Wednesday, December 29, 2010

Ankle Sprains in Basketball Kinesio Tape Vs Traditional rigid athletic tape in treating ankle sprians

Basketbell Players Face High Risk

Researchers at Hacettepe University in Ankara, Turkey, are studying the "Effect of Athletic Taping and Kinesio Taping on Functional Performance in Chronic Inversion Ankle Sprain in Basketball Players." Professor Gul Baltaci, PT., Ph.D., CKTI is working with a team to document and measure the different results for players using Kinesio Tape and traditional rigid athletic tape in treating ankle sprains.

The researchers have worked with 20 male basketball players between 18 and 22 years of age, from whom 15 players met the requirements to participate. These participants were assessed with four different levels of taping: athletic tape, Kinesio Tape, a sham taping, and no tape at all.

So far the study indicates that athletic taping impaired participants' performance on some of the functional performance tests. Unlike the athletic taping method, Kinesio Taping did not cause any decrease on functional performance. Positive influences were seen in some of the functional performance tests. The Hacettepe researchers have noted that "Future researches which focus on functional performance should test taping methods with different performance tests."

Thursday, December 23, 2010

Interferential Current Therapy for Musculoskeletal Pain

Effectiveness of Interferential Current Therapy in the Management of Musculoskeletal Pain: A Systematic Review and Meta-Analysisfrom Physical Therapy current issue by Fuentes, J. P., Armijo Olivo, S., Magee, D. J., Gross, D. P.

Interferential current (IFC) is a common electrotherapeutic modality used to treat pain. Although IFC is widely used, the available information regarding its clinical efficacy is debatable.

The aim of this systematic review and meta-analysis was to analyze the available information regarding the efficacy of IFC in the management of musculoskeletal pain.

Data Sources
Randomized controlled trials were obtained through a computerized search of bibliographic databases (ie, CINAHL, Cochrane Library, EMBASE, MEDLINE, PEDro, Scopus, and Web of Science) from 1950 to February 8, 2010.

Data Extraction
Two independent reviewers screened the abstracts found in the databases. Methodological quality was assessed using a compilation of items included in different scales related to rehabilitation research. The mean difference, with 95% confidence interval, was used to quantify the pooled effect. A chi-square test for heterogeneity was performed.

Data Synthesis
A total of 2,235 articles were found. Twenty studies fulfilled the inclusion criteria. Seven articles assessed the use of IFC on joint pain; 9 articles evaluated the use of IFC on muscle pain; 3 articles evaluated its use on soft tissue shoulder pain; and 1 article examined its use on postoperative pain. Three of the 20 studies were considered to be of high methodological quality, 14 studies were considered to be of moderate methodological quality, and 3 studies were considered to be of poor methodological quality. Fourteen studies were included in the meta-analysis.

Interferential current as a supplement to another intervention seems to be more effective for reducing pain than a control treatment at discharge and more effective than a placebo treatment at the 3-month follow-up. However, it is unknown whether the analgesic effect of IFC is superior to that of the concomitant interventions. Interferential current alone was not significantly better than placebo or other therapy at discharge or follow-up. Results must be considered with caution due to the low number of studies that used IFC alone. In addition, the heterogeneity across studies and methodological limitations prevent conclusive statements regarding analgesic efficacy.

Monday, December 20, 2010



Valid 1 January 2011

All Prohibited Substances shall be considered as “Specified Substances” except Substances in classes S1, S2.1 to S2.5, S.4.4 and S6.a, and Prohibited Methods M1, M2 and M3.


Any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use (i.e. drugs under pre-clinical or clinical development or discontinued) is prohibited at all times.


Anabolic agents are prohibited.

