Aggressive periodontitis is distinguished from chronic periodontitis with respect to, Age of onset Rapid rate of disease progression Nature & composition of the associated subgingival micro flora Alterations in the host’s immune response Familial aggregation of the disease Types of Aggressive Periodontitis Localized Aggressive Periodontitis-LAP Generalized Aggressive Periodontitis-GAP Localized aggressive periodontitis Historical background, Diffuse atrophy of the alveolar bone (Gottlieb-1923) Deep cementopathia (Gottlieb-1928) Parodontitis marginalis progressiva(Wannenmacher- 1938) Periodontosis (world workshop in periodontics -1966) Juvenile periodontitis (Chaput etal-1971) Localized Juvenile periodontitis (world workshop in periodontics- 1989) Localized aggressive periodontitis (International workshop by american academy of periodontology – 1999) Clinical characteristics LAP LAP is localized to first molar or incisor with interproximal attachment loss on at least two permanent teeth ,one of which is a first molar & involving no more than two teeth other than first molars & incisors. Possible reasons for limitation of the destruction After initial colonization of the first permanent teeth( first molars & incisors) Aa evades the host defenses by different mechanisms they are – -PMN chemotaxis inhibiting factors -Endotoxin -Collagenases -Leukotoxin After this initial attack adequate immune defenses are stimulated to produce opsonic antibodies to enhance the clearance & phagocytosis of invading bacteria & neutralize leukotoxic activity there by colonization of other sites may be prevented Bacteria antagonistic to Aa may colonize the periodontal tissues & inhibit Aa from further colonization of periodontal sites in the mouth ,hence Aa infection & tissue destruction is localized Aa may lose its leukotoxin producing ability for unknown reasons A defect in cementum formation may be responsible for the localization of the lesions Clinical features of LAP Age of onset –puberty & around 20 years of age It affects both male & female There will be a lack of clinical inflammation despite the presence of deep periodontal pockets & advanced bone loss The amount of plaque is minimal & is rarely mineralizes to calculus Plaque Contains elevated levels of Aa & Pg The Rate of boneloss is about 3 to 4 times faster than in chronic periodontitis Clinical features of LAP Distolabial migration of the maxillary incisors with concomitant diastema formation Increasing mobility of the maxillary & mandibular incisors & first molars Sensitivity of denuded root surfaces to thermal & tactile stimuli Deep dull radiating pain during mastication Robust antibody response to pathogens Radiographs reveal ‘arc shaped loss of alveolar bone extending from distal surface of the second premolar to the mesial surface of the second molar’ Localized Aggressive periodontitis Generalized Aggressive Periodontitis

1. Aggressive Periodontitis

2. Aggressive periodontitis is distinguished
from chronic periodontitis with
respect to,
 Age of onset
 Rapid rate of disease progression
 Nature & composition of the associated
subgingival micro flora
 Alterations in the host’s immune response
 Familial aggregation of the disease

3. Types of Aggressive Periodontitis
 Localized Aggressive Periodontitis-LAP
 Generalized Aggressive Periodontitis-GAP

4. Localized aggressive periodontitis
Historical background,
 Diffuse atrophy of the alveolar bone (Gottlieb-1923)
 Deep cementopathia (Gottlieb-1928)
 Parodontitis marginalis progressiva(Wannenmacher-
1938)
 Periodontosis (world workshop in periodontics -1966)
 Juvenile periodontitis (Chaput etal-1971)
 Localized Juvenile periodontitis (world workshop in
periodontics- 1989)
 Localized aggressive periodontitis (International
workshop by american academy of periodontology –
1999)

5. Clinical characteristics LAP
 LAP is localized to first molar or incisor with
interproximal attachment loss on at least
two permanent teeth ,one of which is a
first molar & involving no more than two
teeth other than first molars & incisors.

6. Possible reasons for limitation of the
destruction
 After initial colonization of the first permanent
teeth( first molars & incisors) Aa evades the host
defenses by different mechanisms they are –
-PMN chemotaxis inhibiting factors
-Endotoxin
-Collagenases
-Leukotoxin
After this initial attack adequate immune
defenses are stimulated to produce opsonic
antibodies to enhance the clearance &
phagocytosis of invading bacteria & neutralize
leukotoxic activity there by colonization of
other sites may be prevented

7.  Bacteria antagonistic to Aa may colonize the
periodontal tissues & inhibit Aa from further
colonization of periodontal sites in the mouth
,hence Aa infection & tissue destruction is
localized
 Aa may lose its leukotoxin producing ability
for unknown reasons
 A defect in cementum formation may be
responsible for the localization of the lesions

