13.Aggressive Peridontitis.pptx

AGGRESSIVE PERIODONTITIS
Dr.D.Navya,MDS
1

AGGRESSIVE PERIODONTITIS, AS THE NAME IMPLIES IS
A TYPE OF PERIODONTAL DISEASE WHERE THERE IS A
RAPID DESTRUCTION OF PDL AND ALVEOLAR BONE
LEADING TO EARLY LOSS OF TEETH.
THIS OCCURS IN PERSONS OTHERWISE SYSTEMICALLY
HEALTHY AND YOUNGER THAN 30 YEARS AGE BUT ALSO
IN OLDER PEOPLE.
3
Aggressive Periodontitis

Aggressive Periodontitis encompasses distinct types of
Periodontitis that affect people who, in most cases,
Otherwise appear healthy.
It tends to have a familial aggregation and there is a
Rapid rate of disease progression.
(American academy of Periodontology. Glossary of Periodontal
Terms. 4th edn. Chicago. AAP 2001)
4

1. Rapid rate of disease progression seen in otherwise
healthy individual.
2. An absence of large accumulations of plaque &
calculus
3. A family history of aggressive disease suggestive of a
Genetic trait.
(Tonneti & Mombelli-Ann Periodontol,4 ; 39, 1999)
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DIFFERS FROM CHRONIC PERIODONTITIS
PRIMARILY BY

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THREE TYPES OF AgP (Mombelli et. al 2004)
1. Secure or certain form
CAL > 2mm in a year, Rapid bone destruction before 18 yrs.
2. Uncertain or probable form
CAL > 2 mm or severe bone destruction before 30 yrs age.
3. In secure form
CAL with unclear rate of progression of around 2 mm
over a year or bone destruction .

