Aggressive periodontitis is defined as a sub-form of periodontitis attributed to rapid attachment and bone loss in otherwise healthy individuals. The condition features two main subtypes: localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP), with varying prevalence, characteristics, and immune responses. Factors such as specific bacteria, genetic predispositions, and environmental influences, including smoking, contribute to disease progression and necessitate tailored therapeutic interventions.

1. Aggressive
Periodontitis
Chapter 28

2.  The Definition of periodontitis: “an infectious disease resulting
in inflammation within the supporting tissues of the teeth,
progressive attachment loss, and bone loss.”
- There are sub-forms of the disease primarily defined by their
clinical phenotype (i.e., the rate of disease progression and
other features) rather than their etiology.
Aggressive periodontitis:
A sub-form of periodontitis featuring rapid loss of periodontal
attachment and tooth supporting bone in otherwise healthy
patients.

3. Terminology History
- Juvenile periodontitis
“A disease of the periodontium occurring in an otherwise healthy
adolescent which is characterized by a rapid loss of alveolar bone
about more than one tooth of the permanent dentition. The amount
of destruction manifested is not commensurate with the amount of
local irritants.”
- Early onset periodontitis (EOP)
Localized juvenile periodontitis
- Age of onset and distribution of lesions were of primary
importance when making a diagnosis of LJP.

4. Terminology History
The new classification (Aggressive periodontitis)
“To discard classification terminologies that were age-dependent or
required knowledge of rates of progression.”
Subgroups
 Localized & generalized
- The diagnosis is based on clinical, radiographic, and historical
data. These include the age of onset, the involvement of teeth
other than first molars and incisors and the presence of a systemic
antibody response against periodontal pathogens

5. Clinical Characteristics
Three Primary Features:
1) Rapid loss of attachment and tooth-supporting bone. Age is per
se no primary criterion for the diagnosis of aggressive
periodontitis.
2) Subject is otherwise healthy (i.e., not suffering from any systemic
disease or condition that could be responsible for the present
periodontitis). There are systemic diseases that lead to severely
altered host defenses against periodontal pathogens, often
resulting in rapid loss of attachment and tooth loss at an early
age. This disease is designated as: periodontitis as a
manifestation of systemic disease.

6. Clinical Characteristics
Secondary Features:
a) Inconsistency of the low amounts of present etiologic factors and
the observed pronounced tissue destruction
b) Strong colonization by Aggregatibacter actinomycetemcomitans
(A.a) and in some populations: Porphyromonas gingivalis
c) Immunologic differences that do not entail the diagnosis
periodontitis as a manifestation of systemic disease like
hyperresponsive macrophages or abnormalities of neutrophil
function.
a) Self-limiting disease

9. Generalized aggressive periodontitis (GAP)
 Previously classified as generalized juvenile periodontitis (GJP) and rapidly
progressive periodontitis (RPP)
 Highest severity and extent but also with a large heterogeneity.
 Prevalence: 1% - 15%
 Two gingival tissue responses:
• Destructive stage: severe, acutely inflamed tissue, often proliferating, ulcerated,
and fiery red. Bleeding may occur spontaneously or with slight stimulation.
Suppuration may be an important feature. attachment and bone are actively lost.
• Quiescence stage: the gingival tissues may appear pink, free of inflammation,
and occasionally with some degree of stippling, although stippling may be
absent. Despite the apparently mild clinical appearance, deep pockets can be
demonstrated by probing. The bone level remains stationary.

12. Localized aggressive periodontitis (LAP)
 Usually found in younger individuals than those affect by GAP
 More pronounced systemic antibody titers against periodontal pathogens
than found in GAP
• This could indicate that in individuals susceptible to disease, but with the
ability to enact a robust response against pathogens, the disease might
be limited in extent (LAP), whereas in individuals with a lesser humoral
response, the disease would not be limited to the first permanent teeth
(GAP). This would mean that LAP and GAP would merely be phenotypic
variations of the same underlying disease.

