“Jumper's knee,” also called patellar tendinopathy, is a painful condition of the knee, mainly activity-related, caused by small tears in the patellar tendon that mainly occurs in sports requiring strenuous jumping and results in a localized patellar tendon tenderness. The tears are typically caused by accumulated stress on the patellar or quadriceps tendon. As the name implies, the condition is common in athletes from jumping sports where there is a high demand for the speed and power of leg extensors. These sports often lead to high eccentric quadriceps loadings such as volleyball, track (long and high jump), basketball, long-distance running, and skiing. The condition has a male predominance, with a more common occurrence in adolescents and young adults. Contrary to traditional belief, a jumper's knee does not involve inflammation of the knee extensor tendons. Studies dating back 40 years describe jumper's knee as a degenerative condition. Jumper's knee is a clinical diagnosis made through detailed history taking and a physical exam. Ultrasound can facilitate the diagnosis, as this imaging study is readily available and affordable. Treatment mainly revolves around conservative measures such as reducing activities that place loading impact on the knee. Once the pain subsides, restoration of function is achieved through physical and exercise therapy. Surgery usually remains the last resort for chronic refractory cases.
Jumper's knee is an overuse injury of the knee extensor mechanism due to repetitive mechanical stress from athletic activities requiring movements such as jumping, landing, acceleration, deceleration, and cutting. Micro-tearing of the knee extensor tendons can arise after constant repetition of these movements during a single exercise session or if there is insufficient rest between sessions. The component of the knee extensor mechanism most likely to be affected is the inferior pole of the patella where the patellar tendon inserts. Other less frequently involved regions of the knee are at the insertion of the quadriceps tendon to the superior pole of the patella and where the patellar tendon inserts into the tibial tuberosity. For purposes of simplicity, and considering that the majority of the cases for jumper's knee are due to a problem on the patellar tendon at its insertion in the inferior patella, we will use the term patellar tendinopathy interchangeably. It is appropriate to mention that patellar "tendinitis" is a misnomer as the condition is felt by many clinicians to be more tendinosis than it is tendinitis. In published studies, it is noted that classic inflammatory cells are usually absent.
There are several intrinsic factors of the knee that predispose to this pathology. These include ligamentous laxity, quadriceps and hamstring tightness, excessive Q-angle of the knee, abnormal patellar height, previous ongoing inflammation of the knee, and excessive force generation on the knee. Other factors can also lead to the development of the jumper's knee such as excessive volume and frequency of training, the athlete's performance level, and the hardness of the ground where the sport is practiced.Other possible risk factors are the weight, body mass index, waist-to-hip ratio, leg-length difference, the arch height of the foot, quadriceps strength, and vertical jump performance. These factors can result in increased strain on the patellar tendon.
Since sports injuries often are under-reported, it is hard to determine the exact frequency of patellar tendinopathy both in the United States and on an international scale. Jumping sports such as volleyball, basketball, and long and high jumps have a high prevalence of the disease. Studies have shown that patellar tendinopathy is substantially higher in elite versus recreational athletes. Patellar tendinopathy can occur in adolescent athletes to those in their third decade and up. Jumper's knee occurs more often in males.
Multiple theories have been proposed for the pathogenesis of patellar tendinopathy; mechanical, vascular, and impingement related. However, the chronic overload theory is the most commonly reported. Repetitive overload on the knee extensor tendons will cause it to weaken progressively, eventually leading to failure. Microscopic failure occurs within the tendon at high loads and eventually leads to alterations at the cellular level, which undermine its mechanical properties. Tendon micro-trauma may cause individual fibril degeneration due to stress across the tendon. As the fibril degeneration becomes ongoing, chronic tendinopathy will ensue.
Examination of the tendon under ultrasound shows three pathologic changes. At first, there will be edema along the damaged tendon fibers. The affected tissue is swollen and thickened, but still homogenous. The second is a "stage with irreversible anatomical lesions," the tendon has a heterogeneous appearance with hypoechoic and hyperechoic images without edema (granuloma). At this point, the tendinous envelope is still more or less well defined. In the final stage of the lesion, the tendinous envelope is irregular and thickened. Its fibers appear heterogeneous, yet the swelling has disappeared.