CHARACTERISTICS THAT ARE COMMON TO PATIENTS
WITH AGGRESSIVE PERIODONTITIS
(Lang and Bartold)
1. Otherwise clinically healthy patient
2. Rapid attachment loss and bone destruction.
3. Amount of microbial deposits inconsistent with
destruction.
4. Familial aggregation of diseased individuals.
THE FOLLOWING CHARACTERISTICS ARE COMMON
BUT NOT UNIVERSAL
1. Diseased sites infected with A.a.
2. Abnormalities with phagocyte function.
3. Hyper responsive macrophages producing increased
PGE 2 & IL-1.
4. In some cases, self arresting disease progression
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Classified into localized and Generalized forms
Based on the following specific features
Localized form
1. Circum pubertal onset of disease
2. Localized first molar / incisor involvement with proximal
attachment loss on at least two permanent teeth, one of
which is a first molar.
3. Robust serum antibody response to infecting agents.
Generalized form
1. Usually affects persons under 30 yrs of age but may be older.
2. Generalized proximal attachment loss affecting at least three
teeth other than first molars and incisors.
3. Pronounced episodic nature of Periodontal destruction.
4. Poor serum antibody response to infecting agents.
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Localized Juvenile /Aggressive Periodontitis
Defined as “ a disease of the Periodontium occurring in
An otherwise healthy adolescent which is characterized
By a rapid loss of alveolar bone about more than one tooth
Of the permanent dentition. The amount of destruction
Manifested is not commensurate with the amount of
Local irritants “ . (Baer 1971)
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LOCALIZED AGGRESSIVE PERIODONTITIS
Clinical Characteristics
1. Localized aggressive Periodontitis usually has age of
onset around puberty.
2. Clinically it is characterized as having
“localized first molar/ incisor presentation with
inter proximal attachment loss on at least two
permanent teeth , one of which is a first molar, and
involving no more than two teeth other than
first molars and incisors”.
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REASONS FOR PERIODONTAL DESTRUCTION OF ONLY
CERTAIN TEETH IN LAP
1. After Initial colonization of 1st permanent teeth
(first molars & incisors) A.a evades host responses to
initiate periodontal disease.
Then adequate immune defenses are stimulated
to prevent colonization of other sites.
2. Bacteria antagonistic to A.a may colonize tissues
& inhibit A.a from colonizing further sites.
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REASONS FOR PERIODONTAL DESTRUCTION OF ONLY
CERTAIN TEETH IN LAP
3. A.a may lose its leukotoxin producing ability for some
unknown reasons. If this happens then progression
of the disease becomes arrested.
4. The possibility that a defect in cementum formation
may be responsible for localization of lesions has been
suggested. Root surface of teeth extracted from
patients with LAP were found to have hypoplastic cementum.
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• Localized juvenile Periodontitis - "burn out''
Several possible explanations for this:
• Development of an adequate host immune
response is one possibility
• A. actinomycetemcomitans- associated
Periodontitis is strain variations in virulence.
Highly virulent forms of this bacterium could
be associated with progressing periodontal
lesions while less virulent forms could be
associated with non-progressing lesions.
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LAP – CLINICAL FEATURES
1. A Striking feature is lack of clinical inflammation
despite presence of deep Periodontal pockets.
2. The amount of plaque on affected teeth is minimal,
which is inconsistent with the amount of Periodontal
destruction.
3. The plaque that is present forms a thin biofilm on the
teeth and rarely mineralizes to form calculus.
4. Although quantity of Plaque may be limited, it often
contains elevated levels of A. a , and in some patients
P.gingivalis.
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LAP – CLINICAL FEATURES
5. LAP progresses rapidly. Rate of bone loss is about
3-4 times faster than in chronic Periodontitis.
6. Disto labial migration of maxillary incisors with
concomitant diastema formation , increasing mobility
of first molars. Sensitivity of denuded roots to
thermal and tactile stimuli.
7. Deep dull radiating pain and Periodontal abscess with
Regional lymph node enlargement may occur at
later stages.
Not all cases of LAP may progress to this stage and in some patients, progression
of Attachment and bone loss may be self limiting.
(Lang and Bartold ; Ann of Periodontol 1999 ; 4 :53)
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DISTO-LABIAL MIGRATION OF CENTRAL INCISOR
IN LOCALIZED AGGRESSIVE PERIODONTITIS
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LAP with normal gingival tissue and presence of
deep pocket, as shown by probing.
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Advanced bone loss localized
to first molar
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LAP – RADIOGRAPHIC FINDINGS
1. Vertical loss of alveolar bone around
first molars and incisors beginning
around puberty in otherwise healthy
teenagers.
2. Arc shaped bone loss from distal of
2nd premolar to mesial of 2nd molar.
3. Bone defects usually bilateral affecting
first molars and incisors. Least
destruction in Cuspid-Premolar area.
4. Rate of bone loss 3-4 times faster than
chronic Periodontitis.
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Hormand and Frandeen
described three types of bone loss in
patients with Juvenile Periodontitis
Type I - First molars and / or incisors
Type II - First molars and / or incisors and
some additional teeth (less than 14
involved teeth)
Type III - Generalized involvement
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Male ; Female ratio in LAP
Some studies suggested a predilection for female patients
(Hormand J, Frandsen A ; J.Clin Periodontol 1979 ; 6 : 407)
Some studies Report no male-Female differences after
Correction of ascertainment bias
( Hart TC , Marazita MI, Schenkein HA et al.
J.Periodontol 1991; 62 : 745)
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Actinobacillus Actinomycetemcomitans identified by KLINGER 1912
Who first named Actinobacillus actinomycetemcomitans ?
TOPLEY & WILSON IN 1929

