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Etiology Flashcards

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1
Q

Periodontal Pathogenesis
Environment factors:
Microbial factors:
Host factors:

A

smoking
plaque/biofilm
susceptibility

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2
Q

Materia Alba
(4)

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

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3
Q

Dental Plaque
(4)

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

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4
Q

Calculus
(2)

A

*Mineralized dental
plaque forms the hard
deposit
*Generally covered by a
layer of unmineralized
dental plaque

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5
Q

What is
Dental Plaque?

A

The structurally and
functionally organized,
species-rich
microbial biofilms
that form on teeth

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6
Q

Main etiology for
Periodontal diseases

A

Dental caries

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7
Q

Dental Plaque
Composition (3)

A

Water 70%
Microorganisms 70% (dry weight)
Intracellular Matrix 30% (dry weight)

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8
Q

Dental Plaque
Intracellular Matrix
Organic component
(4)

A

Polysaccharides
Proteins
Glycoproteins
Lipids

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9
Q

Dental Plaque
Intracellular Matrix
Inorganic component
(4)

A

Calcium
Phosphorous
Other minerals
Sodium
Potassium
Fluoride

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10
Q

1 gram of plaque contains approximately
— bacteria
(And human body has approximately 1012 bacteria)

A

10^11

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11
Q

More than — distinct microbial species
can be identified with highly sensitive
molecular techniques

A

500

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12
Q

What is dental plaque?

A

B. It is the structurally and functionally organized, species‐rich
microbial biofilm that form on teeth.

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13
Q

Sites of Accumulation
(4)

A

Gingival thirds
Cracks, pits and fissures
Under overhanging restorations
Around malaligned teeth

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14
Q

Classification
based on the position on the
tooth surface toward the
gingival margin (3)

A

Supragingival plaque
Marginal plaque
Subgingival plaque

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15
Q

Subgingival plaque
(3)

A

*Tooth attached
plaque
*Unattached plaque
*Epithelial associated
plaque

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16
Q

Supragingival plaque

A

Gram+ cocci and short rods
Aerobic environment
Slight diversity

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17
Q

Subgingival plaque

A

Gram- rods and spirochete
Anaerobic environment
Great diversity

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18
Q

Supragingival plaque
result

A

Calculus formation and root caries

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19
Q

Marginal plaque
result

A

Direct contact with gingival margin
Initiation and development of gingivitis

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20
Q

Subgingival plaque
result

A

Tissue destruction

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21
Q

Supragingival plaque
Subgingival plaque
Disruption of both is critical during
periodontal treatment.
why?

A

No supragingival plaque control
following disruption of subgingival
microflora allows rapid repopulation of
microorganisms that could lead to
periodontitis.

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22
Q

Formation of Dental Plaque
(3)

A

Step 1:
Formation of the pellicle
Step 2:
Initial colonization of bacteria
Step 3:
Secondary colonization and plaque
maturation

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23
Q

Acquired pellicle:

A

Adsorption of a conditioning film
- An organic material layer coated on all surfaces in
the oral cavity, including hard and soft tissues.

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24
Q

Acquired pellicle
Components derived from

A

saliva and crevicular
fluid.

