Aggressi

ve
periodo
ntitis
A seminar by
Dr. RICHA AGRAWAL
Dept of Periodontology
Introduction
History
1923, Gottlieb -- Case of epidemic influenza
Diffuse atrophy of the alveolar bone!
Loss of collagen fibers in the periodontal
ligament
Replacement by loose connectie tissue
!"tensie bone resorption,
Resulting in a #idened periodontal ligament
space$
%he gingia apparently #as not inoled$
192&, Gottlieb -- inhibition of continuous
cementum formation
Deep cementopathia
Gottlieb's hypothesis of deep cementopathia
(n 193&, )annenmacher - incisor-first molar
inolement
Parodontitis marginalis progressiva in young
patients$
*eeral e"planations
+any -- degeneratie, noninflammatory disease
process , -periodontosis.$
/thers -- denied 00$trauma from occlusion$
%homa and Goldman-- 1arodontosis
/rban 2 )einman, 1eriodontosis3
%hree stages of the disease3
*tage (
*tage ((
*tage (((
%he Committee on 4omenclature of the 551 in
1967 had defined periodontosis as3

-a degeneratie non-inflammatory destruction of
the periodontium originating in one or more of the
periodontal structures characterized by migration
and loosening of the teeth in the presence or absence
of secondary epithelial proliferation and poc8et
formation or secondary gingial disease$.
1999 the )orld )or8shop in 1eriodontics
--concept of periodontosis as a degeneratie entity
#as unsubstantiated and that the term should be
eliminated from periodontal nomenclature$
%he committee did recognize that a clinical entity
different from adult periodontitis might occur
among adolescents and young adults$
"u#enile periodontitis
(ntroduced by Chaput and colleagues in 199: and
;utler in 1999$
(n 19:1, ;aer defined it as, -a disease of the
periodontium occurring in an other#ise healthy
adolescent #hich is characterized by a rapid loss of
aleolar bone about more than one tooth of the
permanent dentition$ %he amount of destruction
manifested is not commensurate #ith the amount of
local irritants$.
Classification systems t$roug$ t$e years
%ear Responsible &ody '$e (ystem
)*++ A A P "P
)*,- A A P "P
.Pre/pubertal0
.Locali1ed0
.Generali1ed0
)*,* AAP 2arly onset
World 3or4s$op periodontitis
)**5 !uropean )or8shop on !arly onset
periodontology periodontitis
<=1,11,R11>
)*** 551 (nternational 5ggressie periodontitis
)or8shop for
Classification
Page and (c$roeder )*,6
1repubertal periodontitis
Generalized
Localized
=uenile periodontitis
Rapidly progressing periodontitis
Grant7 (tern7 and Listgarten7 )*,,
1ost ?uenile
!arly onset
=uenile
Localized
Generalized
(u1u4i7 )*,,
1repubertal periodontitis
=uenile periodontitis
1ost ?uenile periodontitis
Rapidly progressing periodontitis
%ype 5
%ype ;
Ranney7 )**5
2arly/onset periodontitis
Localized early-onset periodontitis
Generalized early-onset periodontitis
!arly-onset periodontitis related to systemic
disease
!arly-onset periodontitis, systemic determinants
un8no#n
(n 19&9 a group of periodontal diseases #ere called
!arly onset periodontitis3
/nset before 36 yrs,
Rapid disease progression and
@istinct etiologic characteristics$
28P included9
1repubertal periodontitis
=uenile periodontitis
Rapidly 1rogressie periodontitis
Prepubertal periodontitis9
Can affect the primary and mi"ed dentition
/nset bet#een eruption of primary teeth and
puberty <before 11 years>
(u1u4i et al .)*,,0 :/, yrs
Lo# caries rate
*eere gingial inflammation rapid bone loss
%ooth mobility
%ooth loss
Page et al )*,5
Generali1ed or locali1ed
Generalised associated 3it$ a systemic disease
1apillon-Lefere syndrome, @o#n syndrome,
Chedia8 Aigashi syndrome, hypophosphatasia,
neutropenias, L5@
Locali1ed // fe#er teeth, slo#er bone loss, minor
inflammation$ +ild defects in neutrophils or
monocytes but not both$
Papillon/Lefe#re syndrome
Palmar plantar 4eratosis
60 Rapidly Progressi#e periodontitis
(n 19&&, *uzu8i has classified this disease as t#o
separate entities-
B 'ype A7
B 'ype &.
