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Table22-1.
and include one’s genetic makeup, congenital disorders (e.g., alkaptonuria), limb
malalignment,gender,aging,neurologicconditions,medicalcomorbidities(e.g.,hypertension),
andsystemicdiseases.
RiskFactorsfortheDevelopmentofTendinopathy
Extrinsic
Overuse
Trainingerrors
Environmentalconditions
Poorequipment
Poorergonomics
Medications/nutritionalsupplementation(e.g.,fluoroquinolones)
Intrinsic
Increasedage
Increasedbodymassindex
Gender
Biomechanicalabnormalities
Priortendonlesions
Limbmalalignment
Geneticmakeup
Medicalcomorbidities
Systemicconditions
The role of genetics in the development of tendinopathy is attributed to a sequence
variation withintheTypeV collagen andTenascin C genes.37 Admittedly, theexactrole of
thesegenesinthepathophysiologyoftendinopathyhasyettobedefined.Aginghasalsobeen
implicatedbecauseofitsadverseeffectsonthemechanicalpropertiesoftendons,whichmay
be dueto reducedblood flow,local hypoxia, free radical production, impairedmetabolism
andnutrition,andadvancedglycosylationendproducts(AGEs).
7
The association between systemic disease and tendinopathy has been described in a
multitude of studies, with diabetes, hypercholesterolemia, hyperuricemia, and obesity all
implicated in the pathogenesis of tendon degeneration. Rheumatoid arthritis, in addition to
manyotherautoimmunediseases,canalsopredisposepatientstotendinopathy.Inthesettingof
diabetes,tendondamage is causedbyanexcessofAGEs,whichcausesanoxidation-driven
cross-linkingofcollagen.Unliketheenzymaticallydrivencross-linkingofcollagen,whichhas
beneficial effects on tendon strength, AGE cross-linking compromises the biologic and
mechanicalintegrityoftendons.38InbothTypeIandTypeIIDM,increasedtendonthickness
andstructuralabnormalitiesoftheplantarfasciaandAchillestendonhavebeenobserved.
Tendonxanthomaisassociatedwithheterozygousfamilial hypercholesterolemia(HeFH).
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This inherited disease involves a mutated low-density lipoprotein (LDL) receptor gene,
leading to defective LDL catabolism.39 The xanthoma, and subsequent tendon degeneration,
occursascholesterolisdepositedboth extracellularlyand inside histiocytesand other foam
cells,triggeringaninflammatoryresponseandfibrousreaction.TheAchillestendon is most
commonlyinvolved.Nonfamilialhypercholesterolemiamayalsocontributetotendinopathy.In
oneinvestigation,theconcentrationofserumlipidswasfoundtobehigherinsubjectswithan
Achilles tendon rupture as compared to controls.40 However, other works refute this,
demonstratingtendonabnormalitiesonlyinsubjectswithfamilialhypercholesterolemia.
41
Hyperuricemia can lead to monosodium urate (MSU) crystal deposition in tendon, in
additionto other softtissues andjoints. These crystals, whichare responsible forgout,can
manifestin tendonsas indolent nodules, which canbechallengingto distinguish from other
subcutaneous nodules, such as those seen in rheumatoid arthritis. In vitro studies have
demonstratedthatatserumuricacidlevelsofapproximately7mgperdL,crystalprecipitation
beginstooccur.42However,theinvivodevelopmentofMSUcrystalsisdependentonother
factors as well; trauma, mechanical stress, decreased blood flow, and lower temperatures
createanenvironmentconducivetocrystaldeposition.
