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Microbiology for Dentists > 20. Periodontal Disease > Flashcards

20. Periodontal Disease Flashcards

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1
Q

Explain plaque-induced periodontal disease

A
  • induced by presence of bacterial plaque
  • inflammatory response to it
  • interaction between micro-organisms in plaque, host tissue and inflammatory cells
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2
Q

Gingivitis is … but periodontitis is not

A

reversible

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3
Q

Key features of dental plaque

A
  • biofilm
  • forms extracellular polysaccharide matrix
  • stable ecology in complex diverse community
  • dynamic community adapting to external stimuli
  • diff constituent flora at aerobic and anaerobic sites
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4
Q

Plaque in health contains what kind of bacteria?

A
  • mainly aerobic gram positive bacteria
  • few species of motile rods
  • cocci
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5
Q

As plaque moves into gingivitis stage, how does bacteria present change?

A
  • increasing heterogeneity of species
  • gram positive rods
  • actinoomyces
  • eventual shift to obligately anaerobic gram negative bacteria
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6
Q

Define ‘ecological plaque hypothesis’

A
  • not one specific pathogen causing disease
  • shifting population of bacteria
  • biofilm in balance
  • virulence of bacterial cells in biofilm and host imflammatory response along with env conditions will dictate progression of disease
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7
Q

How is health and disease balanced with plaque?

A
  • removal of plaque vs ongoing build up
  • resolution of inflammation vs ongoing
  • resolution of disease vs further development
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8
Q

4 stages of periodontitis development

A
  • healthy
  • early
  • moderate
  • severe
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9
Q

Explain initiation of periodontitis

A
  • direct and indirect action by microorganisms in subgingival plaque biofilm
  • dependent on environment and host susceptibility
  • exaggerated host inflammatory and immune response
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10
Q

Environmental changes in periodontal pockets in disease

A
  • flow of gingival crevicular fluid
  • nutrition
  • temp
  • pH
  • oxygen and oxidation-reduction potential
  • aerobic to anaerobic
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11
Q

What do the environmental changes in the periodontal pocket cause in disease?

A
  • changes in homeostasis of subgingival microbiota
  • altered gene expression
  • change in microbial population
  • dysbiosis
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12
Q

Explain the polymicrobial synergy and dysbiosis theory of periodontal disease

A
  • periodontitis is initiated by synergistic and dysbiotic microbiota
  • within which different members or specific gene combinations have distinct roles
  • they converge shape and stabilize the disease-provoking microbiota
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13
Q

Early colonisers in plaque

A
  • streptococci
  • actinomyces
  • veillonella spp.
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14
Q

Late colonisers in plaque

A
  • porphyromonas gingivalis
  • motile G-rods and spirochetes
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15
Q

As plaque moves into periodontitis stage, what happens to bacteria involved?

A
  • mainly anaerobic gram negative organisms
  • more species and motile rods
  • gram-negative rods
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16
Q

How to determine subgingival microflora

A
  • direct sampling
  • cultivation of samples
  • molecular methods
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17
Q

How does checkerboard hybridisation work?

A
  • labelled DNA from samples goes onto specific DNA probes
  • intensity of signal correlates with amount of target organism present in sample
  • quantitative
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18
Q

What bacterial factors are implicated in periodontal disease?

A
  • attachment to host tissues
  • multiplication at susceptible site
  • evasion of host defences
  • direct tissue damage
  • indirect tissue damage
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19
Q

How does attachment of host tissues link to periodontal disease?

A
  • surface components
  • like adhesins and fimbriae
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20
Q

How does multiplication at susceptible site link to periodontal disease?

A
  • protease production to obtain nutrients
  • development of food chains
  • inhibitor production e.g bacteriocins
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21
Q

How does evasion of host defences link to periodontal disease?

A
  • capsules
  • neutrophil-receptor blockers
  • impairment of neutrophil function
  • leukotoxin
  • immunoglobin-specific proeases and complement-degrading protease
  • suppressor T-cell induction
  • degradation of fibrin
22
Q

How does direct tissue damage link to periodontal disease?

