Etiology, Contributing Factors and Link to Systemic Disease Flashcards
(89 cards)
1
Q
Define risk factor
A
A characteristic that places and individual at increased risk of contracting a disease
2
Q
Define risk indicator
A
A probable or putative risk factor that has been identified in cross-sectional correlation studies but not confirmed through longitudinal studies
3
Q
4 risk factors for periodontitis
A
- Diabetes
- Inadequate oral hygiene
- Genetics
- Smoking
4
Q
8 risk indicators for periodontitis
A
- Socio-economic status
- Obesity
- Stress
- Age
- Contraceptives
- Alcohol
- Race
- Sex
5
Q
Define etiology
A
The study or theory of the causation of a disease
A single or a cluster of factors that contribute to disease
6
Q
Role of bacterial plaque in periodontal disease
A
Necessary but not sufficient to cause disease
7
Q
Primary etiologic factor of periodontitis
A
Microbial plaque
8
Q
Secondary etiologic factor of periodontitis
A
Calculus (most significant local contributing factor)
9
Q
3 characteristics of bacteria related to health
A
- Gram positive
- Facultatives anaerobes
- Generally non motile
i.e. streptococcus anguis and mitus, actinomyces viscosus, israelli and naeslundi
10
Q
3 characteristics of bacteria related to disease
A
- Gram negative
- Strict anaerobes
- Motile & non-motile forms
11
Q
What is the pathogenic potential of calculus?
A
- Plaque retention
- Production of an inflammatory reaction in the tissue
12
Q
3 bacterial species in the red category
A
- P. gingivalis
- T. forsythensis
- T. denticola
13
Q
11 local and anatomical factors contributing to periodontal disease
A
- Root morphology
- Furcation
- Cervico-enamel projections (CEP)
- Enamel pearls
- Palatogingival grooves
- Root proximity
- Food impaction/open contacts
- Marginal ridge discrepancy (plunger cusp)
- Restorations (quality of restorative margins, contours, curvatures, etc)
- Position of tooth
- Caries
14
Q
Anatomic variation of furcation that creates a protected environment for plaque and calculus collection
A
Internal intra-radicular root concavities
15
Q
Significance of accessory canals for periodontal disease
A
Communication between the pulp and the furcation
Endo-perio or perio-endo lesions
16
Q
How do cervico-enamel projections contribute to periodontal disease?
A
Acts like a pathway for transferring the plaque to the furcation
17
Q
Define enamel pearls
A
Localized masses of enamel that develop ectopically, typically over the root surfaces in close proximity to the CEJ
18
Q
How do open contacts contribute to periodontal disease?
A
Food impaction
19
Q
Define palato-gingival groove
A
Groove in the enamel of the tooth leading into the gingiva. Site of bacterial and plaque accumulation.
20
Q
7 systemic factors contributing to periodontal disease
A
- Smoking
- Stress
- Medical conditions
- Medications
- Genetics
- Age
- Sex
21
Q
4 effects of smoking on periodontium
A
- Increases the prevalence and severity of destruction
- Increase in PD, CAL and bone loss
- Increased rate of destruction
- Increased number of tooth loss
NOTE: These negative effects are cumulative over time with increased smoking. However, these same effects will decrease with cessation
22
Q
Mechanism of periodontitis associated with diabetes
A
- Altered neutrophil response
- Upregulation of monocutes –> hyper-inflammatory response
- AGE-RAGE interaction may lead to increased production of inflammatory cytokines in the diabetic patient
23
Q
Earlier theory of etiology of periodontal disease (5 points)
A
- All individuals are equally susceptible to periodontitis
- Always starts with gingivitis and if not treated will progress to periodontitis
- As people age the chances of getting periodontitis goes higher
- Plaque, calculus and other local factors are the only contributors to periodontal disease
- NO ROLE OF HOST SUSCEPTIBILITY
24
Q
Today’s theory of etiology of periodontal disease
A
- Not all individuals are equally susceptible to periodontal disease
- Gingivities doesn’t always progress to periodontitis
- Prevalence and severity of periodontal disease increased with age but susceptibility to future periodontal disease is not dependent upon age
- Systemic and environmental factors play a role in progression of the disease
- BUT HOST SUSCEPTIBILITY PLAYS A MAJOR ROLE
25
Define the non-specific plaque hypothesis
Periodontal disease results from the "elaboration of noxious products by the entire plaque flora". If small amounts of plaque are present, the noxious products are neutralized by the host. But if large amounts are present, this overwhelms the host's defenses.
