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PER02-2005 Flashcards

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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
What is materia alba?
Soft accumulation of bacteria, tissue cells and food Loosely attached to tooth surface and oral tissues Easily displaced with fluid flow/rinsing
26
What is the primary aetiological cause of periodontal disease?
Plaque
27
What factors are required for plaque mineralisation?
Saturated solution of calcium and phosphate ions (saliva) Bacteria to initiate crystal growth High pH to promote mineralisation (bicarbonate in saliva)
28
What is the main mechanism for supragingival calculus formation and where is it found?
Precipitation of mineral salts in saliva Found in sites of saliva pooling/duct openings: - behind lower incisors - buccal of upper 6/7s
29
What is the main mechanism of subgingival calculus formation?
Precipitation of mineral salts present in inflammatory exudate
30
Describe calculus.
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
31
Which type of calculus is harder to remove?
Subgingival calculus
32
What are periodontal diseases?
Bacterially-induced, immune-mediated inflammatory diseases of the tissues supporting the teeth
33
What is the difference in the immune response between healthy and diseased periodontal sites?
Healthy = well-defined, precisely-orchestrated, effective immune response Diseased = exacerbated, uncontrolled, detrimental immune response
34
Why are secondary local factors problematic?
Promote accumulation of dental plaque (plaque-traps)
35
What are some examples of secondary local factors?
Calculus Restoration overhangs
36
Why are systemic factors important in periodontal disease?
Modify host-bacteria interactions
37
Give examples of non-modifiable systemic risk factors for periodontal disease.
Age Race Gene polymorphisms Hyper-responsive macrophage phenotype
38
Give examples of modifiable risk factors for periodontal disease.
Smoking Treatable systemic diseases Medication Psychosocial factors
39
What are the prerequisites for periodontal disease initiation and progression?
Virulent periodontal pathogens Suitable local environment Host susceptibility
40
How much damage in periodontal disease is direct and indirect?
Direct (microbes) = 20% Indirect (immune response) = 80%
41
How can bacteria attach to host tissues?
Adhesins Fimbriae
42
How can bacteria evade host defences?
Capsules/slimes PMN-receptor blockers Leukotoxins Immunoglobulin-specific proteases Complement-degrading proteases Suppressor T cell induction
43
What molecules/proteins are involved in direct damage in periodontal disease?
Cytotoxins Enzymes (esp proteases) Bone-resorbing factors
44
What cells produce IL-1 and what does it do?
Macrophages, fibroblasts, epithelial cells Activate osteoclasts PG and IL-6 release from fibroblasts Neutrophil margination TNF production/release
45
What cells produce IL-6 and what does it do?
Monocytes, fibroblasts, epithelial cells Increase bone resorption Activate T and B cells Stimulates antibody production
46
What cells produce IL-8 and what does it do?
Platelets and cells producing IL-6 Strong chemotaxis of neutrophils
47
What cells produce IL-10 and what does it do?
T and B cells Anti-inflammatory functions
48
What cells produce TGF and what does it do?
Most cells Anti-inflammatory repair potential
49
What cells produce PGE2 and what does it do?
Macrophages, neutrophils, mast cells, epithelial cells Increase vascular permeability and vasodilatation Chemotaxis of neutrophils Increase bone resorption
50
What cells produce TNF and what does it do?
Monocytes, macrophages, epithelial cells Increase IL-1 production, PG release and phagocytosis
51
Which cytokines are pro-inflammatory?
IL-1 IL-6 IL-8 PGE2 TNF
52
Which cytokines are anti-inflammatory?
IL-10 TGF
53
What are the theories of periodontal disease pathogenesis?
Non-specific plaque theory Specific plaque theory Ecological plaque theory Keystone pathogen theory Inflammation-mediated polymicrobial emergence and dysbiotic exacerbation (IMPEDE) model
54
Describe the non-specific plaque theory. What practice does it support?
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
Describe the specific plaque theory. What is the flaw in this theory?
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
Describe the ecological plaque theory.
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
Describe the keystone plaque theory.
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
Give an example of a "keystone pathogen" and how it works in periodontal disease.
