Clinical History: A 24 year-old volleyball player presents with anterior knee pain and swelling. (1a) T1-weighted and (1b) Proton density fat-suppressed sagittal images are provided. What are the findings” What is your diagnosis?
Jumper’s Knee refers to a spectrum of disorders that occur in patients with degeneration and/or tearing of the patellar tendon. It is one of the most common tendon abnormalities in athletically active individuals, and as the name implies, is most common in jumping athletes such as basketball and volleyball players. In the non-athlete, rheumatoid arthritis, the seronegative arthropathies, and treatment with exogenous steroids are known to predispose to this condition.
The initial descriptions of the clinical features of Jumper’s Knee were in children, appearing in the 1920’s as described by Sinding-Larson and Johansson.1 Decades later, Smillie described a similar process in adolescents and adults.2 Patients with Jumper’s Knee may experience a combination of proximal patellar tendinopathy and osteochondral reactive marrow changes. Clinical symptoms include pain, perceived swelling or fullness, and a sensation of “weakness” or “giving way”. In severe or extreme cases, partial or full thickness tears, with and without avulsion of the patellar apex, may be identified. MRI provides the most complete depiction of the osseous and soft tissue abnormalities in patients with Jumper’s Knee. The multiplanar capabilities and non-invasive nature of MRI are well suited to evaluate this malady, as pain, hematoma, soft tissue edema and fracture may limit or entirely preclude an adequate clinical exam.
Anatomy and Pathology
The patellar tendon originates from the anterior aspect of the extensor hood, inferior to the patellar apex. The distal portion of the patellar tendon inserts on the tibial tubercle. The patellar tendon is a monotonous band of fibrocartilaginous tissue.3 Though Jumper’s Knee was once referred to as patellar tendonitis, it is now well established in histopathologically and biochemically analyzed tissue samples excised from the patellar tendons of patients with acute symptoms of Jumper’s Knee that inflammatory cellular infiltrates are absent.4,7 This confirms that the mechanism of disease in Jumper’s Knee is that of a degenerative tendinopathy (tendinosis)5,6 rather than that of an inflammatory tendinitis. In the setting of patellar tendinopathy associated with jumper’s knee, the area of abnormal signal intensity on MRI corresponds to a region of tenocyte hyperplasia, angiofibroblastic tendinosis, loss of coherent collagenous architecture and microtears.4 With more advanced disease, macrotears and frank discontinuity may ensue. Rarely, an avulsion fracture at the apical patellar enthesis may be found.
Patellar tendinosis may be classified into four stages of injury. They are as follows:
Stage 1: Pain after activity, without functional impairment
- Pain at beginning of activity
- Pain disappears after warm-up and reappears with fatigue, but still able to perform satisfactorily
- Pain during and after activity that impairs function
- Patient unable to participate in sports at their prior level
Stage 4: Complete tendon rupture requiring surgical repair
To evaluate for the presence of injury, the following test can be conducted:
Ask the patient to lie on unaffected side on a treatment table.
Passively flex the patient’s knee.
A positive sign for jumper’s knee is present if the patient feels pain at 120 degrees passive knee flexion or anytime during resisted knee extension.
Mechanism of Injury
Running, jumping, and other athletic endeavors lead to repetitive traction and overload of the extensor mechanism, including the quadriceps and patellar tendons. Intense quadriceps contractions, which occur with jumping and landing, place a high mechanical load upon the patellar tendon. Jumper’s knee may thus occur in athletes who participate in sports that demand repetitive, violent contraction of the quadriceps mechanism, such as basketball, volleyball, cycling and sprinting.3 Year round strength and speed training limit the body’s ability to heal, and have therefore fueled the increased incidence of chronic patellar tendinosis.9 Anatomic predisposing factors included patellar laxity, leg length discrepancy or femoral anteversion as well as the presence of genu varus or genu valgus. Other contributing factors include systemic, metabolic or inflammatory diseases and extrinsic factors such as improper training and exercising on hard and/or uneven surfaces.13
The ability of MRI to acquire multiplanar images, in concert with its high soft tissue contrast, makes MR imaging the most effective diagnostic modality in the evaluation of Jumper’s Knee. T1, proton density and/or T2-weighted sagittal and axial sequences are employed to evaluate the patellar tendon. Coronal sequences are of limited value due to volume averaging artifacts and the non-orthogonal slice orientation. On MR images, the normal patellar tendon demonstrates homogenous low signal intensity (4a). Exceptions to this rule occur proximally, where the posterior margin of the tendon may show thin, linear, intermediate signal intensity striations, and distally, where mildly increased signal intensity may be noted at the triangle proximal to the tibial tubercle enthesis. A normal patellar tendon should not exceed 7mm in AP diameter.4,9 The tendon is semilunar to half round in geometry, with a convex anterior border. A constant feature is that of a well-defined posterior border (5a).