RAPIDL% PR8GR2((I;2 P2RI8D8<'I'I(9
'%P2 A
1atients usually bet#een 1C and 29 years of age
and een 37 years
Demales affected more than males <231 to 331>
Generalized lesions
+inimal local factors
Caries rate ariable
@epressed neutrophil chemota"is <99 per cent of
patients>
@epressed 5+LR
Genetic implications
1ossible medical considerationsE
/titis media,
(ncreased incidence of respiratory tract
infections,
*8in and fungal infections, and
Durunculosis
+alaise, #eight loss, and mental depression$
RAPIDL% PR8GR2((I;2 P2RI8D8<'I'I(9
'%P2 &
1atients generally oer 29 years of age <29-36>
Generalized lesions
1laFue and calculus present
Caries rate ariable
4eutrophil chemota"is normal or depressed
5+LR #ithin normal limits
Genetic implications not 8no#n
1ossible medical considerations
50 "u#enile Periodontitis
Localized or generalized
1atients bet#een 11-19 years <Glic8man> puberty
and 27 years
%ype 1- ;one destruction limited to first molars and
incisors <1C$9G>
%ype 2- ;one destruction inoling first molars and
incisors and some other teeth <26$6G>
%ype 3- Generalized destruction but #orse around the
first molars and incisors <1C$9G>
%ype C- Generalized inolement of more than 1C teeth
<CC$:G> <Hosof 1997>
+inimal local factors and inflammation
Lo# caries rate
@epressed neutrophil chemota"is <:: per cent of
patients>
5+LR slightly increased
Genetic implications
Rate of bone loss is 3-C times faster than other
periodontitis
(t has also been sho#n that =1 occurs freFuently in
blood group ; <Iaslic8 et al., 19:1>$
Post/"u#enile Periodontitis
29 and 36 years of age
Demales affected more than males <331>
Dirst molar and incisor lesions
1laFue and calculus present
/bious signs of inflammation
;acterial flora resembles chr periodontitis
Caries rate ariable
4eutrophil function not determined
5+LR slightly increased
Genetic implications not 8no#n
Replacement of early onset periodontitis 3it$
aggressi#e periodontitis
Classification and clinical syndromes
5ggressie forms of periodontal disease hae been
defined based on the follo#ing primary features
<Lang et al$ 1999>3
4on-contributory medical history
Rapid attachment loss and bone destruction
Damilial aggregation of cases

*econdary features that are considered to be generally
but not uniersally present are3
5mounts of microbial deposits inconsistent0$$
5 a and in some Dar !ast populations, 1 g$
1hagocyte abnormalities$
Ayper-responsie macrophage phenotype,
including 1G!
2
and (L-l J in response to
bacterial endoto"ins$
1rogression of attachment loss and bone loss
may be self-arresting$
%he international classification #or8shop identified
clinical and laboratory features deemed specific
enough to allo# sub classification of 5g13
Localized and
Generalized forms
<%onetti 2 +ombelli 1999, Lang et al$ 1999>$
Locali1ed aggressi#e periodontitis .LAP0
Circumpubertal onset$
Robust serum antibody response to infecting
agents$
Localized first molarKincisor presentation #ith
interpro"imal attachment loss on at least t#o
permanent teeth, one of #hich is a first molar, and
inoling no more than t#o teeth other than first
molars and incisors$
Clinical features of Locali1ed Aggressi#e
Periodontitis9
Lac8 of clinical inflammation
1resence of deep periodontal poc8ets
5mount of plaFue inconsistent #ith the amount of
periodontal destruction$
1laFue that is present forms a thin biofilm on the
teeth and rarely mineralizes to form calculus$
@istolabial migrationL diastema formation
(ncreasing mobility of the first molars,
*ensitiity of denuded root surfaces to thermal and
tactile stimuli,
5nd deep, dull, radiating pain during mastication,
1eriodontal abscesses may form at this stage,
Regional lymph node enlargement may occur$
Radiograp$ic features
Classic diagnostic sign of localized aggressie
periodontitis ,
Mertical loss of aleolar bone
Dirst molars and incisors
5rc shaped loss of aleolar bone$
Rate of bone loss is about 3-C times faster than in
chronic periodontitis$
Generali1ed aggressi#e periodontitis .GAP0
Nsually affecting persons under 37 years of age,
but patients may be older$
1oor serum antibody response to infecting agents$
Generalized interpro"imal attachment loss
affecting at least three permanent teeth other than
first molars and incisors$
1ronounced episodic nature of the destruction of
attachment and aleolar bone$
G51 represents the most heterogeneous group and
includes the most seere forms of periodontitis$
%hey comprise3
Generalized ?uenile periodontitis,
*eere periodontitis,
Rapidly progressing periodontitis
!ach of these G51 forms, ho#eer, remains highly
heterogeneous in terms of clinical presentation and
response to therapy$
Diagnosis // re=uires t$e absence of systemic
diseases t$at may se#erely impair $ost defenses
and lead to premature e>foliation of teet$??