43
Thereisawell-definedrelationshipbetweenobesityandtendinopathy.44Althoughitwas
oncethoughtthatonlyload-bearingtendonswereaffectedbyobesity,therelationshipbetween
adiposityandtendinopathyisnowrecognizedinnon–load-bearingtendonsaswell.45Thisis
duetoanenhancedunderstandingofthesystemiceffectsofadipose,specificallywithregardto
itsroleintheendocrinesystem.Inotherwords, itisnotsimplytheexcessstressplacedon
tendons thatleads to tendinopathy inthe setting ofobesity, butis also due to the bioactive
peptides and hormones released by adipose tissue, such as chemerin, lipocalin 2, serum
amyloid A3, leptin, and adiponectin.46 These proteins stimulate a low-grade inflammatory
response thatdisrupts the biologic milieucrucial for normal tendon homeostasis.47 Further,
obesity can lead to insulin resistance and the subsequent development of diabetes. As
discussedpreviously,thisdiseaseisalsoimplicatedintendinopathy.
48
DIAGNOSIS
HistoryandPhysicalExamination
A detailed historyisimperativewhenconcernedfortendinopathiesofthefootandankle,as
patients’symptomsareoftenvagueandpresentinsidiously.Acommoncomplaintispaininthe
regionoftheaffectedtendonthatworsenswithsustainedactivityoronweightbearing.Early
on,painisabsentatrest,maydecreaseafterawarm-upperiod,andistriggeredbyspecific
activities. With more advanced disease, patients describe continuous discomfort that is
exacerbatedbyabroaderspectrumofactivities.
Theclinicianmustidentifyanyriskfactorsfortendinopathy,suchasage,obesity,overuse,
training errors, medication side effects, smoking, improper shoe wear, and systemic
conditions.
Althoughpatientsmaydescribeaspecificinjury,participationinanewsportorexercise,
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oranincreaseintheintensityofphysicalactivityprecedingtheonsetofsymptoms,thosewith
tendinopathythatisthemanifestationofasystemicprocessmaynot.Therefore,cliniciansmust
alsoinquireaboutconcurrentmusculoskeletalsymptomsinothertendonsorjoints,whichare
most consistent with a systemic process.
49,50
Admittedly, thecauses of tendinopathy do not
solely occur independent of each other. Clinicians must therefore remember that one’s
presentingsymptomsmaybethecumulativeresultofseveralunderlyingprocesses.
Theaforementionedrelationshipbetweentendinopathyandsystemicdiseaseelucidatesthe
importanceofobtainingthoroughgeneralhealth,medication,andpastmedicalhistoriesfrom
patientsinwhomthereisconcernforatendinopathy.Althoughsomepatientswillpresentwith
a known diagnosis of one of those conditions, others may be unaware. This is commonly
observedwithDM,asapproximately25%ofpatientsareunawarethattheyhavethedisease.
51
Physicalexaminationmustincludeassessmentofthe entire body, as nonspecificfindings
such as body habitus may be of tremendous diagnostic utility. In a study investigating the
relationshipbetweenfatdistributionandtendinopathy,itwasdeterminedthatAchillestendon
pathologyis associatedwithcentral fatdistribution inmenandperipheralfatdistributionin
women.
48
Withregardtothefootandankleexamination,acomprehensiveassessmentiswarranted.
Theexaminationshouldbeginwithvisualinspection,whichmayrevealsubtledifferencesas
compared with the contralateral side. Such findings include swelling, muscle atrophy, skin
breakdown,bruising, and deformity in the region ofthe affectedtendon. With tendinopathy,
discomfort is brought on by palpation along the affected tendon and during assessment of
strength and function, which is usually diminished as well. A patient’s alignment and
neurovascularstatusmustalsobeassessedduringtheexamination.
