Aggressive Periodontitis

1. AGGRESSIVE PERIODONTITIS

2. CONTENTS
• Introduction
• Definition
• History
• Clinical features
• Radiographic features
• Diagnosis
• Classification
• Various forms of aggressive periodontitis
• Etiopathogenesis
» Microbial factors
» Host susceptibility
» Environmental factors
• Treatment
• Conclusion

3. INTRODUCTION

4. • Multifactorial disease
• Comprising of a heterogeneous group of
infectious diseases
• Characterized by the complex host-microbial
interactions in the periodontium.

5. DEFINITION
Disease of the periodontium occurring in an
otherwise healthy adolescent which is
characterized by rapid loss of alveolar bone about
more than one tooth of the permanent dentition.
The amount of destruction is not commensurate
with the amount of local irritants.
Baers 1971

6. HISTORY
1923 Gottlieb “Diffuse atrophy of the
alveolar bone”
1928 Gottlieb “Deep cementopathia”
1938 Wannenmacher “Paradontitis marginalis
progressive”

7. 1940 Thoma KM
Considered this to be
due to degenerative
changes and named
“Periodontosis”
1942 Goldman HM
1947 Orban Β,
Weinmann

8. 1959 Carranza FA “Trauma form occlusion ”
1966 World Workshop
of Periodontics
Periodontosis as a
degenerative entity –
eliminated
1967
1969
Chaput and
colleagues
Butler
“Juvenile perodontitis”

9. 1971 Baer Definition
1989 European
Classification
Pre-pubertal, Juvenile and
Rapidly Progressing
Periodontitis
1993 AAP “Early Onset Periodontitis”

10. 1999 World Workshop
Classification
Aggressive
Periodontitis
……….? ……….? ……….?

11. CLINICAL FEATURES
Prevalence: < 1% of population; 0.9 to 4.5%
0.02% for Caucasians,
0.8% for Afro-Caribbeans and
0.2% for Asians.
Saxby, 1984
Age: 14- 20 yrs
Sweeney et al 1987,
Bimstein et al 1994,

12. Race: African americans
Gender:
• equal distribution among sexes.
Saxby MS 1984
• males slightly higher prevalence
Loe H, Brown in 1991, 1986
• African-American males having a prevalence of 2.9
times more than the females
• For whites, females were 2.5 times more likely to have
the disease than males.

13. CLINICAL CHARACTERISTICS
Primary features:
Lang et al. 1999
•Non-contributory medical history
•Rapid attachment loss and bone destruction
•Familial aggregation of cases

14. • Amounts of microbial deposits inconsistent with the severity
of periodontal tissue destruction
• proportions of A.a & in some Far East populations, P.g
• Phagocyte abnormalities
• Hyper-responsive macrophage phenotype, production of
PGE2 and IL-1 in response to bacterial endotoxins
• Progression of attachment loss and bone loss may be self-
arresting
Secondary features

15. CLASSIFICATION
• Localized aggressive periodontitis
(LAP)
• Generalized aggressive periodontitis
(GAP)

16. Localized aggressive periodontitis
• Circumpubertal onset
• Localized first molar / incisor presentation with
interproximal attachment loss on at least two
permanent teeth, one of which is a first molar, and
involving no more than two teeth other than first
molars and incisors
• Robust serum antibody response to infecting
agents

17. Generalized aggressive periodontitis
• < 30 years of age, but patients may be older
• Generalized inter proximal 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. Clinical features of LAP
Distribution - characteristic but unexplained
1. Initial colonization of Aa the first teeth to erupt
PMN chemotaxis IF
endotoxin,
collagenase,
leucotoxin
Opsonic antibodies Tissue destruction
Zambon JJ, Slots J, Christersson LA 1983

19. 2. Bacteria antagonistic to A.a comitans may
colonize the periodontal sites and inhibit the A.a
from further colonizing the other sites.
Hillman JD, Socransky SS 1982

20. 3. A.a comitans may lose its leukotoxin liberating
capacity by unknown mechanism,
...progression of the disease - arrested or
retarded and colonization of new periodontal
sites averted.
Slots J, Zambon JJ, Rosling BC et al 1982

21. 4. Possibility - defect in cementum formation
• Root surfaces of teeth extracted from patients of
AP - hypoplastic or aplastic cementum.
• This was true not only for the parts exposed but
also on the surface unaffected by disease.
Lindskog S, Blomlof L, 1983,
Page RC, Baab DA, 1985

