AGGRESSIVE PERIODONTITIS PRESENTER DR. REBICCA RANJIT DEPT. OF PERIODONTOLOGY & ORAL IMPLANTOLOGY Why is there localisation of disease to 1st molars and incisors in LAP? Often subjects present with attachment loss that does not fit the specific diagnostic criteria (AP or chronic periodontitis). Schenkein et al. 1995: cigarette smoking was shown to be a risk factor for patients with generalized forms of AgP. Smokers with GAP had more affected teeth and greater mean levels of attachment loss than patients with GAP who did not smoke. IgG2 serum levels as well as antibody levels against A.a. are significantly depressed in subjects with GAP who smoked.

1. AGGRESSIVE
PERIODONTITIS
PRESENTER
DR. REBICCA RANJIT
IIND YEAR RESIDENT

2. Juvenile
periodontitis
Early-onset
periodontitis,
Page & Baab 1989
Deep cementopathia
Gottlieb,1928
Diffuse atrophy of the
alveolar bone
Gottlieb, 1923
1999 AAP International Workshop for Classification Aggressive periodontitis
Chaput & colleagues, 1967
Butler in 1969.
HISTORICAL BACKGROUND

3. Aggressive periodontitis refers to the multifactorial, severe,
& rapidly progressive form of periodontitis, which primarily
but not exclusively affects younger patients.
- Int’l Workshop Classification Of Periodontal
Diseases & Conditions (1999)

4. Aggressive periodontitis
Disease of the periodontium occurring in an
otherwise healthy adolescent
The only teeth
affected are
1. First molars
2. Incisors
Generalized
form, it may
affect most
of the
dentition.
Amount of
destruction
manifested is not
commensurate
with the amount
of local irritants
In 1971, Paul Baer
characterized by a rapid loss of alveolar bone about
more than one tooth of the permanent dentition.
Baer PN. The case for periodontosis as a clinical entity. J Periodontol 1971:42: 516–520.

5. Baer proposed 7criteria to define the disease:-

6. Early onset of the disease during the circumpubertal period
(between 11 and 13 years of age)
1)
Age of the patient per se is not a primary criterion
for the diagnosis of aggressive periodontitis

7.  An arc-shaped loss of alveolar bone,
extending from the distal surface
of 5 to the mesial surface of the 7.
 Occurs bilaterally, depicting
“mirror images” of each other
A distinctive radiographic pattern depicting
vertical alveolar bone loss at the first permanent
molars and at one or more incisor teeth.
Classical case of
aggressive periodontitis
Atypical cases of
aggressive periodontitis
 Show bone loss at only one
proximal surface of 6, or that
 Only the molars are affected
and not the incisors.
2)

8. 3)
A rapid rate of disease progression.
Baer estimated that, typically, an affected tooth can lose 75%
of the alveolar bone support at one or more root surfaces within
5 years of disease initiation.
Atypical cases:- Alveolar bone loss progresses only to a certain
point & 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.
4)
The amount of local etiologic factors is not commensurate with the
severity of periodontal destruction.
5)

10. 6)
The disease has a familial pattern.
7)
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.

11. The 1999 International Workshop for the Classification of
Periodontal Diseases and Conditions defined the entity of AP as
being characterized by “3 primary features”:-
Rapid loss of
attachment
and tooth-
supporting
bone
Presence of
familial
aggregation
Subject is
otherwise
healthy

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

13. American Academy of Periodontology workshop, 1999
Aggressive periodontitis
Localized
aggressive periodontitis
Generalized
aggressive periodontitis

14. Localized aggressive periodontitis (LAP)
In 1989 the World Workshop in Clinical Periodontics, categorized
this disease as:- “Localized juvenile periodontitis” (LJP)

15.  Circumpubertal onset (11 - 13 years of age).
 Localized attachment loss at incisors and first molars; interproximal
attachment loss on at least 2 permanent teeth (one of which is a first
molar) and involving no more than two 0r fewer teeth other than first
molars and incisors.
 Robust serum antibody response to infecting agents.

