Agressive Periodontitis 10/22/15 Flashcards

1
Q

What are the 2 major types of Periodontitis?

A
  • Chronic and Agressive
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2
Q

What are common features of Aggressive Periodontitis?

A
  • Otherwise health patient
  • Characterized by RAPID bone and attachment loss (inconsistent with plaque and Calculus)
  • Familial Aggregation (Genetic)
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3
Q

What are the 2 sub Classifications of A. Periodontitis?

A
  • GAP (Generalized)

- LAP (Localized)

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4
Q

Tell me about LAP…

A
  • Most frequent btw puberty and 20yrs old
  • Pattern = Localized CAL in the first molars/incisors (at least 1 molar MUST be affected)
  • Distribution = No more than 2 teeth other than 1st molars affected.
  • Robust serum antibody response
  • Relatively less intense gingival inflammation
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5
Q

Tell me about GAP…

A
  • Affects individuals under the age of 30 (also older patients)
  • Distribution = at least 3 permeant teeth other than 1st molars and incisors.
  • Pronounced episodic nature of destruction of attachment/bone.
  • Relatively intense gingival inflammation.
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6
Q

What is the Prevalence of A. Periodontitis in Primary dentition?

A
  • Few studies in 5-11 yr-olds

- Prevalence reported between 0.9% and 4.5%

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7
Q

What is the prevalence of A.Periodontitis in Permanent dentition?

A
  • estimates = less than 1% for U.S

- around 2.6 for African americans.

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8
Q

________ is found to be distributed throughout 89-100% of patients with LAP.

A

A. Actinomycetemcomitans (A.a)

*So yes, A.a is associated with LAP.

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9
Q

What are the characteristics and virulence factors for P. Gingivalis?

A
  • Anaerobic
  • Nonmotile
    Virulence factors:
  • Proteinases = Gingipains and Collagenases
  • LPS: activates cells to produce PG’s IL-1B and TNF-alpha
    Inhibits IL-8 (chemotactic factor) = decreased chemotaxis of PMN’s.
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10
Q

What are the Characteristics and Virulence Factors of A.a?

A
  • Facultative Anaerobe
  • Non-motile
    Virulence factors:
  • Leukotoxins = kills PMN’s
  • LPS: activates cells to produce PG’s (IL-B1 and TNF-A)
  • Collagenases = degrade collagen
  • Immunosuppressive factors
    *Can translocate across the JE and invade CE.
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11
Q

What is the Proposed inheritance model for LAP?

A

Autosomal dominant

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12
Q

What is the Host response to LAP?

A
  • Impaired Neutrophil function (know this one!)
  • Significantly higher levels of Prostaglandins in E2 and in GCF.
  • High titers and High avidity of IgG2 in LAP
  • Low levels of Ab against P.g in GAP Patients
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13
Q

Is Smoking a risk factor in GAP?

A

Yes, it increases extent and severity. Also have poorer response to clinical treatment.

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14
Q

What questions should you ask when trying to diagnose AP?

A

Are Crevicular Prostaglandin E2 levels increased? Yes = AP

Are there high titers of IgG2 against A.a? yes = AP

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15
Q

What is the Treatment for Periodontitis?

A

Full Mouth SRP in adjust with systemic antibiotics
Amoxicillin + Metronidazole
or Ciprofloxacin + Metronidazole
*Possible Periodontal surgery

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