periodontal manifestation of systemic diseases.
Clinical features of GAP
%#o gingial tissue responses3
*eere, acutely inflamed tissue, often proliferating,
ulcerated, and fiery red
;leeding
*uppuration
%his is destructie stage, in #hich attachment and bone
are actiely lost$
%issues may appear pin8, free of inflammation, and
occasionally #ith some degree of stippling,
although the last feature may be absent
Het deep poc8ets can be demonstrated by probing$
1age and *chroeder-- to coincide #ith periods of
Fuiescence in #hich the bone leel remains stationary$
*ome patients may hae systemic manifestations
such as #eight loss, mental depression, and general
malaise $
+ay or may not hae local factors
Radiographic features
Radiographs often sho# bone loss that has
progressed since the preious ealuation$
1age and co-#or8ers described sites in generalized
aggressie periodontitis <formerly R11> patients
that demonstrated osseous destruction of 26G to
97G during a 9-#ee8 period$
Despite t$is e>treme loss7 ot$er sites in t$e same
patient sho#ed no bone loss$
Incidental attac$ment loss
/ften sub?ects present #ith attachment loss that
does not fit the specific diagnostic criteria
established for 5g1 or chronic periodontitis$
(t includes3
Recessions associated #ith trauma or tooth position,
5ttachment loss associated #ith impacted third molars,
5ttachment loss associated #ith remoal of impacted
third molars,etc$
(t may include initial clinical presentations of
periodontitis$
%hese patients are a high-ris8 group for 5g1 or chronic
periodontitis$
2PID2@I8L8G%

!arly onset <aggressie> forms of periodontal diseases are
detectable in all age and ethnic groups <1apapanou 1999>$
Primary dentition/
Little eidence -- prealence of 5g1 affecting the
primary dentition$
De# studies from industrialized countries3
B +arginal aleolar bone loss
B 1rimary dentition
B 6 to 11 year olds
B DreFuencies ranging from 7$9 - C$6G of sub?ects <*#eeney et
al$ 19&:, ;imstein et al$ 199C, *?odin 2 +attson 199C>$
1eriodontitis affecting the primary dentition does
not necessarily mean presence of an aggressie
form of periodontitis,
;ut may indicate a chronic form of disease #ith
relatie abundance of local factors <plaFue and
calculus>$
+ore seere cases affecting the primary dentition
--periodontal manifestations of systemic
<hematologic> diseases, such as leu8ocyte adhesion
deficiency$
Permanent dentition
13 to 27-year-old indiiduals, prealence of
periodontitis of O 1G <usually 7$1- 7$2G in
Caucasian populations>$
%he ris8 of deeloping periodontitis at such an
early age, ho#eer, does not seem to be shared
eFually in the population$
5mong N$*$ school children 6-1: years of age, the
prealence of 1eriodontitis has been estimated to
range from about 7$2G for #hites to about 2$9G
for blac8s < Loe 2 ;ro#n 1991 >$
;lac8s #ere at much higher ris8 for localized
aggressie periodontitis
;lac8 males #ere 2$9 times more li8ely to hae the
disease than blac8 females$
)hite females #ere more li8ely to hae localized
aggressie periodontitis than #hite males$
(creening
*creening in children
*creening in adultsK adolescents
Lo# prealence of 5g1
Cost-effectie detection of cases
*ensitie approach
(n 1erio, the most sensitie diagnostic test -
measurement of attachment loss by probing$
5pplication of this diagnostic procedure in the
mi"ed dentition0
(n younger sub?ects-- currently utilized screening
approach3
+easurement of the distance bet#een the
aleolar crest and the cemento enamel ?unction
on bite-#ing radiographs$
5dantage0$
4ormal distance bet#een C!= and the aleolar
crest of primary and permanent molars in : to 9-
year-old children$
;imstein 2 *os8olne 19&&L 4eedleman, +attson
1992
1rimary molars -- 7$& to 1$C mm$
1ermanent molars -- 7 to 7$6 mm apical to the
aleolar crest in : to 9 year olds$
+a?ority of children -- distances significantly O 2-3
mm <#hich is considered normal for the
completely erupted dentitions of adults>$
(n children, significantly greater distances hae
been detected at3
*ites #ith caries,
Dillings or open contacts
(f local factors are absent and the distance is more
