1. Aggressive periodontitis is a rare, severe form of periodontitis typically affecting young individuals under 30 years of age. It is characterized by rapid attachment and bone loss. 2. It is caused by specific pathogens like Aggregatibacter actinomycetemcomitans and has a strong genetic component. Patients often exhibit impaired neutrophil function and hyper-inflammatory responses to bacterial toxins. 3. Aggressive periodontitis is classified into localized and generalized forms depending on the extent of involvement and treated through non-surgical therapies like scaling and root planing along with systemic antibiotics.

1. AGGRESSIVE
PERIODONTITIS-1
Dr. Mayur Kaushik,
Professor & Head of Department
Dept. of Periodontology,
Subharti Dental College & Hospital,
Swami Vivekanand Subharti University,
Meerut, UP

2. Introduction
Classification
Historical background
Clinical features,
Radiographic signs,
Histopathology
Genetic susceptibility,
Enviornmental factors
Diagnosis
Treatment
Conclusion
References
2

3. 3

4. 4

5. 5

6. • Pyorrhea-earlier terminology used
• Involves progressive loss of the
alveolar bone around the teeth.
• Left untreated -loosening and
subsequent loss of teeth.
• Caused by microorganisms that
adhere to and grow on the tooth
surfaces, along with an aggressive
immune response against these
microorganisms.
6

7. • Consensus workshops in North America in
1989 and Europe in 1993 described
following forms of Periodontitis
7
Classifying periodontal diseases
has been a long standing
dilemma.

8. PERIODONTITIS
CHRONIC
LOCALIZED
GENERALIZED
AGGRESSIVE
LOCALIZED
GENERALIZED
8

9. 9
Chronic periodontitis : An infectious disease
resulting in inflammation within the supporting
tissues of the teeth, progressive attachment
loss, and bone loss. (Flemming T.F)
Aggressive periodontitis : Comprises a group of
rare, often severe, rapidly progressive forms of
periodontitis often characterized by an early age of
manifestation and a distinctive tendency to aggregate
in families.

10. Based on disease severity chronic
periodontitis can be classified as:
10
Slight or
mild
periodontitis
Severe
periodontitis
Moderate
periodontitis
1-2 mm of
CAL
3-4mm CAL
>5mm CAL

11. 11

12. 12
1923
• Gottlieb reported a patient with a fatal case of
epidemic influenza “diffuse atrophy of the
alveolar bone”
1928
• “Deep cementopathia”
1938
• Wannenmacher – incisor - first molar
involvement “perodontitis marginalis progressive.

13. 13
• Early onset
periodontitis
• Aggressive
Periodontitis
• Juvenile
Periodontitis
• Degenerative, non-
inflammatory process
- periodontosis
1947
Goldman
1967
Chaput
et al
1989 AAP,
1993
European
Workshop
1999 AAP

14. 14
According to Orban there are 3 stages in
the development of diseases.
Stage I: a)Involves the degeneration of principal fibres of
the periodontal ligament, resorption of the alveolar
bone.
b)In this stage tooth migration occurs without
detectable inflammatory involvement.
Stage II: a)Lack of periodontal ligament fibres.
b)Rapid proliferation of junctional epithelium.
c)Signs of inflammation.
Stage III: a)Progressive inflammation
b)Development of deep infrabony pocket.

15. CRITERIA FOR IDENTIFICATION
15
Primary
features
Lang et al,
1999

16. 16
• Amounts of microbial deposits
inconsistent with destruction.
Elevated proportions of A.a & in some subjects
P. gingivalis
• Phagocyte abnormalities.
• Hyper-responsive macrophage: PGE2 &
IL-1β.
• Progression of bone loss may be self-
arresting.

17. Following
features were
identified-
Localized aggressive periodontitis (LAP) :
• Circumpubertal onset
• Localized first molar / incisor presentation with interproximal
attachment loss on at least two permanent teeth.
• Robust serum antibody response to infecting agents
Generalized aggressive periodontitis (GAP) :
• Under 30 years of age, but patients may be older.
• Generalized interproximal attachment loss affecting at least
three permanent teeth other than first molars and incisors.
• Pronounced episodic nature of the destruction of attachment
and alveolar bone.
• Poor serum antibody response to infecting agents.

18. CLASSIFICATION & CLINICAL SYNDROMES
3 types of aggressive periodontitis have been
described by Mombelli et al 2004.
• A Secure or Certain form
• An Uncertain or Probable form
• In secure form or Possible form.

19. 19
An Uncertain aggressive
periodontitis – CAL or by
severe bone destruction
before the age of 30 years.
A secure aggressive periodontitis is
characterized by clinically documented loss
of attachment of over 2 mm in a year, or by
loss of bone over 2 mm before the age of
18, or by severe bone loss before the age of
18.
Insecure aggressive periodontitis is characterized
by attachment loss with an unclear rate of
progression of around 2 mm in over a year, or by
bone destruction with an unclear rate of
progression.

