Lateral Elbow Tendinopathy: Development of a Pathophysiology-Based Treatment Algorithm

Abstract

Lateral elbow tendinopathy, commonly known as tennis elbow, is a condition that can cause significant functional impairment in working-age patients. The term tendinopathy is used to describe chronic overuse tendon disorders encompassing a group of pathologies, a spectrum of disease. This review details the pathophysiology of tendinopathy and tendon healing as an introduction for a system grading the severity of tendinopathy, with each of the 4 grades displaying distinct histopathological features. Currently, there are a large number of nonoperative treatments available for lateral elbow tendinopathy, with little guidance as to when and how to use them. In fact, an appraisal of the clinical trials, systematic reviews, and meta-analyses studying these treatment modalities reveals that no single treatment reliably achieves outstanding results. This may be due in part to the majority of clinical studies to date including all patients with chronic tendinopathy rather than attempting to categorize patients according to the severity of disease. We relate the pathophysiology of the different grades of tendinopathy to the basic science principles that underpin the mechanisms of action of the nonoperative treatments available to propose a treatment algorithm guiding the management of lateral elbow tendinopathy depending on severity. We believe that this system will be useful both in clinical practice and for the future investigation of the efficacy of treatments.

Keywords: biomechanics; elbow; histopathology; lateral; tendinopathy; tendon healing; tendon injury; treatment.

Figure 1.

Schematic diagram displaying the histological features of (A) healthy tendon and (B) the 4 grades of tendinopathy. In healthy tendon, type 1 collagen fibers are organized and layered side-to-side and end-to-end. They are essentially parallel but with a very slight wave pattern. The tenocytes are elongated and uniform in number. In grade 1 tendinopathy, the tight array of collagen fibers loosens with increasing waviness. There is a relative increase in type 3 collagen and minimal cell proliferation. In grade 2 tendinopathy, there is increasing cell proliferation and clustering as well as angiogenesis. The nuclei of the cells become rounded and the collagen fibers are further disrupted and start to fragment. In grade 3, tendinopathy there is cell death by apoptosis. There is increased cell migration and matrix metalloproteinase (MMP) production. The extracellular matrix begins to breakdown until, in grade 4 tendinopathy, there is structural and mechanical failure.

Figure 2.

The effect of mechanical loading on tendon homeostasis. The black curve represents matrix damage with increasing strain. The red dotted curve represents matrix production by tenocytes. Zone “A” indicates the anabolic zone where matrix production overcomes matrix damage, such that the tendon can maintain its structural integrity. There are 2 “C” zones (catabolic zones) in which matrix disruption overcomes production, leading to tendinopathy. Image adapted from Wang et al with permission.