than 2 mm then0
Radiographic signs of marginal bone loss is a
highly specific sign of periodontitis
;ut #hat about sensitiityP
Lo#er than probing
5s initial intrabony defects are not isible due to
mas8ing effect of intact cortical plates$
(n older adolescents and adults,
5ppropriate screening - periodontal probing not
radiographs$
5 5 1 -- simplified screening e"amination$
%his e"amination is based on a modification of the
C1(%4 <5inamo et al$ 19&2, 5merican 5cademy of
1eriodontology 2 5merican @ental 5ssociation
1992>$
!%(/L/GH 54@ 15%A/G!4!*(*
Characterized by seere destruction of the
periodontal attachment apparatus at an early age$
%his short time of manifestation of clinically
detectable lesions is generally interpreted as being3
%he e"pression of highly virulent causative
agents or
Aigh leels of susceptibility of the individual
patient, or a combination of the t#o$
&acterial etiology
Whether to accept bacterial etiology or not?
@ifficult -- little isible plaFue accumulation$
Listgarten 19:9, )estergaard et al$ 19:&3
+icroscopic studies demonstrated the presence
of a layer of bacterial deposits on the root
surface of adanced 5g1 lesions$
1ioneers #ho attempted to identify the causatie
bacteria using culture techniFues3
4e#man et al$ 19:9
*lots 19:9
4e#man 2 *ocrans8y 19::
Gm /#e organisms comprised appro"imately 6A5
of the isolates from deep periodontal poc4ets$
5nd only )A5 of the isolates in control sites #ith
normal gingia$
%he dominant microorganisms in L=1 included3
5 a,
Capnocytophaga sp,
!$ corrodens,
1$ intermedia and
+otile anaerobic rods, such as C$ rectus$
Gram-positie isolates #ere mostly
streptococci, 5ctinomycetes and
peptostreptococci$
5$a is regarded as a 8ey microorganism in L51$
5s summarized by %onetti and +ombelli, this lin8
is based on the follo#ing eidence3
5$ a is found in high freFuency <appro"imately
97G> in lesions characteristic of L51$
*ites #ith eidence of disease progression often
sho# eleated leels of 5$ a$
1atients #ith the L51 hae significantly eleated
serum antibody titers to 5$a$
Clinical studies sho# a correlation bet#een
reduction in the subgingial load of 5$ a during
treatment and a successful clinical response, and
5$ a produces a number of irulence factors that
may contribute to the disease process$
W$y is t$ere localisation of disease to )
st

molars and incisors in LAPB
5fter initial colonization at the first permanent
teeth to erupt <the first molars and incisors> 5 a
eades the host defense by3
1roduction of 1+4 chemota"is-inhibiting
factors,
!ndoto"in,
Collagenases,
Leu8oto"in,
5nd other factors that allo# the bacteria to
colonize the poc8et and initiate the destruction
of the periodontal tissues$
5fter initial attac8
(mmune defenses stimulated
/psonic antibodies are produced
1hagocytosis of inading bacteria and neutralization
of leu8oto"ic actiity$
Colonization of other sites may be preented$
5 strong antibody response to infecting agents is one
characteristic of L51$
;acteria antagonistic to 5$ a may colonize the
periodontal tissues and inhibit 5$ a from further
colonization of periodontal sites in the mouth$ %his
#ould localize 5$ a infection and tissue destruction$
5$ a may lose its leu8oto"in producing ability for
un8no#n reasons$ (f this happens, the progression
of the disease may become arrested or retarded and
colonization of ne# periodontal sites aerted$
@efect in cementum formation may be responsible
for the localization of the lesions has been
suggested$
Root surfaces of teeth e"tracted from patients #ith
localized aggressie periodontitis hae been found
to hae hypoplastic or aplastic cementum$
%his #as true not only of root surfaces e"posed to
periodontal poc8ets but also of roots still
surrounded by their periodontium$
Dispute on the view that LAP is an A.a. infection

+c4abb et al$ 1992, 199C, Gmur3
5 high prealence of this organism in certain
populations, particularly from deeloping
countries$
*ome patients #ith L=1
4either sho# presence of 5$a$ in the oral
flora
4or hae eleated antibody titers to the
organism <Loesche et al$ 19&6, +oore 19&:>$
A.a.