20. ETIOLOGY &
PATHOGENESIS
 Microbiologic
factors
 Immunologic
factors
 Genetic factors
 Environmental
factors
 Current concepts.
20

21. Microbiologic factors
• Microscopic studies - presence of layer of bacterial
deposits on root surface of AgP lesions
• Identified involved bacteria using culture and found
Gram -ve organisms composed approx. 2/3 of
isolates from deep periodontal pockets, 1/3 Of
isolates in control sites with normal gingiva.
21
Newman and
Socransky
(1977), Slots
(1979).
(Listgarten
(1976))
Westergaarl
et al (1978)

22. MICRO-
ORGANISMS
22
Capnocytophaga
species
Aggregatibacter
Actinomycetemcomi
tans
Porphyromonas
gingivalis
Prevotella
intermedia
Eikenella
corrodens
B. forsythus

23. 23
Nonmotile,
capnophilic,
gram -ve
coccobacillus,
short and
facultatively
anaerobic.
4 lines of
evidence
(Socransky and
Haffajee 1992)

24. 1. A.a. Isolated more than 90% in LAP
patients and less frequent in periodontally
healthy individuals.
2. Demonstration of virulence
factors
3. Finding of immune response towards
A.a.- significantly elevated levels in serum
Antibodies to A.a. In LAP patients.
(Listgarten et al 1981)
4. Clinical studies showing correlation
between treatment outcomes and levels
of A.a. After therapy.

25. 25
Monoclonal antibody technology showed 5 serotyes - a b c d e.
Serotype - variance in virulence
It varies between patients with periodontal disease and
carriers.
• Serotype b has been found particularly often in
patients with LAP
( Zambon et al 1996)

26. Lipopolysachcharides, Bacteriocin (Hammond
et al 1987)
26
Surface associated material (SAM)
(Kamin et al 1986, Wilson et al 1985
Chemotactic inhibition factors ( Van
dyke et al., 1982)
Leukotoxins (Tsai et al., 1984)

27. Leukotoxin
• High leukotoxin - producing strains
have been linked to the etiology of
Ag periodontitis and
• Also Higher prevalence of highly
leukotoxic strain has been reported in
patients with LAP.

28. Identification feature of gram -ve organism –
Lipopolysaccharide
Free when organism die/multiply
Free LPS
Activates host
cells+Macrophages
Production of inflammatory mediators-PGE2,IL-
1β,TNF-α
.
All gram -ve bacteria are enveloped
by two membranes of which the
outer is rich in endotoxin.

29. COLLAGENASES
1. Degradation of collagen
2. Reduce cell growth rate
3. DNA synthesis rate
4. Fibronectin level of human gingival epithelial
cells.
29
Surface Associated Material ( SAM)
 Protein associated with outer
surfaces are potent inducers of
bone resorption and tissue
destruction ( Wilson et al 1995)
 SAM stimulate the production of
PGE2 & collagenase from bone
cells. (Harvey et al 1987).
 SAM's are potent bone resorbing
agents than LPS.

30. PEPTIDE
COMPONENT Fibroblasts IL-6
IL-6 Production
Osteoclast Precursors
Bone
resorption
Stimulates
Produces
Stimulates
Stimulates

31. CHEMOTACTIC INHIBITION FACTORS
 A.a produces factors which inhibit the
chemotaxis of PMNs. These factors could
reduce the no. of PMNs in the local lesions
available to phagocytose and kill these bacteria.
 Extra Cellular Outer Membranes Vesicle
 These vesicles contain the leukotoxin and LPS
 Their small size could easily permit them to cross
epithelial barriers such as the pocket epithelium.

32. DETERMINANTS OF VIRULENCE AND PATHOGENIC
POTENTIAL OF A. ACTINOMYCETEMCOMITANS.
Factor Significance
Leukotoxin Destroys human polymorphonuclear leukocytes
and macrophages
Endotoxin Activates host cells to secrete inflammatory
mediators (prostaglandins, interleukin-1,
tumor necrosis factor-)
Bacteriocin inhibit growth of beneficial species
Immunosuppressive
factors
inhibit IgG and IgM production
Collagenases Cause degradation of collagen
Chemotactic
inhibition factors
inhibit neutrophil chemotaxis

33. HOST RESPONSE TO BACTERIAL
PATHOGENS :
 B cells and antibody-producing plasma cells
represent a significant component of the
mononuclear cell-dominated connective tissue
lesion.
Plasma cells have been
shown to be predominantly
IgG-producing cells, with a
lower proportion of IgA-
producing cells

34.  Subset analysis of local T
cells has indicated a depressed T-helper to T-
suppressor ratio as compared to both
healthy gingiva and peripheral blood. These
findings have been interpreted to suggest the
possibility of altered local immune
regulation.
(Taubman et al.
1988, 1991).

