Common Tendinopathies in theUpper and Lower Extremities

Alexander Scott, PT, MSc, andMaureen C. Ashe, PT, PhD

Corresponding authorAlexander Scott, MSc, PhD

University of British Columbia Department of Family Practice,

David Strangway Building 3rd Floor, 5950 University Boulevard,

Vancouver, BC V6T 1Z3, Canada.

E-mail: ascott@interchange.ubc.ca

Current Sports Medicine Reports 2006, 5:233-241Current Science Inc. ISSN 1537-890xCopyright © 2006 by Current Science Inc.

Overuse tendon injuries (tendinopathies) present achallenge to sports medicine patients and clinicians.Despite the high prevalence of tendinopathy inrecreational and competitive athletes, treatment isoften hampered by contradictory definitions anddescriptions of the underlying pathology, with a lim-ited repertoire of evidence-based treatments. Thisreview provides the clinician with a basic overview oftendon structure and pathophysiology, and highlightsthe most common tendinopathies affecting the upperand lower extremities, including an update on recentadvances in conservative management.

IntroductionIn the past 10 years, there has been a considerable shift inthinking about upper and lower extremity tendinopathies,previously considered to result from cellular or biochemi-cal inflammation. Recent literature has revealed consistentchanges occurring in the most common tendinopathies—neurovascular ingrowth, variable tenocyte density(hyper- and hypocellularity), and abnormal or degenerateextracellular matrix. Despite this improved understand-ing of pathophysiology, the repertoire of evidence-basedtreatments remains limited, even for the more commonlyoccurring conditions. This review provides the clinicianwith an overview of the most common tendinopathiesaffecting the upper and lower extremities. Specifically, wehighlight basic tendon structure and function, discuss thepathophysiology of tendon overuse injuries, and providea foundation for treatment of tendinopathies based onrecent clinical trials.

Tendon StructureThe basic elements of tendon are collagen bundles, tendoncells (tenocytes), and proteoglycans. Collagen providestendons with tensile strength, whereas the proteoglycansprovide structural support for the collagen fibers andregulate the extracellular assembly of procoUagen intomature collagen. Tenocytes are long, branching cells thatform a load-responsive cell signaling network linked bygap junctions. Synthesis of collagen and ground substanceby tenocytes is stimulated by increases in mechanical load,attesting to the adaptive capacity of tendon [1].

The epitenon is a fine connective tissue sheath contain-ing the vascular, lymphatic, and nerve supply. It coversthe tendon and also extends deeply between collagenbundles as the endotenon. The epitenon is surrounded byparatenon, an areolar tissue consisting mainly of type Iand type III collagen, elastin, and an inner synovial lin-ing. Together, the paratenon and epitenon are sometimescalled the peritendon. A two-layer synovial sheath is pres-ent around certain tendons as they pass through areas ofincreased mechanical stress, as in the hand, wrist, andankle. Synovial fluid is produced by the inner lining of thesheath to reduce friction, thereby protecting the glidingsurfaces and reducing their work.

Tendon is supplied with blood by a network ofsmall arterioles and capillaries oriented parallel to thecollagen fibers in the endotenon. It has been postulatedthat tendons may become ischémie in their core regionsduring tensile loading, and recent evidence consistentwith this demonstrates that tensile loading forces waterfrom the tendon's central region toward the paratenon[2]. However, autonomie nerves innervate the arteriesand arterioles and presumably regulate blood flow inresponse to metabolic demand.

Mechanical Loading in TendonThe majority of sports-induced tendinopathies developas a result of either excessive quantity or poor qualityof movement, or both. Strain (deformation) is normallyexperienced by tendons as a result of muscle forces,ground reaction force, and interaction with surrounding

234 Extremity Conditions

structures. In tendon, strain is characterized in threedifferent axes: tensile, compressive, or shear; each canpredispose tissues to injury under certain scenarios.

Tension is the most common force experienced bytendons that are designed to transmit large loads (up to12.5 times hody weight in the Achilles) [3]. Repetitive load-ing of tendon within physiologic range leads to cumulativemicrotrauma, which may require days or weeks to fully self-repair. At a tissue and cellular level, tensile microtrauma invitro is characterized hy dissociation and tearing of fibrils,transverse tearing of fibers and capillaries, fissuring ofcell-matrix boundaries, and tenocyte cell death [4]. Morein-depth study is needed to determine the sequence of earlychanges and the loading thresholds at which such damageis initiated in vivo.

Tendons also undergo compressive and shear loadingat bony wrap-around regions or in narrow areas suchas the acromial space or the carpal tunnel. Compres-sion of the tendon can lead to a change in the characterof the tenocytes and secretion of a stiffer, cartilage-likematrix with type II collagen and aggrecan, and this lossof tensile quality has been suggested to predispose toinjury [5*]. Shearing occurs at points of friction eitherat the tendon's interface with surrounding tissues, orbetween differentially loaded tendon fascicles. Tendonssuch as the supraspinatus that may experience substantialinterfascicular shear forces have longitudinal seams ofproteoglycans between fascicles, possibly as an adaptivemechanism to allows sliding and minimization of shearat multiple joint angles [6]. Partial supraspinatus tears, anincreasingly recognized clinical entity, may occur betweendifferentially loaded tendon fascicles.

