This presentation will equipe you complete knowledge about what is periodontitis, diagnosis and management.

2. Contents
 Introduction
 Historical background
 Baer criteria
 Classification of Aggressive periodontitis
- Localized aggressive periodontitis
- Generalized aggressive periodontitis
 Risk factors
 Treatment
 Conclusion
 Reference

3. Periodontitis is multifactorial in origin associated with involvement of various
risk factors and systemic illness. The disease is caused by an aberrant immune
response to resident microbial communities on the teeth, which extend into the sub
marginal region.
These exaggerated dysbiotic host inflammatory reactions results in the
destruction of the periodontal tissues and can be episodic in nature and nonlinear and
disproportionate to an assorted collection of risk factors.
INTRODUCTION

4. HISTORICAL BACKGROUND
1999 AAP International Workshop for classification of
Aggressive Periodontitis
1. Pre-pubertal periodontitis
2. Juvenile periodontitis
3. RP periodontits
• Diffuse
atrophy of the
alveolar bone
Gottlieb, 1923
• Deep
cementopathia
Gottlieb, 1928
• Juvenile
periodontitis
Chaput & collegues,
1967
Butler in 1969
• Early onset
periodontitis
Page & Baab 1989

5. Aggressive periodontitis refers to the multifactorial, severe
and rapidly progressive form of periodontitis, which primarily but not
exclusively affects younger patients.
- International Workshop Classification Of
Periodontal Disease and Conditions (1999)
Disease of the periodontium occurring in an otherwise healthy individual - Baer

6. Early onset of the disease during the circumpubertal period
(between 11 and 13 years of age)
Age of the patient is not a primary criterion for the diagnosis of
aggressive periodontitis
AGE

7. Radiographic feature
A distinctive radiographic pattern
depicting vertical alveolar bone loss at
the first permanent molars and at one
more incisor teeth
Classical case of aggressive
periodontitis
An arc shaped bone loss
(Bilaterally)
Shows bone loss only at proximal
surface of molars
Atypical cases of aggressive
perioodntitis

8. • A rapid rate of disease progression
• Baer estimated that, typically an affected tooth can lose about 75% of
the alveolar bone support at one or more root surfaces within 5years
of disease initiation.
Atypical cases : Alveolar bone loss progresses only to a certain point and
then may remain quiescent for many years

9. The disease affects only the permanent dentition. The
primary teeth are not affected and are not prematurely
exfoliated because of destructive periodontal disease
The amount of local etiologic factors is not
commensurate with severity of periodontal destruction.

10.  Predominance in female subjects. Baer reported that cases of
aggressive periodontitis have a female to male ratio of
approximately 3 : 1
 Black male teenagers > Black female adolescent > White female
teenagers > White male adolescents
 The disease has a familial pattern

11. In 1999 International workshop for the classification of periodontal disease and
conditions defined the entity of Aggressive periodontitis as being characterized by “3 primary
features”
Rapid loss of
attachment
and tooth
supporting
structures
Presence of
familial
aggregation
Subject is
otherwise
healthy

12. Workshop defined several secondary features :-
1. Inconsistency of the low amounts of present etiological factors
and the observed pronounced tissue destruction.
2. Strong colonization by A.actinomycetemcomitans and in some
populations, Porphyromonas gingivalis
3. Immunological abnormalities:-
a. Hyperresponsive macrophages
b. abnormalities of neutrophil function
4. Self limiting disease

13. Education
Plan

14. LOCALIZED
ATTACHMENT
LOSS AT
INCISORS AND
FIRST MOLARS
LOCALIZED AGGRESSIVE PERIODONTITIS ( LAP )
In 1989 the world workshop in clinical periodontics, categorized this disease as:-
“Localized juvenile periodontitis” (LJP)

15. CLINICAL FEATURES
• Lack of clinical inflammation
• Amount of plaque in consistent with the amount of periodontal destruction
• Presence of deep periodontal pockets

16. • Elevated levels of A.a and P.gingivalis.
• Distolabial migration of maxillary incisors – diastema formation.
• Increasing mobility of maxillary and mandibular incisors and first molars.
• Increased sensitivity of denuded root surfaces to thermal and tactile stimuli.
• Deep, dull, radiating pain during mastication.

17. RADIOGRAPHIC FEATURES
• Classic diagnostic sign of localized aggressive periodontitis vertical “arc
shaped” bone loss in relation to molars and incisors.
• Rate of bone loss is about 3-4 times faster than in chronic periodontitis

18. Production of PMN
chemostasis inhibiting
factors, Endotoxin,
Collagenases, Leukotoxin
Allow the bacteria to
colonize the pocket and
initiate the destruction of
periodontal tissue
After initial attack
Opsonic antibodies are
produced
Phagocytosis of invading
bacteria and neutralization
of leukotoxic activity(may
slow or arrest the disease
process)
Immune defences
stimulated
The possible reason for the localization of disease to first molars and incisors in LAP are…
After initial colonization, A.a. evades the host defence

19. 2. Bacteria antagonistic to A. a may colonize the periodontal
tissues and inhibit it from further colonization of
periodontal sites in the mouth.
3. A.a may lose its leukotoxin-producing ability for unknown
reasons which arrests or impairs the progression of the disease
and may avert the colonization of new periodontal sites

20. 4. Defect in cementum formation may be responsible for the
localization of the lesion. Root surfaces of teeth extracted from patients with
localized aggressive periodontitis have been found to have hypoplastic/aplastic
cementum.