16. •Lack of clinical inflammation
•Amount of plaque inconsistent with the amount of
periodontal destruction.
•Presence of deep periodontal pockets
Clinical features

17. •Elevated levels of A.a and P. gingivalis.
•Distolabial migration of maxillary incisors - diastema formation
•Increasing mobility of maxillary and mandibular incisors & 1st molars
•↑ Sensitivity of denuded root surfaces to thermal and tactile stimuli
• Deep, dull, radiating pain during mastication.

18. • Classic diagnostic sign of localized aggressive periodontitis
Vertical “arc shaped” bone loss irt molars and incisors
• Rate of bone loss is about
3-4 times faster than in
chronic periodontitis.
Radiographic features

19. Why is there localisation of disease
to 1st molars and incisors in LAP?
Some reasons for Site specific
destruction

20. After initial colonization, A.a. evades the host defense
Production of PMN
chemotaxis-inhibiting
factors, Endotoxin,
Collagenases, Leukotoxin
Allow the bacteria to colonize the
pocket and initiate the destruction
of the periodontal tissues.
After initial attack
Immune defenses stimulated
Opsonic antibodies are produced
Phagocytosis of invading bacteria and neutralization of
leukotoxic activity. (may slow or arrest the disease process)
1)

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

22. 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.

23. lesser humoral response
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.

24. “Burn-out phenomenon”
 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 ceasation of disease activity.
 Proposed by Ranney.

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

26. Usually affect <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.

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

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

30. • Often subjects present with attachment loss that does not fit
the specific diagnostic criteria (AP or chronic periodontitis).
It includes:
 Recessions associated with trauma or tooth position,
 Attachment loss associated with impacted third molars,
removal of impacted third molars,etc.
These patients are a high-risk group for AP or chronic
periodontitis.
Incidental attachment loss

31. RISK FACTORS FOR AGGRESSIVE PERIODONTITIS
a) Microbiologic Factors

32. 1. A.a.
2. Capnocytophaga sp
3. E. corrodens
4. P. intermedia
5. Motile anaerobic rods,
such as C. rectus
6. Gram-positive isolates
were mostly
1. Streptococci
2. Actinomycetes
3. Peptostreptococci
Dominant microorganisms
1. Porphyromonas gingivalis,
2. A.a.
3. Bacteroides forsythus
LAP
GAP
(approx. 90%)

33. A. a has been implicated as the primary pathogen associated with LAP. As
summarized by Tonetti and Mombelli, it is based on the following
evidence:
1. A.a is found in high frequency (approx. 90%) in lesions characteristic of LAP.
2. Sites with evidence of disease progression often show elevated levels of A.a
3. Many patients with the clinical manifestations of LAP have significantly elevated
serum antibody titers to A.a.
4. Clinical studies show a correlation between reduction in the subgingival load of A.a
during treatment and a successful clinical response.
5. A.a. produces a number of virulence factors that may contribute to the disease
process.

34. RISK FACTORS FOR AGGRESSIVE PERIODONTITIS
b) Immunologic Factors

35. 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 phagocytose & kill microorganisms.
 Hyperresponsiveness of monocytes from LAP patients involving
their production of prostaglandin E2 in response to LPS
Increased connective tissue or bone loss

36. RISK FACTORS FOR AGGRESSIVE PERIODONTITIS
c) Genetic Factors

37.  Segregation analyses -- autosomal dominant mode of inheritance
(Saxen & Nevanlinna 1984, Beaty et al. 1987, Hart et al. 1992, Marazita
et al. 1994).
 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 IgG2) against A. a may be
race dependent.