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25
Acquired pellicle bacteria
Gram+ facultative microorganisms are involved
26
Initial stage of the development of the plaque
acquired pellicle
27
Formation of the Pellicle
*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
28
Pellicle serves as a
protective barrier
29
Initial Colonization *Adherence - Coadhesion (3)
- Primary colonizers - secondary colonizers - Bacterial mass continue to grow - Alteration in the oxygen gradient, anaerobic conditions emerge in the deeper layers of the deposits
30
SKIPPED Primary colonizers (5)
*Streptococcus spp. *Hemophilus spp. *Neisseria spp. *Actinomyces spp. *Veillonella spp.
31
SKIPPED Secondary colonizers (4)
*Prevotella intermidia. *Capnocytophaga spp. *Fusobacterium nucleatum *Porphyromonas gingivalis
32
Colonization and Maturation Coaggregation (2)
- Secondary colonizers adhere to the bacteria that are already in the plaque mass - A significant feature can be seen by naked eye
33
Maturation (2)
- Through further colonization and growth of additional species - Quorum sensing: cell-cell signaling
34
- Quorum sensing: cell-cell signaling (2)
- Environment modification - metabolic interaction
35
Structure of Dental Plaque --- running through plaque mass Distinct --- produced by matrix Steep --- --- results in bacterial resistance
Open fluid-filled channels microenvironment Chemical gradients (oxygen, pH) Quorum sensing
36
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
37
Dental calculus is
calcified dental plaque, composed primarily of calcium phosphate mineral salts.
38
Calculus Location: Supragingival Detection Color/Texture Source of mineralization Distribution
At or above the gingival margin Visual Creamy-whitish to dark yellow or even brownish mass of moderate hardness Saliva Buccal Max. molars & Lingual Mand. incisors
39
Calculus Location: Subgingival Detection Color/Texture Source of mineralization Distribution
Below the gingival margin Tactile or Radiographic Brownish to black calcified hard mass GCF varies
40
Calculus Composition Organic component (4)
Leukocytes Microorganisms Desquamated epithelial cells Protein polysaccharide complexes
41
Calculus Composition Inorganic component 70 - 90% comprising of (3)
Calcium phosphate Calcium carbonate Magnesium phosphate
42
Calculus Mineralization (2)
- 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.
43
Four main crystal forms:
- Hydroxyapatite (HA) 58% [Ca10(PO4)6(OH)2] - Whitlockite (WHT) 21% [Ca10(HPO4)(PO4)6 ] may contain some Magnesium - Octacalcium phosphate (OCP) 12% [Ca8(PO4)4(HPO4)25HO] - Brushite 9% [CaHPO4-2H2O] only in early stage
44
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.
45
vPlaque mineralization varies between and within individuals and different region of oral cavity. Calcification has been reported as early as
4- 8 hours.
46
Some subjects may form supra- gingival calculus in 2 weeks, at which time the deposit may already contain approximately ---% of the inorganic material found in mature calculus.
80
47
Nevertheless, the formation of dental calculus with the mature crystalline composition of old calculus may require
months to years.
48
Evaluation of calculus by conventional radiography showed - Low sensitivity: - High positive predictive value -
radiographic deposits were detected on only 44% of surfaces that demonstrated calculus microscopically. when you see radiographic calculus, 92% of the surfaces do have calculus microscopically.
49
Four modes of calculus attachment (4)
- Lock into areas of cementum resorption - Attach to irregularities of the cementum surface - By bacterial penetration into the cementum - By an organic pellicle
50
Calculus is a contributing factor or --- etiologic factor
SECONDARY
51
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)
52
It hinders adequate --- control
plaque
53
1900s 1960s 1990s
Nonspecific Plaque Hypothesis Specific Plaque Hypothesis Ecologic plaque Hypothesis
54
Nonspecific Plaque Hypothesis (4)
- 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 - All plaque are not equally pathogenic
55
- All plaque are not equally pathogenic (2)
- 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 the presence of or increase in
specific microorganisms - A. Actinomicetemcomitans in localized aggresive periodontitis
57
Specific Plaque Hypothesis - Targeted treatment strategies aim to
control or eliminate the particular pathogenic organisms
58
Specific Plaque Hypothesis are pathogens present or absent in disease?
!!!Pathogens may be present at the absence of disease!!!
59
microbes to know (3)
P. gingivalis B. forsythus T. denticola
60
microbes present without disease
***B. forsythus ->T. forsythensis ->T. forthysia
61
Ecologic plaque Hypothesis Microbiologic Specificity (3)
- 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
62
Polymicrobial Synergy and Disbiosis