1. Anabolic Androgenic Steroids (AAS)

a. Exogenous* AAS, including:
1-androstenediol (5α-androst-1-ene-3β,17β-diol ); 1-androstenedione (5α-androst-1-ene-3,17-dione); bolandiol (19-norandrostenediol); bolasterone; boldenone; boldione (androsta-1,4-diene-3,17-dione); calusterone; clostebol; danazol (17α-ethynyl-17β-hydroxyandrost-4-eno[2,3-d]isoxazole); dehydrochlormethyltestosterone (4-chloro-17β-hydroxy-17α-methylandrosta-1,4-dien-3-one); desoxymethyltestosterone (17α-methyl-5α-androst-2-en-17β-ol); drostanolone; ethylestrenol (19-nor-17α-pregn-4-en-17-ol); fluoxymesterone; formebolone; furazabol (17β-hydroxy-17α-methyl-5α-The 2011 Prohibited List 18 September 2010 3
androstano[2,3-c]-furazan); gestrinone; 4-hydroxytestosterone (4,17β-dihydroxyandrost-4-en-3-one); mestanolone; mesterolone; metenolone; methandienone (17β-hydroxy-17α-methylandrosta-1,4-dien-3-one); methandriol; methasterone (2α, 17α-dimethyl-5α-androstane-3-one-17β-ol); methyldienolone (17β-hydroxy-17α-methylestra-4,9-dien-3-one); methyl-1-testosterone (17β-hydroxy-17α-methyl-5α-androst-1-en-3-one); methylnortestosterone (17β-hydroxy-17α-methylestr-4-en-3-one); methyltestosterone; metribolone (methyltrienolone, 17β-hydroxy-17α-methylestra-4,9,11-trien-3-one); mibolerone; nandrolone; 19-norandrostenedione (estr-4-ene-3,17-dione); norboletone; norclostebol; norethandrolone; oxabolone; oxandrolone; oxymesterone; oxymetholone; prostanozol (17β-hydroxy-5α-androstano[3,2-c] pyrazole); quinbolone; stanozolol; stenbolone; 1-testosterone (17β-hydroxy-5α-androst-1-en-3-one); tetrahydrogestrinone (18a-homo-pregna-4,9,11-trien-17β-ol-3-one); trenbolone; and other substances with a similar chemical structure or similar biological effect(s).

b. Endogenous** AAS when administered exogenously: androstenediol (androst-5-ene-3β,17β-diol); androstenedione (androst-4-ene-3,17-dione); dihydrotestosterone (17β-hydroxy-5α-androstan-3-one); prasterone (dehydroepiandrosterone, DHEA); testosterone
and the following metabolites and isomers:

5α-androstane-3α,17α-diol; 5α-androstane-3α,17β-diol; 5α-androstane-3β,17α-diol; 5α-androstane-3β,17β-diol; androst-4-ene-3α,17α-diol; androst-4-ene-3α,17β-diol; androst-4-ene-3β,17α-diol; androst-5-ene-3α,17α-diol; androst-5-ene-3α,17β-diol; androst-5-ene-3β,17α-diol; 4-androstenediol (androst-4-ene-3β,17β-diol); 5-androstenedione (androst-5-ene-3,17-dione); epi-dihydrotestosterone; epitestosterone; 3α-hydroxy-5α-androstan-17-one; 3β-hydroxy-5α-androstan-17-one; 19-norandrosterone; 19-noretiocholanolone.

2. Other Anabolic Agents, including but not limited to:

Clenbuterol, selective androgen receptor modulators (SARMs), tibolone, zeranol, zilpaterol.

For purposes of this section:
* “exogenous” refers to a substance which is not ordinarily capable of being produced by the body naturally.
** “endogenous” refers to a substance which is capable of being produced by the body naturally.The 2011 Prohibited List 18 September 2010 4


The following substances and their releasing factors are prohibited:

1. Erythropoiesis-Stimulating Agents [e.g. erythropoietin (EPO), darbepoetin (dEPO), hypoxia-inducible factor (HIF) stabilizers, methoxy polyethylene glycol-epoetin beta (CERA), peginesatide (Hematide)];

2. Chorionic Gonadotrophin (CG) and Luteinizing Hormone (LH) in males;

3. Insulins;

4. Corticotrophins;

5. Growth Hormone (GH), Insulin-like Growth Factor-1 (IGF-1), Fibroblast Growth Factors (FGFs), Hepatocyte Growth Factor (HGF), Mechano Growth Factors (MGFs), Platelet-Derived Growth Factor (PDGF), Vascular-Endothelial Growth Factor (VEGF) as well as any other growth factor affecting muscle, tendon or ligament protein synthesis/degradation, vascularisation, energy utilization, regenerative capacity or fibre type switching;

and other substances with similar chemical structure or similar biological effect(s).