38. RISK FACTORS FOR AGGRESSIVE PERIODONTITIS
d) Environmental factors

39. • Schenkein et al. 1995: cigarette smoking was shown to be a risk factor
for patients with generalized forms of AgP.
• Smokers with GAP had more affected teeth and greater mean levels
of attachment loss than patients with GAP who did not smoke.
• IgG2 serum levels as well as antibody levels against A.a. are
significantly depressed in subjects with GAP who smoked.

40. Non-surgical therapy
Antimicrobial Therapy; Local Delivery
Full-Mouth Disinfection
Host Modulation
Conventional Periodontal Therapy
• Surgical Resective Therapy
• Regenerative Therapy
MANAGEMENT OF AGGRESSIVE PERIODONTITIS

41. Non-surgical therapy
Its effect on aggressive periodontitis is much less clear.
For LAP, the effect of scaling and root planing alone represent the first
phase of a staged combination therapy.
Slots & Rosling
Unsal et al
GAP responds well to scaling & root planing in the short term (upto 6 mths).
However, after 6 months, relapse and disease progression is reported.
Gunsolley et al.
Haas et al,2008
Sigusch et al,1998
SRP reduced the total sub-gingival bacterial counts and the proportions
of certain gram-negative bacteria, but no periodontal pocket became
free of A. actinomycetemcomitans.

42.  Systemic tetracycline (250 mg of tetracycline hydrochloride 4x/day
for at least 1 week) in conjunction with local mechanical therapy.
 If surgery is indicated, systemic tetracycline 1000mg stat should be
prescribed approximately 1 hour before surgery.
 Tetracycline resistant A.a:- Amoxicillin-Metronidazole;
Ciprofloxacin- Metronidazole
Anti-microbial Therapy

43. Doxycycline, 100 mg/day, may be used instead of
tetracycline.
Chlorhexidine rinses should be prescribed and
continued for several weeks to enhance plaque
control and facilitate healing.

44.  Genco et al treated LAP patients with:-
SRP  Systemic administration of tetracycline
(250 mg q.i.d x 14 days every 8 weeks).
Bone loss stopped, 1/3rd of defects demonstrated an increase in bone level
18 months
 Liljenberg and Lindhe treated LAP patients with
Systemic administration of tetracycline (250 mg q.i.d for 2 weeks)
Modified Widman flap
Periodic recall visits (one visit every month for 6 mths, then one visit every 3 mths).
The lesions healed more rapidly and more completely

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

46. Associated Microflora Antibiotic of Choice
Gram-positive organisms Amoxicillin–Clavulanate potassium
(Augmentin)
Gram-negative organisms Clindamycin
Non-oral gram-negative,
facultative rods
Ciprofloxacin
Pseudomonads, Staphylococci
Black-pigmented bacterial,
spirochetes
Metronidazole
Prevotella intermedia,
Porphyromonas gingivalis
Tetracycline
Aggregatibacter
actinomycetemcomitans
Metronidazole-amoxicillin
Metronidazole-ciprofloxacin
Tetracycline
P. gingivalis Azithromycin
Antibiotic Therapy for Aggressive Periodontitis

47. Generalized Aggressive Periodontitis:
Sigusch et al (2001), Xajigeorgiou et al (2006), Guerrero et al (2007)
suggested use of Clindamycin + SRP showed increase in clinical
attachment gain and reduction in pocket depth
Kaner et al (2007) showed use of metronidazole/ amoxicillin given
immediately after SRP will be more effective in resolving deep sites in
GAP patients.

48. 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 antibacterial agents
 Increases the exposure of the target microorganisms to higher
concentrations, of the medication.

49. - Another approach to antimicrobial therapy.
- 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 minute,
 Mouth rinsed with a chlorhexidine solution (0.2%) for 2 minutes,
 Periodontal pockets irrigated with a chlorhexidine solution (1%)
Full-Mouth Disinfection
Significant reductions in periodontal pathogens up to 8 months
after therapy. P. gingivalis and T. forsythia were reduced to levels
below detection.