Mechanisms of Injury and PainTendons (and their linings and insertions) are subject toa spectrum of injuries defined by their acuity, severity,anatomic location, and involvement of associatedstructures. Attempts to classify tendon injuries on thebasis of histology (eg, tendinosis, peritendonitis) havebeen problematic in that microscopic findings overlapin many cases, particularly as the boundaries betweenthese tissue compartments tends to break down withchronic pathology. An important finding arising fromclassic morphologic studies is that in the chronic stage,inflammatory cells are usually absent, leading to thegeneral abandonment of the term tendonitis in favor oftendinopathy. A role for cell-mediated inflammation hasnot been entirely ruled out, however [7«].

In the most common chronic tendinopathies andenthesopathies, frequent microscopic findings are vascu-lar ingrowth, tenocyte death (necrosis and apoptosis) andproliferation (hypercellularity), ahnormal and degener-ated extracellular matrix, and sprouting and ingrowth ofnociceptive nerves implicated in generation of neurogenicinflammation (pain, edema, fibrosis). This constellation of

changes is often referred to as tendinosis, although differenttendons may display different sets of features. For example,in a series of 64 painful patellar tendons in volleyballplayers, 58% demonstrated neovascularization [8].

Molecular and microscopic evidence of prior inflam-mation/repair is frequently seen in chronically painfultendons, including fibrin and fibronectin deposition,increased collagen synthesis and breakdown, withhigher amounts of collagen III (typical of scar tissue orendotendon) and matrix metalloproteinase-1 (interstitialcollagenase) activity, persistent transforming growthfactor-ß, and vascular endothelial growth factor secretion(fibrotic and angiogenic peptides typical of healingwounds), and fibroblastic proliferation and apoptosis [9](Lian OB, et al.; Unpublished data). Tendinopathies inperitendinous structures (including endotendon) displaysimilar, well-recognized signs of chronic injury or fibrosis.Thus, many of the molecular or cellular features of tendi-nosis are consistent with a soft tissue injury in a chronicstage of repair. In addition to the above, features suchas fibrocartilaginous or fatty metaplasia, collagen micro-tears, and persistent neovessels have prompted many toview tendinosis as a failed healing response, whose failuremay result from a relatively poor blood supply and/orongoing mechanical loading of the lesion.

Spectrum of Injuries:Epidemiology of TendinopathyOveruse plays a role in 30% to 50% of all sporting injuriesand the incidence has increased over the past several decades,likely due to the increasing demands on athletes and greaterparticipation in running and recreational sports. In elitesoccer players, overuse injuries and re-injuries constituted37% and 22% of all injuries, and athletes were most at riskof overuse injury during the preseason period [10]. Recentdata have defined thresholds associated with increased riskof injury. Sein et al. [11] report that the combination ofswimming more than 15 hours and 35 km per week predictsthe appearance of supraspinatus tendinopathy in 71% ofelite swimmers. For recreational tennis players, the risk ofelbow tendinopathy is higher in those that play more than2 hours per week [12].

Lower extremityAchilles tendinopathyAchilles tendinopathy (AT) is the most prevalent lowerextremity tendinopathy in the general population, witha 5.9% lifetime cumulative incidence reported amongsedentary people [13]. By comparison, elite enduranceathletes have a lifetime incidence of AT of 50% [13].Nearly a quarter of AT patients demonstrate insertionalproblems, whereas up to two thirds present with periten-donitis (with or witJiout tendinosis) [14]. The majorityof AT patients in sports medicine clinics are involvedin running or jumping sports, attesting to overload as

Common Tendinopathies in the Upper and Lower Extremities Scott and Ashe 235

the major risk factor, compounded with advancing age[15] and training errors such as running on sloping orslippery surfaces. Men have a higher prevalence of ATthan women, although after menopause the incidence ofacute ruptures for women rises to equivalent levels [15].Interestingly, hormone replacement therapy is associ-ated with better tendon structure and lower incidence oftendon pathology (P - 0.056) in active postmenopausalwomen, suggesting a protective effect of estrogen onlower extremity tendons [16].

Various biomechanical abnormalities have been sug-gested to increase the risk of AT, and several have beendemonstrated in prospective studies, including hyper- orhypomobility of the subtalar joint, stiff or slack plantarflexors, decreased plantar flexion strength, and hyper-pronation [17]. The most important recent advance inthe epidemiology of tendinopathies is the finding thatparticular alíeles of the collagen V and tenascin-C genesinfluence the risk of chronic AT [18], in keeping withprior studies that showed a high degree of heritability fortendinopathy. A high level of low-density lipoprotein isanother systemic factor that may predispose to AT [19].

