Tendinosis
Tendinosis | |
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Classification and external resources | |
MeSH | D052256 |
Tendinosis, sometimes called chronic tendinitis, tendinosus, chronic tendinopathy or chronic tendon injury, is damage to a tendon at a cellular level (the suffix "osis" implies a pathology of chronic degeneration without inflammation). It is thought to be caused by microtears in the connective tissue in and around the tendon, leading to an increase in tendon repair cells. This may lead to reduced tensile strength, thus increasing the chance of tendon rupture. Tendinosis is often misdiagnosed as tendinitis due to the limited understanding of tendinopathies by the medical community.[1]
Contents
Diagnosis
Swelling in a region of micro damage or partial tear can be detected visually or by touch. Increased water content and disorganized collagen matrix in tendon lesions may be detected by ultrasonography or magnetic resonance imaging.
Symptoms can vary from an ache or pain and stiffness to the local area of the tendon, or a burning that surrounds the whole joint around the inflamed tendon. With this condition, the pain is usually worse during and after activity, and the tendon and joint area can become stiffer the following day as swelling impinges on the movement of the tendon. Many patients report stressful situations in their life in correlation with the beginnings of pain which may contribute to the symptoms.
Treatment
Ligaments are very slow to heal if injured, and rarely regain their original strength. Partial tears heal by the rapid production of disorganized type-III collagen, which is weaker than normal tendon. Recurrence of injury in the damaged region of tendon is common.
Standard treatment of tendon injuries is largely palliative. Use of non-steroidal anti-inflammatory drugs combined with Physical Therapy, rest and gradual return to exercise is a common therapy, although there is evidence to suggest that tendinosis is not an inflammatory disorder, and that anti-inflammatory drugs are not an effective treatment[2] and that inflammation does not cause tendon dysfunction.[3] There are a variety of treatment options, but more research is necessary to determine their effectiveness. Initial recovery is usually within 2 to 3 months and full recovery is within 3 to 6 months. About 80% of patients will fully recover.[4]
On-going research
Both eccentric loading and extracorporeal shockwave therapy are currently being researched as possible treatments for tendinosis. One study found both modalities to be equally effective in treating tendinosis of the Achilles tendon and more effective than a 'wait and see' approach.[5] Other treatments for which research is on-going includes vitamin E, vitamin B6, nitric oxide and stem cell injections.
Soft Tissue Mobilization
Augmented Soft Tissue Mobilization (ASTM) is a form of manual therapy that has been shown in studies on rats to speed the healing of tendons by increasing fibroblast activity.[6][7] One case study showed ASTM resulting in full recovery in the case of an athlete suffering from chronic ankle pain and fibrosis, after an unsuccessful course of surgery and conventional physical therapy.[8]
Vitamin B6
Various studies have supported the efficacy of vitamin B6 in controlling or preventing pathology to the synovial membrane of affected tendons, which commonly occurs in many cases of chronic tendinitis.[9]
Eccentric loading
Perhaps the most promising avenue of therapy is indicated in a line of research finding dramatic rates of recovery including complete remodeling of chronically damaged tendon tissue with eccentric loading.[10][11][12][13][14][15][4][16]
Inflatable brace
The use of an inflatable brace (AirHeel) was shown to be as effective as eccentric loading in the treatment of chronic Achilles tendinopathy. Both modalities produced significant reduction in pain scores, but their combination was no more effective than either treatment alone.[17]
Shock-wave therapy
Shock-wave therapy (SWT) may be effective in treating calcific tendinosis in both humans[18] and rats.[19] In rat subjects, SWT increased levels of healing hormones and proteins leading to increased cell proliferation and tissue regeneration in tendons. Another study found no evidence that SWT was useful in treating chronic pain in the Achilles tendon.[20]
Tendon Bioengineering
The future of non-surgical care for tendinosis is likely bioengineering. Ligament reconstruction is possible using mesenchymal stem cells and a silk scaffold.[21] These same stem cells were capable of seeding repair of damaged animal tendons.[22]
Vitamin E
Vitamin E has been found to increase the activity of fibroblasts, leading to increased collagen fibrils and synthesis, which seems to speed up the regeneration and increase the regenerative capacity of tendons.[23][24]
Nitric oxide
Nitric oxide (NO) also appears to play a role in tendon healing[25] and inhibition of NO synthesis impairs tendon healing.[26] Supplementing with arginine, the amino acid that the body uses to form NO, may be useful in tendon healing.[27] The use of a NO delivery system (glyceryl trinitrate patches) applied over the area of maximal tenderness was tested in three clinical trials for the treatment of tendinopathies and was found to significantly reduce pain and increase range of motion and strength.[28]
See also
References
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External links
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- ↑ Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
- ↑ Marsolais D, Duchesne E, Côté CH, Frenette J. (2007). "Inflammatory cells do not decrease the ultimate tensile strength of intact tendons in vivo and in vitro: protective role of mechanical loading". J Appl Physiol. 102 (1): 3–4. doi:10.1152/japplphysiol.00162.2006. PMID 16916923.