All beta-2 agonists (including both optical isomers where relevant) are prohibited except salbutamol (maximum 1600 micrograms over 24 hours) and salmeterol when taken by inhalation in accordance with the manufacturers’ recommended therapeutic regime.
The presence of salbutamol in urine in excess of 1000 ng/mL is presumed not to be an intended therapeutic use of the substance and will be considered as an Adverse Analytical Finding unless the Athlete proves, through a controlled pharmacokinetic study, that the abnormal result was the consequence of the use of a therapeutic dose (maximum 1600 micrograms over 24 hours) of inhaled salbutamol.

The 2011 Prohibited List 18 September 2010 5


The following classes are prohibited:

1. Aromatase inhibitors including, but not limited to: aminoglutethimide, anastrozole, androsta-1,4,6-triene-3,17-dione (androstatrienedione), 4-androstene-3,6,17 trione (6-oxo), exemestane, formestane, letrozole, testolactone.

2. Selective estrogen receptor modulators (SERMs) including, but not limited to: raloxifene, tamoxifen, toremifene.

3. Other anti-estrogenic substances including, but not limited to: clomiphene, cyclofenil, fulvestrant.

4. Agents modifying myostatin function(s) including, but not limited, to: myostatin inhibitors.


Masking agents are prohibited. They include:

Diuretics, desmopressin, plasma expanders (e.g. glycerol; intravenous administration of albumin, dextran, hydroxyethyl starch and mannitol), probenecid; and other substances with similar biological effect(s).

Diuretics include:

Acetazolamide, amiloride, bumetanide, canrenone, chlorthalidone, etacrynic acid, furosemide, indapamide, metolazone, spironolactone, thiazides (e.g. bendroflumethiazide, chlorothiazide, hydrochlorothiazide), triamterene; and other substances with a similar chemical structure or similar biological effect(s) (except drosperinone, pamabrom and topical dorzolamide and brinzolamide, which are not prohibited).

The use In- and Out-of-Competition, as applicable, of any quantity of a substance subject to threshold limits (i.e. salbutamol, morphine, cathine, ephedrine, methylephedrine and pseudoephedrine) in conjunction with a diuretic or other masking agent requires the deliverance of a specific Therapeutic Use Exemption for that substance in addition to the one granted for the diuretic or other masking agent.


The following are prohibited:

1. Blood doping, including the use of autologous, homologous or heterologous blood or red blood cell products of any origin.

2. Artificially enhancing the uptake, transport or delivery of oxygen, including, but not limited to, perfluorochemicals, efaproxiral (RSR13) and modified haemoglobin products (e.g. haemoglobin-based blood substitutes, microencapsulated haemoglobin products), excluding supplemental oxygen.


The following is prohibited:

1. Tampering, or attempting to tamper, in order to alter the integrity and validity of Samples collected during Doping Control is prohibited. These include but are not limited to catheterisation, urine substitution and/or adulteration (e.g. proteases).

2. Intravenous infusions are prohibited except for those legitimately received in the course of hospital admissions or clinical investigations.

3. Sequential withdrawal, manipulation and reinfusion of whole blood into the circulatory system is prohibited.


The following, with the potential to enhance sport performance, are prohibited:

1. The transfer of nucleic acids or nucleic acid sequences;

2. The use of normal or genetically modified cells;

3. The use of agents that directly or indirectly affect functions known to influence performance by altering gene expression. For example, Peroxisome Proliferator Activated Receptor δ (PPARδ) agonists (e.g. GW 1516) and PPARδ-AMP-activated protein kinase (AMPK) axis agonists (e.g. AICAR) are prohibited.


In addition to the categories S0 to S5 and M1 to M3 defined above, the following categories are prohibited In-Competition:



All stimulants (including both optical isomers where relevant) are prohibited, except imidazole derivatives for topical use and those stimulants included in the 2011 Monitoring Program*.