}umper's kneeIn a recent study of high-level athletes in a variety ofsports, the overall prevalence of patellar tendinopathy was12%. This varied significantly by sport, with no or veryfew cases among cyclists and runners, and the majorityof cases found among jumping athletes (40% in basket-ball and volleyball players) [20]. In adults, most lesionsare at the inferior pole of the patella, although the mid-substance, paratenon, superior pole, and tibial tuberclecan also be affected. Extrinsic risk factors for patellartendinopathy include increased training volume and hardsurfaces [21], and known intrinsic factors include reducedquadriceps or hamstrings flexibility [22], increasedtibial to stature ratio and external tibial torsion [23-26].Athletes who place more demand on the patellar tendon,as indicated by increased vertical jumping ability anddeeper knee joint angles [27] are at increased risk, as aremen [20]. In contrast to data from the Achilles tendon insoccer players [28], a recent study in volleyball playersfound that baseline ultrasound abnormalities did notpredict the subsequent development of symptoms; in fact,many asymptomatic lesions resolved during the course ofthe season [29].

Upper extremityElbowOne of the most common repetitive injuries to the upperextremity is lateral elbow pain, also known as tenniselbow or lateral epicondylalgia (LE). The prevalence ofLE in the general population is approximately 1% to 3%[30], although it is between 9% and 35% in tennis players[31]. The extensor carpi radialis brevis is the tendon most

Table 1. Clinical risk factors for tendinopathy

Intrinsic

Age

Young: Osgood-Schlatter disease, Sinding-Larssen disease

Old: partial or complete ruptures

Sex

Men: greater overall prevalence

Women: higher risk at wrist and elbow

Biomechanics

Muscle imbalance, joint instability or stiffness

Poor technique, demanding range of motion

Torsional forces

Prior tendon lesion

Extrinsic

Training errors

Sudden increase in volume, excessive hill work

Environmental conditions

Low temperature, hard, slippery or uneven surfaces

Poor equipment

often involved in LE but some patients also have involve-ment of the extensor digitorum communis. Identified riskfactors for elbow injuries include age over 40 years, bodymass index (BMI) over 30, history of carpal tunnel syn-drome, and positioning the affected joints (eg, shoulder,elbow, wrist) in demanding ranges [32,33].

Rotator cuffThe rotator cuff consists of four muscles (supraspinatus,infraspinatus, teres minor, and subscapularis), with thesupraspinatus most commonly injured [34]. Ostor et al.[35] report an age-standardized incidence of shoulder painpresenting to general medical practice of 9.5 per 1000patients; 85% of these presentations are related to a rotatorcuff tendinopathy. Athletes engaged in sports that involveoverhead motions such as throwing, tennis, or swimmingare more susceptible to overuse injury. Risk factors fordeveloping rotator cuff tendinopathy also include high BMIand advancing age [36,37]. The type II or III acromion isassociated with increased incidence of rotator cuff tears,but recent work has suggested that because they are moreprevalent in older individuals, they probably represent asecondary, bony reaction to pathology rather than ananatomic risk factor [36].

Clinical AssessmentFor both the upper and lower extremity a thorough his-tory combined with assessment of risk factors (Table 1) isimportant to understand the mechanism of injury, and thevolume and pattern of loading. The physical examination

236 Extremity Conditions

is usually straightforward for tendinopathies, but anassessment of strength and flexibility throughout thekinetic chain is essential. Outcome measures such asthe disabilities of the shoulder, arm and hand (DASHand Quick DASH) questionnaire, the patient-ratedwrist or elbow evaluation of the upper extremity, andthe Victorian Institute of Sport Assessment (VISA) orVISA-Achilles (VISA-A) questionnaire for the lowerextremity can provide a means to quantify change forthe patient. If sclerosing therapy is to be considered andis available, the presence and extent of neovasculariza-tion must be determined using color Doppler ultrasound.Imaging may also be helpful in confirming the diagnosisand assessing the extent or severity of pathology.

Conservative TreatmentMost tendinopathies are not symptomatic in the earlystages. A variety of treatments have been advocated,but evidence to support them is either preliminaryor nonexistent for many. Results of recent controlledstudies are presented in Tables 2 and 3. A generalstrategy for the chronic stage is one of relative unload-ing and biomechanical correction, controlled andgraduated eccentric loading of the tendon, gradualreintroduction of sport-specific training, and adjuvantmedical treatment.

Lower extremityConservative management for chronic Achilles andpatellar tendinopathies remains challenging, and thisis reflected in the relatively limited evidence base fortreatment (Table 2). A systematic review conducted in2003 for the Achilles concluded that there was weaksupport for the use of topical, but not oral, nonsteroidalanti-inflammatory drugs (NSAIDs), and no support forcorticosteroid injections [38]. More recent literature isencouraging and indicates clinically significant benefitswith eccentric exercise, aprotinin, glyceryl trinitrate(GTN—a nitric oxide donor applied topically), andsclerosing injections for lower extremity tendinopathies.For sclerosing therapy, large randomized controlled tri-als (RCTs) are not currently available but the treatmentappears to allow full return to activity in a remarkablyshort period of time [39]. Aprotinin (a broad-spectrumprotease and matrix metalloproteinase inhibitor injectedinto the paratenon) has RCT support for the Achilles andpatellar tendons, and is reported as superior to cortico-steroid injections in reducing pain and promoting returnto activity [40]. GTN also has RCT-level evidence for ATand is beginning to find wider use among clinicians. Theevidence for extracorporeal shockwave therapy (ESWT)in the lower extremity is conflicting, with one RCTsupporting its use in the patellar tendon, and one RCTagainst its use in the Achilles. Eccentric exercise at pain-ful loads (the "Alfredson program") appears to be more

effective than concentric exercise at improving tendonfunction [41], but care must be taken not to exacerbatepatients during the competitive season as the programhas been shown to worsen knee function in athletes whocontinue to compete [42].

