Etiology Flashcards
(80 cards)
1
Q
Periodontal Pathogenesis Factors
A
2
Q
Periodontal Pathogenesis flow chart
A
3
Q
Materia Alba
A
*White cheeselike accumulation
*A soft accumulation of salivary proteins, bacteria, desquamated epithelial cells, and food debris
*No organized structure
*Easily displaced with a water spray
4
Q
Dental Plaque
A
*Resilient clear to yellow-grayish substance
*Primarily composed of bacteria in a matrix of
salivary glycoproteins and bacterial products
*Considered to be a biofilm
*Impossible to remove by rinsing or spraying
5
Q
Calculus
A
*Mineralized dental plaque forms the hard
deposit
*Generally covered by a layer of unmineralized
dental plaque
6
Q
What is Dental Plaque?
A
The structurally and functionally organized,
species-rich microbial biofilms that form on teeth
7
Q
plaque is main etiology for?
A
Main etiology for
Periodontal diseases
Dental caries
8
Q
Dental Plaque
Composition
A
Water: 70% total
Microorganisms: 70% dry weight
Intracellular Matrix: 30% dry weight
9
Q
Dental Plaque Intracellular Matrix organic components
A
Polysaccharides
Proteins
Glycoproteins
Lipids
10
Q
dental plaque intracell matrix inorganic components
A
Calcium- Phosphorous
Other minerals
Sodium
Potassium
Fluoride
11
Q
- 1 gram of plaque contains approximately
____ bacteria
A
10^11
12
Q
- More than ____ distinct microbial species
can be identified with highly sensitive
molecular techniques in plaque
A
500
13
Q
Sites of Plaque Accumulation
A
Gingival thirds
Cracks, pits and fissures
Under overhanging restorations
Around malaligned teeth
14
Q
dental plaque location classification
A
Classification based on the position on the
tooth surface toward the gingival margin
Supragingival plaque
marginal plaque
Subgingival plaque
15
Q
Subgingival plaque types
A
*Tooth attached plaque
*Unattached plaque
*Epithelial associated plaque
16
Q
Supragingival plaque spp/morph? why? diversity?
A
Gram+ cocci and short rods
Aerobic environment
Slight diversity
17
Q
Subgingival plaque spp/morph? why? diversity?
A
Gram- rods and spirochete
Anaerobic environment
Great diversity
18
Q
Supragingival plaque can lead to:
A
Calculus formation and root caries
19
Q
Marginal plaque leads to:
A
Direct contact with gingival margin
Initiation and development of gingivitis
20
Q
subg plaque leads to:
A
Tissue destruction
21
Q
suprag and subg plaque with perio tx
A
Disruption of both is critical during periodontal treatment.
No supragingival plaque control following disruption of subgingival microflora allows rapid repopulation of microorganisms that could lead to periodontitis.
22
Q
Formation of Dental Plaque steps
A
Step 1: Formation of the pellicle
Step 2: Initial colonization of bacteria
Step 3: Secondary colonization and plaque
maturation
23
Q
Formation of the pellicle
A
24
Q
Initial colonization of bacteria
A
25
Secondary colonization and plaque maturation
26
Acquired pellicle
Adsorption of a conditioning film
- An organic material layer coated on all surfaces in the oral cavity, including hard and soft tissues.
- Components derived from saliva and crevicular fluid.
- Gram+ facultative microorganisms are involved
Initial stage of the development of the plaque
occurs at enamel within 1 min
27
Formation of the Pellicle: binding of 1 colonizers
interactions? effects of this? timeframe?
*Reversible adhesion between the microbial cell surface (adhesins) and the conditioning film (receptors)
- Alters the charge and the free energy of the surface which increases efficiency of the bacterial adhesion
occurs at enamel within 2 hrs
28
Initial Colonization
*Adherence - Coadhesion
- Primary colonizers - secondary colonizers
- Bacterial mass continue to grow
- Alteration in the oxygen gradient, anaerobic
conditions emerge in the deeper layers of the deposits
occurs at enamel with 4-8hrs
29
*Primary colonizers of plaque
mainly gram +
*Streptococcus spp.
*Hemophilus spp.
*Neisseria spp.
*Actinomyces spp.
*Veillonella spp.
She Has Nice Ass Viens
30
Secondary colonizers of plaque
Mainly gram -
*P. intermidia.
*Capnocytophaga spp.
*F. nucleatum
*P. gingivalis
penelope cant find purpose
31
Colonization and Maturation of plaque: coaggregation
seen?
where/when?
*Coaggregation
- Secondary colonizers adhere to the bacteria that are already in the plaque mass
- A significant feature can be seen by naked eye
- at enamel within 4-8hrs
32
plaque maturation
how?
quorum sensing?
when?
