PER02-2005 Flashcards
How many species are part of the oral microbiome in a healthy mouth?
~700-800
What are the three types of bacterial growth?
Planktonic = float in saliva
Sessile = attached to surfaces
Intracellular colonisation = invasion of (epithelial) cells
Describe indigenous/resident oral microflora.
Almost always present in a stable relationship with the host
Do not compromise survival of the host
Describe supplemental species.
Present in small numbers normally but if environment changes, they can become more abundant
Which supplemental species are associated with high caries risk?
Streptococcus mutans
Lactobacilli
Describe transient flora.
Pass through oral cavity but do not become established (eg E. coli)
What is dental plaque?
Complex microbial community that develops on non-shedding, hard surfaces in the mouth
Embedded in a matrix of polymers of bacterial and salivary origin
What are the general stages of plaque formation?
- Acquired pellicle formation
- Attachment of pioneer colonisers
- Microbial succession and syntrophism
- Co-aggregation
- Maturation
Describe the formation of the acquired pellicle.
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
What are some pioneer species of dental plaque?
Streptococci
Actinomyces
Haemophilus
Neisseria
What do pioneer species of dental plaque attach to?
Acquired pellicle
Describe the pioneer colonisation stage of dental plaque formation.
Pioneers attach via receptors to pellicle proteins
Divide and produce extracellular polysaccharides (glucan and fructan)
How do oral bacteria survive the cycle of “feast and famine”?
Take nutrients from diet
Those which ferment carbohydrates produce extracellular polysaccharides as a storage of food
What is the function of the extracellular polysaccharides in plaque?
Food source when host is fasting
Cement-like role (structural integrity)
Protective (tolerance to environment and antimicrobials)
What is the reaction and enzyme in glucan formation?
Sucrose –> glucan + fructose
Glucosyltransferase
What is the reaction and enzyme in fructan formation?
Sucrose –> fructan + glucose
Fructosyltransferase
How can we prevent the growth of plaque through diet?
Eat less sugar/sucrose
Prevents formation of extracellular polysaccharides => plaque cannot grow (as fast)
Describe the microbial succession and syntrophism stage of plaque formation.
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
Why do micro-organisms benefit by being part of a biofilm?
(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
What antagonistic microbial interactions occur in dental plaque?
(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
Describe the co-aggregation stage of plaque formation.
Plaque microflora becomes more diverse and local environment changes due to initial colonisers (receptors, nutrients, fermentation products, CO2…)
Attachment of later colonisers via adhesins
Why is Fusobacterium nucleatum important in biofilm formation?
Acts as a “bridging species” during co-aggregation
Very long bacilli with many adhesins which allow attachment to early colonisers and for later colonisers
Which species are later colonisers?
Veillonella
Eubacterium
Porphyromonas gingivalis
Prevotella intermedia
Treponema
Describe the maturation stage of dental plaque.
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
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
What is the primary aetiological cause of periodontal disease?
Plaque
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)
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
What is the main mechanism of subgingival calculus formation?
Precipitation of mineral salts present in inflammatory exudate
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
Which type of calculus is harder to remove?
Subgingival calculus
What are periodontal diseases?
Bacterially-induced, immune-mediated inflammatory diseases of the tissues supporting the teeth
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
Why are secondary local factors problematic?
Promote accumulation of dental plaque (plaque-traps)
What are some examples of secondary local factors?
Calculus
Restoration overhangs
Why are systemic factors important in periodontal disease?
Modify host-bacteria interactions
Give examples of non-modifiable systemic risk factors for periodontal disease.
Age
Race
Gene polymorphisms
Hyper-responsive macrophage phenotype
Give examples of modifiable risk factors for periodontal disease.
Smoking
Treatable systemic diseases
Medication
Psychosocial factors
What are the prerequisites for periodontal disease initiation and progression?
Virulent periodontal pathogens
Suitable local environment
Host susceptibility
How much damage in periodontal disease is direct and indirect?
Direct (microbes) = 20%
Indirect (immune response) = 80%
How can bacteria attach to host tissues?
Adhesins
Fimbriae
How can bacteria evade host defences?