Upper extremityAt the elbow, several systematic reviews report little

supporting evidence for common interventions (Table 3).Topical NSAIDs and acupuncture are beneficial for LE forshort-term pain relief. A systematic review from Bisset et al.[43] reported that ESWT yielded no benefit over a placebofor pain or functional measures. More recent investigationsreport conflicting results with ESWT (Table 3). It has beendifficult to ascertain the effect of exercise alone as mostinvestigations used exercise in combination with othertreatments. Nonetheless, a recent report by Stasinopoulosand Stasinopoulos [44»] showed superior symptom reliefwith exercise compared with other treatments.

Most studies investigating interventions for shouldertendinopathies are limited by méthodologie issues suchas low numbers of study participants and heterogeneityof treatment groups. As a result, there has been littlesupport for most trialed interventions [45]. More recently,systematic reviews report support for corticosteroidinjection, moderate support for ESWT for treating calcifictendinopathy, but no support for ESWT for noncakifictendinopathy (Table 3). Paoloni et al. [46,47] reportpotential benefits for using topical GTN at the shoulderand elbow.

ConclusionsTendinopathies are common in recreational and pro-fessional athletes, as well as in sedentary populations.Recent advances in the pathophysiology of tendonbreakdown suggest that early proteoglycan-rich lesionsidentified by ultrasound and biopsy are noninflammatoryand asymptomatic, and may either resolve during thesporting season, or progress to become a painful lesion[48«]. Conversely, neurogenic inflammation may play animportant role in the later stages of tendon pathology[49]. Although predisposing and genetic factors havebeen identified, there is currently little evidence tosupport preventive measures for tendinopathy that wouldsupport their value in screening.

As efficacy becomes more firmly established fortendinopathy treatments, the gap in basic scienceunderlying their mechanisms of action becomes moreapparent. Do eccentric exercise, aprotinin, sclerotherapy,and nitric oxide target similar or different processesin tendon? Which combination of treatments wouldbe most effective in a given case? The next few yearsshould see crucial advances as clinicians and research-ers continue to implement and refine the best strategy fordifferent tendinopathies.

Common Tendinopathies in the Upper and Lower Extremities Scott and Ashe 237

Table 2. Recent results for treatment of Achilles and patellar tendinopathy

Study Treatment Outcome Results

Achilles

Systematic reviews

McLauchlan andHandoll [38]

McLauchlan andHandoll [38]

New trials 2004-2006

Brown et al. [52]

Alfredson andOhberg [53]

Paoloni et al. [54]

Bjordal et al. [55]

Costa et al. [56]

Roos et al. [57]

Patellar

NSAIDs

Corticosteroids

Aprotinin injection

Weak support for short-term pain relief fortopical but not oral NSAIDs

No support for corticosteroid injections

Trend toward improved functional outcomes(VISA-A) and return to sport {not significant)

Insufficient evidence todetermine effectiveness

Sclerosing injections Reduced pain and improved patient satisfaction

Topical glyceryltrinitrate

Reduced pain, improved strength and activity

Low-level lasertherapy

Post-treatment reduction in inflammation {pain. Insufficient evidence toprostaglandin levels) of acute tendinopathy; determine effectivenesslong-term follow-up not assessed

Extracorporeal No benefit over placebo; increased incidenceshock wave therapy of rupture in treatment group

Eccentric exercise Reduced pain, increased return to sport +

New trials 2002-2006

Alfredson andOhberg [58]

Giombini et al. [59]

Taunton et al. [60]

Stasinopoulos andStasinopoulos [61]

Stasinopoulos andStasinopoulos [61]

Visnes et al. [42]

Young et al. [62]

Stasinopoulos andStasinopoulos [61]

jonsson et al. [63]

Sclerosing injections Reduced pain, improved return to function

Reduced pain, improved patient satisfaction

Improved VISA score and jump height

Worse outcome than eccentric exercise

Worse outcome than eccentric exercise

Hyperthermia {434MHz microwave)

Extracorporealshock wave therapy

Deep transversefriction

Ultrasound therapy

Eccentric exercise Eccentric training with a decline board givessuperior improvements in VAS and VISAscore at 12 weeks and 1 year, but not whenused in season

NSAID—nonsteroidal anti-inflammatory drug; VAS—visual analogue scale; VISA—Victorian Institute of Sport Assessment;VISA-A—VISA-Achilles.

Given that there is a wide spectrum of presentationand, perhaps, etiology of tendinopathies, one challengeahead for the research and clinical community is tosuccessfully account for this diversity. Strong researchmethodology is essential to improve the specificity andrationale of treatments by 1) targeting specific popula-tions, and 2) measuring relevant physiologic responsesto therapy. Are similar mechanisms responsible for painin a young jumping athlete's patellar tendon, a middle-

aged woman's DeQuervain's tenosynovitis with noobvious cause, or a spontaneous rupture of an asymp-tomatic Achilles tendon with fatty degeneration? Thesame treatment may or may not be warranted for thesedifferent presentations [50]. In general, research intopathophysiology and conservative management of theupper extremity has lagged behind the lower extremity,but some recent studies suggest that a common treatmentparadigm may yet emerge [51«].

