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骨髓炎英文教科书

Chapter52-AcuteandChronicOsteomyelitis

AnthonyRBerendt

CarlWNorden

EPIDEMIOLOGY

Thecharacterofosteomyelitischangedwiththeadventofantibiotics,evolvingfromadiseaseofhighmortalitytoadiseasewithhighmorbidity.Certaintrendsare

apparent.Boneandjointtuberculosishasbecomelesscommoninthedevelopedworld,althoughtheadventofHIV-relateddiseasemaybringaboutareversalinthat

trend.Anincreasingnumberofchronicboneinfectionsarenowassociatedwithtrauma,surgeryandjointreplacementratherthanbeingsecondarytohematogenous

spread.

Theepidemiologyofacutehematogenousosteomyelitishasbeendetailed.

[

1]

Theincidenceishigherinmales,itvariesamonggeographicareas（Fig.52.1）and,in

someareas,classicalacutehematogenousinfectionisinlong-termdecline.

[

2]

Themale-to-femaleratioincreaseswithagefrom1.25inthe0-to4-yearagegroupto

3.69inthe13-to19-yearagegroup.TherearesubstantiallyhigherratesinMaorichildrenfromNewZealandandAboriginalchildrenfromWesternAustraliacompared

bothwithwhitechildrenlivinginthesameareasandwithchildrenlivinginEurope.Althoughalmostcertainlysocioeconomicinorigin,thesedifferencesmayalsobe

influencedbyhostgeneticfactors.

Thereislessclearinformationontheepidemiologyofchronicosteomyelitis,withtheexceptionofdiabeticfootinfections.

[

3]

Thereareanestimated11millionpeoplein

theUSAwithdiabetes;themajorityofthesehavetype2diseaseandhenceareolderadults.Some3%ofdiabeticpeopledevelopafootulcerannuallyand10–30%of

patientswithanulcerwilleventuallyneedanamputation.Ofallamputationsinpeoplewithdiabetes,60%areprecededbyaninfectedulcer.Footproblemshavebeen

estimatedtoberesponsiblefor15%ofthehospitaladmissionsand25%ofthehospitalbedusageamongdiabeticpatients.Theannualhospitalcostsforlimb

amputationsthatarerelatedtodiabetesamounttomorethanUS$350million.

PATHOGENESISANDPATHOLOGY

Microbialfactors

Adhesionistheinitialeventinthelocalizationofinfection.

[

4]

Theinitiallooseadhesiontoboneispotentiallyreversible.However,ifthesolidphaseoffersa

configurationthatisacceptabletothereceptorsofthemicro-organisms,amorepermanentadhesionoccurs.Staphylococcusaureusstrainspossessreceptorsfor

extracellularmatrixcomponentssuchascollagen,fibronectin,bonesialoproteinandosteopontin.

[

5]

[

6]

Itisunclearwhicharecrucialforthegenesisofosteomyelitis,with

conflictingdataontheroleofthecollagenreceptor.Thefibronectin-bindingproteinsappeartoplayaroleinattachmentto,andinvasionof,endothelialcells,events

thatmaybeofrelevanceintheearlieststagesofhematogenousseeding.

[

7]

ItispossiblethattraumaorinjurymayexposebindingsitesforstrainsofS.aureus.

Followingadhesion,firmattachmentandadherentgrowthoccurs.ForstaphylococciandsomeGram-negativeorganisms,synthesisofanexocellularpolysaccharide

（glycocalyx）producesa'biofilm',withinwhichbacteriacanformmicrocolonies（Fig.52.2andFig.52.3）.Adherentgrowthconfersphenotypicresistancetoantibiotics,

probablyasaresultofchangesincellularmetabolism,andtheglycocalyxmayconferprotectionagainstphagocytesandcomplement.

[

8]

Prostaglandinsarepotentboneresorptionagentsthatenhanceosteoclastactivityandcollagensynthesis.Itwasnotedinstudiesofhumanbone,aswellasinstudies

ofexperimentalosteomyelitisinanimals,thatincreasedproductionofprostaglandinE2（themostpotentprostenoidintheresorptionofbone）waspresent.

[

9]

Cytokines,

inparticulartumornecrosisfactor,arealsopotentstimulatorsofosteoclastaction.Finally,ithasbeenrecognizedthatmoleculesreleasedfromanumberofthe

pathogensthatcauseosteomyelitisarepotentstimulatorsofboneresorption,viacytokinereleasefrommonocytesandbystimulationofosteoclastformation.

[

10]

Pathology

Asinmostorgans,aninsulttoboneisfollowedbyvascularandcellularresponses.However,inbonethisprocessismodifiedbytherigidnatureofthebone,because

theincreasedtissuepressurecannotbediffusedintosofttissue.Withincreasedintramedullarypressure,sinusesandcapillariesarecompressedinthemarrow,

producinginfarction.Attheinfarctionedge,thereisreactivehyperemia,whichisassociatedwithincreasedosteoclasticactivity.Thisinturnproduceslossofboneand

localizedosteoporosis.Aninflammatoryprocessbeginsatthemarginoftheinfarctedareaandpenetratesthroughthecortexintothesubperiostealarea.Because

therearefewanchoringfibersintheperiosteumofinfantsandchildren,theperiosteumisreadilystrippedfromthebonesurfacebytheincreasedsubperiosteal

pressure.Thiscanresultindisruptionoftheperiostealbloodsupplytothecortex,andthisleadstocorticalboneinfarction,bonedeathandsequestrumformation.（A

sequestrumisamacroscopicpieceofdeadbonethatisretainedwithintheoverallbonestructure.）Strippingfromunderlyingboneisanosteogenicstimulustothe

periosteum,whichrespondsbylayingdownnewlivingbone.Theendresultisashellofnewbonearoundoraboveadeadsegment,aresponsethatpreservesthe

mechanicalstrengthofthebone,eventhoughpartsofitarenowdead.