*erotypes
Leu8oto"in
!ndoto"in
;acteriocin
Collagenolytic actiity
Dibroblast cytoto"ity
Mesicles
Generalized aggressie periodontitis <G51>, hae
been associated #ith3
1orphyromonas gingialis,
;acteroides forsythus and
5$a$
4on-responding lesions often contain 1$ gingialis in
eleated proportions$
&acterial damage to t$e periodontium
;acteria cause destruction of the marginal
periodontium ia t#o related mechanisms3

@irect action of the microorganisms or their

products on the host tissues

%hey elicit tissue-damaging inflammatory

responses$
5pical spread of bacteria is controlled through a
first line of defense3
Aigh turnoer of =! 8eratinocytes,
/ut#ard flo# of creicular fluid and
@irected migration of 1+4 through the =!
!fficiency of these innate immune mechanisms
is highly enhanced by the presence of specific
antibodies and complement fragments in the
gingial fluid <1age 1997>
Host response to bacterial pat$ogens
Local

*ystemic host responses
Local inflammatory responses-
1olymorphonuclear leucocytes
; cells
5ntibody-producing plasma cells <Lil?enberg 2
Lindhe 19&7>$
B 1redominantly (gG-producing cells$
B Local (gGC producing cells, in particular,
seem to be eleated$
B Lo#er proportion of (g5 producing cells
<+ac8ler et al$ 19::, 19:&, )aldrop et al$
19&1, /ga#a et al$ 19&9>$
% cells$
@epressed %- helper to %- suppressor ratio as compared
to both healthy gingia and peripheral blood$
*uggests the possibility of altered local immune
regulation <%aubman et al$ 19&&, 1991>$
+ononuclear cells- reduced 5+LR
5s #ell as a higher than normal response to ; cell
mitogens$
Local inflammatory responses are characterized by3
1G!2,
(L - 1Q
(L -l J in both creicular fluid and tissue
<+asada et al$ 1997, /ffenbacher et al$ 1993>$
1rostaglandin !2 production, in particular, has
been sho#n to be highly eleated in 5g1
sub?ects #hen compared to periodontally
healthy indiiduals and chronic periodontitis
patients$
Creicular fluid from 5g1 lesions3
*pecific antibodies against 5g1-associated
microorganisms <Lally et al$ 19&7, *teubing et
al$ 19&2, !bersole et al$ 19&C, 19&6>
Cleaed complement fragments < *chen8ein 2
Genco 19::, 1atters et al$ 19&9 >
Creicular fluid titers of antibodies against 5g1
associated microorganisms are freFuently higher
than in the serum of the same patient <!bersole et
al$ 19&C, 19&6>$
*ubstantial titers of antibodies against 5$a$ and 1$
gingialis hae also been detected in the serum of
5g1 patients$
Recent inestigations hae identified the
immunodominant 5$ a antigen to be the serotype
specific carbohydrate
%he ast ma?ority of antibodies reactie #ith this
carbohydrate in 5g1 patients consist of (gG2
<Califano et al$ 1992>$
Aigh titers and high aidity of 5$a$ specific (gG2
hae been demonstrated in L51 patients$
G51 patients are freFuently sero negatie for 5$a$
or display lo# titers and aidity$
5nti 5$a$ serotype polysaccharide (gG2, therefore,
are considered to be protectie against #idespread
5g1 <%e#l et al 1999 >$
1atients freFuently sho#3
Lo# leels of serum antibodies against 1$ g and
Lo# leels of antibody aidity, indicating a specific
inability of some G51 patients to effectiely cope #ith
these bacteria$
1+4 of some L51 and G51 patients present
decreased migration and antibacterial functions
<Genco et al$ 19&7, 19&9, Man @y8e et al$ 19&2,
19&9, 19&&>$
Man @y8e et al$ 19&63
1+4 abnormalities in L51 patients seem to cluster in
families much in the same #ay as 5g1 does$