238 Extremity Conditions

Table 3. Recent results for treatment of elbow and shoulder tendinopathies

Study Treatment Outcome ResultsElbow

Systematic reviews

Green et al. [64]

Bisset et al. [43]

Trinh et al. [65]

Buchbinder et al. [66]

Bisset et al. [43]

Trudel et al. [67]

Bisset et al. [43]

New trials 2004-2006

Manias andStasinopoulos [68]

Rompe et al. [69]

Pettrone and McCall [70]

Chung and Wiley [71]

Lebrun [72]

Martinez-Silvestrini et al. [73] Exercise

Stasinopoulos andStasinopoulos [44*]

Shoulder

Some evidence to support topical but not oralNSAIDS for short-term pain relief (up to 4 weeks)

Orthotics and taping Insufficient evidence to support ordiscourage use

Acupuncture Strong evidence to support acupuncture in theshort-term relief of pain

Extracorporeal shock Conflicting resultswave theray

No added benefit over placebo

Exercise Some evidence to reduce pain

Insufficient evidence to support or discourage use

Insufficient evidence todetermine effectiveness

Insufficient evidence todetermine effectiveness

Insufficient evidence todetermine effectiveness

Ice No added benefit to use ice incombination with eccentric exercises

Extracorporeal shock Reduced pain and increased function comparedwave therapy with placebo

Reduced pain compared with placebo

No difference in pain compared with stretching

No improvement in pain or function comparedwith placebo

No difference in all outcomes compared withstretching and strengthening

Exercise vs Cyriax physiotherapy vs polarizedpolychromatic noncoherent light (bioptron light);exercise had greatest improvement

Systematic reviews

Arroll et al. [74]

Harniman étal. [75]

New trials 2004-2006

Razavi and Jansen [76]

Peters et al. \77\

Sabeti-Aschraf et al. [78]

Moretti et al. [79]

Paoloni et al. [47]

Corticosteroid

ESWT

Acupuncture

ESWT

Topical glyceryltrinitrate

Subacromial injections effective for rotator cufftendinopathy

Moderate evidence that ESWT effective in treatingcalcific rotator cuff tendinopathy; moderate evi-dence that ESWT is not effective to treat noncalcificrotator cuff tendinopathy

In addition to exercise; no added benefit in reduc-ing pain

Calcific: ESWT using different energy levels;significant reduction incalcification and pain comparedwith sham treatment

Calcific: comparison of delivery modes; bothgroups had significant improvement but superiorresults with computer-assisted delivery

Calcific: improvement in pain in all but 7% ofparticipants at 6 months

Significantly improved pain and other outcomescompared with placebo

ESWT—extracorporeal shock wave therapy; NSAID—nonsteroidal anti-inflammatory drug.

Common Tendinopathies in the Upper and Lower Extremities Scott and Ashe 239

AcknowledgmentsThe authors would like to acknowledge those authorswhose work could not be cited due to space limitations,and to thank J.L. Cook for helpful comments on themanuscript.

References and Recommended ReadingPapers of particular interest, published recently,have been highlighted as:• Of importance• • Of major importance

1. Banes AJ, Weinhold P, Yang X, et al.: Gap junctions regulateresponses of tendon cells ex vivo to mechanical loading.Clin Orthop 1999, 367(Suppl):S356-S370.

2. Wellen J, Helmer KG, Grigg P, Sotak CH: Spatialcharacterization of Tl and T2 relaxation times and thewater apparent diffusion coefficient in rabbit Achillestendon subjected to tensile loading. Magn Reson Med2005, 53:535-544.

3. Komi PV: Relevance of in vivo force measurementsto human biomechanics. / Biomech 1990,23(Suppl l):23-34.

4. Scott A, Khan KM, Heer J, et al.: High strain mechanicalloading rapidly induces tendon apoptosis: an ex vivo rattibialis anterior model. Br] Sports Med 1005, 39:e25.

5.« Almekinders LC, Weinhold PS, Maffulli N: Compressionetiology in tendinopathy. Clin Sports Med 2003, 22:703-710.

Novel hypothesis that challenges the prevailing view thattendinopathies result purely from tensile loading.6. Bey MJ, Song HK, Wehrli FW, Soslowsky LJ: Intratendinous

strain fields of the intact supraspinatus tendon: the effect ofglenohumeral joint position and tendon region. / Orthop Res2002,20:869-874.

7.» Schubert TE, Weidler G, Lerch K, et al.: Achilles tendinosisis associated with sprouting of substance P positive nervefibres. Ann Rheum Dis 2005, 64:1083-1086.

Demonstrates increased presence of macrophages in patients with chronicAchilles tendinosis with semiquanitative immunohistochemistry.8. Cook JL, Malliaras P, De Luca J, et al.: Neovascularization

and pain in abnormal patellar tendons of active jumpingathletes. Clin ] Sport Med 2004,14:296-299.