GENERALIZED AGGRESSIVE PERIODONTITIS
A disease of the Periodontium that usually affects
Persons under 30 years of age, but may be older.
Typically, there is generalized inter proximal attachment
loss affecting at least three teeth other than first molars
and Incisors, and there is a pronounced episodic nature of
Destruction of attachment and alveolar bone. There may
also be a poor serum antibody response to infecting
agents.
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CLINICAL CHARACTERISTICS
1. Generalized inter proximal attachment loss affecting at least
three permanent teeth other than first molars and incisors in
individuals less than age 30 but may be older
2. Minimal plaque inconsistent with destruction and presence of
bacteria like P.gingivalis, A.actinomycetemcomitans &
T.forsythia
( Novak KF, Novak MJ. Carranza’s Clinical Periodontology 10th Edn)
3. Two types of Gingival responses- Severe acutely inflamed
tissue with spontaneous bleeding or one with pink gingiva
free of inflammation.
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What are the patient’s complaints ?
1. Recently noticed flaring and progressing spacing of
anterior teeth.
2. Bleeding from gums.
3. Halitosis and discharge from gums.
4. Food impaction, dull nagging pain .
5. Severe pain, mobility of teeth and abscess in later
stages
All these in young patients < 30 years age but may be older
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15 Year old male patient with Generalized Aggressive Periodontitis
Clinically heavy deposits of plaque and calculus with severe gingival
Inflammation and Radio graphically severe bone loss
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RADIOGRAPHIC FINDINGS
• Severe bone loss with generalized involvement &
mostly vertical defects.
• Page and co workers demonstrated osseous
destruction ranged from 20-60% during a range of 9-
week Period.
• Furcation involvement & apical radio lucency in advanced
cases.
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CAN RANGE FROM SEVERE BONELOSS ASSOCIATED WITH
MINIMAL NUMBER OF TEETH –TO- ADVANCED BONE LOSS
AFFECTING THE MAJORITY OF TEETH IN THE DENTITION.
A COMPARISON OF RADIOGRAPHS TAKEN AT DIFFERENT
TIMES ILLUSTRATE THE AGGRESSIVE NATURE OF THIS
DISEASE.
RADIOGRAPHIC FEATURES OF GAP
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Intra bony defect

OPG OF A SEVERE CASE OF GENERALIZED
AGGRESSIVE PERIODONTITIS
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Histopathology of Aggressive Periodontitis is not
Well documented as compared to chronic Periodontitis
Due to less numbers of AgP patients, changing the
Definition of disease entity, and variations in the
Timing of biopsies.
Pretreatment biopsies of LAP showed predominant plasma cell
Inflammatory infiltrate.
( Liljenberg.B, Lindhe.J , J.Clin Periodontol 1980; 7 : 48-61)
Root surfaces of patients with AgP found to be heavily covered
By neutrophils.
(Fine DH, Greene LS, J.Periodontal Res 1984; 19: 152-67)
Enzymatic histochemical investigations of Gingiva of Early onset
Periodontitis – Increase in acid phosphatase positive
Macrophages(Phagocytic macrophages)
( Stambolieva & Bourkova, J.Periodontol 1970 ; 41;532)
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Abundance of plasma cells in gingival connective tissue. This is
Typical of both chronic & Aggressive Periodontitis
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ALTHOUGH THE CLINICAL PRESENTATION OF AGGRESSIVE
PERIODONTITIS APPEARS TO BE UNIVERSAL , THE ETIOLOGIC
FACTORS INVOLVED ARE NOT ALWAYS CONSISTENT
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MICROBIOLOGY
A.a, P.g,Tf ARE ELEVATED AT AFFECTED & PROGRESSING SITES.
ELEVATED ANTIBODY TITERS TO A.a.
IMMUNOLOGY
FUNCTIONAL DEFECTS IN PMN’S & MONOCYTES
HLA A9 & B15 ANTIBODIES ARE ELEVATED IN GAP
MONOCYTES ARE HYPER RESPONSIVE TO LPS
GENETIC
SOME IMMUNOLOGIC DEFECTS MAY BE INHERITED
ENVIRONMENTAL
SMOKING,STRESS
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MICROBIAL ETIOLOGY
BACTERIA
3. Highly leukotoxic clonal type of A.a serotype b was first
isolated from 8 year old male child with LAP in early 1980 s
(Kononen E, Muller HP, Periodontology 2000,2014; 65: 46-78
1. Prevalence of A.a in LAP varies from 70-90 %
(Elamin E, Albander JM et al , J.Periodontal Res 2011 ; 46;285)
2. Six serotypes of A.a (a,b,c,d,e and f) are described based
on the composition of ‘o’ polysaccharide of their LPS. Recently
added serotype fis and JP2 Clone frequency not clear.
(Kononen E, Muller HP. Periodontol 2000,2014; 65: 46-78)
4. There are phenotypically non- sero typeable strains of A.a
which lack expression of serotype specific polysaccharide
antigen.
(Kononen E, Muller HP, Periodontol 2000, 2014;65:46-78)
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Since long time Aa is considered main pathogen especially in LAP