22. Lack of clinical inflammation despite the presence
of deep periodontal pockets.
Plaque:
• Minimal
Listgarten 1976,
Westergard et al 1978
• Thin & rarely under goes calcification

23. Rate of progression
• Burst / random burst / multiple asynchronous
burst hypothesis.
• Rate of progression is 3-4 times that of chronic
periodontitis. Baer PN 1971
• Sub gingival plaque and calculus are significant
predictors of attachment loss
Aass et al 1994

24. Other features
• Distal migration of maxillary teeth - diastema
• Increased mobility of teeth
• Sensitivity of the roots exposed to oral cavity
• Deep dull radiating pain during mastication
• Food impaction.
• Periodontal abscess
• Associated with regional lymphadenopathy

25. LAP

26. Radiographic findings
• Vertical loss of bone around the first molars and incisors,
• Beginning around puberty in an otherwise healthy patient
• Arc shaped loss of alveolar bone

27. Clinical characteristics of GAP
• Represents the most heterogeneous group &
includes the most severe form of disease
• These forms should be considered as a group to
be further defined based on clinical,
microbiological and immunological parameters.
Attstrom and Vander Velden 1993

28. • Given the severity of the
disease and the
heterogeneity of clinical
presentation,
• Each of these cases
deserves individual
consideration.

29. Types of response
Inflamed tissue
Bleeding - spontaneous
Suppuration.
Destructive stage
bone and attachment loss.
Pink, free of inflammation
Stippling
Deep pockets
- Stage of Quiescence
bone level stationary.
Gingival response
Page and Schroeder

30. Systemic manifestation _
• Weight loss
• Mental depression
• General malaise

31. Radiographic findings
• Demonstrated that 25 -60% osseous destruction occurred
in a 9 week period. Page and coworkers 1983

32. Chronic
Periodontitis
Localized
Aggressive
Periodontitis
Generalized
Aggressive
Periodontitis
Most prevalent in
adults
Adolescent;
circumpubertal
onset.
< 30 years of age,
but patients may
be older.
Slow to moderate
rate of progression
Rapid rate of
progression
Rapid rate of
progression
(pronounced
episodic
progressive
periods).

33. Amount of
microbial deposits
consistent with
severity of
destruction
Not consistent
with severity of
destruction.
Sometimes
consistent with
severity of
destruction
Variable
distribution of
periodontal
destruction; no
discernable pattern
Periodontal
destruction
localized to 1st
molars & incisors
Affects many teeth
in addition to
permanent 1st
molars & incisors.
No marked
familial
aggregation
Marked familial
aggregation.
Marked familial
aggregation.

34. DIAGNOSIS
Clinical diagnosis
• Specific medical & dental history
• Clinical examination of periodontium

35. Initial question ……..
• Is there periodontitis?
• Is there loss of periodontal support (loss of clinical attachment
and marginal resorption of alveolar bone)?
• 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 pseudo
pocket formation?

36. • Traumatic injuries
• Removal of impacted teeth
• Tooth position
• Orthodontic tooth movement
• Advance decay
• Subgingival margins of restorations etc.
• In such cases the appropriate clinical diagnosis
may be incidental attachment loss.

37. Does the patient have any systemic condition
that would in itself explain the presence of
periodontitis?
• Diabetes mellitus
• Papillon- Lefevre syndrome
• Hein-Munk syndrome
• Hypophosphatasia.
• Inborn - leukocyte adhesion deficiencies
• Acquired - drug induced granulocytopenia.

38. • Does the patient have signs or symptoms of
necrotizing periodontitis?
• Laboratory tests are utilized to confirm the
diagnosis

39. • Tentative clinical diagnosis is made based on –
• Absence of significant systemic condition,
• Rapid attachment loss and bone destruction,
• Familial aggregation,
• Lack of consistent relation between visible
microbial deposits and severity of periodontal
breakdown.
• Differential diagnoses b/w LAP & GAP

40. RADIOGRAPHIC DIAGNOSIS
• A two point examination of radiographic bone
loss indicates - rate of bone loss.
• Major role in screening

41. MICROBIOLOGICAL DIAGNOSIS
• Microbiological test directed towards AA
Maintenance phase

42. IMMUNOLOGIC DIAGNOSIS
• Crevicular fluid prostaglandin E2
• GAP - decreased ability to mount high titers of
specific IgG2 antibodies to A.a.
• Serum antibody titers - useful in the differential
diagnosis of GAP and LAP

43. ETIOLOGY
Multi factorial
• Microbial factors ………
• Host factors ………
• Environmental factors ……..

44. Microbial Factors Modifying environmental Factors
Genetic factors Modifying Genetic Factors
LAP
GAP
Current understanding eco genetic interactions

45. MICROBIAL FACTORS
• Studies of LAP
• Microscopic studies demonstrating the presence
of a layer of bacterial deposits on the root surface
of advance AgP lesions
Listgarten 1976,
Westergaard et al 1978.