Inthefootandankle,Achilles,posteriortibial,peroneal,tibialisanterior(TA),andFHL
tendinopathies can result from underlying systemic processes. It is therefore important for
clinicianstohaveafamiliaritywiththecommonexaminationfindingsassociatedwitheachof
these.WithAchillestendinopathy,patientsoftenpresentwithpainandswellinginandaround
thetendon,andcanalsohavepalpablenodules,asseeninthesettingofaxanthoma.Posterior
tibial tendinopathy (PTT) is associatedwiththe “too manytoes” sign, which describes the
increasednumberoftoesevidentonthelateralaspectoftheinvolvedfootwhenviewedfrom
behind52(Fig.22-3). In addition, whenaskedto standontiptoe,normalheelvaruswill not
occur,andpainwillensuealongthePTT.Tendinopathyoftheperonealtendonsisfrequently
associatedwithlateralanklepain,instability,andswelling.Thepaincanbereproducedwith
activedorsiflexionandeversionofthefootagainstresistance.InpatientswithTA,abulbous
enlargementofthetendonofthedorsalmedialfootmaybeevident.Ifitisrupturedorseverely
attenuated, patientsmayhaveafoot drop.With FHL tendinopathy, posteromedial anklepain
may be present, andpainalong thetendon will occur when thepatientis askedto flexthe
halluxagainstresistanceandwiththefootinplantarflexion.
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FIGURE22-3.A:Normalposteriorviewofthefoot.B:Evidenceofarchcollapsewith“toomanytoes”sign.
(ReproducedfromUpToDate,WoltersKluwerHealth.)
DiagnosticAdjuncts
Plain radiographs should be the first imaging studies obtained, as they can exclude bony
abnormalities and other pathologies as the cause of symptoms. Radiographs may also
demonstrateosseouschanges consistentwithvarioussystemic disorders,suchas theerosive
changesinthehalluxconsistentwithgout(Fig.22-4). Advancedimaging, such asultrasound
andmagneticresonanceimaging(MRI),iswarrantedifthediagnosisremainsunclearorifa
patientfailstorespondtoconservativeinterventions.
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FIGURE22-4.Anteroposterior(AP)radiographoftheforefootdemonstratingthedestructivechangestothefirst
metatarsophalangealjointconsistentwithgout.(ReproducedfromRubinR,StrayerDS,RubinE,eds.Rubin’s
Pathology:ClinicopathologicFoundationsofMedicine.6thed.Philadelphia,PA:LippincottWilliams&Wilkins;
2012:1263.)
MRI is considered the standard for tendon imaging because of its excellent soft tissue
contrastandvisualization ofintratendinousabnormalities.53It canalso distinguishclinically
similar entities, such as Achilles tendinosis and peritendinitis.53 However, ultrasound has
recently becomeapopularmeansofimagingtendonsasitcanbeperformed atalowercost
andhastheadvantageofdynamicreal-time imaging.54Further,itshigh sensitivity, accuracy,
andpositive predictive valuefor tendon pathology ofthe footand ankle are comparable to
those of MRI.
54,55
When used in conjunction with Doppler techniques, ultrasound becomes
even more advantageous, as it is able to delineate areas of neovascularization that are
associatedwithtendinopathy.18Ingeneral,theultrasoundfindingsconsistentwithtendinopathy
includeincreasedcross-sectionalandanterior–posteriortendondiameter,disruptionofnormal
fibrillarpatternsandirregulartendonstructure,andhypoechoicareaswithinthetendon56(Fig.
22-5).
Laboratorystudiesareindicatediftendinopathyisthoughttohaveresultedfromasystemic
condition.Inadditiontoacompletebloodcountandmetabolicpanel,condition-specificlabs
mustbeobtainedwhentheclinicianisconcernedforanunderlyingmetabolicprocessasthe
cause of one’s tendinopathy. Hemoglobin A1c (HbA1c) is beneficial in the workup for
diabetes,andisrepresentativeofanindividual’sbloodglucosecontrolovertheprevious2to
3months.AnHbA1c>6.5%ontwoseparatetestsisconsistentwiththediagnosisofdiabetes.
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The workup of rheumatoid arthritis and seronegative arthropathies, such as systemic lupus
erythematosus,includesrheumatoidfactor,antinuclearantibody,humanleukocyteantigenB27,
C-reactiveprotein,andanerythrocytesedimentationrate.
