bone loss and patterns of bone loss.ppt1

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2. BONE LOSS AND PATTERNS
OF BONE DESTRUCTION

3. Introduction:
Heightofthealveolarboneisnormallymaintainedby
equilibrium.
Lossofalveolarbonesupportisoneofthe
characteristicsignsofdestructiveperiodontaldisease
andisconsideredtorepresenttheanatomicalsequelto
thespreadofperiodontitis.
Avarietyoffactorsotherthanthemainlocalfactors,ie
plaqueplayaroleinbonedestruction.
Thelevelofboneistheconsequenceofpastpathologic
experiences,whereaschangesinthesofttissueofthe
pocketwallreflectthepresentinflammatorycondition.

4. Factors Responsible for Bone Resorption:
Parathyroid Hormone (PTH):
PTHaffectsbonecellfunction,mayalterbone
remodeling,andcauseboneloss.
PTHactsonbothbone-resorbingcellsandbone-forming
cells.
Theneteffectofthehormonedependsonwhetheritis
administeredcontinuouslyorintermittently.
Whenadministeredcontinuously,itincreases
osteoclasticboneresorptionandsuppressesbone
formation.
However,whenadministeredinlowdosesintermittently,
itsmajoreffectistostimulateboneformation,a
responsethathasbeencalledtheanaboliceffectofPTH.

5. 1, 25-Dihydroxycholecalciferol (I, 25 (OH) 2 D 3):
TheactivemetabolitesofvitaminD3havecomplexeffectson
calciumhomeostasisandboneregulation.
1,25(OH)2D3stimulatesosteoclasticboneresorptioninvitro
andinvivo.
Itincreasesbothosteoclastnumberandactivity,withanincrease
inruffledbordersizeandclear-zonevolume.
Useof1,25(OH)2D3influencesandmodulatescytokine
productionbyimmunecells.

6. Estrogens:
Estrogenclearlyinhibitstheincreaseinboneresorption
associatedwithmenopause.
Followingestrogenwithdrawal,aninitialincreaseinbone
turnovercanbeobserved.
Theeffectsofestrogenaremediatedbyacombinationof
directandindirecteffects.
Thedirecteffectismediatedbyspecificreceptorsfoundin
cellsoftheosteoblastandosteoclastlineages.
Indirecteffectsofestrogenresultfromitsenhancingthe
expressionofgrowthfactorslikeinsulinlikegrowthfactor
(IGF-1)andtransforminggrowthfactor-β(TGF-β)

7. Host and Bacterial Factors Involved in Bone Resorption:
Thesubstancethatcaninduceboneresorptioninperiodontal
diseasecomefrom2sources:BacterialFactors,HostFactors.
BacterialFactors:
SubstancesfrombacteriaincludeLipopolysaccharides(LPS)from
gramnegativebacteria,lipoteichoicacidfromActinomyces
viscosus
Muramylldipeptide(MDP),bacteriallipoproteinandcapsularor
surfaceassociatedmaterial(SAM)fromgram-negativebacteria
havethepotencytocauseresorptioninvitro.

8. Host Factors:
Inflammatorymediators:PGE2,Leukotrienes,
Bradykinin,Cytokines,Interleukin-1,Interleukin–6,
TumorNecrosisFactor.

9. lnterleukin-1(IL-1):
IL-1isapowerfulandpotentbone-resorbingcytokine.
IthasbeenfoundthatIL-1αandIL-1βareequallypotentin
stimulatingboneresorptionandprobablyexerttheireffectson
bone-resorbingcellsinseveralways.
TheeffectsofIL-1probablyoccurbytwomechanisms.
Onemechanismisthestimulationoftheproductionandrelease
ofPGE2,therebystimulatingbone.
ThesecondmechanisminvolvesdirectactionofIL-1on
osteoclastsindependentofPGE2synthesisby80kdareceptor.

10. lnterleukin-6 (IL-6):
IL-6isalsoresponsiblefortheformationofcellswith
anosteoclasticphenotype.
BonecellsalsohavetheabilitytoproduceIL-6,
whichseemstobegreaterwhenthestimulusisby
anothercytokine.

