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Perio MT2 > Aggressive Periodontitis > Flashcards

Aggressive Periodontitis Flashcards

1
Q

What at the 4 overarching characteristics of Aggressive Periodontitis (AP)?

A
  1. Non-contributory medical history (absence of significant systemic conditions
  2. RAPID attachment loss and bone loss
  3. Familial aggregation of cases (genetic component)
  4. Lack of consistency between bacterial deposits and severity of breakdown
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2
Q

Describe how AP can be deceptive in its appearance?

A

Often the gingiva appears clean and thus clinically can be very deceiving. The extent of the damage is often not realized until a radiograph is taken

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3
Q

What is the epidemiological prevalence of AP in the primary dentition?

A

Signs of bone loss in the primary dentition have a prevalence reported in the range of 0.9%-4.5%

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4
Q

What is the epidemiological prevalence of AP in 13-20 year olds with permanent dentition?

A

< 1%

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5
Q

What is the epidemiological prevalence of AP in white people vs black people ages 5-17?

A

Whites: 0.2%
Blacks: 2.6%

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6
Q

Why is it important to catch AP early in life?

A

Because there is an increase in extent and severity with time

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7
Q

What is the normal distance between the CEJ and the Marginal Bone Level (MBL) in 7-9 year olds?

A

< 2.0mm

Anything more and periodontal problem should be suspected

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8
Q

What are some of the very specific indicators for periodontitis?

A

Marginal bone loss PLUS
Clinical attachment loss PLUS
Increased probe depth PLUS
Plaque

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9
Q

Describe what factor would be used to differentially diagnose AP vs. some other cause for the symptoms

A

DD: ABSENCE of systemic disease (ie leukocyte deficiency syndrome, neutropinia)

b/c a systemic disease may severely compromise host response and thus likely be the causative agent for premature exfoliation of teeth

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10
Q

What are the requirements for localized aggressive periodontitis (LAP)

A

-Circumpubertal onset
-No systemic disease present
-RAPID attachment loss and bone destruction
-Localized first molar/incisor presentation
–interproximal attachment loss on at least 2
permanent teeth
–one of which is a molar
–involving no more than 2 teeth other than
first molars and incisors
-Familial history

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11
Q

What is the clinical outcome of untreated LAP?

A

Severe destruction of periodontal tissues in a short time

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12
Q

What are the 2 possible reasons for the destructive process of LAP?

A
  1. Aggressive causative agents and/or

2. High level of suseptibility

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13
Q

What are the 7 host defense mechanisms in the gingival sulcus, used for combating LAP?

A
  1. Intact epithelial barrier and attachment
  2. Salivary flushing action, agglutinins, Ab
  3. Sulcus fluid flushing action, opsinins, Ab, C
  4. Local Ab production
  5. Higher levels of tissue turnover
  6. Presence of normal flora or beneficial species
  7. Emigrating PMNs and other leukocytes
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14
Q

What is the common bacterial etiology seen in LAP (6 species/groups)?

A
  1. AA (facultative anaerobe)
  2. Capnocytophaga sp.
  3. Eikenella corrodens
  4. Prevotella intermedia
  5. Anaerobic rods (ex. campylobacter rectus)
  6. Gram + (Streps, Actinomyces,
    Peptostreptococcus)
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15
Q

What are the 4 roles of Aa in LAP that have been shown in studies?

A
  1. Isolated in more than 90% of LAP patients
  2. Significant Virulance factors
  3. Hyper-response to Aa in LAP patients
  4. Outcome of clinical therapy in LAP – failure linked to failure to reduce Aa load
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16
Q

What are the 6 virulence factors of Aa?

A
  1. Leukotoxin
  2. Endotoxin
  3. Bacteriocin
  4. Immunosuppressive factors
  5. Collagenases
  6. Chemotactic inhibition factors
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17
Q

What does leukotoxin, produced by Aa, do?

A

Kills PMNs and Macrophages

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18
Q

What does endotoxin, produced by Aa, do?

A

Activates cells to produce PGs, IL-1B, & TNF-a

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19
Q

What does bacteriocin, produced by Aa, do?

A

May inhibit growth of “good” species

20
Q

What do the immunosuppressive factors, produced by Aa, do?

A

May inhibit IgG and IgM production

21
Q

What do collagenases, produced by Aa, do?

A

Degrade collagen fibers

22
Q

What do chemotactic inhibition factors, produced by Aa, do?

A

Inhibits PMN chemotaxis

23
Q

Describe the host response to bacterial pathogens in LAP patients (8)

A

Mnemonic: Trying to mount a defense but the “BRITS MIA”

  1. B-cell mitogen evokes an increased response
  2. Recruitment of PMNs is intense
  3. IgG2 plays a special role
  4. Th:Ts ratio depressed compared to in health
  5. Sulcus fluid Ig levels higher than peripheral blood
  6. Mononuclear infiltrate dominated by B-cells and plasma cells
  7. IgG and IgA mostly produced by plasma cells; IgG4 by local cells
  8. Ab levels against Aa very high (not always as extreme with GAP)
24
Q

What is the significance of a depressed Th to Ts ratio?