Stimulants include:

a: Non-Specified Stimulants:
Adrafinil; amfepramone; amiphenazole; amphetamine; amphetaminil; benfluorex; benzphetamine; benzylpiperazine; bromantan; clobenzorex; cocaine; cropropamide; crotetamide; dimethylamphetamine; etilamphetamine; famprofazone; fencamine; fenetylline; fenfluramine; fenproporex; furfenorex; mefenorex; mephentermine; mesocarb; methamphetamine(d-); p-methylamphetamine; methylenedioxyamphetamine; methylenedioxymethamphetamine; modafinil; norfenfluramine; phendimetrazine; phenmetrazine; phentermine; 4-phenylpiracetam (carphedon); prenylamine; prolintane.

A stimulant not expressly listed in this section is a Specified Substance.

b: Specified Stimulants (examples):
Adrenaline**; cathine***; ephedrine****; etamivan; etilefrine; fenbutrazate; fencamfamin; heptaminol; isometheptene; levmetamfetamine; meclofenoxate; methylephedrine****; methylhexaneamine (dimethylpentylamine); methylphenidate; nikethamide; norfenefrine; octopamine; oxilofrine; parahydroxyamphetamine; pemoline; pentetrazol; phenpromethamine; propylhexedrine; pseudoephedrine*****; selegiline; sibutramine; strychnine; tuaminoheptane; and other substances with a similar chemical structure or similar biological effect(s).

* The following substances included in the 2011 Monitoring Program (bupropion, caffeine, phenylephrine, phenylpropanolamine, pipradol, synephrine) are not considered as Prohibited Substances.
** Adrenaline associated with local anaesthetic agents or by local administration (e.g. nasal, ophthalmologic) is not prohibited.
*** Cathine is prohibited when its concentration in urine is greater than 5 micrograms per milliliter.
**** Each of ephedrine and methylephedrine is prohibited when its concentration in urine is greater than 10 micrograms per milliliter.
***** Pseudoephedrine is prohibited when its concentration in urine is greater than 150 micrograms per milliliter.


The following are prohibited:
Buprenorphine, dextromoramide, diamorphine (heroin), fentanyl and its derivatives, hydromorphone, methadone, morphine, oxycodone, oxymorphone, pentazocine, pethidine.

Natural (e.g. cannabis, hashish, marijuana) or synthetic delta 9-tetrahydrocannabinol (THC) and cannabimimetics [e.g. “Spice” (containing JWH018, JWH073), HU-210] are prohibited.

All glucocorticosteroids are prohibited when administered by oral, intravenous, intramuscular or rectal routes.


Alcohol (ethanol) is prohibited In-Competition only, in the following sports. Detection will be conducted by analysis of breath and/or blood. The doping violation threshold (haematological values) is 0.10 g/L.

• Aeronautic (FAI)
• Archery (FITA)
• Automobile (FIA)
• Karate (WKF)
• Motorcycling (FIM)
• Ninepin and Tenpin Bowling (FIQ)
• Powerboating (UIM)

Unless otherwise specified, beta-blockers are prohibited In-Competition only, in the following sports.
• Aeronautic (FAI)
• Archery (FITA) (also prohibited Out-of-Competition)
• Automobile (FIA)
• Billiards and Snooker (WCBS)
• Bobsleigh and Skeleton (FIBT)
• Boules (CMSB)
• Bridge (FMB)
• Curling (WCF)
• Darts (WDF)
• Golf (IGF)
• Motorcycling (FIM)
• Modern Pentathlon (UIPM) for disciplines involving shooting
• Ninepin and Tenpin Bowling (FIQ)
• Powerboating (UIM)
• Sailing (ISAF) for match race helms only
• Shooting (ISSF, IPC) (also prohibited Out-of-Competition)
• Skiing/Snowboarding (FIS) in ski jumping, freestyle aerials/halfpipe and snowboard halfpipe/big air
• Wrestling (FILA)

Beta-blockers include, but are not limited to, the following:
Acebutolol, alprenolol, atenolol, betaxolol, bisoprolol, bunolol, carteolol, carvedilol, celiprolol, esmolol, labetalol, levobunolol, metipranolol, metoprolol, nadolol, oxprenolol, pindolol, propranolol, sotalol, timolol.

