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Classic Lit Fall 2021 > Epidemiology and Pathogenesis of Perio > Flashcards

Epidemiology and Pathogenesis of Perio Flashcards

1
Q

Define Pathogenesis

A

the biological mechanism that leads to the diseased state.

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2
Q

Define Epidemiology

A

The science that studies the patterns, causes, and effects of health and disease in defined populations.

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3
Q

What is Prevalence

A

The proportion of a population who had/have a specific characteristic at a given time - regardless of when they first acquired it

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4
Q

What is Incidence

A

The measure of number of new cases that arise in a population over a given time period

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5
Q

What is the GLOBAL prevalence of periodontal disease?

A

Richards et al. 2014

Data from the Global Burden of Disease

Prevalence of Severe Periodontitis: 11%

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6
Q

What is the prevalence of periodontitis in the US?

A

Eke et al. 2018

Data from the National Health and Nutrition Examination Survey (NHANES)

2009-2014

42% of US has Periodontitis

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7
Q

According to Eke et al. 2018 - how does the prevalence of Mild/Mod/Severe perio change with age?

A

Mild and Moderate prevalence increased with age

Severe prevalence remained below 15% all age groups

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8
Q

According to Eke et al. 2018 what groups is perio most prevalent among?

A

Mexican Americans > non-Hispanic African Americans > …

current smokers, non-regular flossers, non-compliant patients (no dental visit >6mo)

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9
Q

What groups are Severe Perio most prevalent in according to Eke et al. 2018?

A

3x greater prevalence in Mexican Americans, non-Hispanic blacks, and current smokers

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10
Q

What role does age have on development of periodontitis?

A

It is NOT a risk factor

Billings 2018

Combined data from Eke 2018 (NHANES 2009-2014) and the Study of Health in Pomeranian, Germany (SHIP-Trend)

Common pattern in both populations - increased CAL with age

Recession biggest increase 45-49yrs

PD remain constant with age

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11
Q

What is one study that describes the pathogenesis of periodontal disease?

A

Kornman et al. 1997

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12
Q

What are the 4 phases that describe that pathogenesis of periodontal disease?

A

Kornman et al. 1997

  • Acute bacterial challenge phase*
  • Acute inflammatory response phase*
  • Immune response phase*
  • Regulation and resolution phase*
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13
Q

Describe the Acute Bacterial Challenge phase

A

Kornman et al. 1997

0-4 days

  • Epithelial and vascular response to bacteria
    • Bacteria release metabolic products through JE
    • Perivascular mast cells release histamine
    • Vascular endothelial and JE cells release IL-8, IL-1, PGE2, MMPs, TNFα
      • IL-8 + Histamine recruit PMNs
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14
Q

Describe the Acute Inflammatory Response phase

A

Kornman et al. 1997

4-8days

  • Tissue response to early signals
    • Vascular leakage
    • Leukocyte and Monocyte recruitment
    • Activated macrophages produce pro-inflammatory cytokines
    • Neutrophil wall formed between plaque and tissue
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15
Q

Describe the Immune Response phase

A

Kornman et al. 1997

2-3wks

  • Local/systemic immune response shaped by mononuclear cell activation
    • increase in Lymphocytes (T and B), Plasma cells (Antibody response), Macrophages
    • Plasma cells dominate > Produce IGs, IL-6, TNFα
    • Antibodies act locally and systemically
    • Macrophage products alter environment
      • Recruit additional monocytes
      • produce MMP
      • Alter collagen metabolism in local fibroblasts
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16
Q

Describe the Regulation and Resolution phase

A

Kornman et al 1997

no timeline

  • Determinants of protective components balance in the tissue
    • Host response has been impaired
      • Bacteria inhibit T and B cell response
      • Host modifiers (smoking, disease…) lead to more tissue destruction
    • Large number of T cells and Plasma cells
    • Accumulation of inflammatory mediators in local environment
    • Fibroblasts generate cytokines and collagenases (MMPs/TIMPs)

This sets the scene for initiation and progression of periodontitis

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17
Q

How does the proximity of the alveolar bone play a role in periodontal disease?

A

Proximity of bacteria to bone is one of the unique features of the oral cavity.

Graves et al. 2011

If inflammatory infiltrate is in close enough proximity to bone, osteoclastogenesis is stimulated.

If inflammatory infiltrate is at a distance - it is not

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18
Q

What study detailed the events in the progression of Gingivitis?

A

Page & Schroeder 1976

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19
Q

What are the 4 stages of gingivitis described in the landmark article?