46. • Gram –ve organisms …….2/3rds of the isolates
from deep periodontal pockets.
• In contrast these organisms …….1/3rd the
isolates in the control sites with normal gingiva
Newman et al 1976,
Slots 1976,
Newman and Socransky 1977.

47. Organisms associated with LAP
• A.actinomycetemcomitans,
• Capnocytophaga species,
• Eikenella corrodens,
• Prevotella intermedia
• Motile anaerobic rods
• Streptococci,
• Actinomycetes
• Peptostreptococci

48. Actinobacillus Actinomycetemcomitans – primary pathogen
Tonetti and Mombelli, 1999
Socransky & Haffajee 1992
Serotype b is most often found in patients with LAP
Aa – found in in LAP No association
Haffajee et al 1984,
Mandell et al 1987
Loesche et al 1985,
Moore 1987

49. • A successful out come of therapy …… Aa &
converse
Rosling and Slots 1983,
Haffajee et al 1984,
Christersson et al 1985,

50. • Aa - virulent factors
• Leukotoxin
• capable of inducing disease in experimental
animals and non oral sites
Zambon et al 1988,
Slots and Schonfeld 1991

51. • In GAP
• P. gingivalis
• Fusobacterium nucleatum
• A.a.
• P. intermedia
• C. rectus
• Treponema denticola

52. • P.gingivalis -
– Collagenases
– Proteases
– Endotoxin
– Fatty acids
Shah 1993.
• A relationship b/w the clinical outcome of therapy and
bacterial counts
• High local and systemic immune responses against this
bacterium have been demonstrated in patients with GAP
•
Tolo & Schhenck 1985
Vincent et al. 1985

53. Bacterial damage to the periodontium
• The direct action of the microorganisms or their
products on the host tissue,
and /or
• As a result of their eliciting tissue-damaging
inflammatory responses.

54. • Human investigations have indicated that Aa is
able to translocate across the junctional
epithelium and invade the underlying connective
tissue
Saglie et al. 1988.

55. Virulence of the infecting organism
Lipopolysaccharide LPS
• Activate host immune cells & macrophages to
secrete inflammatory mediators
• Prostaglandins,
• Interleukin 1β &
• Tumor necrosis factor α.

56. Bacteriocin
• is capable of inhibiting the growth of some
streptococci & actinomyces
• Interfering with fibroblast proliferation
• Immunosuppressive properties
• Collagenolytic activity
• Inhibition of neutrophil chemotaxis,
Fives-Taylor et al. 1996

57. Virulence
Factor Significance
Leukotoxin Destroys human PMNs & macrophages
Endotoxin Activates host cells to secrete PGE2, IL-
1ß, TNF-α
Bacteriocin Inhibits the growth of beneficial species
Immunosuppres
sive factors
May inhibit IgG & IgM production
Collagenases Cause degradation of collagen
Chemotactic
inhibition
factors
May inhibit neutrophil chemotaxis

58. Host response to bacterial pathogens
• Local responses
• Systemic responses

59. Local responses
• Intense recruitment of PMN leukocytes
– Within tissues
– Periodontal pocket
• B cells & plasma cells represent a significant
component of the mononuclear cell-dominated
connective tissue lesion
Liljenberg & Lindhe 1980

60. • Local IgG4 producing cells, in particular, seem to
be elevated.
Mackler et al. 1977, 1978,
Waldrop et al. 1981
• Depressed T-helper to T-suppressor ratio
Taubman et al. 1988, 1991
• Peripheral blood mononuclear cells exhibit a
reduced autologous mixed lymphocyte reaction
Engel 1996.