Thursday, December 16, 2010

Boxing Bad For The Brain

Boxing Bad For The Brain

Up to 20% of professional boxers develop neuropsychiatric sequelae. But which acute complications and which late sequelae can boxers expect throughout the course of their career? These are the questions studied by Hans Förstl from the Technical University Munich and his co-authors in the current issue ofDeutsches Ärzteblatt International (Dtsch Arztebl Int 2010; 107[47]: 835-9).

Their evaluation of the biggest studies on the subject of boxers’ health in the past 10 years yielded the following results: The most relevant acute consequence is the knock-out, which conforms to the rules of the sport and which, in neuropsychiatric terms, corresponds to cerebral concussion. In addition, boxers are at substantial risk for acute injuries to the head, heart, and skeleton. Subacute consequences after being knocked out include persistent symptoms such as headaches, impaired hearing, nausea, unstable gait, and forgetfulness. The cognitive deficits after blunt craniocerebral trauma last measurably longer than the symptoms persist in the individual’s subjective perception. Some 10–20% of boxers develop persistent neuropsychiatric impairments. The repeated cerebral trauma in a long career in boxing may result in boxer’s dementia (dementia pugilistica), which is neurobiologically similar to Alzheimer’s disease.

Full Article

Monday, December 13, 2010

Nonsteroidal Antiinflammatory Drugs in Tendinopathy: Not so helpful

Clinical Journal of Sport Medicine:
January 2006 - Volume 16 - Issue 1 - pp 1-3

Nonsteroidal Antiinflammatory Drugs in Tendinopathy: Friend or Foe

Magra, Merzesh MRCS; Maffulli, Nicola PhD, FRCS (Orth)

Free AccessAuthor Information

Tendinopathy, a broad term used to describe disorders in and around tendons,1,2 is associated with repetitive tensile forces exerted on tendons.3-5 Rapid increases in the duration and intensity of these forces may cause tendon injuries,6possibly the starting point in the pathogenesis of chronic tendinopathy. The exact incidence of chronic tendinopathy is unknown given the vast population of professional and recreational athletes suffering from this condition at different anatomic sites. Studies on incidence of tendinopathies are usually site7 or sport8 specific, and only provide an approximation of the magnitude of the problem faced by musculoskeletal and sports medicine clinicians in treating this disorder. In addition, a large number of sedentary subjects develop tendinopathy with no apparent history of increased physical activity.

Disorganized, haphazard healing, with frayed, separated, and otherwise disrupted collagen fibrils, are features of tendinopathy.3,9 These lesions are characterized by the absence of inflammatory cells and a poor healing response.1,9 Age-related tendon changes, and not just mechanical overload, may thus play a role in the pathogenesis of tendinopathy, although the exact etiologic, pathophysiologic, and healing mechanisms are still unknown.5,10

Gene expression studies have shown an absence of any inflammatory process in chronic Achilles tendinopathy.11Microdialysis experiments have shown no evidence of intratendinous chemical inflammation, with prostaglandin E2(PGE2) levels being normal in chronic tendinopathies.12Microdialysis has also shown higher levels of glutamate, an excitatory neurotransmitter and a potent modulator of pain in the central nervous system,13 in tendinopathic tendons compared with normal tendons.12,14 The same technique reveals that the local concentration of lactate in the tendinopathic Achilles tendon is almost twice that of the normal Achilles tendon.15

It is possible that there is an ischemic component in the pathogenesis of tendinopathy. Ischemia may precede the start of tendinopathy, but examination of tendinopathic lesions reveals neovascularization16 and increased blood flow in the affected area of the tendon.17 Neovascularization may be a response to a primary injury or may be the result of a metabolic disorder. It is possible that anaerobic conditions exist in areas of tendinopathy that have a poor blood supply, and are the primary cause of neovascularization.15Neovessels and their accompanying nerves, may be responsible for the pain in the tendinopathic tendon,18 which would account for the success of local injection of sclerosants such as Polidocanol in the management tendinopathy.18