Historically, the condition was considered to be inflammatory. A study from 2 decades ago demonstrated the absence of inflammatory cells.
Repetitive microtrauma on the tendons causes microscopic changes. Histologic studies of specimens reveal degeneration, fibrinoid necrosis, pseudocyst change, randomized collagen with neovascularization, tenocyte infiltration, micro-tears of the tendinous tissue, focal degeneration near the bone-tendon insertion, hyaline degeneration, and metaplasia. Repetitive micro-trauma affects tenocytes, altering protein and enzyme production as well as deforming the nucleus. Loading of the tendon fibroblasts increases prostaglandin E2 and leukotriene B4, both of which contribute to tendinopathy. In vitro studies have shown that vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) activity have also been linked to tendon breakdown. In vivo studies show that VEGF may have a role in the neovascularization process. Although several studies have shown neovascularization associated with tendinopathy, there are also conflicting studies showing no association with neovascularity. Diseased tendons also have a higher percentage of cells undergoing apoptosis, as well as multiple pro-apoptotic proteins and genes present.
Patellar tendinopathy is mainly a clinical diagnosis made through a detailed history and meticulous physical examination. Appropriate questions which will cue-in the diagnosis: Sport practiced, schedule of practice and competition, which position the athlete plays, level of performance. The patient will usually complain of well-localized pain and tenderness on the inferior tip of the patella.
Patellar tendinopathy shares other common signs and symptoms of other knee pathologies such as pain with prolonged sitting, squatting, and stair climbing. Also, patients may complain of pain from activities that involve prolonged flexion of the knee, otherwise known as the " Movie Theatre sign". Usually, during activities that store and release energy in the patellar tendon, load-related pain increases with demand on the knee extensors. Sudden tendon pain occurs with loading and usually stops almost immediately when the load is removed. Rarely a patient feels pain when they are resting.
Examination of the knee might reveal a localized swelling overlying the patellar tendon which is tender to palpate. In addition, the following signs have been described; Basset's sign "passive extension – flexion sign" where the examiner palpates the anterior aspect of the fully extended knee and identifies the highest tender point which is usually at the inferior pole of the patella and the proximal part of the patellar tendon. The examination is repeated in 90 degrees of knee flexion and the sign is positive when there is a marked reduction in tenderness to palpation in the flexed knee position. The other sign is the "standing active quadriceps sign" where the whole patellar tendon is palpated whilst the patient is standing and the examination is repeated whilst the patient is standing on the involved extremity with the knee in 30 degrees of flexion. Similarly, the sign is positive if there is a marked reduction in tenderness to palpation whilst the quadriceps muscle is contracted. The concept behind these signs was explained in a cadaveric study that showed when the quadriceps muscle is tensioned as in 90 degrees of knee flexion, the deep fibers of the tendon do not deform to anterior palpation.
A thorough examination of the entire lower extremity is needed to identify relevant deficits at the hip, knee, and ankle/foot region. Often malalignment of the foot, heel, or tibia can place excess stress on the knee extensor tendons increasing the risk of tendinopathy.
There are multiple scales for evaluating tendon overuse. A relatively more accurate scale is the Victorian Institute Sports tendon Assessment (VISA) score. The scale was tailored specifically to evaluate symptoms and functionality in patellar tendinopathy. The scale has good inter and intra-observer reliability and stability. It is a brief questionnaire that assesses symptoms, simple tests of function, and the ability to play sport.
Currently, there is no widely accepted gold standard diagnostic technique.  Ultrasound offers several advantages; it is time and cost-saving, it is non-invasive, repeatable, and accurate, and provides a dynamic image of the knee structures. Both ultrasound and magnetic resonance image (MRI) can be used to detect abnormalities in the patellar tendon itself. Imaging can also be used to guide clinicians as to the severity of the pathology.
