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
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
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’
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
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
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
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