Capsules/slimes
PMN-receptor blockers
Leukotoxins
Immunoglobulin-specific proteases
Complement-degrading proteases
Suppressor T cell induction
What molecules/proteins are involved in direct damage in periodontal disease?
Cytotoxins
Enzymes (esp proteases)
Bone-resorbing factors
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
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
What cells produce IL-8 and what does it do?
Platelets and cells producing IL-6
Strong chemotaxis of neutrophils
What cells produce IL-10 and what does it do?
T and B cells
Anti-inflammatory functions
What cells produce TGF and what does it do?
Most cells
Anti-inflammatory repair potential
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
What cells produce TNF and what does it do?
Monocytes, macrophages, epithelial cells
Increase IL-1 production, PG release and phagocytosis
Which cytokines are pro-inflammatory?
IL-1
IL-6
IL-8
PGE2
TNF
Which cytokines are anti-inflammatory?
IL-10
TGF
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
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
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 !
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
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
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
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
Describe healthy gingivae.
Coral/pale pink, uniform colour
Firm and no swelling
Knife-edged, intact, flat, scalloped margins
Sulci do not bleed on probing
What are the cardinal signs of inflammation?
Redness/rubor
Swelling/tumor
Pain/dolor
Heat/calor
Loss of function/functio laesa
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
What are the histopathological signs of gingivitis?
Dilated blood vessels
Lots of immune cells/inflammatory infiltrate
Junctional epithelium intact at CEJ
What aetiological factors are involved in gingivitis?
Primary = PLAQUE
Local contributing factors = calculus, restoration overhangs, developmental anomalies, patient habits
Systemic factors = diabetes, smoking, immunodeficiency
What are the four stages in periodontal disease?
Initial lesion
Early lesion
Established lesion
Advanced lesion
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
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
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
Describe the advanced lesion in periodontal disease.
Progression to periodontitis in susceptible individuals only
Inflammatory infiltrate causes alveolar bone loss
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)
What are the treatment options for gingivitis?
OHI
Removal of secondary local factors
Raise awareness and control systemic factors
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)
What prevents migration of junctional epithelium in health?
Underlying connective tissue
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
What are the different aspects of managing periodontal disease?
Prevention
Risk assessment
Diagnosis
Communication
Treatment planning
Monitoring treatment outcomes
Which Socransky complexes are associated with gingivitis?
Purple and orange
Which Socransky complexes are associated with periodontitis?
Red and orange
Give examples of bacteria in the red Socransky complex.
Porphyromonas gingivalis
Tanneralla forsythia
Treponema denticola
Which Socransky complex is Fusobacterium nucleatum part of?
Orange
Which bacteria is associated with aggressive periodontitis affecting young populations?
Aggregatibacterium actinomycetemcomitans (actinobacilli)
Give some of the virulence factors of Porphyromonas gingivalis.
LPS
Fimbriae
Proteases like gingipain
Capsule
Give some of the virulence factors of A.a..
Leukotoxin
LPS
Collagenases
What are the general features of necrotising periodontal diseases?
Pain, bleeding
Halitosis
Necrotising inflammation of dental papillae
Grey pseudomembranes
Increased body temp (pyrexia)
What are the risk factors for necrotising periodontal diseases?
Smoking
Poor OH
Poor diet
Immunosuppression
Emotional stress
Fuso-spirochaetal complexes
Which species are involved in fuso-spirochaetal complexes?
Treponema
Prevotella
Fusobacterium
Borrelia vincentii
What process do penicillins inhibit?
Cell wall synthesis
What process do tetracyclines inhibit?
Protein synthesis
What process does metronidazole inhibit?
Nucleic acid synthesis
How can make viewing plaque with the naked eye easier?
Plaque disclosing
Why can plaque be disclosed?
Biofilms can retain large amounts of dye due to interactions with components
Electrostatic with proteins, hydrogen bonds with polysaccharides
Why should a patient rinse before plaque disclosure?
Remove materia alba
What are common dyes used for plaque disclosure?
Iodine
Mercurochrome
Bismark brown
Merbromin
Erythrosine
Fast green
Fluorescin
Two-tone
Basic fuchsin
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
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
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
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
