Current Understanding of Tendinopathies and Treatment Options
Am Fam Physician. 2007 Sep 15;76(6):773-774.
Overuse tendon injuries (i.e., tendinopathies) commonly occur in recreational and competitive athletes but can also occur in nonathletes. In this issue of American Family Physician, the article on lateral epicondylitis by Johnson and colleagues includes numerous treatment options for tendinopathies; however, no clear-cut option emerges as the best evidence-based approach.1 Despite the high prevalence of reported tendinopathies and the many treatment options, the underlying pathology that affects a particular tendon and its surrounding structures can be unclear.
The understanding of tendon injury has evolved over the past decade. Previously, it was thought that tendon injury was caused by inflammation (tendinitis). Tendon injury is now considered to be a spectrum of disorders, and persistent inflammation is not typically associated with overuse tendon injuries.
Acute tendon injuries have a classic inflammatory response; however, it is difficult to determine when the injury has progressed from the inflammatory stage to failed healing or tendinosis. Microscopic changes such as fibrin deposition, lack of neutrophils and macrocytes, neovascularization, and increased collagen synthesis and breakdown commonly occur in chronically painful tendon and peritendinous injuries.2 This failed healing response is thought to be caused by poor blood supply or ongoing mechanical forces on the lesion. The term tendinopathy has been adopted to encompass the various tendon pathologies such as tendinitis, tendinosis, and paratendinitis when histopathologic evidence is unavailable to definitively determine the stage of injury.
Tendons are composed of collagen bundles, tendon cells (tenocytes), and proteoglycans. Collagen provides tensile strength, proteoglycans provide structural support, and tenocytes are a load-responsive network stimulated by increases in mechanical load. The collagen bundles; elastin; and an inner synovial lining surrounded by vascular, lymphatic, and nerve structures form the peritendon.3 Repetitive mechanical forces or poor technique during work- or activity-related movement can break down the peritendinous structures.
Tensile, compressive, or shearing forces cause mechanical loading on the tendon and its associated structures. Tensile forces from repetitive microtrauma are the most common loads placed on tendons.4 This can occur in the elbows of athletes who participate in throwing sports, but it is just as common in the elbows of mothers who carry their babies for long periods. Compressive forces occur when tendons wrap around bony prominences such as the acromion process, or occur within narrow spaces such as the carpal tunnel. Chronic compression of the tendon causes stiffer, less-tensile movement, which predisposes the tendon to injury.5 The effect of shearing forces most often occurs at points of friction.
Treatment options for tendinopathies range from a wait-and-see approach to surgical debridement of chronic lesions.1 The numerous options support the theory that no one treatment stands out as the superior choice.6–8 Questions remain about whether the same treatment approaches can be applied to all types of tendinopathies or if certain treatment combinations are more effective than others.
Physicians should first look for correctable causes of injury such as muscle imbalances, biomechanical issues, or errors in an athlete's training technique. Muscle imbalances commonly contribute to tendinopathies of the rotator cuff, where the chest wall muscles are usually stronger than the back muscles. Physical therapy that focuses on strengthening the scapular and upper back muscles often can help prevent future rotator cuff injury. Similarly, correcting biomechanical issues (e.g., pes planus, leg length discrepancies) with custom-made orthotics can help alleviate many lower extremity tendinopathies.
Educating patients about training techniques related to their sports will help prevent many tendon injuries. Concepts such as gradual increases in training intensity and duration and avoiding the “no pain, no gain” mantra are good starting points. More in-depth advice can be provided by viewing a video of the athlete participating in the sport and analyzing the athlete's gait and motion or by having the athlete participate in expert coaching sessions.
Outside the acute setting, tendon injuries are typically not inflammatory in nature; keeping this in mind may prompt physicians to avoid using nonsteroidal anti-inflammatory drugs alone for the treatment of these injuries. Symptom reduction through the judicious use of modalities such as physical therapy, topical and oral analgesics (including acetaminophen), corticosteroid injections, topical nitrates, bracing, and ultrasonography appears to provide subjective pain relief and improved function. Although there is no strong evidence to support this benefit,6–8 these modalities should be continued if clinically appropriate until better options are available.
Future research is needed to bridge the gap between physicians' basic scientific knowledge and their clinical experience in the treatment of tendinopathies. In the meantime, treatment should focus on the correction of underlying causes to reduce the risk of progression to a chronic condition, and on appropriately controlling the patient's discomfort.
Address correspondence to Carrie A. Jaworski, MD, at firstname.lastname@example.org. Reprints are not available from the author.
Author disclosure: Nothing to disclose.
1. Johnson GW, Cadwallader K, Scheffel SB, Epperly TD. Treatment of lateral epicondylitis. Am Fam Physician. 2007;76:843–8,849,851.
2. Scott A, Khan KM, Roberts CR, Cook JL, Duronio V. What do we mean by the term “inflammation”? A contemporary basic science update for sports medicine. Br J Sports Med. 2004;38:372–80.
3. Scott A, Ashe MC. Common tendinopathies in the upper and lower extremities. Curr Sports Med Rep. 2006;5:233–41.
4. Scott A, Khan KM, Heer J, Cook JL, Lian O, Duronio V. High strain mechanical loading rapidly induces tendon apoptosis: an ex vivo rat tibialis anterior model. Br J Sports Med. 2005;39:e25.
5. Almekinders LC, Weinhold PS, Maffulli N. Compression etiology in tendinopathy. Clin Sports Med. 2003;22:703–10.
6. Newcomer KL, Laskowski ER, Idank DM, McLean TJ, Egan KS. Corticosteroid injection in early treatment of lateral epicondylitis. Clin J Sports Med. 2001;11:214–22.
7. Woodley BL, Newsham-West RJ, Baxter GD. Chronic tendinopathy: effectiveness of eccentric exercise. Br J Sports Med. 2007;41:188–98.
8. Murrell GA. Using nitric oxide to treat tendinopathy. Br J Sports Med. 2007;41:227–31.
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