AGGRESSIVE PERIODONTITIS.ppt

Dr. P. Srujan Kumar MDS Reader

2. Presented by
Dr. P. Srujan Kumar
MDS Reader

3. AGGRESSIVE PERIODONTITIS
LOCALIZED FORM GENERALIZED FORM
LAP GAP

4. LOCALIZED AGGRESSIVE PERIODONTITIS
The term“JUVENILE PERIODONTITIS” was introduced
byCHAPUTin 1967and by BUTLERin1969

5. HISTORICAL BACKGROUND
In 1923 GOTTLIEB reported a fatal case of
influenza and called it as
“ diffuse atrophy of the alveolar bone”
characterized by :
--loss of collagen fibers
--extensive bone loss
--widened pdl space

6. In 1928 GOTTLIEBattributed this condition to
inhibition of continuous cementum formation,
which he termed the disease as
“deep cementopathia”

7. In 1938 WANNENMACHER described incisor-first-molar
involvement and called the disease
“ parodontitis marginalis progressiva”
He considered it as inflammatory process

8. In 1940 THOMA AND GOLDMAN
referred this disease as
“paradontosis”
The initial abnormality was located in the
al.bone rather then in the cementum

9. IN 1942 ORBAN AND WEINMANN
introduced the term
“ periodontosis ”
THREESTAGES
STAGE I
STAGE II
STAGE III

10. STAGE I:
degeneration of principal fibers of pdl
cessation of cementum formation
resorption of the alveolar bone
STAGE II:
rapid proliferation of the JE
earliest signs of inflammation
STAGE III:
progressive inflammation
deep, infrabony periodontal pockets

11. DEFINITION
BAER-1971
“a disease of periodontium occurring in an
otherwise healthy adolescents which is characterized
by a rapid loss of alveolar bone about more than
one tooth of permanent dentition”

12. PREVELENCE
BAER
U.S POPULATION --0.1%
SAXBY
ENGLISH POPULATION --0.1%
MIGLANI
ASIAN POPULATION --0.1%
SAXEN
FRENCH POPULATION --0.1%

13. AGEAND SEXDISTRIBUTION
PUBERTY --21 Yrs OF AGE
MORE PREDILICTION FOR FEMALES
FEMALE : MALE =3.5 :1

14. DISTRIBUTION OF LESIONS
Classic distribution --molar and incisors
Least distribution --cuspid and premolars
THREE TYPES:
1. First molars and incisors
2. First molars and incisors and some
additional teeth [total of < 14 teeth]
3. Generalized involvement

15. POSSIBLE REASONS FOR THE LIMITATIONS OF
PERIODONTAL DESTRUCTION TO 1
st
MOLARS AND
INCISORS ARE:
1]After initial colonisation of 1
st
per.molar and
incisors Aabacilli are phagocytosedby
immune defenses[NEUTROPHILES, MONOCYTES ] and
neutralize destructive factors.[ENDOTOXIN,
LEUCOTOXIN, COLLAGENASE ]

16. 2]Antagonistto Aamay develop there by
decreasing the destruction of the lesions
3] Aa may loose its leukotoxinproducing
ability for unknown reasons. when this
happens the progress of the disease may
become
arrested

17. CLINICAL FINDINGS
1]The most striking feature of early Lap
is lack of clinical inflammation, despite the
presence of deep periodontal pockets
2]There may be a small amount of plaque,
which forms a thin film on tooth and rarely
mineralizes to become calculus

18. 3] Disto-labial migrationof max. incisors,
with diastema formation
4] Root surfaces become sensitiveto thermal
and tactile stimuli
5] Deep, dull radiating painmay occur with
mastication

20. RADIOGRAPHIC FINDINGS
1] Vertical lossof alveolar bone around the
1
st
molars and incisors in healthy teenagers is
a diagnostic sign of classic lap
2] Arc-shapedbone loss extending from the
distal surface of second pm --mesial surface of
2
nd
molar