8. Clinical features of LAP
 Age of onset –puberty & around 20 years of
age
 It affects both male & female
 There will be a lack of clinical inflammation
despite the presence of deep periodontal
pockets & advanced bone loss
 The amount of plaque is minimal & is rarely
mineralizes to calculus
Plaque Contains elevated levels of Aa & Pg
 The Rate of boneloss is about 3 to 4 times
faster than in chronic periodontitis

9. Clinical features of LAP
 Distolabial migration of the maxillary incisors
with concomitant diastema formation
 Increasing mobility of the maxillary &
mandibular incisors & first molars
 Sensitivity of denuded root surfaces to thermal
& tactile stimuli
 Deep dull radiating pain during mastication
 Robust antibody response to pathogens
 Radiographs reveal ‘arc shaped loss of alveolar
bone extending from distal surface of the
second premolar to the mesial surface of the
second molar’

10. Localized Aggressive periodontitis

11. Generalized Aggressive Periodontitis
 GAP is characterized by “‘generalized
interproximal attachment loss
affecting at least three permanent
teeth other than first molars &
incisors’”

12. Clinical features of GAP
 It usually affects individuals under 30 years of age
 It produce poor antibody response to the pathogens
 plaque mainly consists of Pg, Aa & tannerella forsythia
 There will be a severe & acute inflammation of the gingiva
which is fiery red in color, proliferating ,ulcerated, with
bleeding on probing & suppuration at the time of destructive
phase
 At the time of inactive stage gingiva appears pink free from,
inflammation with deep pockets
 Radiographs reveal severe bone loss

13. Generalized Aggressive periodontitis

14. Risk for Aggressive Periodontitis
 Microbiologic factors
Aa is a primary pathogen found in - LAP- 90% along with
capnocytophaga sps, Eikenella corrodens, Prevotella
intermedia & campylobacter rectus.
 Immunologic factors
- Functional defects of PMNs & monocytes leading to defective
chemotaxis & phagocytosis
- Hyperresponsiveness of monocytes to lipopolysaccharides
leads to production of PGE2 (responsible for destruction of
connective tissue & bone)
- Autoimmunity- host antibodies to collagen, DNA & IgG

15.  Genetic factors
- Genetic defects leading to defective
immunologic deficiencies
 Environmental factors
- Smoking

16. prognosis
The prognosis for pts with AP depends on
 Whether the disease is generalized or
localized
 The degree of destruction present at the time
of diagnosis
 Ability to control future progression
 In case GAP prognosis is poor

17. Treatment of Aggressive Periodontitis
Conventional periodontal therapy
o Pt education-regarding causes & risk factors
of the disease
o Oral hygiene maintenance
o Scaling & root planing
o Frequent recall maintenance
o Surgical resective therapy
o Regenerative periodontal therapy using –
bone grafts, GTR, wound healing agents
o Tetracycline root conditioning
o Enamel matrix proteins

18. Bone grafts

19. Barrier membranes-GTR

20. GTR PROCEDURE

21. ENAMEL MATRIX PROTEINS- EMDOGAIN

22. Antimicrobial therapy
Systemic antimicrobial therapy
• Systemic tetracycline 250 mg 4 times
daily for 2 to 8 weeks

23. Based on Bacterial culture & antibiotic
sensitivity
 For Gram positive microbes – amoxicillin-
clavulanate potassium (augmentin)
 For Gram negative microbes – clindamycin
 For Non oral gram negative facultative rods –
ciprofloxacin
 For Spirochetes & black pigmented bacteria-
metronidazole
 For Prevotella intermedia ,pg – tetracycline
 For Aa –metronidazole plus amoxicillin,
metronidazole plus ciprofloxacin,
tetracycline
 For Pg - azithromycin

24. Local drug delivery
Tetracycline fiber Ethyl/ vinyl acetate
copolymer fiber-0.5mm diameter with
12.7mg/ 9 inches
10% doxycycline gel
2% minocycline bioresorbable microspheres
in a gel form
25% metronidazole gel
2.5mg CHX gluconate chip

25. PERIO CHIP

26. ELYZOL GEL

27. ATRIDOX GEL

28. ARESTIN GEL

29. Full mouth disinfection
consists of –
 complete Scaling & root planing within
24 hrs
 Tongue brushing with 1% CHX gel for 1
minute
 Mouth rinsing with 0.2% CHX for 2
minutes
 Irrigation of periodontal pockets with 1%
CHX solution

30. Host modulation Therapy
 Sub antimicrobial dose of doxycycline hyclate 20mg is given
to prevent periodontal destruction by controlling MMPs
released from PMNs & resident cells.
Dental implants
- For replacement of missing or extracted hopeless teeth
Periodontal maintenance
- Is done by recalling the pt at every 3 to 4 weeks