21. LAP Patient GAP Patient
i.e, LAP and GAP would merely be phenotypic variations of the
same underlying disease.
This assumption is backed by several reports that show a
sequence of LAP and GAP in the same individuals over time
Host response

22. Initially it was thought that LAP gradually becomes GAP over time. But
some cases of LAP don’t show any increased bone destruction; are known to
arrest spontaneously, leading to cessation of disease activity
- Ranney
Burn out phenomenon

23. Generalized aggressive periodontitis (GAP)
Encompasses the disease that were previously classified as generalized
juvenile periodontitis and rapidly progressive periodontitis.

24. Tissues appear pink, free of
inflammation and occasionally
with some degree of stippling –
Non destructive stage
1. Deep pockets
2. Bone & attachment levels
relatively stable(Period of
Quiscence)
Severe, acutely inflamed tissue that
is often proliferating, ulcerated and
fiery red - Destructive stage
1. Bleeding
2. Suppuration
3. Active loss of attachment and
bone
Clinical features of GAP
Two gingival tissue responses

26. Education
Plan
Severe bone loss associated with the minimal number of teeth
to advanced bone loss affecting the majority of teeth in the dentition
Radiographic
features

27. RISK FACTORS FOR AGGRESSIVE PERIODONTITIS

28. P. intermedia
A.a comitans (approx.
90%)
Motile anaerobic rods
such as C. rectus
RISK FACTORS FOR AGGRESSIVE PERIODONTITIS
MICROBIOLOGICAL FACTORS – DOMINANT
MICROORGANISMS
1. Porphyromonas
gingivalis
2. A.a comitans
3. Bacteroides forsythus
Capnocytophaga sp
E. corrodens
Gram positive isolates were mostly
a. Streptococci
b. actinomycetes
c. peptostreptococci
L
A
P
G
A
P

29. 1
A.a is found in high
frequency (approx. 90%) in
lesions characteristic of
LAP.
3
Elevated serum antibody titers
to A.a.
Virulence factors that may
contribute to the disease process
2
Sites with evidence of
disease progression often
show elevated levels of A.a
A.a has been implicated as the primary pathogen associated with LAP
5
4
Reduction in the subgingival load
of A.a during treatment
Tonetti and Mombelli et al

30. RISK FACTORS FOR AGGRESSIVE PERIODONTITIS
(IMMUNOLOGICAL FACTORS)
Human leukocyte antigens(HLAs) have been evaluated as candidate markers for
aggressive periodontitis. HLA A9 & B15 antigens are consistently associated with
aggressive periodontitis
Functional defects of PMNs, monocytes or both :-
• Impair the chemotactic attraction of PMNs to the site of infection or their ability to
phagocytosis and kill microorganisms
• Hyper-responsiveness of monocytes from LAP patients involving their production of
prostaglandin E2 in response to LPS ----> Increased connective tissue or bone loss

31. Education
Plan Segregation analysis – autosomal
dominant mode of inheritance (Saxen
& Nevanlinna 1984)
Antibody response to
periodontal pathogens,
particularly A.a, is under
genetic control and that the
ability to mount high titers of
specific, protective antibody
(primarily IgG) against A.a
may be race dependent.
RISK FACTORS FOR AGGRESSIVE PERIODONTITIS
GENETIC
FACTORS

32. Schenkein et al. 1995: cigarette
smoking was shown to be a risk
factor for patients with generalized
forms of Aggressive periodontitis.
Smokers with GAP had more affected
teeth and greater mean levels of
attachment loss than patients with
GAP who did not smoke.
IgG serum levels as well as antibody
levels against A.a. are significantly
decreased in subjects with GAP who
smoked
RISK FACTORS FOR AGGRESSIVE PERIODONTITIS
(ENVIRONMENTAL FACTORS)

33. Past treatment modalities for LAP are:
Standard
periodontal
therapy
Antibiotic
therapy
Extraction
MANAGEMENT OF AGGRESSIVE PEFIODONTITIS

34. Non-surgical
therapy
Antimicrobial
therapy; Local
Delivery
Full mouth
disinfection
Host
modulation
Conventional
periodontal
therapy
MANAGEMENT OF AGGRESSIVE PERIODONTITIS
• Surgical resective therapy
• Regenerative therapy
CURRENT TREATMENT MODALITIES