The control of periodontal disease depends on control of the amount of plaque accumulation
26
Define the specific plaque hypothesis
* Only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microorganisms
* Acceptance of this hypothesis was spurred by the recognition of a.a. as a pathogen in localized aggressive periodontitis
27
Define biofilm
Multi-species community of microorganisms that adhere to each other and a surface, and are encased in an extracellular matrix
28
Define virulence factor
The unique properties which permit a bacterial species to **colonize** a target organ, **defend** itself from the host and cause **tissue damage**
29
2 categories of virulence factors
1. Factors favoring bacterial adherence and colonization
2. Factors which mediate host tissue destruction
30
Adherence factors of subgingival species
Adhesions including fimbriae and cell-associated proteins
31
Define lipopolysaccharides
Large molecules composed of a lipid component (lipid A) and a polysaccharide component. They are found in the outer membrane of gram-negative bacteria. Act as andotoxins and elicit strong immune responses.
32
5 host defense mechanisms that must be overcome to induce periodontitis
* Salivary and gingival crevicular fluid flow
* Mechanical displacement (i.e. tissue desquamation)
* Specific antibodies
* Host products (i.e. glycoproteins that block bacterial cell binding)
* Cells of the immune system
33
2 bacterial mechanisms that may mediate host tissue damage
* Invasion of the tissue by pathogens
* Diffusion of bacterial byproducts from the crevice into the gingival tissues
34
4 examples of bacterial byproducts that may diffuse from the crvice into the gingival tissues to mediate host tissue damage
* Ammonia (NH)
* Hydrogen sulfide (HS)
* Short-chain carboxylic acids (i.e. butyric acid and propionic acid)
* Proteases
35
Define yellow complex bacteria
Early colonizers; most associated with caries formation
36
Complexes that include microorganisms primarily considered to be secondary colonizers
Green, orange or red
37
Complex associated with bleeding probing
Red complex
38
Describe the bacterial properties of P. gingivalis
Gram negative, rod-shaped, anaerobic
39
5 virulence factors of P. gingivalis that make it an aggressive periodontal pathogen
* Fimbriae --\> adhesion
* Capsule --\> protection against phagocytic cells
* Proteases
* Hemolysin
* Collagenase
40
Describe how P. gingivalis is virulent
Can inhibit the migration of PMN's across an epithelial barrier and affects production or degradation of cytokines by mammalian cells. Has the capacity to invade soft tissues
41
Describe the bacterial properties of T. Forsythia
Anaerobic, gram-negative nonmotile, spindle-shaped pathogen
42
2 virulence factors of T. forsythia
* Proteolytic enzymes that destroy immunoglobulins and factors of the complement system
* Induces apoptotic cell death
43
Describe the bacterial properties of T. denticula
* Gram-negative
* Obligate anaerobe
* Motile
* Highly protelytic spichete bacterium
44
4 virulence factors of T. denticula
* Produces proteolytic enzymes that can destroy Ig's (IgA, IgM, IgG) or complement factors
* Has capacity to destroy collagen
* Has ability to travel through viscous media and tissue
* Can pass through GCF and penetrate gingival epithelium and connective tissue
45
Describe the bacterial properties of aggregatibacter actinomycetemcomitans
* Gram-negative
* Facultative nonmotile
* Rod-shaped
46
5 virulence factors of aggregatibacter actinomycetemcomitans
* Very tissue invasive
* Lipopolysaccharide cell wall: endotoxin
* Leukotoxin
* Collagenase
* Proteases that destroy IgG
47
Define leukotoxin
Toxin which creates micro-pores in PMNs, monocytes and some lymphocytes and causes their cell deaths
48
What does the majority of the tissue damage in periodontitis derive from?
The excessive and dysregulated production of a variet of inflammatory mediators and destructive enzymes in response to the presnece of the subgingival plaque bacteria
49
3 key types of mediators of tissue destruction in periodontitis
* Cytokines
* Prostanoids
* Matrix metalloproteinases (MMPs)
50
2 cytokines that play a key role in the initiation, regulation and perpetuation of innate immune responses in the periodontium
IL-1B
TNF-a
51
3 prostanoids
* PGs
* Thromboxanes
* Prostacyclins
52
Effect of PGE2
Vasodilation and induction of cytokine production by a variety of cel types
53
3 upregulators of COX-2
IL-1B
TNF-a
Bacterial LPS
54
Result of upregulation of COX-2
Increased production of PGE2 in inflamed tissues
55
2 cell types that produce PGE2 in the periodontium
Macrophages
Fibroblasts
56
Effect of PGE2 production
Induction of MMPs and osteoclastic bone resorption. Major role in contributing ot the tissue damage that characterizes periodontitis
57
Define MMPs
A family of proteolytic enzymes that degrade extracellular matrix molecules such as collagen, gelatin, and elastin
58
6 cell types that produce MMPs
* Neutrophils
* Macrophages
* Fibroblasts
* Epithelial cells
* Osteoblasts
* Osteoclasts
59
4 histologic stages of gingivitis and periodontitis
* Initial lesion
* Early lesion
* Established lesion
* Advanced lesion
60
3 characteristics of the initial lesion
Clinically healthy gingival tissue:
* Slightly elevated vascular permeability and vasodilation
