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BDS2 PER > PER02-2005 > Flashcards

PER02-2005 Flashcards

1
Q

How many species are part of the oral microbiome in a healthy mouth?

A

~700-800

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2
Q

What are the three types of bacterial growth?

A

Planktonic = float in saliva

Sessile = attached to surfaces

Intracellular colonisation = invasion of (epithelial) cells

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3
Q

Describe indigenous/resident oral microflora.

A

Almost always present in a stable relationship with the host

Do not compromise survival of the host

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4
Q

Describe supplemental species.

A

Present in small numbers normally but if environment changes, they can become more abundant

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5
Q

Which supplemental species are associated with high caries risk?

A

Streptococcus mutans

Lactobacilli

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6
Q

Describe transient flora.

A

Pass through oral cavity but do not become established (eg E. coli)

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7
Q

What is dental plaque?

A

Complex microbial community that develops on non-shedding, hard surfaces in the mouth

Embedded in a matrix of polymers of bacterial and salivary origin

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8
Q

What are the general stages of plaque formation?

A
  1. Acquired pellicle formation
  2. Attachment of pioneer colonisers
  3. Microbial succession and syntrophism
  4. Co-aggregation
  5. Maturation
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9
Q

Describe the formation of the acquired pellicle.

A

Immediately after brushing, positively charged salivary glycoproteins, phosphoproteins and lipids attach to the negatively charged enamel surface

First to attach are low MW proteins = proline-rich proteins and statherins

Followed by higher MW proteins = mucins

Negatively charged molecules can attach by a calcium ion bridge

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10
Q

What are some pioneer species of dental plaque?

A

Streptococci

Actinomyces

Haemophilus

Neisseria

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11
Q

What do pioneer species of dental plaque attach to?

A

Acquired pellicle

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12
Q

Describe the pioneer colonisation stage of dental plaque formation.

A

Pioneers attach via receptors to pellicle proteins

Divide and produce extracellular polysaccharides (glucan and fructan)

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13
Q

How do oral bacteria survive the cycle of “feast and famine”?

A

Take nutrients from diet

Those which ferment carbohydrates produce extracellular polysaccharides as a storage of food

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14
Q

What is the function of the extracellular polysaccharides in plaque?

A

Food source when host is fasting

Cement-like role (structural integrity)

Protective (tolerance to environment and antimicrobials)

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15
Q

What is the reaction and enzyme in glucan formation?

A

Sucrose –> glucan + fructose

Glucosyltransferase

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16
Q

What is the reaction and enzyme in fructan formation?

A

Sucrose –> fructan + glucose

Fructosyltransferase

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17
Q

How can we prevent the growth of plaque through diet?

A

Eat less sugar/sucrose

Prevents formation of extracellular polysaccharides => plaque cannot grow (as fast)

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18
Q

Describe the microbial succession and syntrophism stage of plaque formation.

A

Pioneers produces nutrients that can be used by other micro-organisms (eg lactate for Veillonella)

Plaque becomes enriched as new metabolites are formed using oxygen => decreased oxygen in biofilm and new species adhere

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19
Q

Why do micro-organisms benefit by being part of a biofilm?

A

(Collective strength as a community for survival is greater than sum of components)

Enzyme complementation

Food chains/webs

Co-adhesion

Cell-cell signalling

Gene transfer

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20
Q

What antagonistic microbial interactions occur in dental plaque?

A

(Lead to exclusion of some species)

Bacteriocins toxic to other species

Hydrogen peroxide toxic to anaerobes

Organic acids and low pH not favourable for non-aciduric species

Nutrient competition

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21
Q

Describe the co-aggregation stage of plaque formation.

A

Plaque microflora becomes more diverse and local environment changes due to initial colonisers (receptors, nutrients, fermentation products, CO2…)

Attachment of later colonisers via adhesins

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22
Q

Why is Fusobacterium nucleatum important in biofilm formation?

A

Acts as a “bridging species” during co-aggregation

Very long bacilli with many adhesins which allow attachment to early colonisers and for later colonisers

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23
Q

Which species are later colonisers?

A

Veillonella

Eubacterium

Porphyromonas gingivalis

Prevotella intermedia

Treponema

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24
Q

Describe the maturation stage of dental plaque.

A

Growth rate slows down and continuous production of extracellular polysaccharides

Co-ordination of activities, vertical and horizontal stratification

Shear forces of mucosa limit further expansion (talking, chewing) of supragingival plaque

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25
Q

What is materia alba?

A

Soft accumulation of bacteria, tissue cells and food

Loosely attached to tooth surface and oral tissues

Easily displaced with fluid flow/rinsing

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26
Q

What is the primary aetiological cause of periodontal disease?

