There is an ongoing debate on the role of inflammation and degeneration in tendons, especially from overuse injury. If the primary problem is due to inflammation, then an anti-inflammatory approach is regarded as the answer - but has not been found to be a satisfactory solution.
Biopsy examination of tendons has shown that inflammatory cells are scarce, while degeneration is common. One problem with this statement is that most of the biopsies were taken in the chronic stages, often during surgery. But recent human biopsies of tendons with smaller tears with a less degenerative picture revealed a significant inflammatory infiltrate of mast cells and macrophages.2 Still, it appears that in the chronic stage, the term tendinosis is more applicable than tendinitis.
Abate, et al., state that inflammation and degeneration are not mutually exclusive, but work together in the pathogenic cascade of tendon pathology.3 Depending on factors such as age (rotator cuff pathology up to 50 percent in individuals 70 years and older), traumas from overuse to fractures, genetic background causing abnormal collagen formation (mesenchymal syndrome: patients with multiple problems such as epicondylopathy, carpal tunnel, De Quervian), a combination of localized inflammatory reactions and microdegeneration can occur.
Histopathological studies of tendon pathology, therefore, do not find inflammatory and degenerative changes in isolation, but rather a coexistence of the two changes in adjacent areas of pathological samples. Inflammation in early tendinopathy could represent an innate attempt at tissue repair, while prolonged inflammation could be related to ongoing pathology.
A good example of the combination of inflammation and degeneration is seen in tendons that have a synovial sheath, such as tibialis posterior, peroneal, and extensor and flexor tendons of the wrist and hand. In the acute state, there are increased fibroblasts and fibrinous exudates. At the same time, degenerative changes "proceed in parallel" with the inflammatory and regenerating changes. Adhesions often develop between the tendon and paratenon and in the chronic stages, the fibroblasts develop a contractile ability as they become myofibroblasts, helping to create forces for wound contraction.
Myofibroblasts are also capable of maintaining a "prolonged contracted state in pretendinous adhesions, which, in turn, may lead to constriction of vascular channels, with further impairment of circulation inside the tendon, where a proliferation of new microvessels is frequently present."3
From the medical point of view, the latest approach to tendon disorders is the use of cell therapy; for example, the injection of the patient's platelet-rich plasma into the lesion where inherent growth factors are released from platelets, encouraging tenocyte migration and differentiation at the site of tendon injury. Newer cell therapy techniques are being developed to regenerate the tendon, especially since tendons have a low resident cell population and tissue turnover rate.4
Stem cell techniques do appear promising. Use of the skin as a source of stem cells is very promising since it contains large numbers of fibroblasts that have shown to take on the characteristics of tenocytes and lay down collagen when immersed in a tendon environment. At present, there are no long-term studies, but results look very promising. Then again, just as there are no long-term studies using mechanical load techniques such as Graston, ART, fascial manipulation and other load-based methods, results also look very promising.
- Bisset L, Beller E, Jull G, et al. Mobilisation with movement and exercise, corticosteroid injection, or wait and see for tennis elbow: randomized trial. BMJ, 2006;333.
- Millar NL, Hueber AJ, Reilly JH, Xu Y, et al. Inflammation is present in early human tendinopathy. Amer J Sorts Med, 2010;38(10):2085-91.
- Abate M, Gravare S, Siljeholm C, Di Iorio A, et al. Pathogenesis of tendinopathies: inflammation or degeneration? Arthritis Research & Therapy, 2009;11:235.
- Obaid H, Connell D. Cell therapy in tendon disorders. What is the current evidence? Amer J Sports Med, 2010;38(10):2123-32.
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