Jumper's Knee Clinical Presentation

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