Combines the concepts of “disrupted homeostasis” and “keystone pathogen” but questions the primary importance of the red complex
63
Kochs Postulates Criteria for Identification of Periodontopathogens *Be routinely isolated from *Be grown in *Produce a similar disease when *Be recovered from lesions in a
diseased individuals pure culture in lab inoculated into susceptible lab animals diseases lab animal
64
Socransky’s Criteria *Be --- with disease *Be --- or decreased in sites that demonstrate clinical resolution *Demonstrate a alteration in *Be capable of causing disease in *Demonstrate
associated eliminated host cellular or immune response experimental models virulence factors
65
A. Actinomycetemcomitans Association
Increased in localized aggressive periodontitis lesions. Some in chronic periodontitis lesions.
66
A. Actinomycetemcomitans Elimination
Suppressed or eliminated in successful therapy, can be found in recurrent lesions
67
A. Actinomycetemcomitans Host response
Increased serum and local antibody levels
68
A. Actinomycetemcomitans Animal studies
Capable of inducing disease in gnotobiotic rats
69
A. Actinomycetemcomitans Virulence factors
Host tissue cell adherence and invasion, leukotoxin, protease, collagenase, epitheliotoxin, FIF, bone resorption inducing factors
70
P. Gingivalis Association
Increased in periodontitis lesions, found associated with the crevicular epithelium
71
P. Gingivalis Elimination
Suppressed or eliminated in successful therapy, can be found in recurrent lesions
72
P. Gingivalis Host response
Increased systemic and local antibody levels
73
P. Gingivalis Animal studies
Important in experimental mixed infections
74
P. Gingivalis Virulence factors
Host tissue cell adherence and invasion, trypsin-like enzyme, collagenase, fibrinolysis, phospholipase A, endotoxin, gingipains, factors that affect PMN function
75
P. gingivalis is known as a notorious periodontal pathogen. Which complex of color does it belong to? A. Yellow complex B. Green complex C. Orange complex D. Red complex
D. Red complex
76
Toxins and enzymes
* Bacterial products that promote tissue destruction: lipopolysaccharides(LPS), leukotoxin, gingipains, collagenase, protease
77
Adhesins
* Factors that promote colonization: fimbria, gingipains
78
Evading mechanisms * The production of an extracellular --- * Proteolytic degradation of host immunity components: * Modulate host response: * Invasion of gingival epithelial cells:
capsule gingipains bind serum components on bacterial cell surface lipopolysaccharides(LPS)
79
Bacteria of Gingivitis (8)
Actinomyces spp. Capnocytophaga spp. Campylobacter spp. Streptococcus spp. Parvimonas micra Fusobacterium nucleatum Prevotella intermedia Treponema spp.
80
Bacteria of Periodontitis Specific Bacteria in Disease (8)
Aggregatibacter actinomycetemcomitans (Type b) Porphyromonas gingivalis Prevotella intermedia Parvimonas micra Fusobacterium nucleatum Tannerella forsythia Treponema denticola Spirochetes
81
Bacteria of Necrotizing Periodontal DIsease (4)
Fusobacterium nucleatum Prevotella intermedia Treponema spp. Spirochetes
82
Bacteria Associated with Pregnancy and Puberty (2)
Prevotella intermedia Capnocytophaga spp.
83
Bacteria in Abscess of the Periodontium (5)
Fusobacterium nucleatum Parvimonas micra Prevotella intermedia Porphyromonas gingivalis Spirochetes
84
Health (5)
Gram +ve Cocci Nonmotile Facultative anaerobes Fermenting
85
Disease (5)
Gram -ve Rod Motile Obligate anaerobes Proteolytic
86
Choose correct answer for the specific bacteria observed in correlated periodontal disease A. In diseased sites, more gram positive, nonmotile cocci are observed B. In healthy sites, more orange and red complex bacteria are observed C. A. actinomycetemcomitans and P. gingivalis are highly related to periodontitis D. Capnocytophaga spp. is usually found in periodontal abscess
C. A. actinomycetemcomitans and P. gingivalis are highly related to periodontitis
87
Transmission of Periodontal Pathogens Source: Saliva Bacteria involved: Donor-recipient:
A. actinomycetemcomitans & P. gingivalis Parent to child & Spouse to spouse
88
A ---% chance of transmission between spouses
20-30
89
Does not always result in periodontal disease in the recipient spouse. Stronger bacterial transmission was found from
parent to child
90
!!!Periodontal pathogens are --- but not readily ---!!!
communicable transmissible
91
Goals of Plaque Control (4)
Disrupt ecological succession Reduce degree of organization “Healthy” plaque (G+, aerobic, indigenous flora) Shift in flora compatible with health
92
Future Advances Modulating --- --- Target proteins that are essential for --- Limitation of the identifying the ---
host response (i.e. Resolvins) Antibiotics the maintenance of Biofilm microbial risk markers

Periodontics (13 decks)

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