*uggesting that the L51- associated 1+4 defect may
be inherited$
*hapira et al$ 199C, 5gar#al et al$ 19993
1+4 abnormalities in L51 patients may be, at least in
part, the result of a hyper-inflammatory state resulting
in the presence of pro-inflammatory cyto8ines in the
serum of some 5g1 patients
AL5--regulate immune responses,
candidate mar8ers for 5g 1
AL5-59 and ;16
(ncreased e"pression of type (( +AC molecules$
AL5 @RC $
1olyclonal actiation of ; cells
Genetic aspects of $ost susceptibility
*a"en 2 4eanlinna 19&C, ;eaty et al$ 19&:, Long
et al$ 19&:, ;oughman et al$ 1992, +arazita et al$
199C3 1realence of 5g1 is disproportionately high
among certain families, #here the percentage of
affected siblings may reach C7-67G$
*uch a dramatic familial aggregation of cases
indicates that genetic factors may be important in
susceptibility to 5g1$
Damilial pattern can be partly accounted for by one
or more genes that could predispose indiiduals to
deelop 5g1$
*egregation analyses -- autosomal dominant mode
of inheritance <*a"en 2 4eanlinna 19&C, ;eaty et
al$ 19&:, Aart et al$ 1992, +arazita et al$ 199C>$
+ost of inestigations--in 5frican 5merican
populations$
*egregation analysis3
(nformation about the mode of inheritance of a genetic
trait
4o information regarding specific gene<s> inoled$
Lin8age analysis -- %he chromosomal location of a
gene of ma?or effect for a trait such as 5g1
susceptibility
Lin8age of L51 to the itamin @ binding locus on
region F of chromosome C in a large family of the
;randy#ine population <;oughman et al$ 19&9>$
Aart et al$ 1993
Genetic heterogeneity in L51 forms, and distinct
forms of 5g1 e"ist$
5ll forms of 5g1 are not due to the same genetic
defect <Aart 1999>$
/ther genes may act as modifying genes and
influence clinical e"pression of the disease$
(mpact of genetic control on antibody responses
against specific 5g1 associated bacteria$
Gunsolley et al$ 19&:, 19&&3
%he ability to mount high titers of specific antibodies is
race-dependent and probably protectie
%his has been sho#n to be under genetic control as a
codominant trait, independent of the ris8 for 5g1$
(n indiiduals susceptible to 5g1, the ability to
mount high titers of antibodies < (gG2 in particular>
may be protectie and preent e"tension of disease
to a generalized form < *chen8ein 199C>
5llelic ariations in the Dc receptor for (gG2 hae
also been suggested to play a role in suboptimal
handling of 5$a$ infections$
)ilson 2 Ialmar 19993 1+4 e"pressing the R131
allotype of DcRR((a <i$e$ Dc receptor containing an
arginine instead of a histidine at aminoacid 131>
sho# decreased phagocytosis of 5$a$
2n#ironmental aspects of $ost
susceptibility
*chen8ein et al$ 19963 cigarette smo8ing #as
sho#n to be a ris8 factor for patients #ith
generalized forms of 5g1$
*mo8ers #ith G51 had more affected teeth and
greater mean leels of attachment loss than patients
#ith G51 #ho did not smo8e$
(gG2 serum leels as #ell as antibody leels
against 5$a$ are significantly depressed in sub?ects
#ith G51 #ho smo8ed$
Current concepts
5ggressie forms of periodontitis are currently
considered to be multifactorial diseases deeloping
as a result of comple" interactions bet#een specific
host genes and the enironment$
(nheritance of 5g1 susceptibility is probably
insufficient for the deelopment of disease$
!nironmental e"posure to potential pathogens
endo#ed #ith specific irulence factors is also a
necessary step$
Aost inability to effectiely deal #ith the bacterial