Chronic tendinopathy may well be the final manifestation of a long-standing metabolic process in which inflammation, although an initiator, does not participate in the final histopathologic and biochemical features of chronic tendinopathy. It is important in understanding this hypothesis to recall the mechanism of tendon healing. A tendon heals by undergoing inflammatory (1-7 days of injury), proliferative (7-21 days), and remodeling (3 weeks-1 year) phases.3,19Despite collagen maturation and remodeling, tendons are biochemically and metabolically less active than bone and muscle.3,19 Type III collagen synthesized by fibroblasts in the proliferative phase is gradually replaced by type I collagen from days 12 to 14, with a progressive increase in tensile strength.3

In a rat Achilles tendinopathy model, different populations of inflammatory cells, such as neutrophils and macrophages, accumulate immediately after injury,20 followed by a further macrophage accumulation 1 to 3 days after injury.20Nonsteroidal antiinflammatory drugs (NSAIDs) decrease the accumulation of inflammatory cells in the acute phase of inflammation, but neither prevent tissue damage nor accelerate the overall healing process.21

No studies have been performed to date on animal models with chronic tendinopathy, but we could assume that injury followed by an inflammatory reaction could start a chain of events that ultimately leads to chronic tendinopathy, which, at the point of clinical relevance, does not show inflammatory features.1,9 From our understanding of the etiology and development of this condition, we believe that there is no scientific basis to manage chronic tendinopathy with NSAIDs.

Back to Top | Article Outline


NSAIDs inhibit tissue inflammation by repressing cyclooxygenase (COX) activity, with a reduction in the synthesis of proinflammatory prostaglandins.22

Management of an anatomically defined medical condition is ideally based on an understanding of its pathophysiology. Although, as noted earlier, tendinopathy is a noninflammatory condition, NSAIDs are widely used in attempts at treatment.23-27 Ironically, the analgesic effect of NSAIDs28allows patients to ignore early symptoms, possibly imposing further damage on the affected tendon and delaying definitive healing. Topical Naproxen gel produced a marginal advantage in relieving symptoms after 3 and 7 days in patients with acute tendinopathies who had symptoms for less than 48 hours.29 Although NSAIDs may provide some pain relief in such patients, they do not actually result in sustained improvement in the healing process.2 It is still not known whether NSAIDs actually change the natural history of tendinopathy or whether they merely exert an analgesic action.2 Recent studies on rats with acute tendon injuries show that NSAID administration does not prevent collagen degradation and loss of tensile force in tendons.21 It is therefore questionable whether NSAIDs should be used to alleviate pain in so-called acute tendinopathy.21

NSAIDs are not effective in athletes with tendinopathy.23Most studies of NSAID treatment of tendinopathy have a short follow-up.2 Double-blind, randomized, placebo-controlled clinical trials of NSAIDs used in the management of tendinopathies based on clinical symptoms and signs only have shown no beneficial effects.30 Even these placebo-controlled clinical studies are difficult to interpret because of the inability to control for the severity of the lesion, level of athletic participation, and other variables.

NSAIDs could theoretically benefit patients with tendinopathy by increasing the tensile strength of tendons via accelerated formation of cross-linkages between collagen fibers.23,28,31 In animal models, COX inhibitors do show a beneficial effect on tendon regeneration after transection, in exactly this fashion.32 However, these studies were conducted on rats with Achilles tendons that had been surgically divided, a situation that does not reflect the conditions encountered in chronic tendinopathy. Another study using a rat model showed that, in the first few days after Achilles tendon transection, the inflammatory response was necessary for normal repair, and should not be inhibited.33 Early NSAID administration led to a reduction in the amount of force and stress required for the tendon to fail.33 During remodeling, on the other hand, inflammation has a negative influence, and NSAIDs such as COX-2 inhibitors might be valuable for the final outcome.33 Indeed, late treatment with COX-2 inhibitors leads to increased tensile strength, although they do not change the histopathologic picture.33 COX-2 inhibitors should therefore be avoided in the early period after tendon injury, given their deleterious effect on tensile strength.

