Management of Tendinopathy: no longer “one size fits all”

Keynote Lecture by Hans Zwerver, The Netherlands

Introduction

Tendon disorders comprise 30-50% of all sports-related injuries. The clinical presentation is straightforward in many cases—the patient presents with tendon pain during or after activity. In the early stages of the condition, athletes can "run through" the pain or the pain disappears when they warm up, only to return after exercise when they cool down. The athlete is able to continue to train fully, however when continuing normal training routines function will be progressively impaired. Loading tests demonstrate increased pain with increased load and palpation can localize tendon pain accurately and reveals thickening of the tendon. Although there have been advances in the understanding of the multifactorial etiology, histopathology, imaging techniques, and both conservative and surgical treatment for this condition over the past two decades, successful management of athletes with tendinopathy remains a major challenge for both the practitioner and patient. The high prevalence, the impairment of function and the chronic character of this condition mean that tendinopathy might have substantial impact on an athlete's career. For some athletes it is even a reason to retire from sports.

Pathophysiology and pain

Mechanical loading of tendon tissue is anabolic by increasing synthesis of collagen. This peaks around 24 hours after exercise and remains elevated for up to 70 to 80 hours. However, exercise also results in degradation of collagen proteins, although the timing of this catabolic peak occurs earlier than the anabolic peak. This results in a net loss of collagen around the first 24 to 36 hours after training, followed by a net gain in collagen. Thus, a certain restitution time interval in between exercise bouts is critical for the tissue to adapt and to avoid a net catabolic situation.

Repetitive microtrauma due to overload and insufficient restitution time may be considered as the initial disease factor; microruptures of tendon fibers occur and several molecules are expressed including inflammatory cytokines, which act as disease mediators, while other released factors promote the healing process. Neural in-growth that accompanies the neovessels might explain the occurrence of pain and triggers neurogenic-mediated inflammation. This complex and not fully elucidated pathophysiologic process of (neuro)inflammatory and degenerative changes finally leads to a painful tendon with a failed healing response.

However, this rather simplified description of a complex pathophysiologic process does not fully explain the heterogeneity in presentation and pain, and variability in recovery. Cook and Purdam proposed a model of tendinopathy, which is based on available evidence from pathology, clinical and imaging studies. This "continuum of tendon pathology" describes three stages (1) reactive tendinopathy, tendon disrepair (failed healing) and (3) degenerative tendinopathy. The load applied to the tendon is the crucial factor in this continuum.

Clinical and imaging features allow a tendon to be classified as one of these stages. One should keep in mind that there is continuity between these stages and that combined stages can exist within a tendon.

However, the problem of tendon pain is that the relation between pain and evidence of tissue disruption is variable. Many clinical features are consistent with tissue disruption—the pain is localised, persistent and specifically associated with tendon loading, whereas others are not—investigations do not always match symptoms and painless tendons can be catastrophically degenerated. As such, the question 'what causes a tendon to be painful?' remains unanswered. Without a proper understanding of the mechanism behind tendon pain, it is no surprise that treatments are often ineffective. Thus investigation into mechanisms for tendon pain and should extend beyond local tissue changes and include peripheral and central mechanisms of nociception modulation.

Ultrasound Tissue Characterization

Ultrasonographic tissue characterisation (UTC) is a new promising imaging modality that can quantitatively evaluate tendon structure and differentiate pathology. UTC is based on a transducer in transverse position that is displaced stepwise in the longitudinal direction. In this way, contiguous transverse images provide longitudinal information. By precise matching of UTC processed images with exactly corresponding tendon sections, echo-types were verified with use of histology as reference test: (I) intact and aligned tendon bundles; (II) less integer and waving tendon bundles; (III) mainly fibrillar tissue and (IV) a mainly amorphous matrix with loose fibrils, cells or fluid. These echo-types fairly match with the different pathology stages of the tendon pathology continuum described above. Recent studies have shown that UTC is able to detect training load related changes in tendons of elite athletes.Therefore UTC might be a useful tool in monitoring tendon structure in relation to tendon load, important for the prevention and management of tendinopathy.

Management of tendinopathy

Treating tendinopathy remains a challenge for all practitioners. Ideally, strategies employed to manage tendinopathy should be individually tailored depending on stage of tendon disease, understanding of the underlying pain mechanism, timing in or out of competition season, and addressing the different etiologic factors including individual genetic profile (personalized medicine). Management strategies that control pain and maintain performance are required in season. These include load management, both reducing aggravating loads and introducing pain-relieving loads, medications and adequate monitoring to detect a deteriorating tendon. Out of season interventions with a more regenerative focus are required to promote tendon healing and to restore tendon function, so athletes can compete to their full potential again. 


Keep Me Updated