With Jumper’s Knee, the most reliable MRI finding is focal proximal 3rd tendon thickening with an associated increase in AP diameter greater than 7mm.9 Focal T2 hyperintensity within the proximal tendon is most commonly seen involving the medial one-third of the tendon (6a),4 and may extend to involve the central third of the tendon. Mild, subtle tendonopathy may not affect the entire A-P diameter of patellar tendon (7a). More severe tendinopathy demonstrates full thickness involvement by intrasubstance signal and T2 hyperintensity (8a,8b). In addition, an indistinct posterior tendon border may also be seen. Edema may be present within the adjacent Hoffa’s fat pad, with irregular T2 hyperintensity replacing normal fat signal. Partial thickness (9a,10a) and complete tears may also occur (11a,11b).
Numerous approaches have been applied to the treatment of Jumper’s Knee. The optimal treatment approach is likely still evolving. Both conservative and operative management may be employed. These strategies are in large part empirically based and often lack scientific evidence, relying on clinical experience.7 The RICE regimen (rest, ice, compression, elevation) may help alleviate soreness. Non-steroidal anti-inflammatory medication, such as aspirin or ibuprofen, and ice massage after activity help control swelling and inflammation. COX-2 inhibitors may prove more effective in limiting local inflammation by limiting the release of prostaglandin E2 at the site of tendinosis. Excellent results have also been reported employing eccentric quadriceps training for twelve weeks, as outlined by the Victorian Institute of Sport Assessment.10
In cases of jumper’s knee refractory to conservative therapy, chronic patellar tendinosis may be treated surgically. Both arthroscopic and open repairs consisting of surgical excision of a longitudinal strip of pathologic patellar tendon may be utilized. In one study, in patients at an average of 3.5 years surgical follow-up, eighty-six percent of individuals achieved excellent results.12 Finally, in patients who have completely ruptured their patella, the Dall-Miles cable procedure may be employed. End-to-end sutures which incorporate a medial and lateral retinaculum repair are performed, with a cable placed through the patella and tibial tubercle for reinforcement.13
Jumper’s Knee is among the most common tendon disorders in athletic individuals. The clinical diagnosis may be challenging, as in many cases the physical exam is difficult or confusing due to pain and guarding. In milder cases, patient symptoms may mimic those of meniscal tear, osteochondral injuries, or quadriceps pathology. Fortunately, MRI’s multiplanar capabilities and excellent soft-tissue contrast make it ideally suited for the definitive diagnosis, allowing excellent characterization of patellar tendinosis and related injuries in patients with Jumper’s Knee.
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2 Smillie, I.S. Injuries of the knee joint. 1970 Edinburgh: Churchill Livingstone.
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10 Bahr R, Fossan B, Loken S, Engebretsen L. Surgical treatment compared with eccentric training for patellar tendonopathy (Jumper’s Knee). Randomized, controlled trial. J Bone Joint Surg Am. 2006 Aug; 88 (8): 1689-98
11 Jonsson P; Alfredson H. Superior results with eccentric compared to concentric quadriceps training in patients with jumper’s knee: a prospective randomized study. Br J Sports Med. 2005; 39 (11): 847-50
12 Griffiths GP, Selesnick FH. Operative treatment and arthroscopic findings in chronic patellar tendonitis. Arthroscopy 1998 Nov-Dec; 14 (8): 836-9.
13 Shelbourne KD; Darmelio MP, Klootwyk TE. Patellar tendon rupture repair using Dall-Miles cable. Am J Knee Surg. 2001; 14(1): 17-20;