A

Page & Schroeder 1976

Initial Lesion (2-4days)

Early Lesion (4-7days)

Established Lesion (14-21days)

Advanced Lesion (>21days)

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20
Q

Describe the Initial Lesion

A

Page & Schroeder 1976

2-4 Days

Location: Gingival Sulcus (JE and coronal aspect of CT)

Vascularity: Vasculitis

Cells: PMNs dominate (Macrophages and lymphocytes also present)

Collagen affected: Perivascular

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21
Q

Describe the Early Lesion

A

Page & Schroeder 1976

4-7 Days

Location: Gingival Sulcus (JE and small portion of CT)

Vascularity: more pronounced vasculitis

Cells: Lymphoid Cells make up 75%

Collagen affected: 60-70% lost - Dentogingival fibers supporting JE and gingival margin are lost

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22
Q

Describe the Established Lesion

A

Page & Schroeder 1976

2-3 weeks

Location: Gingival sulcus (JE and coronal aspect of CT

Vascularity: vascular proliferation

Cells: Plasma cells dominate

Collagen affected: Further loss - Fibrosis and Scarring

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23
Q

Describe the Advanced Lesion

A

Page & Schroeder 1976

>3wks

Location: Extends apically/laterally causing alveolar bone loss (Periodontitis)

Vascularity: “Acute exudative vasculitis”

Cells: Dense infiltrate of Plasma/Lymphocytes/Macrophages

Collagen affected: Continued loss adjacent to the pocket - Fibrosis and Scarring

24
Q

Name 2 landmark Experimental Gingivitis studies

A

Loe 1965

Theilade 1966

25
Q

Briefly describe the earliest Experimental Gingivitis study

A

Loe 1965

12 participants (9 dental students)

Refrained from OH and monitored inflammatory changes

Progression to gingivitis:
3 subjects: 10 days
9 subjects: 15-21 days

Inflammation was resolved within 1 week of resuming OH

First study to show that plaque causes gingivitis!

26
Q

Briefly describe the 2nd Experimental Gingivitis study

A

Theilade 1966

11 dental students

No OH

Progression to gingivitis:

  • Group 1: 9-13 days*
  • Group 2: 15 days*
  • Group 3: 17-21 days*

“Rapidly returned to pre-experimental levels” on reinstitution of OH

27
Q

How does the subgingival microbial profile change from health to disease?

A

Loe 1965 and Theilade 1966 both show:

Health

Gram (-) Rods and Cocci
-
Filamentous bacteria
-
Spirochetes

Disease

28
Q

What is primary etiology of periodontal disease?

A

Bacterial dysbiosis in a susceptible host

29
Q

Do all gingivitis cases progress to periodontitis? (Citation)

A

NO

Loe et al. 1986

30
Q

Describe the Sri Lankan tea laborer study

A

Loe et al. 1978/1986

1978 - compared Norwegian cohort (dental care) to Sri Lankan cohort (no dental care)
Found a continuous and even pace of progression (true today???)

1986 - followed up with Sri Lankan cohort to see rate of progression:

  • No progression: 11% (0.05-0.09mm/yr)
  • Moderate progression: 81% (0.05-0.5mm/yr)
  • Rapid progression: 8% (0.1-1mm/yr)
31
Q

What are the different plaque hypotheses?

A

Non-Specific Plaque Hypothesis

Specific Plaque Hyopothesis

Updated Non-Specific Plaque Hypothesis

Ecological Plaque Hypothesis

Polymicrobial Synergy and Dysbiosis

32
Q

What is the Non-Specific Plaque Hypothesis?

A

Miller 1890

Dental infection is caused by the non-specific overgrowth of all bacteria in dental plaque

33
Q

What is the Specific Plaque Hypothesis?

A

Loesche 1976 | Socransky et al. 1998

Dental infection is a result of specific bacteria in the dental plaque.

34
Q

What is the Updated Non-Specific Plaque Hypothesis?

A

Theilade 1986

Took into consideration that some indigenous bacteria can be more virulent than others, and that there is a change in the community from health to disease.

However, it remained that all bacteria in plaque contribute to the virulence by having a role in either colonization/evasion of defense/provocation of inflammation.

35
Q

What is the Ecological Plaque Hypothesis?

A

Marsh 1994

Disease is a result of an environmental shift in the plaque (pH, redox potential, nutrient availability) which aids certain (more virulent) pathogens

36
Q

What is the Polymicrobial Synergy and Dysbiosis Model?

A

Hajishengallis & Lamont 2012

Different members within the community fulfill distinct roles that converge to shape and stabilize a disease-provoking microbiota.

These communities require a ‘keystone pathogen’ to modulate the host response in ways that impair immune surveillance and tip the balance from homeostasis to dysbiosis.