Although in vitro studies on human tendon fibroblasts treated with NSAIDs have shown a decreased expression of PGE2, they also show an increased expression of leukotriene B4(LTB4).34 The reduction in PGE2 may give patients some pain relief; increased LTB4, however, could potentially exacerbate the situation via increased neutrophilic infiltration and lymphocyte activation,35 paradoxically causing inflammatory and degenerative changes in the tendon. Thus, in tendinopathy, leukotriene pathway activation occurs after cyclical strain on tendons, and treatment with NSAIDs may actually worsen the condition.34

Back to Top | Article Outline


Pharmacologic management strategies for tendinopathies vary considerably, and are frequently based on empirical evidence. Can the continued use of NSAIDs for the treatment of tendinopathies be justified? The available literature would suggest that in the absence of an overt inflammatory process, there is no rational basis for the use of NSAIDs in chronic tendinopathy, because they are unlikely to change its still ill-defined natural history. Despite this reality, many clinicians still anticipate a quicker and better recovery using these agents. There is no biologic basis for NSAID effectiveness in treating this condition, and no evidence of any benefit. NSAIDs appear to be effective, to some extent, for pain control. This causes patients to ignore early symptoms, and thus may lead to further damage of the tendon and delay definitive healing. Early NSAIDs administration after an injury may have a deleterious effect on long-term tendon healing. It would thus seem reasonable to shift our research efforts to other forms of conservative management. Examining strategies that promote the migration and activation of tenocytes to influence tendon healing and function might be an appropriate first step. It is equally appropriate to limit our use of NSAIDs in the management of tendinopathy. What may appear clinically as an acute tendinopathy is actually a well-advanced failure of a chronic healing response in which there is neither histologic nor biochemical evidence of inflammation.

Back to Top | Article Outline


1. Khan KM, Cook JL, Kannus P, et al. Time to abandon the tendonitis myth. Painful overuse tendon conditions have a non-inflammatory pathology. BMJ. 2002;324:626-627.

2. Almekinders LC, Temple JD. Etiology, diagnosis, and treatment of tendonitis: an analysis of the literature. Med Sci Sports Exerc. 1998;30:1183-1190.

3. Jozsa L, Kannus P. Human tendons. Champaign, IL: Human Kinetics; 1997.

4. Kannus P. Etiology and pathophysiology of chronic tendon disorders in sports. Scand J Med Sci Sports. 1997;7:78-85.

5. Almekinders LC, Deol G. The effects of ageing, anti-inflammatory drugs, and ultrasound on in vitro response of tendon tissue. Am J Sports Med. 1999;27:417-421.

6. Nicholas JA. Clinical observations on sports-induced soft tissue injuries. In: Leadbetter WB, Buckwalter JA, Gordon SL, eds. Sports-Induced Inflammation. Park Ridge, IL: American Academy of Orthopaedic Surgeons; 1990:129-148.

7. Kujala UM, Sarna S, Kaprio J. Cumulative incidence of Achilles tendon rupture and tendinopathy in male former elite athletes. Clin J Sport Med. 2005;15:133-135.

8. Taunton JE, Ryan MB, Clement DB, et al. A retrospective case-control analysis of 2002 running injuries. Br J Sports Med. 2002;36:95-101.

9. Khan KM, Cook JL, Bonar F, et al. Histopathology of common tendinopathies. Update and implications for clinical management. Sports Med. 1999;27:393-408.

10. Riley GP, Curry V, DeGroot J, et al. Matrix metalloproteinase activities and their relationship with collagen remodelling in tendon pathology. Matrix Biol. 2002;21:185-195.

11. Alfredson H, Ljung BO, Thorsen K, et al. In vivo investigation of ECRB tendons with microdialysis technique-no signs of inflammation but high amounts of glutamate in tennis elbow. Acta Orthop Scand. 2000;71:475-479.

12. Alfredson H, Lorentzon M, Bäckman S, et al. cDNA-arrays and real-time quantitative PCR techniques in the investigation of chronic Achilles tendinosis. J Orthop Res. 2003;21:970-975.