Whenconcernedthatatendinopathyisduetocholesterolmetabolism,alipidpanelshould
beperformed.Infact,Beeharryetal.57suggestthatallyoungpatientscomplainingofsevere
Achillestendonpainforfourormoredaysshouldhavetheirserumcholesterolchecked,asthis
is a common finding in patients with HeFH, as compared to control subjects. In another
investigation,Gaidaetal.45foundthatindividualswithsymptomaticAchillestendinopathyhad
highertriglyceridelevelsandlowerhigh-densitylipoproteinlevelsascomparedwithgender,
age,andbodymassindex–matchedcontrols.
FIGURE22-5.UltrasoundoftheAchillestendondemonstratingenthesitis(arrow),tendonitis(arrowhead),and
retrocalcanealbursitis(*).(ReproducedfromUpToDate,WoltersKluwerHealth.)
A serum uric acid level must be obtained when the clinician’s differential diagnosis
includes MSU crystal deposition. In the work by Pineda et al.,58 Achilles tendinopathy
secondary to MSU deposition was more common in hyperuricemic as compared to
normouricemicpatients(15%vs.1.9%,respectively).
TREATMENT
Available modalities for the treatment of foot and ankle tendinopathies range from
conservativeinterventionstosurgery.Althoughorthopedicsurgeonsandothermusculoskeletal
cliniciansaretypicallyabletomanagesuchtendinopathiesandtheintrinsicandextrinsicrisk
factorsmostoftenresponsible(e.g.,overuse),thoseoccurringinthesettingofsystemicdisease
oftennecessitateamultidisciplinaryapproach.Withouttreatmentoftheunderlyingcondition,a
patient’ssymptomsmayfailtoresolve,worsen,orrecurfollowingtreatment.Further,systemic
diseasessuchasobesityanddiabetespredisposepatientstoinferioroperativeoutcomesand
complications.59 In such instances, perioperative optimization is recommended with the
assistanceofapatient’sendocrinologist,internist,orotherspecialist.
Mostpatientsdiagnosedwithtendinopathyareinitiallytreatedwitha2-to6-weekperiod
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ofrestwithorwithoutimmobilization.However,thereisnoconsensusontheexactperiodof
rest needed, which is dependent on the extent of injury and the patient’s level of activity.
Medications such as nonsteroidal anti-inflammatorydrugs (NSAIDs) andacetaminophenare
also used atthis time. Although NSAIDs provide short-termpainrelief,theyhavenotbeen
showntoaffectlong-termoutcomes.Further,thereisnoevidencetosuggestthatNSAIDsare
moreeffectivethanacetaminophenforthetreatmentoftendinopathy.
60
Followingtreatmentwiththesemodalities,asupervisedphysicaltherapyprogramcanbe
initiated that is focused on stretching and strengthening (Figs. 22-6 to 22-8). Eccentric
stretching and strengthening promotes the formation ofnewcollagen and is associated with
excellentresults,particularlyinthemanagementofAchillestendinopathy.61Ultrasound,laser,
massage,andelectricalstimulationhave beenusedtosupplementthe rehabilitationprocess,
butno conclusive evidenceexistsregardingthebenefitsof these modalities.
62–64
Other less
traditionalinterventions,suchasextracorporealshockwavetherapy(ESWT)andplatelet-rich
plasma(PRP),havebeguntoreceiveattentionasnoveltechniquesdesignedtoimprovetendon
biologyandmechanicalintegrity.
Repetitivelow-energyESWTis analternativetosurgeryforbothchronictendinopathies
thathavefailedotherconservativeinterventions.
65–67
Itworksbyintroducingpressurewaves
atadiseasedsitewhichareconvertedintobiochemicalsignals.Thesesignalsinturnstimulate
the release of growth factors, increase vascularity, and enhance extracellular matrix
production.68Ina systematicreviewbyAl-Abbadetal.,benefitsofESWT inthe setting of
chronic Achilles tendinopathy were consistently observed.65 Rasmussen et al. found that
patientswithAchillestendinopathywhowere treatedwithESWTimprovedtheir American
Orthopaedic Foot and Ankle Society (AOFAS) scores to a significantly greater extent than
thoseinashamgroupat3monthsfollow-up.66Further,ESWTmaybeofgreaterclinicalutility
when combined with an eccentric loadingprogram, as described by Rompe etal.67 Future
researchisneededregardingtheoptimalenergylevelsandthenumberoftreatmentsnecessary
to achieve good results with ESWT. Studies with longer term follow-up would also be
beneficial,asmostliteraturehasontheshort-termbenefits.