Radiographs including anteroposterior, lateral, and skyline views are recommended to exclude any acute bony injuries or pathologies. Radiographic changes on the tendon might be noted such as elongation of the involved pole of the patella, calcification, inferior traction spur known as enthesophyte in chronic cases, and increased density within the patellar tendon matrix. However, these changes are rare in the first six months of symptoms. MRI scan would be indicated in chronic cases and for surgical planning. It can show thickening of the patellar tendon which is more diagnostic than the presence of edema. Foci of increased signal intensity in both T1 and T2 images have been observed. In chronic cases, MRI scans may reveal the absence of the posterior border of the fat pad. It is often the proximal part of the tendon which is affected and thickened. Although not usually indicated, a bone scan can be used in the initial stages of the disease. This test will demonstrate increased pooling of blood and localized tracer activity in the affected region.
There is no evidence-based, preferred treatment of choice for jumper's knee. Refractory response to treatment is also typical for the condition which often leaves the health professional and patients searching for alternative therapies.
Most patients with jumper's knee are managed through medical and rehabilitative treatment in the initial stages of the disease. Early recognition and diagnosis of jumper’s knee are vital as it can have a progressive course. Although non-steroidal anti-inflammatory drugs were used traditionally, these have recently become less judicious as more physicians come to realize that the disease is not inflammatory. Hence, NSAIDs may not provide a significant long-term benefit in tendinopathy. Corticosteroid injections are contraindicated as they bear a risk of patellar tendon rupture.
Non-surgical treatment focusing on the following: Relative rest rather than immobilization to avoid tendon and muscle atrophy. Cryotherapy provides analgesia and antagonizes the neovascularization process which contributes to the pathology. Modification of activities, and sports training including adequate warm-ups, and physiotherapy to increase the flexibility of quadriceps and hamstring muscles. Eccentric training has been suggested to play a key role in the rehabilitation of a jumper's knee. Eccentric training has been shown to have equally efficacious results to that of surgical treatment. It is recommended that eccentric training should be tried for twelve weeks before offering surgical treatment. According to Rodriguez-Merchan eccentric training appears to be the treatment of choice for patients suffering from patellar tendinopathy. Athletes must avoid activities such as excessive jumping or impact loading of the knee which only aggravates the situation. As the pain begins to subside, the intensity of rehabilitation therapy and sport-specific training can be slowly increased. Reduction of strain across the patellar tendon can be helpful using taping or infrapatellar straps. It reduces patellar tendon strain by altering the angle between the patella and patellar tendon.Given the refractory response to many initial treatments, new methods have recently emerged. These include dry-needling, sclerosing injections, platelet-rich plasma therapy, extracorporeal shock wave treatment, Aprotinin injection which is a strong inhibitor of matrix metalloproteinases, and hyperthermia thermotherapy.
Surgical treatment is usually indicated in cases of partial tendon tears and Blazina stage III where pain continues during rest and activities. Also, it remains the last resort for chronic refractory cases unresponsive to conservative treatment. Traditionally, the gold standard for surgical treatment of patellar tendinopathy involved open debridement of the inferior pole of the patella, as well as debridement of the patellar tendon by excising the angiofibroblastic and degenerative areas. This is followed by reattachment of the tendon using sutures or anchors as indicated. Recently, knee arthroscopy has gained popularity for tissue debridement and release. The arthroscopic procedure has been described to be performed through a direct inferior patellar portal.
Jumper's knee can be mistaken for other injuries or pathologies such as Osgood-Schlatter disease, meniscal injuries, patellofemoral syndrome, quadriceps injury, knee bursitis (superficial and deep infrapatellar bursae), osteochondritis dissecans, patellar subluxation, pathologies of the knee fat pad, chondromalacia, or a patellar tracking problem.
Blazina et al. first used the term jumper's knee in 1973. They also classified the pathology by stage according to the onset of pain in relation to physical activity. This classification along with its modifications is still widely employed. Blazina et al. suggest 4 stages.
It may be useful to classify the pathology into 3 stages according to the duration of symptoms.
