Aetiology of Periodontitis Flashcards

1
Q

Definition of aetiology

A

The science behind the study of factors causing disease - contribute, modify or cause development.

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2
Q

Prevention and treatment

A

Relationship between the aetiological factors and pathogenesis

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3
Q

What is the main aetiological factor in the development and progression of inflammatory periodontal disease?

A

Dental biofilm - no plaque control contributes to increase prevalence and severity.

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4
Q

What are the plaque theories?
(WALTER LOESCH 1976)

A
  1. Specific Plaque theory
  2. Non-specific Plaque theory
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5
Q

Non-specific plaque hypothesis states that:

A

The degree of gingival inflammation = to the amount of plaque present as well as all plaque has the same potential to cause disease.

MORE PLAQUE –MORE DISEASE

Hypothesis?
Sometimes Less plaque have more periodontal destruction
Sometimes more plaque causes less destruction.

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6
Q

Specific Plaque Theory

A

Only certain plaque is pathogenic and its pathogenicity depends on the presence of or an increase in specific microorganisms”

Further studies lead to the realisation that the microflora in affected and non infected areas differ in composition

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7
Q

Dental Plaque definition

A

Specific but highly variable structural entity that develops due to sequel of events of micro-organism inhabitation of tooth structures, restoration and other parts of oral cavity. Composed of: salivary components - mucins, micro-organisms, debris, desquamated epithelial cells that are embedded in extracellular matrix.

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8
Q

Composition of Dental Plaque:

A

1) WATER 80%
2) MICRO- ORGANISMS INTERCELLULAR MATRIX 20% (20-30% OF PLAQUE MASS)

-INORGANIC MATERIALS:
Calcium, phosphorus
Sodium, potassium
fluoride

-ORGANIC MATERIALS:
Polysaccharides,
glycoproteins, proteins,
lipids

-BACTERIA
MYCOPLASMA
PROTOZOA
YEAST
VIRUSES

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9
Q

What are the 4 categories of bacteria characteristics?

A

1) Cell wall composition
2) Oxygen environment
3) Metabolism
4) Morphotypes (group of bacterial strains within a single species that are distinguishable by morphological characteristics)

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10
Q

Cell wall
characteristics of bacteria

A

Gram-positive (Gr +ve) and gram-negative bacteria (Gr -ve). Named according to permeability of cell wall.

Gr -ve = external membrane lipopolysaccharide layer(LPS layer) under capsule. Release of LPS layer (endotoxin) causes tissue destruction.

G +ve bacteria have NO LPS layer.

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11
Q

Bacterial Metabolism types

A
  1. Saccharolytic (fermenting) - break down CHOs (carbohydrates)
  2. Asaccharolytic (non-fermenting) - uses amino-acids, peptides & proteins to grow.
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12
Q

Oxygen environment of bacteria

A

O2 availability influences ability of bacterial growth and number.

  1. Aerobic organisms need O2.
  2. Facultative anaerobes can use O2, can also grow anaerobically.
  3. Aerotolerant anaerobes do not use O2 but can tolerate an oxidizing environment.
  4. Obligate anaerobes cannot survive in an O2-rich environment.
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13
Q

Morphotypes of bacteria

A

Structural properties.
Name usually describes form:
Cocci = spherical
Bacilli = rods, filaments
Spirochetes = spiral formed

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14
Q

Plaque as biofilm

A

Bacteria binds to surface developing sessile, mushroom-shaped colonies attached with narrow bases. The microcolony has various types of bacteria that are compatible and independent.

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15
Q

Steps for supragingival plaque development into dental biofilm:

A

1 Pellicle formation:
An amorphous membrane that coats all surfaces of oral cavity, made up of glycoproteins (saliva).
Attaches to Ca and PO4 ions of the hydroxyapatite of tooth.

2 Initial colonization of the pellicle:
Within hours, Bacteria in saliva contact and bind by using receptor- molecules.
Initially bacteria are mainly cocci, binding in a mono layer and later proliferate to form colonies.
Bacilli and filaments attach to the cocci. Colonies become larger leading to a bacterial mass.