9. Hazelman BL, Riley G, Speed GA: Soft tissue rheumatology.Oxford: Oxford University Press; 2006.

10. Waiden M, Hagglund M, Ekstrand J: Injuries in Swedish elitefootball—a prospective study on injury definitions, risk forinjury and injury pattern during 2001. Scand] Med Sci Sports2005,15:118-125.

11. Sein ML, Walton JR, Linklate J, et al.: Supraspinatustendinosis and elite swimming training. Proceedings ofthe American Academy of Orthopaedic Surgeons AnnualMeeting. Washington, DG; July 14-17, 2005.

12. Gruchow HW, Pelletier D: An epidemiologic study of tenniselbow. Incidence, recurrence, and effectiveness of preventionstrategies. Am] Sports Med 1979, 7:234-238.

13. Kujala UM, Sarna S, Kaprio J: Gumulative incidence ofAciiilles tendon rupture and tendinopathy in male formerelite athletes. Clin ] Sport Med 2005,15:133-135.

14. Kvist M: Achilles tendon injuries in athletes. Ann ChirGynaecol 1991, 80:188-201.

15. Maffulli N, Waterston SW, Squair J, et al.: Ghangingincidence of achules tendon rupture in Scotland: a 15-yearstudy. Clin] Sport Med 1999, 9:157-160.

16. Gook JL, Bass SL, Black JE: Hormone therapy is associatedwith smaller Achilles tendon diameter in active post-menopausal women. Scand] Med Sci Sports 2006, in press.

17. Maffulli N, Wong J, Almekinders LG: Types andepidemiology of tendinopathy. Clin Sports Med 2003,22:675-692.

18. Mokone GG, Schwellnus MP, Noakes TD, Gollins M:The Gol5Al gene and Achilles tendon pathology.Scand] Med Sci Sports 2006, 16:19-26.

19. Ozgurtas T, Yildiz G, Serdar M, et al.: Is high concentrationof serum lipids a risk factor for Achilles tendon rupture?Clin Chim Acta 2003, 331:25-28.

20. Lian OB, Engebretsen L, Bahr R: Prevalence of jumper's kneeamong elite athletes from different sports: a cross-sectionalstudy. Am ] Sports Med 2005, 33:561-567.

21. Eerretti A: Epidemiology of jumper's knee. Sports Med1986, 3:289-295.

22. Gook JL, Kiss ZS, Khan KM, et al.: Anthropometry, physicalperformance, and ultrasound patellar tendon abnormality inelite junior basketball players: a cross-sectional study.Br] Sports Med 2004, 38:206-209.

23. Gaida JE, Gook JL, Bass SL, et al.: Are unilateral andbilateral patellar tendinopathy distinguished by differencesin anthropometry, body composition, or muscle strengthin elite female basketball players? Br ] Sports Med 2004,38:581-585.

24. Khan KM, Gook JL, Kiss ZS, et al.: Patellar tendon ultra-sonography and jumper's knee in female basketball players:a longitudinal study. Clin] Sport Med 1997, 7:199-206.

25. Gigante A, Bevilacqua G, Bonetti MG, Greco E:Increased external tibial torsion in Osgood-Schlatterdisease. Acta Orthop Scand 2003, 74:431-436.

26. Sen RK, Sharma LR, Thakur SR, Lakhanpal VP: Patellarangle in Osgood-Schlatter disease. Acta Orthop Scand1989, 60:26-27.

27. Lian O, Engebretsen L, Ovrebo RV, Bahr R: Characteristicsof the leg extensors in male volleyball players with jumper'sknee. Am ] Sports Med 1996, 24:380-385.

28. Eredberg U, Bolvig L: Significance of ultrasonographicallydetected asymptomatic tendinosis in the patellar and Achillestendons of elite soccer players: a longitudinal study. Am ]Sports Med 2002, 30:488-491.

29. Malliaras P, Gook J, Ptasznik R, Thomas S: Prospectivestudy of change in patellar tendon abnormality on imagingand pain over a volleyball season. Br ] Sports Med 2006,40:272-274.

30. Smidt N, Assendelft WJ, van der Windt DA, et al.:Gorticosteroid injections for lateral epicondylitis:a systematic review. Pain 2002, 96:23-40.

31. Pluim BM, Staal JB, Windier GE, Jayanthi N: Tennisinjuries: occurrence, aetiology, and prevention. Br ] SportsMed 1006, 40:415-413.

32. Werner RA, Eranzblau A, Gell N, et al.: Predictors ofpersistent elbow tendonitis among auto assembly workers./ Occup Rehabill005,15:393-400.

33. Tanaka S, Petersen M, Gameron L: Prevalence and riskfactors of tendinitis and related disorders of the distal upperextremity among U.S. Workers: comparison to carpal tunnelsyndrome. Am ] Ind Med 2001, 39:328-335.

34. Li XX, Schweitzer ME, Bifano JA, et al.: MR evaluation of sub-scapularis tears. / Comput Assist Tomogr 1999,23:713-717.

35. Ostor AJ, Richards GA, Prévost AT, et al.: Diagnosis andrelation to general health of shoulder disorders presenting toprimary care. Rheumatology (Oxford) 2005, 44:800-805.