37
Q

How does periodontal disease progress?

A

Can cycle from states of homeostasis to activity and back again - often in unpredictable ways

38
Q

What are 3 landmark studies on periodontal disease progression?

A

Socransky 1984

Jeffcoat and Reddy 1991

Teles et al. 2018

39
Q

What are the 3 models for disease progression in S84?

A

SoCRAnsky 1984

Continuous model

Random burst model

Asynchronous multiple burst model

40
Q

What is the Continuous Model of disease progression?

A

Socransky 1984

Some sites show progressive attachment loss over time while others sho no pregression.

41
Q

What is the Random Burst model of disease progression?

A

Socransky 1984

Activity is depicted as occurring at random at any site - some sites show no activity, while others show one or several bursts

42
Q

What is the Asynchronous Multiple Burst model of disease progression?

A

Socransky 1984

Several sites show repeated bursts of activity over a finite period, followed by prolonged inactivity before another burst.

43
Q

Jeffcoat and Reddy 1991

A

6mo prospective study measuring pockets

76% Linear progression
12% Burst (followed by quiescence)
12% Exacerbation/Remission (up-down-up-down)

29% of pockets had active disease

44
Q

Teles et al. 2018

A

Progression happens most on molars (50%) and interproximals (72%)

Main mode of progression: pocketing

Mean rate of progression in active site : 0.35mm/yr

45
Q

How does maintenance impact tooth loss over time?

A

Toothloss/year

Becker 1984a (perio tx + maintenance) 0.11/year

Becker 1984b (perio tx) 0.22/year

Becker 1979 (No tx) 0.36/year

46
Q

Name an important plaque index and explain it

A

Sillness and Loe 1964

0 - No plaque

1 - plaque confined to gingival margin not visible to the eye but w/ disclosing solution of probe

2 - plaque along the gingival margin that can be seen with the naked eye

3 - abudence of soft matter within the pocket or on the tooth into the interproximal zones

47
Q

What is an important Gingival Index?

A

Loe & Sillness 1963

0 - no inflammation

1 - mild inflammation/edema but no BOP

2 - moderate inflammation/glazing/redness/edema with BOP

3 - Severe inflammation/marked redness/ulcueration w/ possible spontaneous bleeding

48
Q

What is the Modified Gingival Index?

A

Lobene 1986

No BOP considered, just inflammation

0 - Normal

1 - Mild inflammation/slight change of a portion of the gingival unit

2 - Mild inflammation of entire unit

3 - Moderate inflammation of entire unit

4 - Severe inflammation of entire unit

49
Q

What is the Comunity Periodontal Index? Citation?

A

Ainamo 1982

CPITN - CPI for Treatment Needs (TN0/½/3)

0 - No pockets/BOP/Calc (no Tx/TN0)

1 - BOP (improve OH/TN1)

2 - Calc or overhang (scaling/improve OH/remove overhang/TN2)

3 - PD 4-5mm (scaling/improve OH/TN2)

4 - PD 6+mm (advanced treatment/TN3)

50
Q

What is the prevelance of Periodontitis according to CDC/AAP vs WW2017?

A

61.9% vs 100%!!!

488 participants from NHANES 2009-2010

Germen et al. 2021

51
Q

Which classification is better for epidemiological studies? Why and citation

A

CDC/AAP - Greater challenge in applying new case definitions to NHANES Data - lack of clinical data on case complexity - (mob, FI)

Ortigara et al. 2021

52
Q

What are some challenges with epidemiological studies?

A

Wide thresholds for disease

Full vs Partial mouth recording

Cross sectional data

Large dataset management

Not longitudinal

Sample selection (NHANES is black/non white while NIDR is employed)

Sample variation (age/sex/smoking…)

53
Q

Hirschfield & Wasserman 1978

A

Perio treatment provided!

Well maintained: 0-3 teeth lost (83%)

Downhill: 4-9 teeth lost (13%)

Extreme Downhill: 10+ Teeth lost (4.2%)

Mean tooth loss: 0.08/yr

Most common tooth lost - Max 2nd molar

Least common tooth lost - Mand canine

54
Q

How many years follow up was the Hirschfield & Wasserman study? How many teeth were lost per person in each group?

A

22yrs

  1. 68/person
  2. 7/person
  3. 3/person
55
Q

What trend with questionable teeth was seen in the Hirschfield & Wasserman study?

A

In the WM group, only 17% of teeth initially called questionable were lost and they made up the large majority of teeth lost

In the D and ED groups, Nearly all initially questionable teeth were lost by final follow up, and the made up less and less of the total (lost more normal teeth also)`

Classic Lit Fall 2021 (29 decks)

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