A

Plaque

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27
Q

What factors are required for plaque mineralisation?

A

Saturated solution of calcium and phosphate ions (saliva)

Bacteria to initiate crystal growth

High pH to promote mineralisation (bicarbonate in saliva)

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28
Q

What is the main mechanism for supragingival calculus formation and where is it found?

A

Precipitation of mineral salts in saliva

Found in sites of saliva pooling/duct openings:

  • behind lower incisors
  • buccal of upper 6/7s
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29
Q

What is the main mechanism of subgingival calculus formation?

A

Precipitation of mineral salts present in inflammatory exudate

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30
Q

Describe calculus.

A

Secondary, local, plaque-retentive factor

Creamy white to dark yellow or brownish

Mineralised plaque formed of calcium phosphate crystals

Requires professional removal

May take 2-14 days to form

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31
Q

Which type of calculus is harder to remove?

A

Subgingival calculus

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32
Q

What are periodontal diseases?

A

Bacterially-induced, immune-mediated inflammatory diseases of the tissues supporting the teeth

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33
Q

What is the difference in the immune response between healthy and diseased periodontal sites?

A

Healthy = well-defined, precisely-orchestrated, effective immune response

Diseased = exacerbated, uncontrolled, detrimental immune response

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34
Q

Why are secondary local factors problematic?

A

Promote accumulation of dental plaque (plaque-traps)

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35
Q

What are some examples of secondary local factors?

A

Calculus

Restoration overhangs

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36
Q

Why are systemic factors important in periodontal disease?

A

Modify host-bacteria interactions

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37
Q

Give examples of non-modifiable systemic risk factors for periodontal disease.

A

Age

Race

Gene polymorphisms

Hyper-responsive macrophage phenotype

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38
Q

Give examples of modifiable risk factors for periodontal disease.

A

Smoking

Treatable systemic diseases

Medication

Psychosocial factors

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39
Q

What are the prerequisites for periodontal disease initiation and progression?

A

Virulent periodontal pathogens

Suitable local environment

Host susceptibility

40
Q

How much damage in periodontal disease is direct and indirect?

A

Direct (microbes) = 20%

Indirect (immune response) = 80%

41
Q

How can bacteria attach to host tissues?

A

Adhesins

Fimbriae

42
Q

How can bacteria evade host defences?

A

Capsules/slimes

PMN-receptor blockers

Leukotoxins

Immunoglobulin-specific proteases

Complement-degrading proteases

Suppressor T cell induction

43
Q

What molecules/proteins are involved in direct damage in periodontal disease?

A

Cytotoxins

Enzymes (esp proteases)

Bone-resorbing factors

44
Q

What cells produce IL-1 and what does it do?

A

Macrophages, fibroblasts, epithelial cells

Activate osteoclasts

PG and IL-6 release from fibroblasts

Neutrophil margination

TNF production/release

45
Q

What cells produce IL-6 and what does it do?

A

Monocytes, fibroblasts, epithelial cells

Increase bone resorption

Activate T and B cells

Stimulates antibody production

46
Q

What cells produce IL-8 and what does it do?

A

Platelets and cells producing IL-6

Strong chemotaxis of neutrophils

47
Q

What cells produce IL-10 and what does it do?

A

T and B cells

Anti-inflammatory functions

48
Q

What cells produce TGF and what does it do?

A

Most cells

Anti-inflammatory repair potential

49
Q

What cells produce PGE2 and what does it do?

A

Macrophages, neutrophils, mast cells, epithelial cells

Increase vascular permeability and vasodilatation

Chemotaxis of neutrophils

Increase bone resorption

50
Q

What cells produce TNF and what does it do?

A

Monocytes, macrophages, epithelial cells

Increase IL-1 production, PG release and phagocytosis

51
Q

Which cytokines are pro-inflammatory?

A

IL-1

IL-6

IL-8

PGE2

TNF

52
Q

Which cytokines are anti-inflammatory?

A

IL-10

TGF

53
Q

What are the theories of periodontal disease pathogenesis?

A

Non-specific plaque theory

Specific plaque theory

Ecological plaque theory

Keystone pathogen theory

Inflammation-mediated polymicrobial emergence and dysbiotic exacerbation (IMPEDE) model

54
Q

Describe the non-specific plaque theory. What practice does it support?

A

Dental infections are caused by non-specific over-growth of all bacteria in the dental plaque

Quantity > virulence

Host has a threshold capacity to detoxify bacterial products and disease only develops if threshold surpassed

Supports importance of oral hygiene and brushing to remove plaque

55
Q

Describe the specific plaque theory. What is the flaw in this theory?