• A. actinomycetemcomitans (A.a) – key
microorganism in LAP.
Four lines of evidence (Socransky & Haffajee
1992):
i. Association studies, linking
the organism to the disease
ii Demonstration of virulence factors
iii Findings of immune responses towards
this bacterium
Iv correlation between treatment outcomes
and levels of A.a after therapy
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LAP GAP
1.Fusobacterium spp Fusobacterium spp
2.Actinomyces naeslundii Actinomyces naeslundii
3.Campylobacter Rectus Fusobacterium Nucleatum
4.Veillonella parvulla Lactobacillus spp
5.Aggregatibacter
actinomycetemcomitans
Aggregatibacter
actinomycetemcomitans
Porphyromonas gingivalis
Tannerella forsythia
Bacterial profile of LAP and GAP
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• Several potent enzymes, in particular
Collagenases , proteases, and endotoxins .
• Relationship between the clinical outcome
of therapy and bacterial counts=
documented
• Non-responding lesions often contain this
organism in elevated proportions.
• High local and systemic immune responses
against this bacterium have been
demonstrated in patients with GAP. (Shah
1993)
ROLE OF PORPHYROMONAS GINGIVALIS IN GAP
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BACTERIAL INVASION OF PERIODONTAL
TISSUES
• Human investigations have indicated that
A.a is able to translocate-across the
junctional epithelium and invade the
underlying connective tissue (Saglie et al.
1988).
• These data support the hypothesis that
direct bacterial invasion may be responsible
for some of the observed tissue breakdown.
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MICROBIAL ETIOLOGY
Role of Viruses in Aggressive Periodontitis
Herpes Viruses , especially Epstein Barr virus(EBV) and
Human cytomegalo virus (HCV) have been suggested
To play a role in the onset of Aggressive Periodontitis
By interacting with Periodontitis associated bacteria,
Such as A.actinomycetemcomitans, P.gingivalis,
T.forsythia, C.rectus and Dialister pneumosintes.
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HEALTHY GINGIVA
BACTERIAL PLAQUE
GINGIVITIS
Influx of inflammatory cells
Containing latent Herpes viruses
HERPES VIRUS ACTIVATION
Immuno suppression, infection , stress and
hormonal
PERIHODONTOPATHIC PROPERTY
Cytokines, immuno suppression, overgrowth of
bacteria
DESTRUCTIVE PERIODONTAL DISEASE
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Systemic neutrophil abnormalities
associated with aggressive Periodontitis
CONDITION NEUTROPHIL
ABNORMALITY
PERIODONTAL
MANIFESATIONS
1. Neutropenia,
Agranulocytosis
Increased number of
neutrophil
Severe aggressive
Periodontitis
2. Chediak-Higashi
syndrome
Decreased
neutrophil Chemo
taxis and secretion.
Neutrophil granules
fuse to form
characteristic giant
granules called
megabodies
Aggressive
Periodontitis & oral
ulceration. The
syndrome is caused
by a mutation in the
vesicle trafficking
regulator gene,
LYST.
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ABNORMALITY
PERIODONTAL
MANIFESATIONS
3.Papillon- Lefebvre
Syndrome
Multiple functional
neutrophil defects including
myeloperoxidase deficiency
as well as defective
chemotaxis & phagocytosis
Severe aggressive periodontal
destruction at an early age,
which may involve the primary
and permanent dentition.
Recently associated in
affected individuals with a
mutation in the cathepsin-C
gene..
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ABNORMALITY
PERIODONTAL
MANIFESATIONS
4. Leukocyte adhesion
deficiency
Type – I
Defects in leukocyte
function due to lack of
integrin 2 subunit ( CD18 ).
Neutrophil defects include
impaired migrations &
phagocytosis.
Histologically, almost no
extra vascular neutrophils
are evident in periodontal
lesions
Aggressive Periodontitis at
an early age affecting
primary & permanent
dentition, in individuals who
are homozygous for the
defective gene.
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ABNORMALITY
PERIODONTAL
MANIFESATIONS
5. Leukocyte adhesion
deficiency
Type –II
Neutrophils fail to express
the ligand ( CD15 )
Selectins, resulting in
impaired transendothelial
migration in response to
inflammation
Aggressive Periodontitis at a
young age.
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ASSOCIATED WITH SYSTEMIC CONDITION
PAPILLON-LEFEVRE SYNDROME
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HUMAN LEUKOCYTE ANTIGENS
Human leukocyte antigens play an important role
In Regulating immune response.
HLA-A 9, HLA-A23, HLA-A24 , HLA-A 28, HLA-A 33, and
HLA-B 15, HLA-DR4 increased in patients with AgP
Risk of AgP in HLA-A9 and B-15 positive individuals is
1.5 to 3.0 times than those lacking these antigens.
Negative correlation between HLA-A2 and HLA-A12
And localized aggressive Periodontitis.
Few studies show there is no link between AgP and HLA
Cullinan et al J.Periodont Res 1980, 15; 177-184)
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Modified from Page RC, Kornman KS. The pathogenesis of human
Periodontitis-An introduction. Periodontol 2000 1997;14:9-11