- ↑ 4.0 4.1 Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
- ↑ Rompe JD, Nafe B, Furia JP, Maffulli N (2007). "Eccentric loading, shock-wave treatment, or a wait-and-see policy for tendinopathy of the main body of tendo Achillis: a randomized controlled trial". Am J Sports Med. 3 (35): 374–83. doi:10.1177/0363546506295940. PMID 17244902.
- ↑ Craig J. Davidson et. al., "Rat tendon morphologic and functional changes resulting from soft tissue mobilization", Medicine & Science in Sports & Exercise, Mar. 1997, Vol. 29, No. 3, pp. 313-319.
- ↑ Gale M. Gehlsen, "Fibroblast responses to variation in soft tissue mobilization pressure", Medicine & Science in Sports & Exercise, Apr. 1999, Vol. 31, No. 4, pp. 531-535.
- ↑ Thomas J. Melham et. al., "Chronic ankle pain and fibrosis successfully treated with a new noninvasive augmented soft tissue mobilization technique (ASTM): a case report", Medicine & Science in Sports & Exercise, Jun. 1998, Vol. 30, No. 6, pp. 801-804.
- ↑ Template:Cite author=Ellis, John M
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- ↑ Petersen W, Welp R, Rosenbaum D (June 14, 2007). "Chronic Achilles Tendinopathy: A Prospective Randomized Study Comparing the Therapeutic Effect of Eccentric Training, the AirHeel Brace, and a Combination of Both". Am J Sports Med. 35 (10): 1659–67. doi:10.1177/0363546507303558. PMID 17569792.
- ↑ Cacchio A, Paoloni M, Barile A, Don R, de Paulis F, Calvisi V, Ranavolo A, Frascarelli M, Santilli V, Spacca G (2006). "Effectiveness of radial shock-wave therapy for calcific tendinosis of the shoulder: single-blind, randomized clinical study". Phys Ther. 5 (86): 672–82. PMID 16649891.
- ↑ Chen YJ, Wang CJ, Yang KD, Kuo YR, Huang HC, Huang YT, Sun YC, Wang FS (2004). "Extracorporeal shock waves promote healing of collagenase-induced Achilles tendinosis and increase TGF-beta1 and IGF-I expression". J Orthop Res. 22 (4): 854–61. doi:10.1016/j.orthres.2003.10.013. PMID 15183445.
- ↑ Costa ML, Shepstone L, Donell ST, Thomas TL (2005). "Shock wave therapy for chronic Achilles tendon pain: a randomized placebo-controlled trial". Clin Orthop Relat Res. 440: 199–204. doi:10.1097/01.blo.0000180451.03425.48. PMID 16239807.
- ↑ Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
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- ↑ Erickson, Laurie (2002-07-01). "Future Treatments". Retrieved 2007-04-02.
- ↑ Murrell GA. (2007). "Using nitric oxide to treat tendinopathy". Br J Sports Med. 41 (4): 227–31. doi:10.1136/bjsm.2006.034447. PMC 2658939 Freely accessible. PMID 17289859.