A

Dental disease caused by specific periopathogens

Development of anaerobic hood allowed cultivation of strict anaerobes which led to this theory

5 Socransky complexes of bacteria based on association with periodontal disease

! High pathogenicity bacteria were found in healthy mouths !

56
Q

Describe the ecological plaque theory.

A

Disease caused by imbalance in total microflora due to ecological stress resulting in enrichment of some “oral pathogens” (disease-related micro-organisms)

Changes in plaque microbial composition influenced by changes in local environment

Changed in local environment may be attributed to early colonisers being facultative anaerobes that use O2 and produce CO2 and H+ which give strict anaerobes the chance to grow

57
Q

Describe the keystone plaque theory.

A

Certain species have an effect on their environment which is disproportional to their overall abundance

Certain low-abundance microbial pathogens can increase quantity of normal microbiota by changing its composition or the host response

58
Q

Give an example of a “keystone pathogen” and how it works in periodontal disease.

A

Porphyromonas gingivalis

Manipulates innate immune system to facilitate its own and the entire microbial community’s survival and growth

59
Q

Describe the IMPEDE model of periodontal disease.

A

Stage 0 = health

Overgrowth of Gram-positive bacteria in susceptible individuals = gingivitis

Stage 1 = inflammation of gingiva alters subgingival environment

Stage 2 = polymicrobial emergence

  • host immune response, genetic predisposition and environment able to “contain” infection => gingivitis
  • further dysregulated host inflammation and tissue damage => deepens pocket

Overgrowth of “periodontal pathogens” in subgingival biofilm

Stage 3 = inflammation mediated dysbiosis
- host immune response, genetic predisposition and environment unable to “contain” infection => early periodontitis

Stage 4 = late stage periodontitis

60
Q

Describe healthy gingivae.

A

Coral/pale pink, uniform colour

Firm and no swelling

Knife-edged, intact, flat, scalloped margins

Sulci do not bleed on probing

61
Q

What are the cardinal signs of inflammation?

A

Redness/rubor

Swelling/tumor

Pain/dolor

Heat/calor

Loss of function/functio laesa

62
Q

What are the characteristics of gingivitis clinically?

A

Signs and symptoms confined to free gingiva

Presence of dental plaque along gingival margin

Inflammation

Stable attachment/JE and no bone loss

Removal of aetiology reverses disease

63
Q

What are the histopathological signs of gingivitis?

A

Dilated blood vessels

Lots of immune cells/inflammatory infiltrate

Junctional epithelium intact at CEJ

64
Q

What aetiological factors are involved in gingivitis?

A

Primary = PLAQUE

Local contributing factors = calculus, restoration overhangs, developmental anomalies, patient habits

Systemic factors = diabetes, smoking, immunodeficiency

65
Q

What are the four stages in periodontal disease?

A

Initial lesion

Early lesion

Established lesion

Advanced lesion

66
Q

Describe the initial lesion in periodontal disease.

A

24-48 hours of plaque accumulation

Gram-positive anaerobes provoke immune response

Vasodilatation

Increase in neutrophils and gingival crevicular fluid

Infiltrate confined to small area of connective tissue under junctional epithelium and minimal tissue damage

67
Q

Describe the early lesion in periodontal disease.

A

4-7 days of plaque accumulation

Increase in inflammatory infiltrate - mainly PMNs and lymphocytes

Loss of fibroblasts and collagen in infiltrated area due to enzymes and microbial products

Proliferation and rete peg formation in junctional epithelium

Increased production of GCF and PMNs accumulate in gingival crevice

May observe bleeding on probing

68
Q

Describe the established lesion in periodontal disease.

A

2-3 weeks of plaque accumulation, may persist for years

Gingival connective tissue largely replaced by inflammatory infiltrate

Large and increasing numbers of PMNs, lymphocytes and plasma cells

Blood stasis => insufficient nutrients to epithelial cells

Ulceration of junctional and sulcular epithelium

69
Q

Describe the advanced lesion in periodontal disease.

A

Progression to periodontitis in susceptible individuals only

Inflammatory infiltrate causes alveolar bone loss

70
Q

What are the differences between the gingival sulcus, gingival pocket and periodontal pocket?

A

Sulcus = ≤3mm with no bleeding

Gingival pocket = >3mm with bleeding, signs of inflammation

Periodontal pocket = >3mm with bleeding, apical migration of junction epithelium

Pockets have more anaerobic, Gram-negative bacteria and proteolytic species and pH is 6.9-7.8 (> saliva)

71
Q

What are the treatment options for gingivitis?