Porphyromonas gingivalis Manipulates innate immune system to facilitate its own and the entire microbial community's survival and growth
59
Describe the IMPEDE model of periodontal disease.
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
Describe healthy gingivae.
Coral/pale pink, uniform colour Firm and no swelling Knife-edged, intact, flat, scalloped margins Sulci do not bleed on probing
61
What are the cardinal signs of inflammation?
Redness/rubor Swelling/tumor Pain/dolor Heat/calor Loss of function/functio laesa
62
What are the characteristics of gingivitis clinically?
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
What are the histopathological signs of gingivitis?
Dilated blood vessels Lots of immune cells/inflammatory infiltrate Junctional epithelium intact at CEJ
64
What aetiological factors are involved in gingivitis?
Primary = PLAQUE Local contributing factors = calculus, restoration overhangs, developmental anomalies, patient habits Systemic factors = diabetes, smoking, immunodeficiency
65
What are the four stages in periodontal disease?
Initial lesion Early lesion Established lesion Advanced lesion
66
Describe the initial lesion in periodontal disease.
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
Describe the early lesion in periodontal disease.
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
Describe the established lesion in periodontal disease.
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
Describe the advanced lesion in periodontal disease.
Progression to periodontitis in susceptible individuals only Inflammatory infiltrate causes alveolar bone loss
70
What are the differences between the gingival sulcus, gingival pocket and periodontal pocket?
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
What are the treatment options for gingivitis?
OHI Removal of secondary local factors Raise awareness and control systemic factors
72
Describe the critical pathway model.
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
What prevents migration of junctional epithelium in health?
Underlying connective tissue
74
What occurs on a cellular and molecular level in the tissues during periodontitis?
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
What are the different aspects of managing periodontal disease?
Prevention Risk assessment Diagnosis Communication Treatment planning Monitoring treatment outcomes
76
Which Socransky complexes are associated with gingivitis?
Purple and orange
77
Which Socransky complexes are associated with periodontitis?
Red and orange
78
Give examples of bacteria in the red Socransky complex.
Porphyromonas gingivalis Tanneralla forsythia Treponema denticola
79
Which Socransky complex is Fusobacterium nucleatum part of?
Orange
80
Which bacteria is associated with aggressive periodontitis affecting young populations?
Aggregatibacterium actinomycetemcomitans (actinobacilli)
81
Give some of the virulence factors of Porphyromonas gingivalis.
LPS Fimbriae Proteases like gingipain Capsule
82
Give some of the virulence factors of A.a..
Leukotoxin LPS Collagenases
83
What are the general features of necrotising periodontal diseases?
Pain, bleeding Halitosis Necrotising inflammation of dental papillae Grey pseudomembranes Increased body temp (pyrexia)
84
What are the risk factors for necrotising periodontal diseases?
Smoking Poor OH Poor diet Immunosuppression Emotional stress Fuso-spirochaetal complexes
85
Which species are involved in fuso-spirochaetal complexes?
Treponema Prevotella Fusobacterium Borrelia vincentii
86
What process do penicillins inhibit?
Cell wall synthesis
87
What process do tetracyclines inhibit?
Protein synthesis
88
What process does metronidazole inhibit?
Nucleic acid synthesis
89
How can make viewing plaque with the naked eye easier?
Plaque disclosing
90
Why can plaque be disclosed?
Biofilms can retain large amounts of dye due to interactions with components Electrostatic with proteins, hydrogen bonds with polysaccharides
91
Why should a patient rinse before plaque disclosure?
Remove materia alba
92
What are common dyes used for plaque disclosure?
Iodine Mercurochrome Bismark brown Merbromin Erythrosine Fast green Fluorescin Two-tone Basic fuchsin
93
What is special about the two-tone dye for plaque disclosure?
Stains early biofilm (<3 days) with reddish-pink and mature biofilm (>3 days) with blue
94
What are the advantages of plaque disclosure?
Allows visualisation for taking plaque indices Guides biofilm removal Motivational and educational tool Personalisation of OHI Self-evaluation and maintenance
95
Describe the Silness and Loe, 1964 plaque index.
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
Describe the O'Leary plaque score.
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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