35.  Local inflammatory responses are
characterized by high levels of
prostaglandin E2, interleukin-1 and
interleukin-1 in both crevicular fluid and
tissue (Masada et al. 1990, Offenbacher et
al. 1993).
 Prostaglandin E2 production, has been
shown to be highly elevated in AgP
subjects when compared to periodontally
healthy individuals and chronic periodontitis
patients.

36.  Immunodominant A.a antigen to be the
serotype specific carbohydrate;
 Vast majority of antibodies reactive with this
carbohydrate in AgP patients consist of IgG2
(Califano et al. 1992).
36

37.  GAP patients are frequently sero negative
for A.a. or display low titers and avidity
against P.gingivalis.
 Both titers and avidity of antibodies reacting
with P.gingivalis can be improved as a result
of therapy.
Anti A.a. serotype polysaccharide IgG2,
therefore, are considered to be protective
against widespread AgP.
(Tew et al. 1996).

38. 1
• Chemotactic attraction of PMN to the site of infection
or their ability to phagocytose and kill
microorganisms.
2
• Hyperresponsiveness of monocytes from LAP
patients with respect to their production of PGE2 in
response to LPS.
3
• Poorly functional inherited forms of monocyte, have
been shown to be disproportionately present in
patients with LAP.
4
• Defects may be induced by the bacterial infection or
may be genetic in origin.
38

39. 39
Neutrophils from patients with
aggressive periodontitis had
significantly increased
adherence and this suggests
that hyperadherence could
inhibit the migration of
neutrophils from the
circulation to the infection site
( Hurttia et al 1998)

40. Leucocytes use the selectin -
glycoprotein and integrin superfamily
interactions to migrate from blood vessels
to sites of infection. In particular selectin-
glyooprotem interactions are responsible
for the initial rolling adhesion between
leucocyte and vascularendothelium.
P selectin L selectin
E selectin

41.  Autoimmunity has been considered to have a
role in generalized aggressive periodontitis
according to Anusaksathien and Dolby, who
found host antibodies to collagen, DNA, and
immunoglobulin G (IgG).
 Possible immune mechanisms include an
increase in the expression of type II MHC
molecules, HLA DR4, altered helper or
suppressor T-cell function, polyclonal
activation of B cells by microbial plaque, and
genetic predisposition.

42. 42
An investigation utilizing linkage analysis
methodology reported linkage of LAP to the
vitamin D binding locus on region q of
chromosome 4 in a large family of the
Brandywine population (Boughman et al. 1986).

43.  Such data are currently considered to support the
existence of genetic heterogeneity in LAP forms, and
of distinct forms of AgP.
 Although formal genetic studies of AgP support the
existence of a gene of major effect, it is unlikely that
all forms of AgP are due to the same genetic defect
(Hart 1996).

44. The ability to mount high titers of
specific antibodies is race-dependent
and probably protective.
In individuals susceptible to AgP,
therefore, the ability to mount high titers
of antibodies (IgG2 in particular) may be
protective and prevent extension of
disease to a generalized form
PMN expressing the R131 allotype of
FcRIIa (i.e., an Fc receptor containing
an arginine instead of a histidine at
aminoacid 131) show decreased
phagocytosis of A.a.

45.  Tonetti MS, Mombelli A. Early onset
periodontitis. Annals of Periodontol. 1999;4:39.
 Armitage GC, Cullinan MP. Comparison of the clinical
features of chronic and aggressive periodontitis.
Periodontology 2000, 2010;53:12.
 Christersson LA, Wikesjo UM, Albini B, Zambon JJ,
Genco RJ. Tissue localization of Actinobacillus
actinomycetemcomitans in human periodontitis. II.
Correlation between immunofluorescence and culture
techniques. J Periodontol. 1987;58:540.

46.  Haffajee AD, Socransky SS, Gunsolley JC. Systemic anti-
infective periodontal therapy. A systematic review. Annals
of Periodontol. 2003;8:115.
 Jorgensen MG, Slots J. Practical antimicrobial periodontal
therapy. Compend Contin Educ Dent.2000;21:111.
 Armitage GC. Development of a classification system for
periodontal diseases and conditions.
 Ann Periodontol 1999;4:1-6. 2. Parameter on aggressive
periodontitis.
 American Academy of Periodontology. J Periodontol
2000;71:867-9. 3. Sachdeo A, Haffajee AD, Socransky SS.
Biofilms in the edentulous oral cavity. J Prosthodont
2008;17:348-56.