21. 3] Resorption of rootsof 1
st
molar and incisors
4] Bilaterally symmetrical type of bone loss
resembling that of “ mirror images ”

22. CLINICAL COURSE
Lap progresses rapidly and rate of bone loss
is about 3-4times faster than in periodontitis
Bone resorption progresses until the
teeth are treated, exfoliated or extracted which
is termed as “burn out” phenomenon

23. Rate of bone loss
= CP Age
= AP

26. GENERALIZED AGGRESSIVE PERIODONTITIS
CLINICAL FEATURES
under the age of 30 years
poor antibody response to the pathogens
generalized interproximal attachment loss
affecting at least three permanent teeth
other than first molars and incisors

27. occur episodically with periods of advanced
destruction followed by periods of quiescence
small amounts of bacterial plaque associated
with affected
teeth

28. TWO GINGIVAL TISSUE RESPONSES
ONEIS
severe, acutely inflamed, fiery red,
proliferating, ulcerated tissue
bleeding occur spontaneously
suppuration

29. SECONDIS
gingival tissues appear pink,
free of inflammation
despite mild clinical appearance,
deep pockets can be probed

30. RADIOLOGICAL FEATURES
generalized severe bone loss
osseous destruction of 25%--60%during a
9–weekperiod

32. PREVALENCE / AGE AND SEX DISTRIBUTUON
SRILANKA --8%
U.SADOLESCENTS AGED 14 -17 yrs --0.13%
BLACKS --HIGHER RISK >WHITES
MALES --MORE LIKELY > FEMALES

33. ETIOLOGY: [RISK FACTORS]
1. HEREDITY
Baerdescribed the disease in twins, siblings
and first cousins as well as in parentsand offspring
Transmitted as x-linked dominantdisease
[if the father and mother has APsons and daughters
has AP]

34. 2. BACTERIOLOGY
GRAM --VEANEROBIC RODS
MINIMAL --ATTACHED PLAQUE
LARGER --UNATTACHED PLAQUE
PREDOMINANT BACTERIA :
aggregatibacter actinomycetem comitans
capnocytophaga

35. TWOCLASSIFICATIONS
1
ST
CLASSIFICATION
GRAM –VE
1 Aa
2 capnocytophaga sub-species sputegena
3 Motile anaerobic rods
a,spirochetes b,mycoplasma
c,ekenella d,wolionella
e, black pigmentedbacteroids
GRAM + VE
1 streptococcus
2 pepto streptococcus

36. 2
nd
CLASSIFICATION
3 GROUPS
GROUP 1: Aa
GROUP 2: Aa, capnocytophaga
GROUP 3: Eubacterium saberium

37. 3. IMMUNOLOGY
Functional defects of PMNs and monocytes
These defects can impair:
Chemo tacticattraction of PMNs to the site
Phagocytosis of microorganisms

38. Aabacillus produce
4.VIRULENCE FACTORS
Bring about destructive process

39. iLEUKOTOXIN:
Destroys PMNs and monocytes there by inhibit
host defense
mechanism
ii ENDOTOXIN: [LPS]
Stimulate osteoclast --bone resorption
iii COLLAGENASE :
Destroys gingival CT [collagen]
iv EPITHELIOTOXIN:
Facilitates penetration ofAa into CT throughJE
and destroy collagen

40. v FIBROBLAST INHIBITING FACTOR :
Impair collagen formation
vi OSTEOCLAST ACTIVATING FACTOR [ OAF] :
Brings about resorption of Al. bone
vii POLYCONAL B-LYMPHOCYTE ACTIVATING FACTOR :
Mediate inflammatory reaction by stimulatingOAF
and bring about bone resorption

41. 5. ENVIRONMENTAL FACTORS
Patients withGAP who smoke have more affected teeth
and loss of clinical attachment than non smokers
Smoking may not have the same impact on patients with LAP