aggression and to aoid inflammatory tissue
damage results in the initiation of the disease
process$
(nteractions bet#een the disease process and
enironmental <e$g$ cigarette smo8ing > and
genetically controlled < e$g$ (gG2 response to 5$a$ >
modifying factors are thought to contribute to
determining the specific clinical manifestation of
disease$
@iagnosis
DIAG<8(I(
Clinical diagnosis is based on
*pecific medical and dental history
Clinical e"amination of the periodontium$
*upplementation #ith other, more adanced aids
to properly diagnose, treatment plan and monitor
these diseases$
Cirst establis$ t$e presence of periodontitis
Dind out the cause for attachment loss
Rule out other causes of attachment loss
5g 1
Ch 1
41
5ccor to current classification 3
Clinical pres
Rate of progression
Damilial aggregation
*ystemic causes
Rule out systemic factors
Rule out 41
Ch 1 K 5g1
Clinical presentation suspect 5g 1
Aistory
Confirmed by lab inestigations
%entatie diagnosis is based on3
4o systemic inolement
Rapid attachment loss
Damilial aggregation
Less amt of local factors #hen compared to the
amount of destruction
@icrobiological diagnosis
Loo8 for presence of 5a <secondary feature to
differentiate from chr periodontitis>
Loo8 for presence of 5a and 1g
5ppropriate antibiotics
Nseful3 at initial diagnosis
3 at re-ealuation and recall phase
5a and 1g , transmitted to other family members
+icrobial testing of spouses and other family
members0$$
2#aluation of $ost defenses
1+4 , phagocytosis, chemota"is
Nnnoticed until lab testing
@efects are related to specific populations
GCD 1G!
2
--

++1 actiation
(gG2 titers in L51 and G51
Genetic diagnosis
!aluation of siblings and other family members
Construct a pedigree of the 5g1 trait
PRI<CIPL2( 8C 'H2RAP2D'IC
I<'2R;2<'I8<
5pproach in the past
Current approac$
*uccessful treatment dependent on3
!arly diagnosis,
@irecting therapy to#ards elimination or
suppression of the infecting microorganisms and
1roiding an enironment conducie to long-
term maintenance$
5$a$ is difficult to eliminate by conentional
mechanical therapy$
*lots 2 Rosling 19&3, Christersson et al$ 19&6,
Iornman 2 Robertson 19&63
*R1 in =1 lesions could not suppress 5$a$ belo#
detection leels$
Christersson et al$ 19&63
*oft tissue curettage and access flap therapy also had
limited success in eliminating 5$a$
5d?unctie administration of antibiotics3
%etracyclines K @o"ycycline
+etronidazole
Ciproflo"acillin
+etronidazole S amo"icillin
+etronidazole plus Ciproflo"acillin
5ugmentin
5zithromycin
+echanical therapy
C-9 #ee8s reassess
+icrobial samples from the deepest poc8et
5ppropriate surgical proceduresK mech instru
*ystemic antimicrobial therapy
+icrobiology testing repeated at 1-3 months later
5fter resolution of infection, the patient should be
placed on an indiidually tailored maintenance care
program
/ptimal plaFue control by the patient is of
paramount importance for a faorable clinical and
microbiologic response to therapy$
Conclusion
References
Glic8man
Lindhe
@C45 5pril 19&&
5nnals 1999
+anson 2 !lley
1erio 2777 @iagnostics- 277C ol 3C
5ntimicrobials for treatment of aggressie periodontitis-
/ral @iseases 2773L9361-63
1eriodontal diseases in the child and adolescent3 =ournal
/f Clinical 1eriodontology Molume 29 (ssue 6 1age
C77 L+ay 2772
Aerpesiralbacterial interactions in aggressie
periodontitis3 =ournal /f Clinical 1eriodontology Molume
37 (ssue 6 1age C27 L +ay 2773