11. Tumor necrosis factor (TNF) and Lymphotoxin:
Theyarebothmulti-functionalcytokinesproducedby
activatedLymphocytes,andtheysharethesamereceptor.
Theirmajoreffectonboneistostimulateosteoclasticbone
resorption.
IthasbeensuggestedthatpartoftheeffectofTNFismediated
byPGE2,aswellasbyIL-6.

12. Gamma interferon (IFN-γ):
Gammainterferonisamulti-functionalcytokinewhichhas
effectssimilartoTNFαorIL-1inmostbiologicalsystem.
GammainterferonismoreeffectiveininhibitingIL-1orTNF-
αthansystemichormoneslikePTHor1,25-(OH)2D3.
Further,ithasbeenfoundinlong-termmarrowcellcultures
thatgammainterferoninhibitstheformationofcellswiththe
osteoclastphenotype.

13. Other Products of Inflammation:
Heparinfrommastcellscanenhanceboneresorption
intissueculturesysteminducedbyLPSand
lipoteichoicacid,butcannotinduceboneresorption
onitsown.
Thrombin,aninflammatorymediatorandendproduct
ofthebloodcoagulationcascadeisapotentbone-
resorbingagent.
Anotherinflammatoryagent,bradykinin,evokes
similareffectsanditisindependentofprostaglandin
production.

14. ETIOLOGY OF BONE LOSS:
INFLAMMATION:
Theextensionofinflammationtothesupportingstructuresofa
toothmaybemodifiedbythepathogenicpotentialofplaqueor
bytheresistanceofthehost.
Thelatterincludesimmunologicactivityandothertissue-
relatedmechanisms,suchasthedegreeoffibrosisofthe
gingiva,probablythewidthoftheattachedgingiva,andthe
reactivefibrogenesisandosteogenesisthatoccurperipheralto
theinflammatorylesion.
Thepathwayofthespreadofinflammationiscriticalbecause
itaffectsthepatternofbonedestructioninperiodontaldisease.

15. Pathway of Inflammation:
Pathwaysofinflammationfromthe
gingivaintothesupporting
periodontaltissuesinperiodontitis.
A,Interproximally,fromthegingiva
intothebone(1),fromtheboneinto
theperiodontalligament(2),and
fromthegingivaintotheperiodontal
ligament(3).
B,Faciallyandlingually,fromthe
gingivaalongtheouterperiosteum
(1),fromtheperiosteumintothe
bone(2),andfromthegingivainto
theperiodontalligament(3).
A B

16. Afterinflammationreachesthebonebyextension
fromthegingiva,itspreadsintothemarrowspaces
andreplacesthemarrowwithaleukocytes,fluid
exudate,newbloodvessels,andproliferating
fibroblasts.
Multinuclearosteoclastsandmononuclearphagocytes
areincreasedinnumber,andthebonesurfacesare
linedwithresorptionlacunae.

17. Inthemarrowspaces,resorptionproceeds
startsfromwithin,causingfirstathinningof
thesurroundingbonytrabeculaeand
enlargementofthemarrowspaces,followed
bydestructionoftheboneandareductionin
boneheight.
Normallyfattybonemarrowispartiallyor
totallyreplacedbyafibroustypeofmarrowin
thevicinityoftheresorption.

18. RadiusofAction:
Locallyproducedboneresorptionfactorsmayhavetobe
presentintheproximityofthebonesurfacetobeabletoexert
theiraction.
PageandSchroeder(1982),onthebasisofWaerhaug's(1980)
measurementsmadeonhumanautopsyspecimens,postulated
thatthereisarangeofeffectivenessofabout1.5to2.5mm
withinwhichbacteria/plaquecaninducelossofbone.
Beyond2.5mmthereisnoeffect;interproximalangular
defectscanappearonlyinspaceswiderthan2.5mmbecause
narrowerspaceswouldbedestroyedentirely.
Tal(1984)-Largedefectsfarexceeding2.5mmfromthetooth
surfacemaybecausedbythepresenceofbacteriainthe
tissues.

19. Mechanisms of Bone Destruction:
Thereareseveralpossiblepathwaysbywhichproductsinplaque
absorbedbyperiodontaltissuescouldcausealveolarboneloss
(Hausman,1974).
1.Absorbableproductsfromplaquecouldstimulatebone
progenitorcellsintheperiodontiumtodifferentiateinto
osteoclasts,whichresorbalveolarbone.
2.Absorbableproductsfromplaqueas,forexample,complexing
agentsandhydrolyticenzymescoulddestroyalveolarbone
throughnon-cellularmechanismbydissolvingbonemineraland
hydrolyzingtheorganicmatrix.