- Through further colonization and growth of additional species
- Quorum sensing: cell-cell signaling: Environment modification and metabolic interaction
- within 12hrs
33
bacterial detatchment from plaque
can detatch and colonize elsewhere
34
cell-cell comms in plaque
can comm to establish favorable environment (metabolics)
35
fluid channels in plaque
Open fluid-filled channels running through plaque mass, movement of nutrients
36
microenvironment of plaque
Distinct microenvironment produced by matrix
Steep chemical gradients (oxygen, pH)
37
Quorum sensing results in:
Quorum sensing results in bacterial resistance
38
Periodontal Microbiology:
Corn-cob formation
Coccal‐shaped cells attach along the tip of gram negative filamentous organisms
An example of inter-bacterial adherence or coaggregation
39
Dental calculus is:
calcified dental plaque, composed primarily of calcium phosphate mineral salts.
40
locations of calc
supra and sub g
41
supra vs subg calc
location?
detection?
color/texture?
source of mineral?
distribution?
42
Calculus Composition organic component
Leukocytes
Microorganisms
Desquamated epithelial cells
Protein polysaccharide complexes
43
Calculus Composition inorganic component
70 - 90% comprising of Calcium phosphate,
Calcium carbonate, Magnesium phosphate
44
Calculus Mineralization
- The mineralization starts in centers which arise intracellularly in bacterial colonies or extracellularly from matrix with crystallization nuclei
- At least 2/3 of the inorganic component is crystalline in structure.
45
main crystal forms of calculus
- Hydroxyapatite (HA) 58%
- Whitlockite (WHT) 21% may contain some Magnesium
- Octacalcium phosphate (OCP) 12%
- Brushite 9% only in early stage
46
supra vs subg calc deposition
- Supragingival calculus is deposited in layers;
Subgingival calculus is commonly deposited in
rings or ledges on root surfaces, but it may also
appear on veneers.
47
Plaque mineralization variabilty
reported as early as?
- Plaque mineralization varies between and within individuals and different region of oral cavity. Calcification has been reported as early as 4- 8 hours.
48
- Some subjects may form supra- gingival calculus in ___ weeks, at which time the deposit may already contain approximately ___% of the inorganic material found in mature calculus.
- Some subjects may form supra- gingival calculus in 2 weeks, at which time the deposit may already contain approximately 80% of the inorganic material found in mature calculus.
49
the formation of dental calculus with
the mature crystalline composition of old calculus may require how much time?
the formation of dental calculus with
the mature crystalline composition of old calculus may require months to years.
50
calculus on radiographs
- Low sensitivity: radiographic deposits were detected on only 44% of surfaces that demonstrated calculus microscopically.
- High positive predictive value - when you see radiographic calculus, 92% of the surfaces do have calculus microscopically.
51
Calculus Attachment Modes
1. Lock into areas of cementum resorption
2. Attach to irregularities of the cementum surface
3. By bacterial penetration into the cementum
4. By an organic pellicle
52
Calculus
Clinical Implications
- etiologic factor?
- It is always covered by? sphere influence?
tissues)
- It hinders?
- Calculus is a contributing factor or SECONDARY etiologic factor
- It is always covered by unmineralized viable
bacterial plaque. It extends the sphere of influence of bacterial plaque (keeps it in close contact with tissues)
- It hinders adequate plaque control
53
Microbiologic Specificity thru time
54
Nonspecific Plaque Hypothesis
- Direct relationship between?
- Concept inherited?
- Standard of care?
- Direct relationship between the total amount of plaque and the amplitude of the pathogenic effect
- Concept inherited: Control of periodontal disease depends on control of plaque accumulation
- Standard of care: oral hygiene measures, non-
surgical/ surgical debridement
55
Nonspecific Plaque Hypothesis contraindictions
- equally pathogenic?
- Gingivitis develop into destructive periodontitis?
- Site specificity?
- All plaque are not equally pathogenic
- Not all Gingivitis develop into destructive periodontitis
- Site specificity in the pattern of disease was demonstrated in some individuals with periodontitis
56
Specific Plaque Hypothesis
- The pathogenicity depends on?
- A. Actinomicetemcomitans?
- Targeted treatment?
