Epidemiology Flashcards

1
Q

Periodontitis prevalence

A

~42% of US population >30y/o
11.2% global prevalence (severe perio)

Kassebaum et al 2014

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2
Q

2017 AAP definition of periodontitis

A

Interproximal CAL at ≥ 2 non-adjacent teeth

OR

Buccal or facial CAL ≥ 3mm with PD > 3mm in non-interproximal surfaces in at least 2 teeth.

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3
Q

Gingival Index

Loe and Silness 1963

A
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4
Q

Plaque Index

Silness and Loe 1964

A
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5
Q

Modified gingival index

Lobene 1986

A
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6
Q

Community Periodontal Index for Treatment Needs (CPITN)

Ainamo 1982

A

CPITN probe: 0.5mm ball at tip, 3.5-5.5 mm markings

Used for PSR

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7
Q

Perio prevalence; Eke et al 2018

NHANES study (2009-14)

A
  • 42% of population has periodontitis (8% severe)
  • Most prevalence in mexican americans, then black peorple
  • prevalence increased with age
  • more prevalent in active smokers, noncompliant pts
  • More severe CAL: smokers, diabetics, lower SES
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8
Q

Eke et al 2018 probe/perio classification

A
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9
Q

Challenges of epidemiology studies in perio

Borrell and Papapanou 2005

A
  1. Wide threshold in defining perio
  2. Full mouth recordings vs partial (Ramfjord teeth: 3, 8, 12, 19, 24, 28)
  3. x-sectional studies
  4. Lack of longitudinal data
  5. Large dataset management
  6. Sample selection (NHANES reflects non-whites; NIDR is employed adults)
  7. Sampling variation
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10
Q

Ways to improve epi studies

2015 American & European periodontal epidemiology workshop

A
  1. Study design should include non-response and drop-out
  2. Full mouth probing protocol
  3. Perio probe should be UNC15
  4. Examiner reliability should be reported (kappa statistic)
  5. Report all perio risk factors
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11
Q

Kornman 1976

A
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12
Q

Non-specific plaque hypothesis

Loesche 1976, Theilade 1986

A

Amount of bacteria determines pathogenecity and destruction of periodontium

Problem is amount of plaque did not correlate with amount of destruction

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13
Q

Specific plaque hypothesis

Loesche 1976, Socransky 1998

A

Only a limited few bacterial species were capable of causing periodontal disease

Problem: not all could be cultivated, therefore bias to easily cultivatable bacteria

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14
Q

Ecological hypothesis

Marsh, 1994

A

Ecological stress triggers a shift in the resident microflora

Should target host response in addition to bacteria

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15
Q

Keystone pathogen hypothesis

Hajishengallis 2012

A

Host immunity plays critical role. Authors promoted term “dysbiosis”, meaning certain bacteria have the capacity to alter immune response, even if they exist in small numbers.

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16
Q

Loe 1978

Periodontal disease progression

A

Compared two cohorts, Noreweigens (with annual recalls and 90% compliance) and Sri-Lankan laborers with no preventive or treatment

Mean CALoss:

Nor: 0.08 mm interprox; 0.1mm buccal
SL: 0.3 mm interprox ; 0.2 mm buccal

17
Q

Loe et al 1986

Sri lankan follow-up

A
18
Q

Ramseier et al 2017

Follow-up on Loe 1986 study

A

Moderate progression: 92%, Rapid progression 8%

CALoss <1.81 mm was 80%ppv for presence of at least 20 teeth at age 60

19
Q

Goodson et al 1982

22 patients followed monthly for a year

A

82.8% –> no change
11.5% –> became shallower
5.7% –> became deeper

20
Q

Socranksy 1984

Untreated perio patient disease progression

A

CALoss of >2mm:

Baseline: 12%
3 years: 40%

Continuos model: some sites show progessive CALoss over time
**Random burst model: **activity at random on any site
Asynchronous multiple burst model: several sites show repeaeted bursts of activity, followed by inactivity

21
Q

Teles et al 2018

A
22
Q

Becker 1984

Rate of tooth loss

A