Regarding the staging classification in patellar tendinopathy, Blanzina et al. (1973) reported the first classification, which has been used over 40 years. Except for stage 4, which is complete tendon rupture, they classified three stages based on symptoms and dysfunction. In the twenty-first century, Cook and Purdam et al. (2009) classified tendinopathy into three stages, namely, reactive tendinopathy, early or late tendon disrepair, and degenerative tendinopathy. This classification was based on microstructural changes of the damaged tendon; thus, it can indicate the degree of microstructural damage that requires treatment intervention. They divided these three stages into two groups. For the tendinopathies in the first group, including reactive tendinopathy, only load management was enough for healing, whereas for the tendinopathies in the second group, including degenerative tendinopathy, treatment intervention, including eccentric exercise, should be applied. If the tendinopathies in the second group were resistant to eccentric exercise, more-invasive treatments such as extracorporeal shockwave therapy and surgery are necessary.

Patellar tendinopathy is one of the most popular tendinopathies. Generally, the region of pathological change in patellar tendinopathy is the posteromedial tendon substance at the insertion to the inferior patellar pole (Johnson et al. 1996; Lavagnino et al. 2008; Khan et al. 1996) (Fig. 28.2). This region specificity is closely related with the mechanical and structural characteristics of the patellar tendon. First, the proximal patellar tendon cross-sectional area (CSA) was smaller than the mid- or distal tendon CSA (Kongsgaard et al. 2007). Therefore, the force per unit area at the proximal patellar tendon was larger than that at the mid- or distal tendon. This is one of the reasons for the tendency of patellar tendinopathy to occur at the proximal tendon attachment to the patella. Second, some reports investigated the mechanism of pathological changes in the posterior potion of the proximal patellar tendon (Basso et al. 2002; Dillon et al. 2008; Pearson and Hussain 2014; Hansen et al. 1985). In both cadaveric and experimental studies, mechanical stress was higher at the posterior region than at the anterior region of the proximal tendon owing to the lever arm (Basso et al. 2002; Dillon et al. 2008). The finite element model findings also showed maximum strain at the classical tendinopathy lesion, at the posterior region of the proximal patellar tendon attachment to patella (Lavagnino et al. 2008). Moreover, regarding the mechanical properties of the proximal tendon, posterior fascicles were markedly weaker and micro-damages are likely to occur at the posterior tendon (Hansen et al. 1985). Finally, the reason why most tendinopathy lesions are located at the medial side was explained in the study on regional structural differences at the enthesis of the proximal patellar tendon. Toumi et al. (2006) reported that bone quality, trabecular thickness, and uncalcified fibrocartilage were greatest medially and that the subchondral plate was thinner laterally. These results indicate that mechanical stress at the proximal patellar tendon enthesis is greater on the medial than on the lateral side, leading to the tendency of exposure with overload on the proximal medial tendon. Overall, the posteromedial site of the proximal patellar tendon has weak mechanical properties with large mechanical stress, which explains why the lesion of proximal patellar tendinopathy occurs at the posteromedial portion.

Although many treatment methods are available for patellar tendinopathy, evidence-based therapies are limited. Therefore, no consensus has been reached on the appropriate use of these therapies. According to a recent systematic review (Larsson et al. 2012), only eccentric exercise has strong evidence for patellar tendinopathy. Moderate evidence was found on heavy slow resistance training as an alternative to eccentric exercise. Moreover, evidence is limited for sclerosing injection, shockwave therapy, and surgery (Table 28.1).