13. Dickenson AH, Chapman V, Green GM. The pharmacology of excitatory and inhibitory amino acid mediated events in the transmission and modulation of pain in the spinal cord. A review. Gen Pharmacol. 1997;28:633-638.

14. Alfredson H, Forsgren S, Thorsen K, et al. In vivo microdialysis and immunohistochemical analyses of tendon tissue demonstrated high amounts of free glutamate and glutamate NMDAR1 receptors, but no signs of inflammation, in jumper's knee. J Orthop Res. 2001;19:881-886.

15. Alfredson H, Bjur D, Thorsen K, et al. High intratendinous lactate levels in painful chronic Achilles tendinosis. An investigation using microdialysis technique. J Orthop Res. 2002;20:934-938.

16. Öhberg L, Lorentzon R, Alfredson H. Neovascularisation in Achilles tendons with painful tendinosis but not in normal tendons: an ultrasonographic investigation. Knee Surg Sports Traumatol Arthrosc. 2001;9:233-238.

17. Åström M, Westlin N. Blood flow in the human Achilles tendon assessed by laser Doppler flowmetry. J Orthop Res. 1994;12:246-252.

18. Alfredson H. Chronic tendon pain-implications for treatment: an update. Curr Drug Targets. 2004;5:407-410.

19. Leadbetter WB. Cell-matrix response in tendon injury. Clin Sports Med. 1992;11:533-578.

20. Marsolais D, Côté CH, Frenetta J. Neutrophils and macrophages accumulate sequentially following Achilles tendon injury. J Orthop Res. 2001;19:1203-1209.

21. Marsolais D, Côté CH, Frenetta J. Nonsteroidal anti-inflammatory drug reduces neutrophil and macrophage accumulation but does not improve tendon regeneration. Lab Invest. 2003;83:991-999.

22. Vane JR. Introduction: mechanism of action of NSAIDs. Br J Rheumatol. 1996;(suppl 1)35:1-3.

23. Weiler JM. Medical modifiers of sports injury. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) in sports soft-tissue injury. Clin Sports Med. 1992;11:625-644.

24. Curwin S. The aetiology and treatment of tendinitis. In: Harries M, Williams C, Stanish WD, et al, ed. Oxford Textbook of Sports Medicine. Oxford: Oxford University Press; 1994:512-528.

25. Leadbetter WB. Anti-inflammatory therapy and sports injury: the role of non-steroidal drugs and corticosteroid injection. Clin Sports Med. 1995;14:353-410.

26. Teitz CC, Garrett WE Jr, Miniaci A, et al. Tendon problems in athletic individuals. J Bone Joint Surg Am. 1997;79:138-152.

27. Saltzman CL, Tearse DS. Achilles tendon injuries. J Am Acad Orthop Surg. 1998;6:316-325.

28. Almekinders LC. The efficacy of non-steroidal anti-inflammatory drugs in the treatment of ligament injuries. Sports Med. 1990;9:137-142.

29. Thorling J, Liden B, Berg R, et al. A double blinded comparison of Naproxen gel and placebo in the treatment of soft tissue injuries. Curr Med Res Opin. 1990;12:242-248.

30. Åström M, Westlin N. No effect of piroxicam on Achilles tendinopathy. A randomised study of 70 patients. Acta Orthop Scand. 1992;63:631-634.

31. Vogel HG. Mechanical and chemical properties of various connective tissue organs in rats as influenced by non-steroidal antirheumatic drugs. Connect Tissue Res. 1977;5:91-95.

32. Forslund C, Bylander B, Aspenberg P. Indomethacin and celecoxib improve tendon healing in rats.Acta Orthop Scand. 2003;74:465-469.

33. Virchenko O, Skoglund B, Aspenberg P. Parecoxib impairs early tendon repair but improves later remodeling. Am J Sports Med. 2004;32:1-5.

34. Li Z, Yang G, Khan M, et al. Inflammatory response of human tendon fibroblasts to cyclic mechanical stretching. Am J Sports Med. 2004;32:435-440.

35. Baud L, Perez J, Denis M, et al. Modulation of fibroblast proliferation by sulfidopeptide leukotrienes: effect of indomethacin. J Immunol. 1987;138:1190-1195.