AGGRESSIVE PERIODONTITIS

In chronic periodontitis the bone loss and

attachment loss occurs at a slow rate.

In chronic periodontitis, due to plaque

accumulation the pathogenic microflora causes
ulceration of the epithelium and it enters into the
connective tissue evading the host. So all these steps
are occurring at a slow rate in chronic
periodontitis.

But in aggressive periodontitis, there is presence of

very less amount of plaque and the bone
destruction is quite aggressive.

So, aggressive periodontitis is:

✓ Rare
✓ Severe
✓ Rapidly progressing
✓ Early onset
✓ Familial
 HISTORY

1923- GOTTLIEB
✓ Coined AP
c/a diffuse atrophy of alveolar bone
= excess loss of collagen
✓ widening of pdl space
excess bone loss
= Gingiva looked quite normal

1928- GOTTLIEB
✓ Renamed it as DEEP CEMENTOPATHIA

✓ Due to a disease in eruption > cementum initiate

a host response > production of antibody >
exfoliation of teeth > excess bone loss

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1938-WANNEMACHER
Called it as PARODONTITIS MARGINALIS PROGRESSIVA
Affects incisor and first molar

1967-CHAPUT & BUTLER 1969

Called it as JUVENILE PERIODONTITIS

1977-AAP-AMERICAN ASSOCIATION OF PERIODONTOLOGY

Adopted the name JUVENILE PERIODONTITIS

1986-AAP CLASSIFIED JUVENILE PERIODONTITIS

1.PRE-PUBERTAL LOCALISED PERIODONTITIS

2.GENERALISED PERIODONTITIS

1989-AAP removed JUVENILE PERIODONTITIS and called

it as EARLY ONSET PERIODONTITIS

1993-EWWP-EUROPEAN WORLD WORKSHOP OF

PERIODONTOLOGY

Defined early onset periodontitis as a disease

that occurs before the fourth decade of life
that is before 40 years of life and it is rapid
onset disease.

Called it as defect in host response > host can't

fight with microbes >rapid destruction even by
little amount of plaque

1999-AAP – introduced AP-AGGRESSIVE PERIODONTITIS

2017 CLASSIFICATION SYSTEM-REMOVED AP

let's now talk about the aggressive periodontitis
in detail..

1999-LANG ET AL

Gave primary and secondary features of AP

1° (should be present to qualify as AP)

1-No underlying medical condition to be present
like diabetes,osteoporosis
2-Rapid attachment loss and bone loss
3-Familial history seen

2° (These features may or may not be seen but are

usually present)
1. Amount of microbial deposition doesn't
depend on severity of PDL destruction
2. High level of AA-Aggregatibacter
actinomycetemcomitans and PG-Porphyromonas
gingivalis
3. Neutrophils hyper-responsive but abnormal
phagocytosis
4. High level of PGE2 and IL 1 BETA
5. Rapid attachment loss and bone loss

Bone loss and attachment loss in periodontitis

is 3-4 times more than chronic periodontitis
 So in the 1999 classification, aggressive periodontitis
was further classified into two categories.

CLASSIFICATION:-
1. LAP- Localised aggressive periodontitis
2. GAP- Generalised aggressive periodontitis

LAP-
-localised to first permanent molar and incisors
-Interproximal attachment loss on at least two
permanent teeth-one of which is the first molar
and It involves no more than two teeth, other
than the first molar and the incisor.

If it becomes more than two teeth, say three

teeth, other than the Molars and the incisors are
involved, then it becomes a case of generalized
aggressive periodontitis.

Incisor

:
Molars
CLINICAL FEATURES

1. AGE- Puberty-20 yrs

2. SEX- F:M=1:3
3. SITE- First molar and incisors
4. PREVALENCE- BY BEAR-0.1%
5. RACE- Black males>black females>white
females>white males
6. No inflammation in gingiva
7. Deep periodontal pockets
8. Heavy destruction with rapid progression
9. Plaque-only a thin biofilm
10. Max CI-midline flaring-midline diastema
11. Tooth mobile
12. Sensitive denuded root surface to
thermal and tactile stimulus
13. Deep,dull radiating pain
14. PDL abscess
15. Regional lymphadenopathy
RADIOLOGICAL FEATURES:-
1. Vertical bone loss around first molar and
incisors (classic diagnostic sign of LAP)

2. Arc shaped bone loss-from distal surface of

second premolar to mesial surface of second molar

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GAP-
-Affects three or more or most of the teeth apart
from molar and incisors
-Generalised interproximal attachment loss and
bone loss

So here, if you can see, this is, a clinical picture

taken from a 35 year old female. And if you can see
there is hardly any plaque which is seen. But if we
probe this particular patient then the probing
depths ranged somewhere between 8 to 10 mm

So there was huge attachment loss and bone loss,

even in presence of such less amount of plaque.
And as you can see, she already lost her lower
incisors. So the bone loss was so much that the
teeth became mobile and they exfoliated as well. So
this is the advanced or the rapid bone loss seen even
in presence of less amount of plaque.

>
 CLINICAL FEATURES

1. AGE- puberty-35 yrs,old age can be affected

2. SEX- M > F
3. RACE- Black > white
4. PREVALENCE-
1. LOE ET AL- 8% in Sri Lankian tea workers (0.1-1mm
attachment loss/yr)
2. US Study- 0.13% -7-17 yrs age

5. EX-35 yr old female showing

Small specks of calculus

¥
Very little plaque
Probing depth-8-10 mm
Excess bone loss-mand incisors lost
Tooth-mobile and exfoliated

↳
 6. Gingival response-
I case
✓ Acute inflammation

= Proliferation
Ulcers
Fiery red
= Suppuration
✓
Spontaneous bleeding
II case-

= No inflammation
Pink
✓ Deep probing depth

7.Systemic changes-mental depression,wt loss,malaise

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 RADIOLOGICAL FEATURES:-
1. Severe bone loss in one or two teeth to advanced
bone loss in most teeth
2. PAGE ET AL-Stated 25-60% bone destruction in 9
week span

RISK FACTORS AFFECTING AP:-

1. MICROBIAL FACTORS-
✓ AA-Aggregatibacter
actinomycetemcomitans-1°pathogen
✓
GAP-AA,Porphyromonas gingivalis,spirochete
✓ LAP-AA

✓ Cause epithelial ulceration,invade connective

tissue,evade host response,bone loss

2. IMMUNOLOGICAL FACTORS-
LAP-75% Show abnormal neutrophils-no chemotaxis
But strong antibody response

3. GENETIC FACTORS-Familial aggregation by LANG ET AL

4. ENVIRONMENTAL FACTORS-Smoking
Rate of destruction-
Smoker > non-smoker
*
Why is LAP localised?

4 reasons

1. Robust serum antibody response:-

AA colonise first molar and incisors as they are
first to erupt-B cells activated-antibody IgG serotype
II released-quickly kill AA- No spread-localised

2. Bacterial antagonist may colonise PDL tissue and

inhibit AA from colonisation

3. AA may lose its LEUKOTOXIN(damage tissues)

producing ability

4. Defect in cementum formation of molars and

incisors-AA colonise only these.

This phenomenon of self-limiting activity of LAP

that attachment loss and bone destruction do not
spread to other teeth is c/a BURNOUT PHENOMENON.
 IMPORTANT QUESTIONS

LONG Q-
AP- Intro, etiology, classification, c/f, r/f, diagram

SHORT Q-
AP- write in Small points
LAP
GAP

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