3.Growth and maturation of plaque:
Unpleasant odor/Maturity
Inter-microbial matrix formed from:
- saliva material
- gingival exudate
- other microbial substances

Non-specific bacteria also caught in this extra-cellular matrix.

These bacteria are different from initial colonizers. Colonization and growth of new bacterial species
Change in initial aerobic environment: gram positive - gram negative.

  1. Bacterial co-aggregation:

2 bacteria species becoming one.
Brought about by the direct interaction between the surface components of two species.
E.g. Filaments covered with cocci, called “corncob” formation; others resemble test-tube brushes, where filamentous bacterium acts as central axis and gram negative rods forming the hairs of a brush

5 Bacterial succession:

With plaque maturation - initial bacteria proliferate(rapid increase in number) and grow.
- the environment changes – this allows new and different types of bacteria to move into developing plaque.

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16
Q

Forces involved in pellicle formation:

A

Van der Waal forces
Electrostatic forces
Hydrophobic forces

17
Q

UNDISTURBED PLAQUE WILL:

A
  • Increase in Thickness
  • Increase in Amount of bacteria
    -Increase in different types of bacteria
    -be visible after 24hrs (no food required)
18
Q

Late bacteria colonizers:

A
  1. motile gram-negative rods
  2. Porphyromanas gingivalis
19
Q

Early bacteria colonizers:

A
  1. Streptococci
  2. Capnocytaphaga species
  3. gram positive rods
  4. actinomyces species
20
Q

Sub-gingival plaque formation steps:
(More aggressive organisms)

A
  1. Initiated by mature supra-gingival plaque
  2. Leads to gingival inflammation that may lead to gingival attachment loss
  3. Supra-gingival plaque then grows apically into the sulcus
  4. = Sub-gingival plaque
  5. Bacteria multiply as the environment changes
21
Q

Iatrogenic factors

A

orthodontic brackets
partial dentures
restorations
crowns
pontics

22
Q

Tooth position &
anatomy factors

A

enamel pearls
grooves
malocclusion

23
Q

Poor plaque control factors

A

ignorance
retardation
economic

24
Q

Systemic factors

A

alcohol
diet
smoking
saliva

25
Q

Tooth pathology factors

A

caries

26
Q

Inorganic composition of calculus: (70-80%)

A

EARLY CALCULUS
Brucite

LATER CALCULUS
Octacalcium phosphate

MATURE CALCULUS
Hydroxyapatite &
Whitlokite

27
Q

Organic structure (10-15%)

A

PROTEINS
POLYSACCHARIDE COMPLEXES
DESQUAMATED EPITH CELLS
LEUCOCYTES
VARIOUS M/ORGANISMS

28
Q

BOOSTER CONCEPT Calculus Theory

A

Mineral precipitation results from a local rise in the degree of saturation of calcium and phosphate ions
A rise in the pH of the saliva causes the precipitation of calcium phosphate salts by lowering the precipitation constant.

29
Q

BACTERIOLOGICAL THEORY

A

Oral microorganisms are the primary cause of calculus formation.
Involved in the attachment to the tooth surface.

30
Q

INHIBITION THEORY

A

Calcification at specific sites - because of inhibiting mechanism at non-calcifying sites.

Alkaline pyrophosphatase enzyme involved in controlling mechanism.
Pyrophosphate inhibits calcification - prevents the initial nucleus from growing, possibly by poisoning the growth centers of the crystals.

31
Q

TRANSFORMATION THEORY

A

Hypothesis - hydroxyapatite need not arise exclusively via epitaxis or nucleation.

32
Q

EPITACTIC CONCEPT

A

According to this concept, seeding agents induce small foci of calcification which enlarge and coalesce to form a calcified mass.

33
Q

Enzymatic theory

A

Calculus formation is the resultant of the action of phosphatases derived from either oral tissues or oral microorganism on some salivary phosphate containing complex.