13. Localized aggressive periodontitis (LAP)
 Prevalence: less than 1%
 Affects both males and females and is seen most frequently in the period
between puberty and 20 years of age.
 Blacks are at much higher risk and black male teenagers were 2.9 times
more likely to have the disease than black female adolescents. White
female teenagers were more likely to have LAP than white male
adolescents.
 the highest prevalence of LAP: black males > black females > white

17. Pathobiology and Risk Factors
Microbiology
Host response
Genetics
Environmental factors

18. Microbiology
 The observed higher rate of disease progression in aggressive
versus chronic periodontitis could possibly be explained by the
presence of specific microorganisms (within-family
transmission) that cause and perpetuate tissue destruction.
 Differences exist in the microbiologic composition between:
(1) LAP and both GAP and chronic periodontitis
(2) GAP and chronic periodontitis

19. Specific Bacteria in LAP:
 A. actinomycetemcomitans: has been associated with and predicts the
development of LAP.
 The highly leukotoxic A.a (serotype b) strain JP2 that leads to a 10 to 20 fold
higher production of leukotoxin, was found to be directly related to the
occurrence of LAP in children in northern Africa.
 A recent study on the occurrence of JP2 clone strains in aggressive periodontitis
patients shows a high incidence in both LAP and GAP.
 Note: as with all entities of periodontitis, LAP is clearly not a mono-infection with
A.a but features a polymicrobial biofilm. There are reports of cases of LAP that
did not carry A.a.

20. Host Response to Bacterial Challenge
 The inflammatory response toward pathogens is responsible for a larger
proportion of the tissue destruction in periodontitis than the invading
pathogens themselves.
 The rapid progression of aggressive periodontitis implies that, in addition
to the composition of the subgingival microbiologic flora, specific
properties of inflammatory response renders the individuals both more
susceptible to disease and more prone to lose more attachment in a
shorter time.

21. Host Responses Specific to Aggressive Periodontitis
 In GAP, one review concluded that “there appears to be no difference
between aggressive and chronic periodontitis in terms of their
histopathology and immunopathology.”
 This could mean that “the differences between both disease entities only
reflect variations in the degree of severity of susceptibility rather than
actual different immune-pathologies.”
 Stronger activation of natural killer cells and natural killer T cells has been
suggested to be causative for the more pronounced tissue destruction in
aggressive periodontitis.

22. Abnormalities in LAP
 Earlier work: an inherited defect of neutrophil function, leading to a dampened
immune response against the microflora inhabiting the periodontal pocket.
Specifically, when challenged with periodontal pathogens, the LAP neutrophils
showed impaired chemotaxis, phagocytosis, and killing of bacteria. Alternatively,
it was also hypothesized that these impaired defense properties were in fact
acquired defects caused by prolonged exposure to an inflammatory
microenvironment.
 Today, the understanding is that neutrophils arriving at a site with uncontrolled
periodontal inflammation are primed to attack the invading pathogens by
releasing lytic enzymes that accelerate tissue destruction.
 It is hypothesized that the observed dampened neutrophil function in deep
aggressive periodontitis lesions is due to the heavy commitment of primed
neutrophils to debridement, so that less potency remains for chemotaxis and

23. Genetics
 Family studies: a familiar aggregation is often, but not always found in
aggressive periodontitis. Twin studies shows a strong genetic component
with likely autosomal dominant inheritance mode and a 70% (African
Americans) to 73% (Caucasians) penetrance.
 Polymorphisms: there is evidence for a strong genetic component in
aggressive periodontitis. A number of common susceptibility loci for
myocardial infarction and aggressive periodontitis could be identified.

24. Environmental Factors Affecting Susceptibility
 The amount and duration of smoking are important variables
that can influence the extent of destruction seen in young
adults.
 Patients with GAP who smoke have more affected teeth and
more CAL than non-smoking patients with GAP.
 Smoking may not have the same impact on attachment levels in
younger patients with LAP.

25. Therapeutic Considerations
 Anti-infective Therapy: adjunctive use of systemic antibiotics
 Surgical Therapy: individuals with aggressive periodontitis, especially LAP, have to
undergo surgical therapy more often than the average periodontitis patient, due to: (1)
the often much more pronounced loss of attachment with deep periodontal pockets that
are challenging to instrument, and (2) the high prevalence of vertical defects, notably in
LAP, that need to be resolved.
 Supportive Periodontal Therapy: optimize the self-performed oral hygiene to minimize
the amount of plaque that could eventually lead to a new, rapid loss of attachment.
Performing supportive periodontal therapy, including regular assessments of periodontal
parameters, at least every 3 months is recommended.
 Implant therapy: Peri-implantitis risk is linked to a history of periodontal disease and