20. Periods of Destruction:
Periodontaldestructionoccursinanepisodic,intermittent
fashion,withperiodsofinactivityorquiescence.
Thedestructiveperiodsresultinlossofcollagenandalveolar
bonewithdeepeningoftheperiodontalpocket.
Burstsofdestructiveactivityareassociatedwithsubgingival
ulcerationandanacuteinflammatoryreaction,resultingin
rapidlossofalveolarbone.

21. BONE LOSS IN PERIODONTITIS:
CHRONIC PERIODONTITIS:
Thecharacteristicfindingsinslowlyprogressive
periodontitisaregingivalinflammation,whichresults
fromtheaccumulationofplaque,andlossof
periodontalattachmentandalveolarbone,which
resultsinformationofapocket.
Pocketdepthsarevariable,andbothhorizontaland
angularbonelosscanbefound.
Toothmobilityoftenappearsinadvancedcaseswhen
bonelosshasbeenconsiderable.
Radiographicallybonelossisusuallyhorizontal

22. AGGRESSIVE PERIODONTITS:
Clinically,thereisasmallamountofplaque,which
formsathinbio-filmonthetoothandrarely
mineralizestobecomecalculus.
Themostcommoninitialsymptomsaremobilityof
thefirstmolarsandincisors,distolabialmigrationof
theincisors.
Bonelossisabout3-4timesfasterthaninchronic
periodontitis.
Theprogressionofbonelossandattachmentlossmay
beself-arresting.
Verticallossofalveolarbonearoundthefirstmolars
andincisorsisseen.An"arc-shaped"lossofalveolar
boneextendingfromthedistalsurfaceofthesecond
premolartothemesialsurfaceofthesecondmolar.

23. TRAUMA FROM OCCLUSION:
Traumafromocclusioncanproducebonedestruction
intheabsenceorpresenceofinflammation.
Intheabsenceofinflammation,thechangescaused
bytraumafromocclusionvaryfromincreased
compressionandtensionoftheperiodontalligament
andincreasedosteoclastsofalveolarbone,necrosisof
theperiodontalligamentandbone,andresorptionof
boneandtoothstructure.
Traumafromocclusionresultsinfunnel-shaped
wideningofthecrestalportionoftheperiodontal
ligament.

24. FOOD IMPACTION:
Interdentaldefectsoftenoccurwhereproximal
contactsisabnormalorabsent.
Pressureandirritationfromfoodimpaction
contributestoinversearchitecture.
Insomeinstancesthepoorproximalrelationship
maybetheresultofshiftinbonepositionbecauseof
extensivebonedestructionprecedingfoodimpaction.
Insuchcasesfoodimpactionisthecomplicating
factorratherthanthecauseofbonedestruction.
SMOKING:
Variousstudiesrecentlyhaveadvocatedandproven
theadverseeffectofsmokingonperiodontiumand
subsequentlyonbone.

25. STRESS:
Therearemany
formsofstress,suchas
trauma,drugintoxication,and
muscularfatiguethatmay
compromisethehealthofan
individual.

27. Prichard (1965) classification:
Interproximalcraters.
Inconsistent margins.
Hemisepta.
Furcationinvolvement.
Intra bony defect (with three osseous walls).
Combination of above.
Fenestration.
Dehiscence.
Glickman (1964):
Osseous craters.
Intra bony defect.
Bulbous bony contours.
Hemisepta.
Inconsistent margins.
Ledges.

28. Nomenclature of deformities of the
alveolar process:
The proposed system of nomenclature for
bony deformities caused by non-uniform
loss of bone is based on the following
basic terms:
OSSEOUS CRATERS:

29. MOAT:Whenthe
previouslydescribed
deformityinvolvesall
foursurfacesoftoothit
isdescribedasamoat.
RAMP:Initspurest
formthetermramp
describesdeformitythat
resultswhenboth
alveolarboneandits
supportingbonearelost
tothesamedegreein
suchamannerthatthe
margins of the
deformityareat
differentlevels.

