Epidemiology and Pathogenesis of Perio Flashcards
Define Pathogenesis
the biological mechanism that leads to the diseased state.
Define Epidemiology
The science that studies the patterns, causes, and effects of health and disease in defined populations.
What is Prevalence
The proportion of a population who had/have a specific characteristic at a given time - regardless of when they first acquired it
What is Incidence
The measure of number of new cases that arise in a population over a given time period
What is the GLOBAL prevalence of periodontal disease?
Richards et al. 2014
Data from the Global Burden of Disease
Prevalence of Severe Periodontitis: 11%
What is the prevalence of periodontitis in the US?
Eke et al. 2018
Data from the National Health and Nutrition Examination Survey (NHANES)
2009-2014
42% of US has Periodontitis
According to Eke et al. 2018 - how does the prevalence of Mild/Mod/Severe perio change with age?
Mild and Moderate prevalence increased with age
Severe prevalence remained below 15% all age groups
According to Eke et al. 2018 what groups is perio most prevalent among?
Mexican Americans > non-Hispanic African Americans > …
current smokers, non-regular flossers, non-compliant patients (no dental visit >6mo)
What groups are Severe Perio most prevalent in according to Eke et al. 2018?
3x greater prevalence in Mexican Americans, non-Hispanic blacks, and current smokers
What role does age have on development of periodontitis?
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
What is one study that describes the pathogenesis of periodontal disease?
Kornman et al. 1997
What are the 4 phases that describe that pathogenesis of periodontal disease?
Kornman et al. 1997
- Acute bacterial challenge phase*
- Acute inflammatory response phase*
- Immune response phase*
- Regulation and resolution phase*
Describe the Acute Bacterial Challenge phase
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
Describe the Acute Inflammatory Response phase
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
Describe the Immune Response phase
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
Describe the Regulation and Resolution phase
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)
- Host response has been impaired
This sets the scene for initiation and progression of periodontitis
How does the proximity of the alveolar bone play a role in periodontal disease?
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
What study detailed the events in the progression of Gingivitis?
Page & Schroeder 1976
What are the 4 stages of gingivitis described in the landmark article?
Page & Schroeder 1976
Initial Lesion (2-4days)
Early Lesion (4-7days)
Established Lesion (14-21days)
Advanced Lesion (>21days)
Describe the Initial Lesion
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
Describe the Early Lesion
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
Describe the Established Lesion
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
Describe the Advanced Lesion
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
Name 2 landmark Experimental Gingivitis studies
Loe 1965
Theilade 1966
Briefly describe the earliest Experimental Gingivitis study
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!
Briefly describe the 2nd Experimental Gingivitis study
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
How does the subgingival microbial profile change from health to disease?
Loe 1965 and Theilade 1966 both show:
Health
Gram (-) Rods and Cocci
-
Filamentous bacteria
-
Spirochetes
Disease
What is primary etiology of periodontal disease?
Bacterial dysbiosis in a susceptible host
Do all gingivitis cases progress to periodontitis? (Citation)
NO
Loe et al. 1986
Describe the Sri Lankan tea laborer study
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)
What are the different plaque hypotheses?
Non-Specific Plaque Hypothesis
Specific Plaque Hyopothesis
Updated Non-Specific Plaque Hypothesis
Ecological Plaque Hypothesis
Polymicrobial Synergy and Dysbiosis
What is the Non-Specific Plaque Hypothesis?
Miller 1890
Dental infection is caused by the non-specific overgrowth of all bacteria in dental plaque
What is the Specific Plaque Hypothesis?
Loesche 1976 | Socransky et al. 1998
Dental infection is a result of specific bacteria in the dental plaque.
What is the Updated Non-Specific Plaque Hypothesis?
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.
What is the Ecological Plaque Hypothesis?
Marsh 1994
Disease is a result of an environmental shift in the plaque (pH, redox potential, nutrient availability) which aids certain (more virulent) pathogens
What is the Polymicrobial Synergy and Dysbiosis Model?
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.
How does periodontal disease progress?
Can cycle from states of homeostasis to activity and back again - often in unpredictable ways
What are 3 landmark studies on periodontal disease progression?
Socransky 1984
Jeffcoat and Reddy 1991
Teles et al. 2018
What are the 3 models for disease progression in S84?
SoCRAnsky 1984
Continuous model
Random burst model
Asynchronous multiple burst model
What is the Continuous Model of disease progression?
Socransky 1984
Some sites show progressive attachment loss over time while others sho no pregression.
What is the Random Burst model of disease progression?
Socransky 1984
Activity is depicted as occurring at random at any site - some sites show no activity, while others show one or several bursts
What is the Asynchronous Multiple Burst model of disease progression?
Socransky 1984
Several sites show repeated bursts of activity over a finite period, followed by prolonged inactivity before another burst.
Jeffcoat and Reddy 1991
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
Teles et al. 2018
Progression happens most on molars (50%) and interproximals (72%)
Main mode of progression: pocketing
Mean rate of progression in active site : 0.35mm/yr
How does maintenance impact tooth loss over time?
Toothloss/year
Becker 1984a (perio tx + maintenance) 0.11/year
Becker 1984b (perio tx) 0.22/year
Becker 1979 (No tx) 0.36/year
Name an important plaque index and explain it
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
What is an important Gingival Index?
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
What is the Modified Gingival Index?
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
What is the Comunity Periodontal Index? Citation?
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)
What is the prevelance of Periodontitis according to CDC/AAP vs WW2017?
61.9% vs 100%!!!
488 participants from NHANES 2009-2010
Germen et al. 2021
Which classification is better for epidemiological studies? Why and citation
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
What are some challenges with epidemiological studies?
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…)
Hirschfield & Wasserman 1978
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
How many years follow up was the Hirschfield & Wasserman study? How many teeth were lost per person in each group?
22yrs
- 68/person
- 7/person
- 3/person
What trend with questionable teeth was seen in the Hirschfield & Wasserman study?
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)`
