3. Definition
• Defined as a disease of the periodontium occurring in an
otherwise healthy individual 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
factors
4. CLASSIFICATION
• According to 1999 international world workshop periodontitis
is classified into
• chronic periodontitis
• Aggressive periodontitis
• Periodontitis modified by systemic diseases
5. INTRODUCTION
Aggressive periodontitis is characterized by---
1) Age of onset
2) Rapid rate of disease progression
3) Nature and composition of subgingival microflora
4) Alteration in host's immune response
4) Familial aggregation
7. LOCALISED AGGRESSIVE PERIODONTITIS-
HISTORY
• 1923- Gottilieb reported a case of diffuse atrophy of alveolar
bone characterized by loss of collagen fibers in periodontal
ligament & alveolar bone
• 1928 Gottilieb attributed this condition to the inhibition of
cementum formation termed as cementopathia
8. • 1938 Wannenmacher described it as incisors and
first molar involvement & called it periodontitis
marginalis progressiva.
• The term juvenile periodontitis was introduced by
chat put& colleagues in --1967
9. • In 1971 BAER defined it “a disease of periodontium occurring
in an other wise healthy adolescent which is characterized by
rapid loss of alveolar bone about more than one tooth of
permanent dentition and the amount of destruction does not
commensurate with amount of local irritants
• 1989 world work shop this disease was categorized
• 1.L.J.P. 2.G.A.P 3.R.P.P
• 1999 world workshop it was classified in to
•
• 1.L.A.P 2.G.A.P.
10. CLINICAL FEATURES
Age of onset : circumpubertal
Systemic health status : pt is otherwise systemically
healthy
Progression of disease : Rate of progression is 3-4 times
faster than CP
Familial pattern : Familial aggregation
Presence of local factors : Minimal amount of local factors
which is inconsistent with magnitude of destruction
11. • Distribution : Localised first molar| incisor
Interproximal attachment loss on at least two permanent
teeth, one of which is a first molar
Serum antibody response : Robust serum antibody response
to the infective agents(Aa)
Causative specific microbes – Aa
Gingival inflammation – lack of clinical inflammation
despite the presence of deep periodontal and advanced
bone loss
Pathological migration : Distolabial migration of maxillary
incisors
12. CONT…CLINICAL FEATURES
Increase mobility
Increase sensitivity
Deep dull radiating pain during mastication
Formation of periodontal abscess
Regional lymph node enlargement
Burnt – out phenomenon- Disease appears to be self
limiting as the age advances
15. REASON FOR THE LIMITATION OF PERIODONTAL
DESTRUCTION ARE…
First molar / incisors are the first permanent teeth to be erupted
Production of opsonizing antibodies against A.a called-,burn-out
phenomenon
Bacterial antagonist to A.a may colonize the periodontal tissue,
decreasing further colonization
A.a may loose their leukotoxin producing ability
Defect in cementum formation (Hypoplastic or Aplastic
cementum)
16. RADIOGRAPHIC FINDINGS
Vertical /angular bone loss around first molars /incisors
Arc- shaped loss of alveolar bone extending from distal
surface of 2nd premolar to mesial surface of 2nd molar
19. GENERALISED AGGRRESIVE
PERIODONTITIS
under 30 yrs of age ,but older pts may also be affected
Poor antibody response to the pathogens.
clinically characterized by generalized interproximal
attachment loss affecting at least 3 permanent teeth other
than first molars and incisors.
Episodic manner of destruction.
Plaque mainly consist of A.a, P.g. Tannarella forsythia.
20.
21. TWO TYPES OF GINGIVAL
RESPONSE ARE
1. 1)Severe acutely inflammed often proliferating
,ulcerated and fiery red, bleeding on slight stimulation
and suppuration – destruction
• 2) The gingival tissue appear pink, free of
inflammation, occasionally with some degree of
stippling - quiescence
• Page and Schroder suggested that tissue response
coincides with period of destruction and quiescence.
22. RADIOGRAPHIC FINDINGS
Range from severe bone loss associated with the minimal
number of teeth to advanced bone loss affecting majority
of teeth
25. MICROBIOLOGICAL FACTORS
A.a has been implicated as primary pathogen
associated with L.A.P
90% of the lesion shows high frequency of A.a
Sites with disease progression shows elevated levels of
A.a.
Increase serum antibody titer to A.a is seen in many
patients.
26. Studies has shown correlation between reduction in
subgingival load and successful clinical response
A.a produce number of virulence factor that may
contribute to the disease process.
27. Virulence factors produced by
(Aa)
• Production of exotoxin , leukotoxin that can destroy
PMNs and monocytes (apoptosis)
• Chemotactic inhibition factor
• Surface associated material(SAM) – stimulates bone
resorption
• LPS endotoxin – bone resorption
• Proteases that degrade immunoglobulin's (IgG)
• Collagenases that degrade the CT
28. IMMUNOLOGICAL FACTORS
HLA which regulates immune response has been evaluated
as candidate marker(HLA-9, B-15)
Functional defect in PMN , monocytes or both.
Hyper responsiveness of monocytes to produce PGE2 in
response to LPS.
poorly functional inherited form of monocytes receptor
(FCRR11) to IGg2
29. GENETIC FACTORS
• Vandyke has suggested a familial cluster neutrophil
abnormality
Antibody response to A.a is under genetic control.
30. ENVIRONMENTAL FACTORS
• Smokers with generalized aggressive periodontitis exhibit
more number of teeth affected by loss of clinical
attachment than non smokers with generalized aggressive
periodontitis
• The protective antibody (IgG2) response to Aa in GAP
pts with smoking is significantly reduced
31. Treatment
• Early diagnosis – very crucial for
successful treatment
• Elimination of causative organisms
• Providing an environment conducive to
long term maintenance
32. Non – Surgical treatment
Phase 1 therapy
• Motivation and education of pt
• Oral hygiene instructions
• Scaling and root planing
• Correction of anatomical factors
• Occlusal correction
• Recall appointments for maintenance
33. Full mouth disinfection
(Quirynen et al)
• Full mouth scaling and root planing ( two visits within 24
hrs)
• Brushing of dorsum of tongue by pt for 60 sec with 1%
Chx gel
• Spraying peritonsillar region twice daily with Chx
• Subgingival application of 1% Chx solution in to full
depth of periodontal pocket three times in 10 minutes
• Rinsing of mouth with 0.2% Chx for 2 minutes
34. Antibiotic therapy
• Systemic antibiotics
• Tetracycline are effective , when administered as an
adjunct to scaling and root planing
• Doxycycline 100 mg, twice daily for two weeks (LAP)
• Metronidazole 200 mg , tds for 10 days in combination
with scaling and root planing – effective in eradicating Aa
• Metronidazole 250mg + amoxicillin 250 mg tds for 7
days + surgical therapy – effective in microbial resistant
cases
• Local drug delivery
35. Host modulation therapy
• Administration of agents that modulate the
host response
• Administration of sub antimicrobial –dose
doxycycline (SDD)-20mg – prevent tissue
destruction by controlling the activation of
matrix metalloprotienases (MMPs)
36. Photodynamic therapy
• Broad spectrum antibacterial therapy for
aggressive periodontitis
• Procedure involves eradication of
periodontal pathogens by reactive oxygen
particles produced by means of photo
desensitising compounds (toludine blue)
instilled in periodontal pocket which is
activated by laser
37. Surgical therapy
• Modified widman flap surgery
• Ressective osseous surgery
• Regenerative osseous surgery
• Root resection hemisection of affected
first molar
• Auto transplantation of 3rd molar
• Implant therapy