36. Worland RL, Lee D, Orozco GG, et al.: Gorrelation ofage, acromial morphology, and rotator cuff tear pathologydiagnosed by ultrasound in asymptomatic patients. / SouthOrthop Assoc 2003,12:23-26.

37. Wendelboe AM, Hegmann KT, Gren LH, et al.: Associationsbetween body-mass index and surgery for rotator cufftendinitis. / Bone ]oint Surg Am 2004, 86-A:743-747.

38. McLauchlan GJ, Handoll HH: Interventions for treating acuteand chronic Achilles tendinitis. Cochrane Database Syst Rev2001, GD000232.

240 Extremity Conditions

39. Gisslen K, Ohberg L, Alfredson H: Is the chronic painful 55.tendinosis tendon a strong tendon? A case study involvingan Olympic weightlifter with chronic painful jumper's knee.Knee Surg Sports Traumatol Arthrose 2006, in press.

40. Capasso G, Testa V, Maffulli N, Bifuico G: Aprotinin,corticosteroids and normosaline in the management of 56.patellar tendinopathy in athletes: a prospective randomizedstudy. Sports Exere Injury 1997, 3:111-115.

41. Alfredson H, Pietila T, Jonsson P, Lorentzon R: Heavy-loadeccentric calf muscle training for the treatment of chronic 57.Achilles tendinosis. Am ] Sports Med 1998, 26:360-366.

42. Visnes H, Hoksrud A, Cook J, Bahr R: No effect ofeccentric training on jumper's knee in volleyball playersduring the competitive season: a randomized clinical trial.Clin J Sport Med 2005, 15:227-234. 58.

43. Bisset L, Paungmali A, Vicenzino B, Beller E: A systematicreview and meta-analysis of clinical trials on physicalinterventions for lateral epicondylalgia. BrJ Sports Med2005, 39:411-422.

44.« Stasinopoulos D, Stasinopoulos I: Comparison of effects 59.of Cyriax physiotherapy, a supervised exercise programmeand polarized polychromatic non-coherent light (bioptronlight) for the treatment of lateral epicondylitis. Clin Rehabil2006,20:12-23. 60.

Demonstrates superiority of exercise to traditional (Cyriax)physiotherapy.45. GreenS, Buchbinder R,HetrickS: Physiotherapy interven- 61.

tions for shoulder pain. Coehrane Database Syst Rev 2003CD004258.

46. Paoloni JA, Appleyard RC, Nelson J, Murrell GA: Topicalnitric oxide application in the treatment of chronic extensor 62.tendinosis at the elbow: a randomized, double-blinded, placebo-controlled clinical trial. Am } Sports Med 2003, 31:915-920.

47. Paoloni JA, Appleyard RC, Nelson J, Murrell GA: Topicalglyceryl trinitrate application in the treatment of chronicsupraspinatus tendinopathy: a randomized, double-blinded, 63.placebo-controlled clinical trial. Am J Sports Med 200533:806-813.

48.» Cook JL, Feller JA, Bonar SF, Khan KM: Abnormal tenocytemorphology is more prevalent than collagen disruption in 64.asymptomatic athletes' patellar tendons. / Orthop Res 200422:334-338.

Reports the ability to detect early, asymptomatic tendinosis lesionsby ultrasound and biopsy—methods that may help shed light on 65early pathogenesis.49. Danielson P, Alfredson H, Forsgren S: Distribution of general

(PGP 9.5) and sensory (substance P/CGRP) innervations in the 66.human patellar tendon. Knee Surg Sports Traumatol Arthrose2006,14:125-132.

50. MaffulliN, Testa V, Capasso G, etal.: Surgery for chronic 67.Achilles tendinopatliy yields worse results in nonathleticpatients. Clin J Sport Med 2006, 16:123-128.

51.« Jonsson P, Wahlstrom P, Ohberg L, Alfredson H: Eccentric 68.training in chronic painful impingement syndrome ofthe shoulder: Results of a pilot study. Knee Surg SportsTraumatol Arthrose 2006, 14:76-81.

Highlights a novel method of eccentrically loading the supraspinatus ^^tendon, with promising preliminary results.52. Brown R, Orchard J, Kinchington M, et al.: Aprotinin in

the management of Achilles tendinopathy: a randomised 7Qcontrolled trial. Br ] Sports Med 2006, 40:275-279.

53. Alfredson H, Ohberg L: Sclerosing injections to areasof neo-vascularisation reduce pain in chronic Achilles jitendinopathy: a double-blind randomised controlled trial.Knee Surg Sports Traumatol Arthrose 2005, 13:338-344.

54. Paoloni JA, Appleyard RC, Nelson J, Murrell GA: Topicalglyceryl trinitrate treatment of chronic noninsertionalAchilles tendinopathy. A randomized, double-blind,placebo-controlled trial. / Bone loint Sure Am 2004,86-A:916-922.