61. • Specific antibodies against Ag P-associated
microorganisms
• Cleaved complement fragments
Lally et al. 1980,
Steubing et al. 1982,
Ebersole et al. 1984,1985a,b

62. Systemic responses
• Substantial titers of antibodies against A.a. and
P.g have also been detected in the serum of AgP
patients
Ebersole 1990, 1996
Immunodominant A.a antigen to be the serotype
specific carbohydrate;
Majority of antibodies reactive with this
carbohydrate in Agp patients consist of IgG2
Califano et al. 1992

63. • HLA - immune responses; candidate markers for
aggressive periodontitis.
• Many HLA have been inconsistent, HLA-A9 &
B15 antigens are consistently associated with
aggressive periodontitis.

64. Mechanisms in gingival sulcus
• Intact epithelial barrier attachment
• Salivary flushing action, agglutinins, antibodies
• Sulcular fluid flushing action, opsonins antibodies
• Local Ab production
• High levels of tissue turnover
• Presence of normal flora
• Emigrating PMNs

65. GENETIC FACTORS
• Familial pattern of alveolar bone loss
Butler JH 1969
Tonetti and Mombelli 1999
• Pattern of disease transmission is consistent with
Mendelian mode of inheritance of a major disease
gene
• Autosomal Dominant Mode Of Inheritance
Saxen and Nevanlinna 1984,
Boughman et al 1992,

66. • Vitamin D binding locus on the region q of
chromosome 4 in large family of Brandywine
population
Boughman et al 1986

67. • Allelic variations in the Fc receptor for IgG2
immunoglobulins have also been suggested to
play a role in suboptimal handling of A.a
infections.
• PMN expressing the R131 allotype of FcγRIIa
showed decreased phagocytosis of A.a
Wilson and Kalmer 1996
The role of specific genes remains to be elucidated.

70. ENVIRONMENTAL FACTORS
• Patients with GAP who smoke have more affected
teeth
• Depression of IgG2 in smokers
Schenkein JA,
Gunsolley JC et al 1995

71. TREATMENT
Principles of therapeutic intervention:
• Early diagnosis
• Directing treatment towards suppressing or
eliminating the infecting organisms
• Providing an environment conductive for long
term maintenance.

72. • Extraction - Transplantation of third molar
• Standard periodontal therapy
• Scaling and root planing,
• Curettage,
• Flap surgery with or with out bone grafts,
• Root amputation,
• Hemi sections,
• Occlusal adjustments
• Strict plaque control measures
• Frequent maintenance visits

73. Antibiotic therapy
• Tetracycline - 250mg four times daily for 14
days every 8 weeks
Magnusson I, Low SB et al 1994
Genco and colleagues 1981
• If surgery is indicated antibiotics should be
prescribed 1hr before the surgery.
• Refractory then antibiotic susceptibility tests
• Monitoring the patient every 3 weeks or less is
suggested while the disease is in an active state.

74. Lindhe’s stages approach in management of AgP
• An initial phase of mechanical therapy
• Introduction of meticulous oral hygiene.
• After 6 weeks - appropriate surgical procedures
and administration of antibiotics.
• Microbial samples from deeper pocket from each
quadrant

75. • Microbial testing may be repeated at 1-3 months
after completion of therapy
• Individually tailored maintenance care
programme
• Recurrence of the disease --- repetition of
microbiological test

76. CONCLUSION
• Age is not the criteria
• Etiology multifactorial
• Control factors which influence the expression
• Early diagnosis
• Recurrence – managed appropriately
• Research – genetic aspect of disease

77. References
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• Jan Lindhe, Thorkild Karring, NiklausP Lang Clinical
Periodontology and Implant Dentistry; 4th edition
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Aggressive periodontitis. Annals Periodontol 1999;4:53
• Mombelli Gray C. Armitage and Peter M Loomer; Diagnostics;
Perio 2000 vol. 34; 2004
• Bonfil JJ, Dillier FL, Mercier P, A case control study on the role
HLA DR4 in severe and rapidly

78. • Rapidly progressing periodontitis. Identification of types and
subtypes using molecular biology. J Clinical Periodontology 1999;
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• Sachenkein JA, Gunsolley JC, Koertge et al, Smoking and its
effects on early onset periodontitis. J American dental association
1995; 126: 1107.
• American Academy of Periodontology, Position Paper:
Periodontal disease in childhood and adolescents. J Periodontology
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Periodontology 1996; 67:355-366.
• Schenkein H, van Dyke T, Early onset periodontitis. Systemic
aspects of etiology and pathogenesis. Perio 2000; 6: 7-25.
• Internet resources