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Aggressive periodontitis
Dr.Haddadi
Reference:
• Carranza clinical periodontology, 2015, chapter 25.
primary features of aggressive periodontitis:
1. The rapid loss of attachment and tooth-supporting bone :
To evaluate this, the evaluation of clinical or radiographic data from
earlier points in time is necessary.
The age of the patient is not a primary criterion for the diagnosis of
aggressive periodontitis.
The neglect of oral hygiene in a periodontitis-susceptible individual will
lead to severe attachment loss, even with a slow rate of progression.
On the other hand, severe attachment loss in an older individual is not
necessarily the result of long-lasting, slowly progressing disease.
2. The subject is otherwise healthy (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 the rapid loss of
attachment and tooth loss at early age. This disease is designated
“periodontitis as a manifestation of systemic disease”
3. The presence of familiar aggregation
It can be evaluated via medical and dental history, questionnaires and by
interviewing the patient.
It is advisable to verify similar cases in the family, if possible, because
many individuals may not be fully aware of their diagnoses
secondary features that are generally found in aggressive periodontitis
cases but that are not universally necessary to diagnose the disease
entity:
1. Inconsistency of the low amounts of present etiological factors and
the pronounced tissue destruction.
2. Strong colonization by Aggregatibacter actinomycetemcomitans and,
in some populations, Porphyromonas gingivalis
3. Immunological differences:
a. Hyperresponsive macrophages
b. Abnormalities of neutrophil function
4. Self-limiting disease
Subgroups:
• Aggressive periodontitis can be subclassifed into localized and
generalized forms.
• The diagnosis of the subcategory is based on clinical, radiographic,
and historical data. These include:
• The age of onset,
• The involvement of teeth other than first molars and incisors (the first
permanent teeth to erupt),
• The presence of a systemic antibody response against periodontal
pathogens.
Generalized Aggressive Periodontitis
• GAP was previously classified as generalized juvenile periodontitis and
rapidly progressive periodontitis.
1. Usually affecting persons under 30 years of age, but patients may be older
2. Generalized interproximal attachment loss affecting at least three
permanent teeth other than first molars and incisors
3. Pronounced episodic nature of the destruction of attachment and alveolar
bone
4. Poor serum antibody response to infecting agents.
• Acutely inflamed tissue that is often proliferating, ulcerated, and fiery
red. Bleeding may occur spontaneously or with slight stimulation,
and suppuration may be an important feature. This tissue response
is thought to occur during the destructive stage, in which attachment
and bone are actively lost .
• The gingival tissues may appear pink, free of inflammation, and
occasionally with some degree of stippling, although stippling may be
absent. However, despite the apparently mild clinical appearance, deep
pockets can be demonstrated by probing.
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 agent
Prevalence:
• The prevalence of aggressive periodontitis of approximately 1% to
15% among subjects who are 35 years old or younger.
• LAP was reported to affect both males and females, and it is
seen most frequently in the period between puberty and 20 years
of age.
• Several studies have found the highest prevalence of LAP among
black males, who are followed in descending order by black females,
white females, and white males.
Microbiology
• The higher rate of disease progression in aggressive versus chronic
periodontitis could possibly be explained by the presence of specific
microorganisms that cause and perpetuate tissue destruction.
• The microbiology of GAP is similar to chronic periodontitis.
• In patients with LAP, several lines of evidence point to a strong role of
specific microorganisms, most notably A. actinomycetemcomitans (A.a)
• LAP is clearly not a mono-infection with A. actinomycetemcomitans , LAP
features a poly-microbial biofilm.
Host Response to Bacterial Challenge
• The inflammatory host response toward pathogens is responsible for
a larger tissue destruction in periodontitis than the invading
periodontal pathogens themselves.
• With regard to GAP, a recent review concluded that “there appears to
be no difference between aggressive and chronic periodontitis in
terms of their histopathology and immunopathology.”
• The differences between both disease entities only reflect variations
in the degree of severity of susceptibility rather than actual different
immune-pathologies.
• Specifically, when challenged with periodontal pathogens, the LAP
neutrophils were reported to show impaired chemotaxis, phagocytosis,
and killing of bacteria.
• To assess the familiar component of the disease, twin studies were
performed, and these demonstrated a strong genetic component with a
likely autosomal-dominant inheritance pattern and a 70% penetrance.
• 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
loss of clinical attachment than nonsmoking patients with GAP.
• However, smoking may not have the same impact on attachment
levels in younger patients with LAP.
Diagnosis
• Assessment of Clinical Presentation
The diagnosis of aggressive periodontitis in the clinic is made by jointly
assessing the primary and secondary features of aggressive periodontitis.