Bjordal JM, Lopes-Martins RA, Iversen VV: A randomised,placebo controlled trial of low level laser therapy for activatedAhilles tendinitis with microdialysis measurement ofperitendinous prostaglandin E2 concentrations. Br I SportsMed 2006,40:76-80.Costa ML, Shepstone L, Donell ST, Thomas TL: Shockwave therapy for chronic Achilles tendon pain: a random-ized placebo-controlled trial. Clin Orthop Relat Res 2005440:199-204.Roos EM, Engstrom M, Lagerquist A, Soderberg B: Clinicalimprovement after 6 weeks of eccentric exercise in patientswith mid-portion Achilles tendinopathy — a randomizedtrial with 1-year follow-up. Seand] Med Sei Sports 2004,14:286-295.Alfredson H, Ohberg L: Neovascularisation in chronicpainful patellar tendinosis—promising results aftersclerosing neovessels outside the tendon challenge the needfor surgery. Knee Surg Sports Traumatol Arthrose 2005,13:74-80.Giombini A, Di Cesare A, Casciello G, et al.: Hyperthermiaat 434 MHz in the treatment of overuse sport tendinopathies:a randomised controlled clinical trial. Jnt] Sports Med 200223:207-211.Taunton KM, Taunton JE, Khan KM: Treatment of patellartendinopathy with extracorporeal shock wave therapy.BC Med} 2003, 45:500-507.Stasinopoulos D, Stasinopoulos I: Comparison of effectsof exercise programme, pulsed ultrasound and transversefriction in the treatment of chronic patellar tendinopathy.Clin Rehabil 2004, 18:347-352.Young MA, Cook JL, Purdam CR, et al.: Eccentricdecline squat protocol offers superior results at 12 monthscompared with traditional eccentric protocol for patellartendinopathy in volleyball players. Br J Sports Med 200539:102-105.Jonsson P, Wahlstrom P, Ohberg L, Alfredson H: Eccentrictraining in chronic painful impingement syndrome of theshoulder: Results of a pilot study. Knee Surg Sports TraumatolArthrose 2006,14:76-81.Green S, Buchbinder R, Barnsley L, et al.: Non-steroidalanti-inflammatory drugs (NSAIDs) for treating lateralelbow pain in adults. Coehrane Database Syst Rev 2002,CD003686.Trinh KV, Phillips SD, Ho E, Damsma K: Acupuncture forthe alleviation of lateral epicondyle pain: a systematic review.Rheumatology (Oxford, England) 2004, 43:1085-1090.Buchbinder R, Green S, White M, et al.: Shock wavetherapy for lateral elbow pain. Coehrane Database Syst Rev2002, CD003524.Trudel D, Duley J, Zastrow I, et al.: Rehabilitation forpatients with lateral epicondylitis: a systematic review./ Hand Ther 2004, 17:243-266.Manias P, Stasinopoulos D: A controlled clinical pilottrial to study the effectiveness of ice as a supplement to theexercise programme for the management of lateral elbowtendinopathy. Br ] Sports Med 2006, 40:81-85.Rompe JD, Decking J, Schoellner C, Theis C: Repetitive low-energy shock wave treatment for chronic lateral epicondylitisin tennis players. Am J Sports Med 2004, 32:734-743.Pettrone FA, McCall BR: Extracorporeal shock wave therapywithout local anesthesia for chronic lateral epicondylitis./ Bone Joint Surg Am 2005, 87:1297-1304.Chung B, Wiley JP: Effectiveness of extracorporeal shockwave therapy in the treatment of previously untreated lateralepicondylitis: a randomized controlled trial. AmJ Sports Med2004, 32:1660-1667.

Common Tendinopathies in the Upper and Lower Extremities Scott and Ashe 241

72. Lebrun CM: Low-dose extracorporeal shock wave therapy forpreviously untreated lateral epicondylitis. Clin } Sport Med2005,15:401-402.

73. Martinez-Silvestrini JA, Newcomer KL, Gay RE, et al.:Chronic lateral epicondylitis: Comparative effectivenessof a home exercise program including stretching aloneversus stretching supplemented with eccentric or concentricstrengthening. / Hand Ther 2005, 18:411-419, quiz 420.

74. ArroU B, Goodyear-Smith F: Corticosteroid iniections forpainful shoulder: a meta-analysis. Br ] Gen Pract 2005,55:224-228.

75. Harniman E, Carette S, Kennedy C, Beaton D: Extracorporealshock wave therapy for calcific and noncalcific tendonitisof the rotator cuff: a systematic review. ] Hand Ther 2004,17:132-151.

76. Razavi M, Jansen GB: Effects of acupuncture and placebotens in addition to exercise in treatment of rotator cufftendinitis. Clin Rehabil 2004,18:872-878.

77. Peters J, Luboldt W, Schwarz W, et al.: Extracorporealshock wave therapy in calcific tendinitis of the shoulder.Skeletal Radiol 2004, 33:712-718.

78. Sabeti-Aschraf M, Dorotka R, GoU A, Trieb K: Extra-corporeal shock wave therapy in the treatment of calcifictendinitis of the rotator cuff. Am } Sports Med 2005,33:1365-1368.

79. Moretti B, Garofalo R, Genco S, et al.: Medium-energyshock wave therapy in the treatment of rotator cuffcalcifying tendinitis. Knee Surg Sports Traumatol Arthrose2005,13:405-410.