Its very important for dentists to differentiate aggressive periodontitis and chronic periodontitis. This presentation includes basics of Aggressive periodontitis which can be very useful for undergraduate students of dental school for reference.

1. AGGRESSIVE
PERIODONTITIS
DR. MONALI SHAH

2. Aggressive periodontitis generally
affects systemically healthy
individuals less than 30 years old,
although patient may be older
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Dr. Monali Shah

3. Definition:
 Aggressive periodontitis (AgP) comprises
a group of rare, often severe, rapidly
progressive forms of periodontitis often
characterized by an early age of clinical
manifestation and a distinctive tendency
for cases to aggregate in families.
(Clinical Periodontology and Implant
Dentistry 4th edition)
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Dr. Monali Shah

4. How does it differ from
chronic periodontitis ???
Age of onset
Rate of disease progression
Nature & composition of microflora
Alteration in host immune response
Familial aggregation
Hart
TC.1996
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Dr. Monali Shah

5. Aggressive periodontitis
describes three of the diseases
formerly classified as
Juvenile Periodontitis.
Early onset periodontitis
Periodontosis
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Dr. Monali Shah

6. Aggressive
periodontitis
Localised Generalised
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Dr. Monali Shah

7. Localized aggressive
periodontitis
A disease of periodontium occuring in
otherwise healthy adolescent which is
characterised by rapid loss of alveolar
bone about more than one tooth of
permanent dentition
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Dr. Monali Shah

8. Clinical Characteristics
Age of onset around puberty
Localized first molar/incisor presentation
with interproximal attachment loss on
atleast two permanent teeth, one of which
is a first molar, and involving no more than
two teeth other than first molars and
incisors
(Ann Periodontol 1999)
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Dr. Monali Shah

9. Other Clinical Characteristics
Distolabial migration of the maxillary incisors
with concomitant diastema formation
Increased mobility of first molars
Sensitivity of denuded root surfaces
Deep and dull radiating pain during mastication
Periodontal abscesses and regional lymph node
enlargement
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Dr. Monali Shah

10. 10
Diseased sites infected with Aggregatibacter
actinomycetumcomitans
Abnormalities in phagocyte function
Hyper responsive macrophages, producing
increased PGE2 and IL-1
Self arresting disease progression
Lack of clinical inflammation despite the presence
of deep periodontal pockets
Amount of plaque Vs Amount of periodontal
destruction
Characteristics which are common but
not universal
Dr. Monali Shah

11. Radiographic findings
Arc shaped loss of alveolar bone extending
from the distal surface of the second premolar
to the mesial surface of the second molar.
Loss of alveolar bone may become generalized
as the disease progresses but remains less
pronounced in the premolar areas.
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Dr. Monali Shah

12. Possible reasons for the limitation
of periodontal destruction to
certain teeth
Actinobacillus actinomycetumcomitans,
colonizes the first permanent teeth to erupt.
Bacteria antagonistic to A.a
A.a may lose its leukotoxin producing ability
for unknown reasons
Defect in cementum formation
(Hillman JD et al ;
1982)
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Dr. Monali Shah

13. Generalized Aggressive
Periodontitis
 Affects individuals under the age of 30, but older
patients also may be affected.
 Generalized interproximal attachment loss affecting
atleast three permanent teeth other than first molars
and incisors.
 GAp produces a poor antibody response to pathogens
present
(Ann. Periodontol 1999)
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Dr. Monali Shah

14. Clinical Characteristics
Pronounced episodic nature of
periodontal destruction
Radiograph shows bone loss that has
progressed since previous evaluation
Often have small amount of plaque
associated with affected teeth
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Dr. Monali Shah

15. Microbiologic characteristics
Bacteria s frequently found in
GAp plaque
P. gingivalis
A. actinomycetamcomitans
B. forsythus
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Dr. Monali Shah

16. 17 Radiographic findings
Severe bone loss associated with
the minimal number of teeth.
Advanced bone loss affecting the
majority of teeth in the dentition.
Dr. Monali Shah

17. Clinical Diagnosis
Clinical diagnosis is based on
information derived from a specific
medical and dental history and
from the clinical examination of the
periodontium
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Dr. Monali Shah

18. Case History And
Clinical Features
Chronic
Periodontitis
Aggressive
Periodontitis
Age of onset or
detection
Relatively older
and elderly
individuals
Relatively young
individuals
Rates of
progression
Slow Rapid
Signs of
inflammation
Consistent with
presence of local
factors
Minimal
Relative amounts
of plaque and
calculus
Consistent with
periodontal
destruction
Not consistent with
periodontal
destruction
Patterns of
destruction
Usually uniform with
horizontal bone loss
Usually variable
with vertical bone
loss
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Dr. Monali Shah

