Tendons that transmit the contractile force from muscles to bone are often a clinical problem, especially when dealing with the shoulders, elbows, knees and ankles. Tendons attach to muscles at the myotendinous area and to the bone at the teno-osseous junction.
Tendinopathy is a common medical problem that accounts for approximately 48 percent of occupational illnesses in the United States.2 Sixteen percent of the general population and 21 percent of the elderly suffer with shoulder problems, most of the time due to rotator cuff lesions.3,4 The term "tendinopathy" has replaced the terms tendinitis and tendinosis, since the "itis" or "osis" can only be confirmed by biopsy. Most biopsies of tendons in the chronic stage are performed after four or more months of symptoms, when surgery is a consideration. At four months, inflammatory cells rarely are present; mucoid degeneration, a loss of the tightly bundled collagen, fibrosis and neovascularization are present, all of which point to a tendinosis and failure of healing, rather than a tendonitis.
It is thought that within the first two weeks, there may be some inflammatory reaction5 before the degenerative process begins. It has been shown that cyclic stretching of fibroblasts, which may occur in early injury, produces inflammatory mediators and early tendonitis. Since in tendinosis, tendon degeneration is often asymptomatic, initial symptoms rarely are due to what the patient thinks recently caused the problem, but more likely are due to the already-present degeneration. Tendinitis usually is relieved within two weeks, while tendinosis may not repair fully for months. Often, patients must be made aware that complete relief may take some time.
An important question which is not fully answered is, since we are dealing with a degenerative rather than an inflammatory problem, where does the pain originate? One theory is that the cause of pain is neurogenic. Chronic repetitive loading can stimulate sensory fibers. Anoxia is another cause of pain. It has been found that the sympathetics may be involved, creating an abnormal vasomotor response and eventual anoxia, which triggers painful C fibers.6 Inflammatory mediators also are present, although an actual inflammatory process is not taking place.
There is controversy regarding the etiology of tendinopathy. Currently, it is thought to be multifactor. A mechanical theory is based on repeated microtrauma; but if so, why would exercise improve the condition, and why would exercise in a physiological range harm a tendon?2 The mechanical theory also may include training errors and poor technique. A tendon should be able to adapt to the load placed upon it, but if someone is out of shape and less load has been placed on the tendon, a rapid increase in training load may affect a tendon that cannot adapt fast enough to the new stress, and minimal injury may occur. The tendon may be able to heal, but if the training is increased with excess load, causing a plastic deformation, the healing may be overtaxed and a more severe injury may occur.
Recent studies question this mechanical tensile failure theory of tendons. When the most loaded areas of tendons are evaluated, it appears that those particular areas are not affected initially with tendinopathy. The joint side of the supraspinatus tendon is involved more often than the bursal side, and measurements have shown that the strain of the supraspinatus on the joint side is lower than the bursal side; i.e., the side affected by tendinopathy was found to be "stress-shielded."1 Therefore, the tensile stress theory has to be questioned.
A vascular theory is based on pathology occurring at hypovascular areas (for example, in the Achilles tendon or supraspinatus), but a study by Brooks, et al.,7 found that the "critical zone" (lack of circulation) of the supraspinatus is equally bad in the infraspinatus. Another theory states that rather than vascular compromise, hyperthermia may adversely affect the tendon cells. Lesions of the Achilles tendon usually are located in the central core region, where the greatest temperature increase occurs.8 This may be related to a poor blood supply, since adequate blood supply cools overheated tissue, although repeated episodes of thermally induced damage and repair may be primary. When exercise levels cause the temperature to exceed 42.5° C, fibroblasts lose their viability. Fibroblasts are necessary for healing and repair.
There is also a neurological theory. For example, there is an association between radiculopathy and Achilles tendinopathy.9 The association of nerve-cell endings within tendons and mast cells can be causative, because when neurally mediated mast cells are deregulated, substance P (a nociceptive neurotransmitter) is released. Substance P can be a pro-inflammatory mediator and has been found in rotator-cuff tendinopathy.2
There are many types of treatments for tendinopathy, but few are supported with adequate evidence. Corticosteroid injections for tennis elbow, for example, were found effective only in the short term (two to six weeks); no long-term benefits have been shown.10 Even ultrasound has little clinical evidence as to its efficacy.4 Manual techniques such as Graston technique (GT), friction massage and Active Release have shown clinical results with tendinopathy. The results achieved with deep friction and GT have been explained by their ability to increase fibroblastic proliferation and the establishment of new collagen to replace the old. The most recent study on the use of eccentric exercise has proven to be extremely valuable. A randomized, controlled study was performed on Achilles tendinosis patients who performed eccentric exercises for 12 weeks, while the control group performed concentric exercises. Twelve of 15 patients scheduled for surgery found it unnecessary. In a study on eccentric exercises for supraspinatus tendinopathy, after 12 weeks, 56 percent of patients waiting for surgery improved and rejected surgery.11 Extracorporeal shock-wave therapy has shown mixed results.12
References
- Maganaris CN, Narici MV, Almekinders LC, Maffulli N. Biomechanics and pathophysiology of overuse tendon injuries: ideas on insertional tendinopathy. Sports Med 2004;34(14):1005-1017.
- Li Z, Yang G, Khan M, Stone D, Woo SL, et al. Inflammatory response of human tendon fibroblasts to cyclic mechanical stretching. Am J Sports Med 2004;32:435-40.
- Urwin M, Symmons D, Alison T, et al. Estimating the burden of musculoskeletal disorders in the community: the comparative prevalence of symptoms at different anatomical sites, and the relationship to social deprivation. Ann Rheum Dis 1998;57:649-55.
- Rees JD, Wilson AM, Wolman RL. Current concepts in the management of tendon disorders. Rheumatology 2006,45:508-521.
- Marr CM, McMillan I, Boyd JS, Wright NG, et al. Ultrasonographic and histopathological findings in equine superficial digital flexor tendon injury. Equine Vet J 1993;25:23-29.
- Smith RW, Papadopolous E, Mani R, Cawley MI. Abnormal microvascular responses in a lateral epicondylitis. Br J Rheumatol 1994:33:1166-68.
- Brooks CH, Revell WJ, Heatly FW. A quantitative histological study of the vascularity of the rotator cuff tendon. J of Bone & Joint Surg 1992;74-B(1):151-153.
- Wilson AM, Goodship AE. Exercise-induced hyperthermia as a possible mechanism for tendon degeneration. J Biomech 1994;23:306-312.
- Maffulli N, Irwin AS, Kenward MG, et al. Achilles tendon rupture and sciatica: a possible correlation. Br J Sports Med 1998;32:174-177.
- Hay EM, Paterson SM, Lewis M, et al. Pragmatic randomized controlled trial of local corticosteroid injection and naproxen for treatment of lateral epicondylitis in primary care. Br Med J 1999;319:964-8.
- Jonsson P, Wahlstrom P, Ohberg L, et al. Eccentric training in chronic painful impingement syndrome of the shoulder: results of a pilot study. Knee Surg Sports Traumatol Arthrosc 2006;14:76-81.
- Sabeti-Aschraf M, Dorotka R, Goll A, Trieb K, et al. Extracorporeal shock wave therapy in the treatment of calcific tendonitis of the rotator cuff. Am J Sports Med 2005;33:1365-8.
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