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ENVIRONMENTAL FACTORS AS RISK
FOR AGGRESSIVE PERIODONTITIS
1. SMOKING IS A MAJOR RISK FACTOR
2. ASSOCIATED WITH  LEVELS OF Tf, Aa
AND Pg IN PERIODONTAL POCKETS.
3. ALTERED NEUTROPHIL CHEMOTAXIS AND PHAGOCYTOSIS AND
ELEVATED LEVELS OF TNF-, PGE 2 AND MMP 8
4. IL-I GENOTYPE POSITIVE HAS 2.7 TIMES INCREASED RISK FOR
TOOTH LOSS AND COMBINED EFFECT OF POSITIVE GENOTYPE
PLUS HEAVY SMOKING INCREASE RISK OF TOOTH LOSS BY 8
FOLD. (Meisel P et al J Dent Res 2003;82:189)

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SEVERE ATTACHMENT AND BONE LOSS IN GAgP
PATIENT WHO IS A SMOKER

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POLYMORPHISM GENE
1. IL 1A(+4845), IL-1B(+3854) IL-1 GENE
2 IL-4 PROMOTERS &
INTERONS POLYMORPHISM
IL-4 GENE
3 FC ¥ R III b-NA2 allele
FC ý R III A-158 F
FC Receptor gamma
4 Gc LOCUS CHROMOSOME 4 q UNKNOWN
5 FMLP RECEPTOR N-FMLP
POLYMORPHISM
6 VDR POLYMORPHISM N-FMLP
POLYMORPHISM,
VIT D RECEPTOR
POLYMORPHISM
GENES ASSOCIATED WITH AGGRESSIVE PERIODONTITIS RISK

TENTATIVE CLINICAL DIAGNOSIS OF AP
• Absence of significant systemic conditions.
• Rapid attachment loss and bone destruction.
• Familial aggregation of cases.
• Lack of consistency between clinically visible
bacterial deposits and severity of periodontal
breakdown.
• The international classification workshop consensus - not
all listed primary and secondary features need to be
present - the diagnosis may be based on clinical,
radiographic and historical data alone.
• laboratory testing, although helpful, might not be
essential in making an Aggressive Periodontitis
diagnosis.
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PROGNOSIS DEPENDS ON
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S.NO PHASES TREATMENT
1 SYSTEMIC PHASE Review of medical history, Lab investigations
Medical consultation if needed, Identification/
modulation of risk factors(smoking, stress etc)
2 INITIAL PHASE Emergency treatment, if needed, Explanation of
the disease process, occlusal analysis &
correction Bacterial sampling, Extraction of
hopeless teeth, SRP, Local & systemic antibiotics
3 RE-EVALUATION 4-6 weeks interval. Gingival status, pockets,
exudation and Bleeding on probing
4 SURGICAL PHASE Resective & Regenerative surgeries with adjunct
systemic antibiotics
5. RESTORATIVE PHASE All permanent restorations
6 MAINTENANCE
PHASE
Every month recall for first 6 months, Bi monthly
for next 6 months and at 3 months interval later.
Full mouth SRP with adjunctive antibiotics
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SERIAL OR COMBINATION ANTIBIOTICS
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Mombelli and von Winkelhoff
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EMPIRICAL THERAPY VERSUS MICROBIAL TESTING
Choice of Antibiotic can either be empiric or guided by
Information about the nature of involved pathogen and
their Antibiotic sensitivity profile.
There is no evidence that microbiologic diagnosis
And targeted selection of antibiotic provides an additional
Benefit compared to empirical use.
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CONCLUSION

13.Aggressive Peridontitis.pptx

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13.Aggressive Peridontitis.pptx