* GCF flows out of the sulcus
* Migration of leukocytes, primarily neutrophils, in relatively small numbers through the gingival connective tissue, accross the junctional epithelum and into the sulcus
61
5 characteristics of the early lesion
Corresponds to early gingivitis that is evident clinically:
* Increased vascular permeability, vasodilation, and GCF flow
* Large numbers of infiltrating leukocytes
* Degeneration of fibroblasts
* Collagen destruction --\> collagen depleted areas of connective tissue
* Proliferation of the junctional and sulcular epithelium into collagen-depleted areas
62
2 main leukocytes present in early lesion
Neutrophils and lymphocytes
63
5 characteristics of established lesion
Corresponds to established, chronic gingivitis
* Dense inflammatory cell infiltrate
* Accumulation of inflammatory cells in the connective tissues
* Elevated release of MMPs and lysosomal contents from neutrophils
* Significant collagen depletion and proliferation of epithelium
* Formation of pocket epithelium containing large numbers of neutrophils
64
3 cell types in the inflammatory cell infiltrate of the established lesion
Plasma cells, lymphocytes and neutrophils
65
5 characteristics of the advanced lesion
Marks the transition from gingivitis to periodontitis
* Predominance of neutrophils in the pocket epithelium and in the pocket
* Dense inflammatory cell infiltrate in the connective tissues
* Apical migration of junctional epithelium to preserve intact epithelial barrier
* Continued collagen breakdown --\> large areas of collagen depleted connective tissue
* Osteoclastic resorption of alveolar bone
66
Primary cell type in inflammatory cell infiltrate of the advanced lesion
Plasma cells
67
Body's first response to injury
Inflammation
68
5 characteristics of acute inflammation
* Redness
* Swelling
* Heat
* Altered function
* Self-perpetuating
69
One important inflammation marker found in the blood
C-reactive protein (CRP)
70
Significance of elevated CRP
It's a risk factor for several chronic inflammatory diseases
71
3 diseases of aging for which inflammation appears to be a common link
Heart disease
Arthritis
Periodontitis
72
Purpose of inflammation
To contain the injury to the local site in an immediate reaction in order to protect the body from further damage
73
When does chronic inflammation occur?
When there is sustained infection (i.e. periodontitis)
74
How does periodontitis affect your general systemic health?
It is a significant contributor to the total inflammatory burden on your body and can adversely affect your systemic health. It shares common inflammatory processes similar to diabetes, CVD and stroke
75
What is the link between periodontitis and cardiovascular disease?
* Inflammation contributes to heart attacks as much as or more than cholesterol
* Artherosclerosis always begins with injury to the endothelium of blood vessels
* Periodontal pathogens have been found in atherosclerotic lesions
76
3 distinct pathways through which gingival inflammation may influence atherosclerosis
* Local inflammation processes from periodontal pockets produce micro-ulcerations through the pocket epithelium, promoting risks for distant-site infection and transient bacteremia
* Bacteria release biologically active molecuels (i.e. LPS, endotoxins, chemotactic peptides, proteins, organic acids) that may enter the systemic circulation
* These products can trigger the host inflammatory response and elevate serum concentrations of acute-phase reactants and inflammatory mediators
77
7 inflammatory mediators that may be elevated when periodontal bacteria release biologically active molecules
* CRP
* Serum amyloid A
* Fibrinogen
* Haptoglobin
* TNF-a
* IL-6
* IL-8
78
5 inflammatory diseases with which periodontal disease has a relationship
* CVD
* Arthritis
* Alzheimer's Disease
* Diabetes
* Cancers
79
Effect of chronic periodontal disease exposure on risk of developing Alzheimer's disease
It quadruples the individual's risk
80
Effect of hyperglycemia on inflammation
Inhibition of resolution of inflammation
81
Effect of CRP on insulin resistance
High CRP promotes insulin resistance
82
Link between diabetes and likelihood of having periodontal disease
Patients with diabetes are 3 times more likely to have periodontal disease
83
Specific interaction in diabetes that leads to the exaggerated inflammatory response and periodontal tissue destruction
AGE-RAGE interaction
NOTE: AGEs directly and indirectly promote inflammation
84
2 cancers with a positive correlation between risk of development and presence of periodontal disease
Pancreatic cancer
Head and neck cancers
85
Link of obesity to periodontitis
* Patients with higher BMI tend to have higher levels of CRP
* Calorie reduction --\> decreased gingival bleeding and rate of periodontal disease progression
86
4 inflammatory mediators associated with adverse pregnancy outcomes
* IL-1
* IL-6
* TNF-a
* PGE2
87
3 types of systemic risk factors for periodontal disease
* Biologic
* Genetic
* Behavioral
88
3 ways genetic risk factors can be minimized
* Proper diet
* Exercise
* Oral hygiene
89
5 behavioral risk factors for periodontal disease
* Poor oral hygiene
* Smoking (specifically, nictine intake)
* Stress
* Sleep deprivation
* Poor diet