A

Depressed ratio compared to healthy subjects suggests an altered local response in LAP pateints

25
Q

What are the two most LAP specific features of a host response to Aa?

A
  1. Ab levels against Aa extremely high

2. IgG2 seems to play a special role

26
Q

What is a possible reason for the huge amount of Ab against Aa seen in LAP patients, but not so much of an extreme in GAP patients?

A

-Likely that their Abs do not work as well as they should, thus more are more are recruited. -Thought that the high level of Abs is a protective defense.

27
Q

Describe the genetic patterns seen with LAP

A
  1. Familial aggregation
  2. Mendelian inheritance pattern
  3. 1+ genes predispose to EOP
  4. Likely substantial genetic polymorphism
  5. LAP trait is likely Autosomal Dominant
28
Q

T/F: Smoking is not an important factor on localized form of AP

A

TRUE!!

29
Q

Describe the 2 etiologically significant findings regarding smokers and GAP

A

Smokers have significantly higher:

  1. Extant (% sites with Perio AL >5 mm)
  2. Severity (Perio AL)
30
Q

Approx what % of adult Ohioans are smokers

A

27%

AA>HA>EA

31
Q

Approx what % of ohio middle school students use at lease 1 form of tobacco?

A

16%

32
Q

Approx what % of ohio high school students use at least 1 form of tobacco?

A

28%

33
Q

What are the 4 hallmarks of GAP?

A
  1. Usually affects persons under 30 but patients may be older
  2. Poor serum antibody response to infecting agents
  3. Pronounced episodic nature of destruction of attachment and bone
  4. Generalized interproximal attachment loss affecting at least 3 permanent teeth other than first molars and incisors.
    * *Also, as with all APs…
    - systemically healthy, rapid AL and bone destruction, and familial aggregation
34
Q

LAP and GAP are _____ diseases

A

Multifactorial

35
Q

LAP and GAP are the result of imbalance between ___ and ___

A

Imbalance b/t Host Genes and Environment

36
Q

What is necessary in terms of pathogen and host’s response in order to get LAP/GAP?

A
  1. Exposure to the pathogen by the host

2. Host’s inability to deal with it to avoid damage

37
Q

In what 2 ways is LAP/GAP phenotype determined?

A
  1. Modifying environmental factors (smoking)

2. Modifying Genetic factors (IgG2)

38
Q

Describe the series of events leading from normal periodontium to LAP to GAP

A

Normal –> (genetic predisposition + Exposure/Infection of Aa) –> LAP –> (genetic modifying factors + smoking or other bacteria) –GAP

39
Q

T/F only genetics play a role in development of LAP because it is often seen in kids

A

FALSE! Both LAP and GAP are due to both environmental and genetic factors

40
Q

Dr. T said to look over Dr. M’s lecture on AP….so in light of that…what are some Secondary features associated with LAP?

A
  1. Microbial deposits are inconsistent with the amount periodontal destruction
  2. Elevated Aa and Pg
  3. Phagocyte abnormalities
  4. Hyper-responsive macrophage phenotype (elevated levels PGE2 and IL-1B)
  5. Progression may be self-arresting
41
Q

What 6 questions must be answered to diagnose LAP/GAP?

A
  1. Is there periodontitis?
  2. Does the amt of plaque/calculus/local factors match the degree of periodontal destruction?
  3. Is there a systemic component?
  4. What is the patient’s microbial diagnosis?
  5. Are other family members affected?
  6. What are the host defenses like?
42
Q

What questions should you ask to determine if periodontitis is present when differentially diagnosing for LAP/GAP (5)?

A
  1. CAL and bone loss?
  2. Is CAL assoc w/ pocket or recession?
  3. Other explanations for CAL besides periodontitis?
  4. Is the pattern localized or generalized?
  5. Has there been previous perio treatment?
43
Q

What percent of patients with LAP progress to GAP?

A

~30% or 1/3

44
Q

What you be looking for in a microbiological diagnosis when trying to determine if a patient has LAP/GAP?

A

Aa, Pg, both or neither

45
Q

What 3 questions regarding the host defense could be helpful in the diagnosis of LAP/GAP?

A
  1. Are crevicular PGE2 levels largely increased?
  2. What are the other local inflammatory mediators?
  3. If GAP, IgG2 titers against Aa
46
Q

What are the 4 treatment principals for LAP/GAP?

super generalized answer….doesn’t tell you squat really

A
  1. Referral to periodontist
  2. Elimination (Sc/RP) forllowed by suppression (antibiotics) of microflora
  3. Address environmental factors
  4. Provide environment conducive to long term maintenance.

Perio MT2 (5 decks)

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