Tendinopathy in sport

Abstract

Context: Tendinopathy is increasing in prevalence and accounts for a substantial part of all sports injuries and occupational disorders. Despite the magnitude of the disorder, high-quality scientific data on etiology and available treatments have been limited.

Evidence acquisition: The authors conducted a MEDLINE search on tendinopathy, or "tendonitis" or "tendinosis" or "epicondylitis" or "jumpers knee" from 1980 to 2011. The emphasis was placed on updates on epidemiology, etiology, and recent patient-oriented Level 1 literature.

Results: Repetitive exposure in combination with recently discovered intrinsic factors, such as genetic variants of matrix proteins, and metabolic disorders is a risk factor for the development of tendinopathy. Recent findings demonstrate that tendinosis is characterized by a fibrotic, failed healing response associated with pathological vessel and sensory nerve ingrowth. This aberrant sensory nerve sprouting may partly explain increased pain signaling and partly, by release of neuronal mediators, contribute to the fibrotic alterations observed in tendinopathy. The initial nonoperative treatment should involve eccentric exercise, which should be the cornerstone (basis) of treatment of tendinopathy. Eccentric training combined with extracorporeal shockwave treatment has in some reports shown higher success rates compared to any therapies alone. Injection therapies (cortisone, sclerosing agents, blood products including platelet-rich plasma) may have short-term effects but have no proven long-term treatment effects or meta-analyses to support them. For epicondylitis, cortisone injections have demonstrated poorer long-time results than conservative physiotherapy. Today surgery is less indicated because of successful conservative therapies. New minioperative procedures that, via the endoscope, remove pathologic tissue or abnormal neoinnervation demonstrate promising results but need confirmation by Level 1 studies.

Conclusions: Novel targeted therapies are emerging, but multicenter trials are needed to confirm the results of exercise and mini-invasive treatments.

Keywords: pain; tendinopathy; tendinosis; tendon.

Figure 1.

Diagram depicting collagen synthesis and degradation after acute exercise in humans. The first 24 to 36 hours after exercise results in a net loss of collagen. However, 36 to 72 hours after exercise, a net synthesis of collagen follows. Hence, repetitive training without enough resting time in between may result in a net catabolic situation with degradation of the matrix and lead to tendinopathy. Reproduced with permission from Magnusson et al.

Figure 2.

Patellar tendon of healthy control (A) and painful tendinopathy (B) after hematoxylin and eosin staining. Arrows denote tenocytes. The healthy tendon has homogeneous, organized parallel collagen structure and thin, elongated tenocytes (A). Tendinopathy, in contrast, is characterized by collagen disorganization, increased cell count, transformed tenocytes, and vascular ingrowth (V) in the tendon proper (B). Bar, 50 µm. Reproduced with permission from Lian et al.

Figure 3.

Achilles tendon of healthy control (A) and painful tendinopathy (B) after immunostaining for substance P (SP); picture taken with immunofluorescence microscopy. Arrows denote free nerve endings. The micrograph illustrates SP-positive nerve fibers in close vicinity to a proliferated vessel (B). v = blood vessel. Bar = 50 μm. Reproduced with permission from Ackermann et al.

Figure 4.

Eccentric squats exercises for the patellar tendon in an experimental setup for (A) free weight, decline board and (B) overload, decline board experiments. Reproduced with permission from Frohm et al.^-

Figure 5.

Achilles tendon subjected to 3 levels of physical activity during 4 weeks postrupture. Rats were post Achilles tendon rupture treated with a plaster cast (IMMOB), freely mobilized (MOB), or wheel-running (RUN). (A) Midtendon mediolateral diameter of new organized collagen in the healing area. (B) Area occupied by nerve fibers (%) immunoreactive to a sensory nerve marker, calcitonin gene related peptide (CGRP) in relation to total area, of the Achilles tendon proper. Increased physical activity seems to accelerate sensory nerve retraction from the tendon proper. Mean + SD. ^*P < 0.05; ns, P > 0.05. Reproduced with permission from Bring et al.