Classificationsystemsforosteomyelitis

ThemostfrequentlyusedclassificationsystemisthatofWaldvogeletal.

[

11]

Inthisclassification,infectionsareclassifiedashematogenous,secondarytoacontiguous

focusofinfectionorrelatedtovascularinsufficiency.Forchroniclongboneosteomyelitis,asecondclassificationsystem,developedbyCierneyandMader,

[

12]

combinesfourstagesofanatomicdiseaseandthreecategoriesofphysiologichost（Fig.52.4）.Thisclassificationisusefulfordescribingseverityandlocationof

infectionandforplanningtreatment,anditisamenabletostudy.Thethreecategoriesofhostare:

¦normalexceptforosteomyelitis

¦systemicorlocalcompromise,and

¦treatmentwouldbeworsethanthedisease.

572

Figure52-1Acutehematogenousosteomyelitisinpreschoolchildren.DatafromGillespie.

[

1]

Figure52-2Endosteumofboneshowingstaphylococcineartheendostealhaversiancanal.In-vitroincubationofbonechipswithStaphylococcusaureusinterruptedat48

hours（scanningelectromicrograph）.FromNordenCW,GillespieWJ,NadeS.Infectionsinbonesandjoints.BlackwellScientificPublications;1994,withpermission.

Figure52-3Staphylococcienmeshedinglycocalyxnearthehaversianosteum.In-vitroincubationofbonechipswithStaphylococcusaureusinterruptedat48hours（scanning

electromicrograph）.FromNordenCW,GillespieWJ,NadeS.Infectionsinbonesandjoints.BlackwellScientificPublications;1994,withpermission.

Figure52-4Anatomicclassificationofosteomyelitisinadultlongbones.AdaptedwithpermissionfromMaderJT,CalhounJ.Osteomyelitis.In:

MandelG,BennetJ,DolinR,eds.

Infectiousdiseases.NewYork:

Churchill-Livingstone;1995:

1039–52.

Causativeagentsofosteomyelitis

Inacutehematogenousosteomyelitisinchildren,S.aureusaccountsformorethanhalfoftheorganismsisolated.

[

13]

Thenextmostfrequentgroupofisolatesare

streptococci.Inosteomyelitisorosteochondritisduetopuncturewoundstothefoot,Pseudomonasaeruginosaisisolatedfrequentlyandisassociatedwiththewearing

ofsneakers.Theorganismisfoundinthesoleofthesneakerandispresumablycarriedintothefootbythepuncturingnail.

[

14]Salmonellaspp.,althoughaninfrequent

overallcause,arestronglyassociatedwithsicklecelldisease.Indiabeticpatientswithfootinfections,S.aureus,Staphylococcusepidermidis,enterococci,other

streptococciandCorynebacteriumspp.areamongthemostfrequentaerobicorganismsthatareisolatedfrombone.Anaerobicorganismsarealsofrequentlyisolated,

withPeptostreptococcusspp.beingmostcommon.Fungi,mycoplasma,mycobacteria,brucella,treponema,actinomycosisandparasiteshavealsoallbeenassociated

withosteomyelitis.

573

Pathogenesisofdiabeticfootosteomyelitis

Thepathogenesisofosteomyelitisinthediabeticfootisanimportantproblemthatmeritsadditionalconsideration.Diabeticpatientsdevelopfootulcersbecauseofa

combinationofmotor,sensoryandautonomicneuropathyinteractingwithchangesinthemechanicalpropertiesofthesofttissuesofthefoot.Motorneuropathycauses

ahigh-archedfootwithclawingofthetoes,andthisdeliversexcessivepressurestothemetatarsalheads,theheelandtheendsofthetoes.Subluxationatthe

metatarsophalangealjointsnotonlybringsthemetatarsalheadintoamoreprominentweight-bearingpositionbutalsocausesthefibrousmetatarsalpadstoslipout

fromunderthemetatarsalheads.Sensoryneuropathyreducestheresponsetopain,sothatforeignbodiesintheshoesareneglected,andcloudstherecognitionthat

itistimetochangeanill-fittingpairofshoesorrestthefeet.Autonomicneuropathyisassociatedwithexcessivefissuringandcrackingfromdry,poorlylubricatedskin,

anidealportalofentry.Nonenzymaticglycosylationofcollagenleadstocross-linking,withincreasedstiffness.

Thesefactorstogethercanreadilyleadtoulceration,whichmayleaddowntoajointorbone.Lossofperiosteumcausesdeathofthesuperficialpartofthecortexof

thebone.Infectioncantrackthroughthecorticalboneintothemedullaandspreadrapidlyupinsidethelongaxisofthebone.Boneinfarctionandreactiontoinfection

thenproceedsjustasinlargerbones.Ischemiafromperipheralvasculardiseasecompound