A

OHI

Removal of secondary local factors

Raise awareness and control systemic factors

72
Q

Describe the critical pathway model.

A

Non-pathogenic commensal bacteria in harmony with immune system - removed by brushing

Poor OH leads to pathogenic low microbial mass which produce virulence factors

Innate defence succeeds = gingivitis

Innate defence fails = increase microbial mass and penetration into connective tissue

Adaptive immune response with release of cytokines

  • success = gingivitis
  • failure = continued growth of bacteria and increased infiltration of PMN and lymphocytes

Tissue destruction, pocket formation and bone loss (periodontitis) creates more area for more pathogenic mass (cycles back to low microbial mass)

73
Q

What prevents migration of junctional epithelium in health?

A

Underlying connective tissue

74
Q

What occurs on a cellular and molecular level in the tissues during periodontitis?

A

Breakdown of collagen fibres and damaged fibroblasts

Build up of host and bacterial factors in connective tissue

Necrotic cementum due to blood stasis

Bacterial products (eg LPS) stimulate release of cytokines, leukotrienes, prostaglandins to activate osteoclasts = bone resorption

Secretion of inflammatory mediators

Direct damage due to bacterial products also occurs

75
Q

What are the different aspects of managing periodontal disease?

A

Prevention

Risk assessment

Diagnosis

Communication

Treatment planning

Monitoring treatment outcomes

76
Q

Which Socransky complexes are associated with gingivitis?

A

Purple and orange

77
Q

Which Socransky complexes are associated with periodontitis?

A

Red and orange

78
Q

Give examples of bacteria in the red Socransky complex.

A

Porphyromonas gingivalis

Tanneralla forsythia

Treponema denticola

79
Q

Which Socransky complex is Fusobacterium nucleatum part of?

A

Orange

80
Q

Which bacteria is associated with aggressive periodontitis affecting young populations?

A

Aggregatibacterium actinomycetemcomitans (actinobacilli)

81
Q

Give some of the virulence factors of Porphyromonas gingivalis.

A

LPS

Fimbriae

Proteases like gingipain

Capsule

82
Q

Give some of the virulence factors of A.a..

A

Leukotoxin

LPS

Collagenases

83
Q

What are the general features of necrotising periodontal diseases?

A

Pain, bleeding

Halitosis

Necrotising inflammation of dental papillae

Grey pseudomembranes

Increased body temp (pyrexia)

84
Q

What are the risk factors for necrotising periodontal diseases?

A

Smoking

Poor OH

Poor diet

Immunosuppression

Emotional stress

Fuso-spirochaetal complexes

85
Q

Which species are involved in fuso-spirochaetal complexes?

A

Treponema

Prevotella

Fusobacterium

Borrelia vincentii

86
Q

What process do penicillins inhibit?

A

Cell wall synthesis

87
Q

What process do tetracyclines inhibit?

A

Protein synthesis

88
Q

What process does metronidazole inhibit?

A

Nucleic acid synthesis

89
Q

How can make viewing plaque with the naked eye easier?

A

Plaque disclosing

90
Q

Why can plaque be disclosed?

A

Biofilms can retain large amounts of dye due to interactions with components

Electrostatic with proteins, hydrogen bonds with polysaccharides

91
Q

Why should a patient rinse before plaque disclosure?

A

Remove materia alba

92
Q

What are common dyes used for plaque disclosure?

A

Iodine

Mercurochrome

Bismark brown

Merbromin

Erythrosine

Fast green

Fluorescin

Two-tone

Basic fuchsin

93
Q

What is special about the two-tone dye for plaque disclosure?

A

Stains early biofilm (<3 days) with reddish-pink and mature biofilm (>3 days) with blue

94
Q

What are the advantages of plaque disclosure?

A

Allows visualisation for taking plaque indices

Guides biofilm removal

Motivational and educational tool

Personalisation of OHI

Self-evaluation and maintenance

95
Q

Describe the Silness and Loe, 1964 plaque index.

A

0 = following air drying, plaque is not visible nor can be wiped off with explorer

1 = following air drying, plaque is not visible but can be wiped off with explorer

2 = plaque visible along gingival margin, with or without air drying

3 = thick plaque visible along gingival margin

Uses buccal and lingual surfaces of specific teeth in each sextant, scored by worst situation

Overall score is the sum of 12 values

96
Q

Describe the O’Leary plaque score.

A

0 = no plaque, 1 = plaque (or fill in a chart)

Qualitative only of all 4 surfaces of teeth after disclosing

% of total surfaces with plaque

BDS2 PER (4 decks)

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