• Patients who are at risk for developing aggressive periodontitis should be
more closely monitored. These are primarily subjects with a known familiar
aggregation of aggressive periodontitis.
• The diagnosis of systemic health is made by checking the medical history of
the patient, usually with the use of a questionnaire and interview.
• Assessment of Radiographic Presentation
Radiographic evidence of periodontal bone loss is a very specific but
not very sensitive diagnostic sign of periodontitis.
To screen for bone loss in younger children and adolescents with the
use of the bite-wing radiographs that are regularly obtained for the
early detection of dental caries.
A distance of 2 mm between the cemento-enamel junction and the
alveolar bone crest in these patients could be a sign of
periodontitis and may warrant a more thorough examination.
• The vertical loss of alveolar bone around the first molars and incisors,
which begins around puberty in otherwise healthy teenagers, is a
classic diagnostic sign of LAP.
• Radiographic findings may include an “arc-shaped loss of alveolar
bone extending from the distal surface of the second premolar to the
mesial surface of the second molar.”
• Bone defects are usually wider than those that are usually seen with
chronic periodontitis.
Arc-shape bone loss
Assessment of Microbiology
• There are available tests for sampling the subgingival microbiota. These
tests most often assess the presence and estimate the relative numbers of
3 to 20 prominent periodontal pathogens.
• However, the sensitivity and specificity of these tests is disputed.
• In patients with aggressive periodontitis, the test results will likely not
change standard treatment protocols, which most often include the
prescription of systemic antibiotics as adjuncts to anti-infective therapy.
• Therefore, some authors suggest that microbial testing can be omitted.
Anti-infective Therapy of Aggressive
Periodontitis
• Anti-infective therapy in patients with aggressive periodontitis
seems to benefit strongly from the adjunctive use of systemic
antibiotics.
• Antibiotic of choice: amoxicillin + metronidazole
Surgical Therapy of Aggressive Periodontitis
• In general, individuals with aggressive periodontitis, especially
LAP, have to undergo surgical therapy more often than the average
patient with periodontitis.
(1) The often much more pronounced loss of attachment with deep
periodontal pockets that are challenging to instrument.
(2) the high prevalence of vertical defects, most notably in patients
with LAP, that need to be resolved.
Maintenance phase:
• Recall visits every 3-4 months.
Any question..?

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Aggressive periodontitis

  • 1.
  • 3. Reference: • Carranza clinical periodontology, 2015, chapter 25.
  • 4. primary features of aggressive periodontitis: 1. The rapid loss of attachment and tooth-supporting bone : To evaluate this, the evaluation of clinical or radiographic data from earlier points in time is necessary. The age of the patient is not a primary criterion for the diagnosis of aggressive periodontitis. The neglect of oral hygiene in a periodontitis-susceptible individual will lead to severe attachment loss, even with a slow rate of progression. On the other hand, severe attachment loss in an older individual is not necessarily the result of long-lasting, slowly progressing disease.
  • 5. 2. The subject is otherwise healthy (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 the rapid loss of attachment and tooth loss at early age. This disease is designated “periodontitis as a manifestation of systemic disease”
  • 6. 3. The presence of familiar aggregation It can be evaluated via medical and dental history, questionnaires and by interviewing the patient. It is advisable to verify similar cases in the family, if possible, because many individuals may not be fully aware of their diagnoses
  • 7. secondary features that are generally found in aggressive periodontitis cases but that are not universally necessary to diagnose the disease entity: 1. Inconsistency of the low amounts of present etiological factors and the pronounced tissue destruction. 2. Strong colonization by Aggregatibacter actinomycetemcomitans and, in some populations, Porphyromonas gingivalis 3. Immunological differences: a. Hyperresponsive macrophages b. Abnormalities of neutrophil function 4. Self-limiting disease
  • 8. Subgroups: • Aggressive periodontitis can be subclassifed into localized and generalized forms. • The diagnosis of the subcategory is based on clinical, radiographic, and historical data. These include: • The age of onset, • The involvement of teeth other than first molars and incisors (the first permanent teeth to erupt), • The presence of a systemic antibody response against periodontal pathogens.
  • 9. Generalized Aggressive Periodontitis • GAP was previously classified as generalized juvenile periodontitis and rapidly progressive periodontitis. 1. Usually affecting persons under 30 years of age, but patients may be older 2. Generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors 3. Pronounced episodic nature of the destruction of attachment and alveolar bone 4. Poor serum antibody response to infecting agents.