69
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FIGURE22-6.A:EccentricAchillesstrengtheningexercisepart1:standingbilateralplantarflexion.B:Eccentric
Achillesstrengtheningexercisepart2:standingunilateralcontrolledlowering.(ReproducedfromLotkePA,Abboud
JA,EndeJ.Lippincott’sPrimaryCareOrthopedics.Philadelphia,PA:WoltersKluwer;2013.Figures76-10,76-11,
withpermission.)
Biologictherapies, such asPRP, attempttofacilitatethehealingofdegenerative tendons
throughtheintroductionofahighconcentrationofplateletsandtheirrespectivegrowthfactors
toareasofdiseasedtendon.
The growth factors derived from these platelets include platelet-derived growth factor,
transforming growth factor β, vascular endothelial growth factor, epidermal growth factor,
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insulin-like growthfactors I and II, and fibroblastgrowth factor,which stimulatea healing
response.70 Specifically, they promote the formationofextracellular matrix andgranulation
tissueandstimulatecellgrowth,proliferation,angiogenesis,andcellmigration.Plateletsare
foundin extremelyhigh concentrations inPRP as compared to normal plasma. Although the
normalconcentrationofplateletsisapproximately200,000perµL,inPRP,itisapproximately
2millionperµL.
71
FIGURE22-7.Anexampleofaposteriortibialtendonstrengtheningexercisewitharesistanceband.(Reproduced
fromUpToDate,WoltersKluwerHealth.)
Monto72evaluatedtheroleofPRPintreatingchronicAchillestendinopathy,andfounditto
be a beneficial intervention. At 6 months following treatment, abnormalities in MRI and
ultrasoundhadresolvedin27of29patients.At24monthsposttreatment,theaverageAOFAS
scorewas88;itwas34pretreatment.71However,otherinvestigationshavenotfoundPRPto
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beadvantageous.InarandomizedcontrolledtrialbydeVosetal.,73eccentricexerciseswitha
PRP injection did not result in greater improvement in pain and activity as compared to
eccentric exercises witha saline placebo injection. As such, future researchis required to
enhanceourunderstandingofPRPasatreatmentfortendinopathy.
Surgicalinterventionisindicatedifapatienthascontinuedsymptomsafter3to6monthsof
conservative treatments or ifa tendon rupture has occurred. The general principles include
debridementofabnormaltendon,thereleaseoffibrousadhesions,andrepairortubularization
of the remaining viable tendon. Tendon transfers and autograft- or allograft-based tendon
reconstruction are used in severe cases of tendinopathy. Osseous procedures, such as the
calcaneal osteotomies performed for PTT and pes planus, are designed to correct the
underlyingdeformityandanymalalignment.
FIGURE22-8.Exercisesfortherehabilitationofperonealtendinopathy.A:Isometriccontractionagainstawallwith
footeverted.B:Resistancebandeccentricexercise.C:Heeldropandraiseonstep.(ReproducedfromUpToDate,
WoltersKluwerHealth;CourtesyofTimothyDraper,DO,AAFP,CAQSportsMedicine.)
CONCLUSION
Tendinopathies of the footand ankle havetraditionallybeen thought ofas overuseinjuries.
Although this remains one of the most common causes of symptomatic lower extremity
tendinopathy, the role of systemic disease must also always be considered, as metabolic
derangementscanadverselyaffectthemechanicalandphysiologicintegrityoftendon.Asthe
prevalenceof metabolic disorders, such asDM andobesity, continues torise inthe United
States, so too will the sequelae ofthese conditions.
73,74
Practitioners must therefore have a
familiaritywiththedeleteriousmusculoskeletaleffectsofsuchdiseases.
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