50. Host Modulation
A novel approach in the treatment of aggressive periodontitis
and difficult-to-control forms of periodontal disease.
Modulates the host response to disease.
Tetracyclines
Growth
factors
Enamel matrix
proteins
BMPs
Bisphosphonates
NSAIDS

51. Access surgery
• Modified Widman flap procedure effective in reducing PPD.
Christersson et al, 1985
• SRP  Tetracycline administration  MWF surgery
Lindhe & Liljenberg, 1984

52. Surgical Resective Therapy
 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 on a case-by-case basis.

53. Regenerative surgery
• Bone grafting,
o Guided tissue regeneration using membranes,
 The use of biologic modifiers &
 Combinations of the above
Designed for the regeneration of steep vertical defects & have very
specific indications :- defect morphology, tooth mobility & furcation
involvement.

54. Bone grafting
Yukna & Sepe, reported an average defect fill of 80% with FDBA in 12
patients with LAP at re-entry after 12 months.
Evans et al evaluated a 4:1 ratio combination of -tricalcium phosphate/
tetracycline, hydroxyapatite/tetracycline or freeze-dried bone
allograft/tetracycline in patients with LAP which showed significant
decrease in defect depth & pocket depth were detected for each graft
material.
Hydroxyapatite/tetracycline  -tricalcium phosphate/ tetracycline.

55. OTHERS
1. Autogenous bone chips (Oshrains and Kaslick – 1981)
2. Osseous coagulum (Burnette and Steroark - 1969)
3. Frozen autogenous hip marrow (De Marco and Scaletter-1970)

56. PD reduction & clinical attachment gain significantly greater
in the PTFE membrane-treated defects than in osseous surgery
-treated defects.
Sirirat M, Kasetsuwan J, Jeffcoat MK. Comparison between 2 surgical techniques for the
treatment of early-onset periodontitis. J Periodontol 1996:67: 603–607
Guided tissue regeneration
Esposito et al(2003) reported that use of emdogain can improve clinical
attachment level(1.3mm) and reduction in probing depth(1.0mm) compared
to flap debridement alone.
Enamel matrix proteins

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

58. Ozonized water in treatment of AP
Effect of ozonized water on oral microorganisms & dental plaque was
studied by Nagayoshi et al., (2002).
Useful in reducing the infections caused by oral microorganisms in
dental plaque.
Ramzy et al assessed the clinical and antimicrobial effect of ozonized
water in management of aggressive periodontitis, found that ozone
has a potent antibacterial effect explained by the fact that it causes
disruption of the envelope integrity through peroxidation of
phospholipids.

59.  The duration between recall visits should be usually short during
the period after completion of therapy, generally no longer than 3-
month intervals.
 Monitoring as frequently as every 3 - 4 weeks may be necessary
when the disease is thought to be active.
 If signs of disease activity and progression persist despite
therapeutic efforts, frequent visits and good patient compliance,
microbial testing may be indicated.

60. CONCLUSION
Aggressive periodontitis is the multifactorial, severe, & rapidly
progressive form of periodontitis, which primarily but not
exclusively affects younger patients where the amount of
destruction manifested is not commensurate with the amount of
local irritants.
Surgery and tetracycline is the best option for treatment as
the procedure involves the removal of granulation and connective
tissue infected with Aggregatibacter actinomycetemcomitans.

61. REFERENCES

62. Carranza, 10th & 12th Edition
Albandar, J. M. (2014), Aggressive periodontitis: case definition and
diagnostic criteria. Periodontology 2000, 65: 13–26.
Könönen, E. and Müller, H.-P. (2014), Microbiology of aggressive
periodontitis. Periodontology 2000, 65: 46–78.
Kulkarni, C. and Kinane, D. F. (2014), Host response in aggressive
periodontitis. Periodontology 2000, 65: 79–91.
Teughels, W., Dhondt, R., Dekeyser, C. and Quirynen, M. (2014),
Treatment of aggressive periodontitis. Periodontology 2000,
65: 107–133.

63. THANK YOU