  • 10. • Acutely inflamed tissue that is often proliferating, ulcerated, and fiery red. Bleeding may occur spontaneously or with slight stimulation, and suppuration may be an important feature. This tissue response is thought to occur during the destructive stage, in which attachment and bone are actively lost . • The gingival tissues may appear pink, free of inflammation, and occasionally with some degree of stippling, although stippling may be absent. However, despite the apparently mild clinical appearance, deep pockets can be demonstrated by probing.
  • 11.
  • 12.
  • 13. 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 agent
  • 14.
  • 15.
  • 16. Prevalence: • The prevalence of aggressive periodontitis of approximately 1% to 15% among subjects who are 35 years old or younger. • LAP was reported to affect both males and females, and it is seen most frequently in the period between puberty and 20 years of age. • Several studies have found the highest prevalence of LAP among black males, who are followed in descending order by black females, white females, and white males.
  • 17. Microbiology • The higher rate of disease progression in aggressive versus chronic periodontitis could possibly be explained by the presence of specific microorganisms that cause and perpetuate tissue destruction. • The microbiology of GAP is similar to chronic periodontitis. • In patients with LAP, several lines of evidence point to a strong role of specific microorganisms, most notably A. actinomycetemcomitans (A.a) • LAP is clearly not a mono-infection with A. actinomycetemcomitans , LAP features a poly-microbial biofilm.
  • 18. Host Response to Bacterial Challenge • The inflammatory host response toward pathogens is responsible for a larger tissue destruction in periodontitis than the invading periodontal pathogens themselves. • With regard to GAP, a recent review concluded that “there appears to be no difference between aggressive and chronic periodontitis in terms of their histopathology and immunopathology.” • The differences between both disease entities only reflect variations in the degree of severity of susceptibility rather than actual different immune-pathologies.
  • 19. • Specifically, when challenged with periodontal pathogens, the LAP neutrophils were reported to show impaired chemotaxis, phagocytosis, and killing of bacteria. • To assess the familiar component of the disease, twin studies were performed, and these demonstrated a strong genetic component with a likely autosomal-dominant inheritance pattern and a 70% penetrance.
  • 20. • 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 loss of clinical attachment than nonsmoking patients with GAP. • However, smoking may not have the same impact on attachment levels in younger patients with LAP.
  • 21. Diagnosis • Assessment of Clinical Presentation The diagnosis of aggressive periodontitis in the clinic is made by jointly assessing the primary and secondary features of aggressive periodontitis. • Patients who are at risk for developing aggressive periodontitis should be more closely monitored. These are primarily subjects with a known familiar aggregation of aggressive periodontitis. • The diagnosis of systemic health is made by checking the medical history of the patient, usually with the use of a questionnaire and interview.
  • 22. • Assessment of Radiographic Presentation Radiographic evidence of periodontal bone loss is a very specific but not very sensitive diagnostic sign of periodontitis. To screen for bone loss in younger children and adolescents with the use of the bite-wing radiographs that are regularly obtained for the early detection of dental caries. A distance of 2 mm between the cemento-enamel junction and the alveolar bone crest in these patients could be a sign of periodontitis and may warrant a more thorough examination.
  • 23. • The vertical loss of alveolar bone around the first molars and incisors, which begins around puberty in otherwise healthy teenagers, is a classic diagnostic sign of LAP. • Radiographic findings may include an “arc-shaped loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar.” • Bone defects are usually wider than those that are usually seen with chronic periodontitis.
  • 24.
  • 26. Assessment of Microbiology • There are available tests for sampling the subgingival microbiota. These tests most often assess the presence and estimate the relative numbers of 3 to 20 prominent periodontal pathogens. • However, the sensitivity and specificity of these tests is disputed. • In patients with aggressive periodontitis, the test results will likely not change standard treatment protocols, which most often include the prescription of systemic antibiotics as adjuncts to anti-infective therapy. • Therefore, some authors suggest that microbial testing can be omitted.
  • 27. Anti-infective Therapy of Aggressive Periodontitis • Anti-infective therapy in patients with aggressive periodontitis seems to benefit strongly from the adjunctive use of systemic antibiotics. • Antibiotic of choice: amoxicillin + metronidazole
  • 28. Surgical Therapy of Aggressive Periodontitis • In general, individuals with aggressive periodontitis, especially LAP, have to undergo surgical therapy more often than the average patient with periodontitis. (1) The often much more pronounced loss of attachment with deep periodontal pockets that are challenging to instrument. (2) the high prevalence of vertical defects, most notably in patients with LAP, that need to be resolved.
  • 29. Maintenance phase: • Recall visits every 3-4 months.
  • 30.