Jumpers Knee

Etiology

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.[2] 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.[3] For simplicity and considering that most 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.[4]

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.[5] Other possible risk factors are body 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.[6]

Epidemiology

Since sports injuries are often under-reported, it is hard to determine the exact frequency of patellar tendinopathy in the United States and internationally. Jumping sports such as volleyball, basketball, and long and high jumps have a high disease prevalence.[3] Studies have shown that patellar tendinopathy is substantially higher in elite versus recreational athletes.[7][8] Patellar tendinopathy can occur in adolescent athletes to those in their third decade and up.[9] Jumper's knee occurs more often in males.[1] Approximately 45% of elite jumping athletes and up to 14% of recreational jumping athletes will have jumper's knee symptoms at any point during their career.[1]

Pathophysiology

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.[10]

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.[2]

Histopathology

Historically, the condition was considered to be inflammatory. A study from 2 decades ago demonstrated the absence of inflammatory cells.[11]

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.[2] Repetitive micro-trauma affects tenocytes, altering protein and enzyme production and 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.[10]

History and Physical

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, and level of performance. The patient will usually complain of well-localized pain and tenderness on the inferior tip of the patella.[12][2] 

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."[13] 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.[14]

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 at 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 while the patient is standing, and the examination is repeated while 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 while 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.[15]

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.[14]

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 function tests, and the ability to play sports.[16]

Evaluation

Currently, there is no widely accepted gold standard diagnostic technique.[17] Ultrasound offers several advantages; it is time and cost-saving, non-invasive, repeatable, and accurate, and provides a dynamic image of the knee structures.[2] Both ultrasound and magnetic resonance imaging (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.[18]

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 scans 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.[19] 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.[20]

Treatment / Management

There is no evidence-based, preferred treatment of choice for a jumper's knee. Refractory response to treatment is also typical for the condition, often leaving the health professional and patients searching for alternative therapies.[21]

Most patients with jumper's knee are managed through medical and rehabilitative treatment in the initial stages of the disease.[22] Early recognition and diagnosis of jumper's knee are vital as they can have a progressive course. Although non-steroidal anti-inflammatory drugs were used traditionally, these have recently become less judicious as more physicians have come to realize that the disease is not inflammatory. Hence, NSAIDs may not provide a significant long-term benefit in tendinopathy.[4] 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.[23] Cryotherapy provides analgesia and antagonizes the neovascularization process, contributing to the pathology.[24] 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 rehabilitating a jumper's knee.[25][26][2] Eccentric training has been shown to have equally efficacious results as surgical treatment. It is recommended that eccentric training should be tried for twelve weeks before offering surgical treatment.[27] According to Rodriguez-Merchan eccentric training appears to be the treatment of choice for patients suffering from patellar tendinopathy.[28] (A1)

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.[2] 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.[29] 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, a strong inhibitor of matrix metalloproteinases, and hyperthermia thermotherapy.[30][21] More recently, a three stages rehabilitation protocol has been proposed with a focus on pain reduction followed by progressive loading. The three stages include; Modulation of pain and load management, followed by strengthening exercises and load progression, and finally, functional strengthening and return to sports.[31](B2)

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 as being performed through a direct inferior patellar portal.[32][21](B3)

Differential Diagnosis

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.[7]

Staging

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 four stages.

1. Pain after sports activity 
2. Pain at the beginning of sports activity that disappears with warm-up and sometimes reappears with fatigue
3. Pain at rest and during activity, along with the deterioration of performance
4. Rupture of the tendon[33]

Classifying the pathology into three stages according to the duration of symptoms may be useful.

1. Acute when symptoms have been present for 0 to 6 weeks
2. Sub-acute when symptoms have been present between 6 to 12 weeks
3. Chronic after more than three months[34] 

Prognosis

Most cases of patellar tendinopathy will resolve with nonoperative management.[10] 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.[35]

Rudavsky and Cook say that the process of returning to sports play is slow. This process is often dependent on various 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.[7] 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.[36] 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 mean time to return to play was 4.03 plus or minus 3.18 months.[37]

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 was that eccentric squat-based therapy, shockwave, or PRP could be used as monotherapies or 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.[38] 

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 compared to their asymptomatic counterparts, in which only 7% quit.[35]

Complications

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.[14]