Patellar tendinopathy or “jumper’s knee,” first described by Blazina and colleagues [1] in 1973, is primarily a chronic overuse injury of the patellar tendon resulting from excessive stress on the knee extensor mechanism. Athletes involved in sports requiring repetitive jumping, running, and kicking (e.g., volleyball, basketball, tennis, track) are at greatest risk. For example, volleyball players have an increased incidence compared with other sports of 22% to 39% [2]. Acceleration, deceleration, takeoff, and landing generate eccentric forces that can be three times greater than conventional concentric and static forces. These eccentric forces may exceed the inherent strength of the patellar tendon, resulting in microtears anywhere along the bone-tendon interface [2–4]. With continued stress, a cycle of microtearing, degeneration, and regeneration weakens the tendon and may lead to tendon rupture.

As in other overuse injuries, the predisposing factors in jumper’s knee include extrinsic causes, such as errors in training, and intrinsic causes, such as biomechanical flaws. Training errors include improper warm-up or cool-down, rapid increase in frequency or intensity of activity, and training on hard surfaces [3,4]. Biomechanical imbalances, such as tight hamstrings and excess femoral anteversion [3], and jumping mechanics [2,5] have been implicated as increased risk factors for development of patella tendinopathy (jumper’s knee). Finally, an increased incidence of Osgood-Schlatter disease and idiopathic anterior knee pain during adolescence has been identified in patients with jumper’s knee [3].

Because histologic studies of the patellar tendon reveal collagen degeneration with little or no evidence of acute inflammation, many authors argue that “patellar tendinopathy or tendinosis” is a more accurate description than “patellar tendinitis.” [6–8] This distinction has important implications for rehabilitation. In treatment of patellar tendinosis and other chronic overuse tendinopathies, the treatment team should emphasize restoration of function rather than control of inflammation. This is an overuse syndrome that has no age or gender predilection.

Symptoms

Patients typically report a dull, aching anterior knee pain, initially noted after a strenuous exercise session or competition, that is insidious in onset and well localized [7]. The bone-tendon junction at the inferior pole of the patella is most frequently affected (65% of cases), followed by the superior pole of the patella (25%) and the tibial tubercle (10%) [6]. Other symptoms may include stiffness or pain after prolonged sitting or climbing stairs [3], a feeling of swelling or fullness over the patella, and knee extensor weakness [1]. Mechanical symptoms of instability, such as locking, catching, and give-way weakness, are uncommon.

Four phases have been described in the progression of jumper’s knee: phase 1, pain is present after activity only and is not associated with functional impairment; phase 2, pain is present during and after activity but does not limit performance and resolves with rest; phase 3, pain is present continually and is associated with progressively impaired performance; and phase 4, complete tendon rupture [1].

As the disease progresses, the pain becomes sharper, more severe, and constant (present not only with athletic endeavor but also with walking and other everyday activities). If it is not treated, the disorder may result in tendon rupture, a sudden painful event associated with immediate inability to extend the knee [7].

Physical Examination

The hallmark of jumper’s knee is tenderness at the site of involvement, usually the inferior pole of the patella [7]. This sign is best elicited on palpation of the knee in full extension [7], and the pain typically increases when the knee is extended against resistance [3]. On occasion, there may be swelling of the tendon or the fat pad, although a frank knee joint effusion is not typically present [3]. Mild patellofemoral crepitus and pain with compression of the patellofemoral joint have been noted [3]. In advanced disease, patients may have quadriceps atrophy without detectable weakness on manual muscle testing and hamstring tightness [3,7]. Test results for knee ligamentous laxity are negative. The examiner should also expect normal findings on neurologic examination.