- The pathogenicity depends on the presence of or increase in specific microorganisms
- A. Actinomicetemcomitans in localized aggresive periodontitis
- Targeted treatment strategies aim to control or eliminate the particular pathogenic organisms
57
Specific Plaque Hypothesis contraindication
Pathogens may be present at the absence of disease
58
Ecologic plaque Hypothesis
- Both the total amount of dental plaque and the specific microbial composition of plaque
may contribute
- Environmental factors drives the selection and enrichment of specific bacteria
- Microbial homeostasis: the state of the dynamic equilibrium
59
Polymicrobial Synergy and Disbiosis
Combines the concepts of “disrupted
homeostasis” and “keystone pathogen” but questions the primary importance of the red complex
current concept we use today
60
three bacteria to know
P gingivalis
P denticola
T forsynthia
61
Kochs Postulates
*Be routinely isolated from diseased individuals
*Be grown in pure culture in lab
*Produce a similar disease when inoculated into susceptible lab animals
*Be recovered from lesions in a diseases lab animal
62
Socransky’s Criteria
*Be associated with?
*Be eliminated or decreased?
*Demonstrate a alteration in?
*Be capable of causing disease in?
*Demonstrate?
*Be associated with disease
*Be eliminated or decreased in sites that demonstrate clinical resolution
*Demonstrate a alteration in host cellular or immune response
*Be capable of causing disease in experimental models
*Demonstrate virulence factors
63
criteria for Identification of Periodontopathogens
Kochs Postulates and Socransky’s Criteria
64
A. Actinomycetemcomitans
Association:
Elimination:
Host response:
animal studies:
VF:
Association: Increased in localized aggressive periodontitis lesions. Some in chronic periodontitis lesions.
Elimination: Suppressed or eliminated in successful therapy, can be found in recurrent lesions
Host response: Increased serum and local antibody levels
Animal studies: Capable of inducing disease in gnotobiotic rats
Virulence factors: Host tissue cell adherence and invasion, leukotoxin, protease, collagenase, epitheliotoxin, FIF, bone resorption inducing factors
65
P. Gingivalis
Association
Elimination
Host response
Animal studies
Virulence factors
Association: Increased in periodontitis lesions, found associated with the crevicular epithelium
Elimination: Suppressed or eliminated in successful therapy, can be found in recurrent lesions
Host response: Increased systemic and local antibody levels
Animal studies: Important in experimental mixed infections
Virulence factors:Host tissue cell adherence and invasion, trypsin-like enzyme, collagenase, fibrinolysis, phospholipase A, endotoxin, gingipains, factors that affect PMN function
66
Toxins and enzymes of bacteria
* Bacterial products that promote tissue destruction:
lipopolysaccharides(LPS), leukotoxin, gingipains,
collagenase, protease
67
Adhesins of bacteria
* Factors that promote colonization: fimbria, gingipains
68
Evading mechanisms of bacteria
* The production of an extracellular capsule
* Proteolytic degradation of host immunity components: gingipains
* Modulate host response: bind serum components on bacterial cell surface
* Invasion of gingival epithelial cells: lipopolysaccharides(LPS)
69
Virulence
Factors of bac
Toxins and enzymes
Adhesins
Evading mechanisms
70
Bacteria of Gingivitis
Actinomyces spp.
Capnocytophaga spp.
Campylobacter spp.
Streptococcus spp.
Parvimonas micra
Fusobacterium nucleatum
Prevotella intermedia
Treponema spp.
71
Bacteria of Periodontitis
Aggregatibacter actinomycetemcomitans (Type b)
Porphyromonas gingivalis
Prevotella intermedia
Parvimonas micra
Fusobacterium nucleatum
Tannerella forsythia
Treponema denticola
Spirochetes
72
Bacteria of Necrotizing Periodontal DIsease
F. nucleatum
P. intermedia
Treponema spp.
Spirochetes
for penelope this sucks
73
Bacteria Associated with Pregnancy and Puberty
Prevotella intermedia
Capnocytophaga spp.
Gingival inflammation results from an increased secretion of sex steroid hormones during puberty/pregnancy
74
Bacteria in Abscess of the Periodontium
Fusobacterium nucleatum
Parvimonas micra
Prevotella intermedia
Porphyromonas gingivalis
Spirochetes
75
Bacteria of peri-implantitis
Comparable microbiota to that of periodontitis
76
Healthy Versus Diseased Sites environments
gram? shape? motility?
aerobic? metabolism?
77
Transmission of Periodontal Pathogens
source? pathogens? routes?
Periodontal pathogens are communicable but not readily transmissible
78
Goals of Plaque Control
Disrupt ecological succession
Reduce degree of organization
“Healthy” plaque (G+, aerobic, indigenous flora)
Shift in flora compatible with health
79
future individualization of tx
Modulating host response (i.e. Resolvins)
Antibiotics
Target proteins that are essential for the maintenance of Biofilm
Limitation of the identifying the microbial risk markers
80
future individualization of tx
Modulating host response (i.e. Resolvins)
Antibiotics
Target proteins that are essential for the maintenance of Biofilm
Limitation of the identifying the microbial risk markers