Most cases of patellar tendinopathy will resolve with nonoperative management. Nevertheless, mild to moderate pain may persist for 15 years in adult athletes with patellar tendinopathy but does not appear to limit leisure-time physical activity.
Rudavsky and Cook say that the process of returning to sports play is slow. This process is often dependent on a variety of factors ranging from the severity of pain, grade of dysfunction, the sport practiced, the quality of rehabilitation, the athlete's performance level, and the presence of intrinsic and extrinsic factors. A previous study that used imaging technology to classify the severity of the lesion said that mild pathologies might take anywhere from 20 days for the patient to return to sport, whereas more severe cases might take 90 days. Other experts mention that athletes with severe dysfunction might need anywhere from 6 to 12 months to recover. Lang and coworkers published a study where they analyzed patients who were treated surgically (arthroscopic patellar release). They determined that the meantime to return to play was 4.03 plus or minus 3.18 months.
Joshua et al. performed a systemic search of previous studies to compare the efficacy of treatment for commonly used invasive and non-invasive treatment options. The conclusion reached was that eccentric squat-based therapy, shockwave, or PRP could be used as monotherapies or as adjunct therapies to accelerate recovery. Surgery or shockwave can be considered for patients who fail to improve after six months of conservative treatment. Since patellar tendinopathy is not inflammatory, corticosteroid injections should not be used.
Patellar tendinopathy may cause long-lasting symptoms that can lead to the athlete's early retirement from the sport. In a small prospective case-control study, Kettunen et al. found that 53% of their symptomatic subjects with Jumper's knee had quit their sport when compared to their asymptomatic counterpart in which only 7% quit.
Athletes, clinicians, coaches, and athletic trainers need to understand that the treatment for patellar tendinopathy can be a slow and sometimes frustrating process. There are multiple pitfalls to be aware of, including the failure to control pain. The athlete’s beliefs about pain and pathology may influence the development and management of unresponsive tendinopathies. Because some athletes may have been told that they have weakened tendons due to tears and degeneration, and hence an increased risk of rupture, they may develop fear-avoidance behavior, which can be associated with poorer functional outcomes in individuals suffering from lower-limb tendinopathy. Over-reliance on non-invasive therapies like shockwave therapy and injections instead of including rehabilitation exercises as part of the treatment plan can also lead to complications. Failure to address the athletes' landing kinematics can also bring difficulties. Athletes should have their jump-landing mechanics retrained after adequate rehabilitation.
Patients who undergo patellar tendon debridement and repair should be immobilized in full extension for 2 weeks. This should be followed by a progressive range of motion and rehabilitation exercises. Full weight-bearing as tolerated is permissible from day one.
There is currently insufficient evidence for preventative interventions specific to patellar tendinopathy. Some of the proposed preventive measures are proprioception training, eccentric training and stretching of the patellar tendon, reducing the training duration or frequency, and bracing or taping.
Managing patellar tendinopathy is a job for physicians trained in the care of musculoskeletal conditions along with other members of the interprofessional healthcare team. Sports medicine physicians, physiatrists, and rheumatologists provide the first line of care. Orthopedic surgeons are consulted for refractory cases or when the knee extensor tendons are partially or completely torn. A team of professionals from multiple disciplines including athletic trainers, physical therapists, sports biomechanists, and sports psychologists is needed since the condition commonly affects athletes. The orthopedic specialty nurse is often responsible for the coordination of care and follow up and reporting concerns to the clinician.
Initially, the physical therapist must work at hand with physicians to implement a nonoperative regimen consisting of therapy with isometric or eccentric exercises as the mainstay treatment. In a level 2 study, at 12 weeks, patients undergoing an eccentric exercise program showed significant improvement compared with those undergoing a concentric exercise program. As the treatment progresses, plyometrics and sport-specific training is required to return the athlete to sport at the highest level
Alternative medical treatments have been studied at different levels of evidence, demonstrating mixed and inconclusive results. Acceptable outcomes have been obtained from surgical interventions in refractory cases.
An interprofessional team approach involving clinicians, specialists, orthopedic nursing, and therapists will yield the best results.
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