30. PLANE:Thistermisappliedwhenbothalveolarboneandsupporting
boneislosttothesamedegreesuchthatthemarginsofthedeformityareat
thesamelevel.Itcanbeconsideredhorizontalbonelossaboutonetoothor
portionofatooth.
HEMISEPTA:Ahemiseptumoftenisassociatedwithaninconsistent
osseousmargin.Hemiseptaoccurbetweenanterioraswellasposterior
teeth,andtheyarefoundincombinationwithallothertypesofbony
deformities.

31. REVERSEDARCHITECTURE :Thesedefectsareproducedbylossof
interdentalbone,includingthefacialand/orlingualplates,withoutconcomitant
lossofradicularbone,therebyreversingthenormalarchitecture.Suchdefects
aremorecommoninthemaxilla.

32. LEDGES:Ledgesare
plateau-likebonemargins
causedbyresorptionof
thickenedbonyplates.
BULBOUS BONE
CONTOURS:Theseare
bonyenlargementscausedby
exostoses,adaptationto
functionorbuttressingbone
formation.Theyarefound
morefrequentlyinthemaxilla
thaninthemandible.

33. FENESTRATIONS AND
DEHISCENCE:

34. FURCATION INVOLVEMENT:

35. THICKENEDMARGIN:Anenlargementoffacial
orlingualmarginalalveolarplate,insteadofathin,
tapering,slightlyroundedbonymargin.Irregular
bonemarginisseenwherethereareabrupt
irregularitiesinthescallopedlevelofmarginalbone
andinterdentalsepta.
MARGINAL GUTTER:Ashallowlineardefect
betweenmarginalboneoftheradicalcorticalplateor
interdentalcrest,extendingthelengthofoneormore
rootsurfaces,usuallyformedbyresorptionofthe
socketsideoftheplateanddepositiononthefacial
surface.

36. HORIZONTAL BONE
LOSS:Thisisthemost
commonpatternofbone
lossinperiodontaldisease
theboneisreducedin
height,butthebonemargin
remains roughly
perpendiculartothetooth
surface.
Theinterdentalseptaand
facialandlingualplatesare
affected,butnotnecessarily
toanequaldegreearound
thesametooth.

37. VERTICAL BONELOSSOR
ANGULAR DEFECTS:Vertical
orangulardefectsarethosethat
occurinanobliquedirection,
leavingahollowed-outthroughin
thebonealongsidetheroot;the
baseofthedefectislocatedapical
tothesurroundingbone.

40. DIAGNOSIS:
CLINICAL:
Periodontalprobingandexplorationarekeyaspectsofclinical
examination.Carefulprobingrevealsthepresenceofpocket
depthgreaterthanthatofanormalgingivalsulcus.
Thelocationofthebaseofthepocketinrelativetothe
mucogingivaljunctionandattachmentlevelonadjacentteeth,
thenumberofbonywallsandthepresenceoffurcation
defects.
Transgingivalprobing,orsounding,underlocalanesthesia
confirmstheextentandconfigurationoftheintrabony
componentofthepocketoroffurcationdefects.
Theprobeshouldbe"walked"alongthetissue-toothinterface,
soastofeelthebonytopography.
Theprobemayalsobepassedhorizontallythroughthetissue
toprovidethree-dimensionalinformationregardingbony
contours.

41. RADIOGRAPHIC DIAGNOSIS:
Dentalradiographsarethetraditionalmethodusedto
assessthedestructionofalveolarboneassociatedwith
periodontitis.
Althoughradiographscannotaccuratelyreflectthe
bonymorphologybuccalandlingual,theyprovide
usefulinformationoninterproximalbonelevels.
However,evenatthislevel,theexacttopographyof
defectscannotbeassessedaccuratelyfrom
radiographs.
Variousmethodsofradiographicdiagnosisinclude
photodensitometricanalysisdigitalradiography,
subtractionradiography,CADIA,,nuclearmedicine.

42. Conclusion:
“Preventionisbetterthancure”sothereis
aneedforearlydiagnosisandidentificationof
thesefactorssuchaslocalfactors,TFO,
Smoking,Stress,SystemicDisordersetc
preventionofwhichwouldfurtherprevent
progressionofthedisease”.