-specific training, including high-level plyometric exercises, should then be initiated.

Surgical Intervention

Surgical intervention is indicated for stage IV, as well as refractory stage III tendinopathy (see Acute Phase above).

Maintenance Phase

Rehabilitation Program

Physical Therapy

An in-depth, stage-specific description of a conservative therapy program is described above (see Acute Phase). Briefly, once in the maintenance phase, the athlete should complete a sport-specific training program before returning to competition. The physician and physical therapist can assist the athlete in determining when to return to competition based on the patient's symptoms, current physical examination findings, and functional test results. Once the athlete returns to play, he or she must work to maintain gains in flexibility and strength.

Surgical Intervention

Surgical intervention is indicated for stage IV disease (see Acute Phase above).



Medication Summary

Nonsteroidal anti-inflammatory drugs (NSAIDs) may be used judiciously in the acute phase of jumper's knee in conjunction with nonpharmacologic modalities for pain relief and anti-inflammatory effects.

Nonsteroidal Anti-inflammatory Drugs

Class Summary

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action of these agents is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation and various cell membrane functions. Many NSAIDs are currently on the market. In general, the mechanism of action of these agents is the same. No evidence exists that one NSAID is more efficacious than another; however, individual response may differ.

Naproxen (Aleve, Anaprox, Naprelan, Naprosyn)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Ibuprofen (Motrin, Advil, Excedrin IB, Ibuprin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.



Return to Play

Return to play for those recovering from jumper's knee (patellar tendinopathy, patellar tendinosis, patellar tendinitis) should be based on an athlete's ability to safely and skillfully perform sport-specific activities. When symptoms persist despite exhaustive conservative or even surgical treatment, the athlete must weigh the benefits and the consequences of playing in pain.

Functional testing at the end of the recovery phase of rehabilitation, administered by a physical therapist, athletic trainer, or physician, is helpful in determining the athlete's readiness to return to his or her sport.


The most common complication of jumper's knee is persistent pain during jumping that may result in activity avoidance.


Sport-specific training and physical fitness before competition may help prevent jumper's knee. To the author's knowledge, no research validates any particular preventive training regimen more so than any other.


The prognosis for jumper's knee stage I or II is typically excellent with conservative treatment. Stage III carries a guarded prognosis for a full-recovery, whereas those few with stage IV injury (complete tendon rupture) require surgical repair of the tendon and are least likely to return to competitive play.


Jumper's knee affects jumping athletes. It is nearly always amenable to conservative treatment with a comprehensive rehabilitation program. The persistence of pain during and after play guides the staging and treatment of this disorder. Judicious use of relative rest, reducing pain and inflammation, and alternative conditioning methods help to expedite an athlete's return to competition.