35. • Its effect on aggressive periodontitis is much less clear.
• SRP reduced the total sub-gingival bacterial counts
• GAP responds well to scaling and root planning in the short term(up
to 6 months). However after 6months relapse and disease
progression is reported – Gunsolley et al 2008

36. Anti-microbial therapy
• Systemic tetracycline (250mg of tetracycline hydrochloride 4x/day for
atleast 1week) in conjunction with local mechanical therapy.
• If surgery is indicated, systemic tetracycline 100mg should be
prescribed approximately 1hour before surgery)
• Tetracycline resistant A.a:- Amoxicillin-Metronidazole; Ciprofloxacin-
Metronidazole

37. • Genco et al treated LAP patients with;-
SRP + Systemic administration of tetracycline (250 mg q.i.d × 14days).
Bone loss stopped, 1/3rd of defects demonstrated an increase in bone
level.
• Liljenberg and Lindhe treated LAP patients with
Systemic administration of tetracycline (250mg q.i.d for 2weeks)
Modified widman flap
Periodic recall visits (one visit every month for 6months, then one visit
every 3months)
The lesions healed more rapidly and more completely

38. MICROBIAL TESTING
In practice, antibiotics are often used empirically without microbial testing
Empiric use of antibiotics such as a combination of amoxicillin and
metronidazole, may be more clinically sound and cost effective than bacterial
identification and antibiotic sensitivity testing

39. 01
 Sigusch et al (2001), Guerrero et al (2007) suggested use
of clindamycin + SRP showed increase in clinical
attachment gain and reduction in pocket depth.
02
 Kaner et al(2007) showed use of metronidazole /
amoxicillin given immediately after SRP will be more
effective in resolving deep sites in GAP patients.
GENERALIZED AGGRESSIVE PERIODONTITIS
GAP

40. Local delivery agents including solutions, gels, fibers, chips
 Smaller dosages of topical agents can be delivered inside the
pocket
 Avoidance the side effects of systemic antimicrobial agents
 Increases the exposure of the target microorganisms to higher
concentrations of the medication

41. Full-mouth Disinfection
The concept described by Quirynen et al, consists of:-
 Full mouth debridement completed in 2 appointments within a 24 hour period
 The tongue is brushed with a chlorhexidine gel(1%) for 1 minutes
 Mouth rinsed with a chlorhexidine solution (0.2%) for 2 minutes
 Periodontal pockets irrigated with a chlorhexidine solution(1%)
Significant reductions in periodontal pathogens upto 8months after therapy. P.gingivalis
and T.forsythia were also reduced to levels below detection

42. Education
Plan
HOST MODULATION
.
NSAIDS
Bisphosphonates
BMP’s
Tetracyclines
Growth factors
Enamel matrix
proteins
• A novel approach in the treatment of aggressive periodontitis
• Modulates the host response to disease
.

43. ACCESS SURGERY
 Modified widman flap procedure effective in reducing
PPD – Christersson et al, 1985
 SRP + Tetracycline administration + MWF surgery –
Lindhe & Liljenberg, 1984

44. Surgical Resective Technique
 Effective to reduce or eliminate pocket depth
 Difficult to accomplish if adjacent teeth are
unaffected (in cases of LAP)
 Careful evaluation of the risks versus the benefits of
surgery must be considered.

45. Regenerative Surgery
 Bone grafting
 Guided tissue regeneration using membranes
 The use of biologic modifiers and combination of the
above
Designed for the regeneration of steep vertical defects and have very
specific indications:- defect morphology, tooth mobility and furcation
involvement.

46. Study by Rafael R. de Oliveira et al (2009) concluded that PDT and
SRP showed good results in the treatment of aggressive periodontitis

49. Aggressive Periodontitis both generalized and localised are
severe in the rate of progression and extent. Early diagnosis is very
essential for the successful treatment and good prognosis. It could be
prevented in families with history of Aggressive Periodontitis with
periodontal screening, maintaining good oral hygiene, eliminating the
risk factors and the causative micro organisms.
CONCLUSION

50. REFERENCES…
 Mani A, James R, Mani S. Etiology and Pathogenesis of Aggressive Periodontitis: A Mini Review.
Galore International Journal of Health Sciences and Research. 2018;3(2):4-8.
 Fine DH, Patil AG, Loos BG. Classification and diagnosis of aggressive periodontitis. Journal of
clinical periodontology. 2018 Jun;45:S95-111.
 Armitage GC, Cullinan MP. Comparison of the clinical features of chronic and aggressive
periodontitis. Periodontology 2000. 2010 Jun 1;53:12-27.
 Könönen E, Müller HP. Microbiology of aggressive periodontitis. Periodontology 2000. 2014
Jun;65(1):46-78.
 Albandar JM. Aggressive periodontitis: case definition and diagnostic criteria. Periodontology 2000.
2014 Jun;65(1):13-26.

51. Thank You