19. IN THE DIAGNOSIS OF AGP THE INITIAL
QUESTION THAT THE CLINICIAN SHOULD ASK
IS
Is there
periodontitis?
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Dr. Monali Shah

20. Correctly answering this question requires
systematic collection of clinical
information regarding the following items
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 Is there loss of periodontal support
 Is the loss of attachment accompanied by
pocket formation or mostly the result of
recession?
 Is there a plausible cause for attachment loss
other than periodontitis?
 Is there another process imitating periodontal
disease by pseudopocket formation?
Dr. Monali Shah

21. After establishing the
presence of periodontitis -
---------the clinician should
determine which clinical
diagnosis best describes
the disease in the
individual patient
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Dr. Monali Shah

22. 24
A tentative clinical diagnosis of
AgP is made based on the
following criteria
1. Absence of significant systemic conditions
2. Rapid attachment loss and bone destruction
3. Familial aggregation of cases
4. Lack of consistency between clinically visible
bacterial deposits and severity of periodontal
breakdown.
Dr. Monali Shah

23. Microbiologic diagnosis
The international classification workshop
indicated that the presence of specific
microorganisms and A.a. in particular
represent one of the secondary features
of AgP
Microbiologic diagnosis can be useful at
different stages of the treatment plan
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Dr. Monali Shah

24. Aggressive Periodontitis
Its one of the diagnostic challenge in
periodontology but careful clinical
examination can help to solve this
diagnostic dilema
Once diagnosed not difficult to treat
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Dr. Monali Shah

25. Immunologic factors
 Human leukocyte antigen (HLA)
 Regulates immune response
 Evaluated as candidate marker for AP
 HLA- A9 & B15 consistently associated with AP
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Dr. Monali Shah

26. Functional defect of PMNs,
monocytes or both
Impair either
1) Chemotactic attraction of PMNs
to site of infection
2) Ability to phagocytose and kill
organism
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Dr. Monali Shah

27. Hyperresponsiveness of monocytes
 Production of PGE2 in response to
lipopolysaccride
 Leading to connective tissue and bone
loss
 Defects may be induced by bacterial
infection or genetic in origin
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Dr. Monali Shah

28. Genetic factor
Results from several studies supports the
concept that all individuals are not
equally susceptible to aggressive
periodontits
Several authors has describe a familial
pattern of alveolar bone loss and have
implicated genetic factors in aggressive
periodontitis
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Dr. Monali Shah

29. TREATMENT PLANNING:
• Prognosis depends on
Localised or generalised
Degree of destruction
If associated with systemic diseases –
worse prognosis
• Important to obtain and retain earlier
radiograph to assess the stage of the
disease
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Dr. Monali Shah

30. TREATMENT FOR AGGRESSIVE
PERIODONTITIS:
EXTRACTION:
• involved teeth – if prognosis is hopeless
NON-SURGICAL PHASE:
• scaling
• root planing , curettage
• Occlusal adjustment
• splinting
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Dr. Monali Shah

31. SURGICAL PHASE:
• Flap surgery with & without bone
graft
• Root amputation
• Hemisection
MAINTENANCE PHASE:
• Strict plaque control
• Host Modulation
• Follow up
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Dr. Monali Shah

32. ANTIBIOTIC THERAPY
• Aggrigatibacter actinimycetemcomitence (A.a) a
main culprit
• Penetrates the tissue
• Regimens including the adjunctive administration of
tetracyclines or metronidazole, have been tested for
the treatment of LAP and other forms of AgP.
(PRAKASAM A et al)
 CHOICE OF THE ANTIBIOTIC:
• Metronidazole in combination with amoxicillin may
suppress A.a. more effectively than single antibiotic
regimes
 COMBINATION THERAPIES INCLUDE:
• Metronidazole/amoxicillin
• Amoxicillin/doxycycline
• Clindamycin
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Dr. Monali Shah

33. HOST MODULATION THERAPY:
• Administration of agents that modulate the host response.
• Subantimicrobial dose doxycycline (SDD) : help to
prevent the destruction of PDL attachment by controlling
the activation of MMP’s, primarily collagenase and
gelatinase, from both infiltrating cells and resident cells of
periodontium, primarily neutrophils.
• SDD as an adjunct to repeated mechanical debridement
resulted in clinical improvement in patients with
generalized aggressive periodontitis.
• Other agents such as flubriprofen, indomethacin, and
maproxen may reduce inflammatory mediator production.
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Dr. Monali Shah

34. Conclusion
 Early diagnosis is very important
 Should not underestimate tissue invasive
micro-oganisms
 Antimicrobial therapy and host
modulation is very helpful
 Regenerative therapy gives result but less
predictable than chronic periorodntitis
 Meticulous maintenance is required
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Dr. Monali Shah