A
  • enzymes (protease, collagenase, hyaluronidase)
  • bone resorbing factors (lipotechoic acid, LPS, capsule)
  • cytotoxins (butyric and proprionic acids, amines, ammonia, volatile sulphur compounds)
23
Q

How does indirect tissue damage link to periodontal disease?

A

inflammatory response to plaque antigens

24
Q

Key periodontal pathogens

A
  • streptococcus spp.
  • fusobacterium nucleatum
  • treponema denticola
  • prophyromonas gingivalis
25
Q

How is fusobacterium nucleatum a key pathogen in periodontitis?

A
  • gram-neg, proteolytic, anaerobic, long rod-shaped cells
  • coaggregates with early colonisers like strep sp. and late colonisers like T. denticola
  • can invade host epithelial cells
  • present in high numbers in subgingival plaque (over 20% of total bacteria)
26
Q

All red complex bacteria are …

A
  • fastidious
  • gram-negative
  • proteolytic
  • anaerobes
27
Q

How is prophyromonas gingivalis a red complex bacteria?

A
  • short rods
  • produces black and brown porphyrin (haem-containing) pigments
  • highly proteolytic, adheres to certain oral strep
  • one of the most thoroughly studied oral bacteria
  • plays disproportionate important role in disease relative to numbers in community
28
Q

How is tannerella forsythia a red complex bacteria?

A
  • short rods with tapered ends
  • difficult to grow in monoculture - growth facilitated by other bacteria
  • possesses glycosylated S-layer on outside, which hides cells from immune system
  • invades epithelial cells
29
Q

How is treponema denticola a red complex bacteria?

A
  • spirochaete
  • highly motile - flagellum is located in periplasm and winds around cell
  • outer sheath primarily consisting of major sheath protein for adhesion
  • highly proteolytic
30
Q

3 examples of animal models produced for periodontitis

A
  • rodents
  • dogs
  • primates
31
Q

Infections with a variety of bacteria cause disease in animal models. Co-infection often results in what?

A
  • greater damage than infection with either organism alone
32
Q

Give Koch-Henle postulates

A
  • organism must be present in all cases of disease
  • organism must be located in pure culture
  • isolated organism must cause disease in suitable animal
  • organism must be re-isolated from infected animal
33
Q

With periodontal disease, organism isn’t always present in all cases of disease. What rules do we follow then?

A
  • if no infecting organism is detected
  • if bacteria cannot be grown in culture
  • if no suitable animal model is available
  • if more than one species of bacterium is involved
  • if level rather than just presence of infecting bacterium is important
34
Q

How do virulence factors link to Koch-Henle postulates?

A
  • provide additional evidence for involvement in disease
  • if the organism can be cultured
35
Q

Virulence factors of P.gingivalis

A
  • adhesins/invasins like minor and major fimbriae
  • capsule (highly virulent)
  • LPS
  • haemagglutinins
  • porteases
36
Q

How are P.gingivalis’
- adhesins/invasins
- capsule
- LPS
virulence factors?

A
  • minor fimbriae for coaggregation, major for adhesion/invasion
  • capsule resists host immunity (phagocytosis, complement activation)
  • LPS are pro-inflammatory
37
Q

P.gingivalis have several proteases - most important being …

A
  • extracellular ones or gingipains
  • calleed Arg-Xaa specific protease (RGP) or Lys-Xaa specific protease (KGP)
38
Q

Roles of P.gingivalis proteases

A
  • major antigens in infections
  • for nutrition and processing bacterial proteins
  • cleave host proteins in connective tissue (laminin, fibronectin, collagen)
  • secondary functions (haemagglutination, adhesion)
  • roles in evasion of host immune response
39
Q

What does aggregatibacer actinomyctemcomitans do?
Give structure and function

A
  • facultative anaerobe
  • gram-neg, capnophilic, coccobacillus, Haemophilus related
  • involved in more aggressive forms of periodontal disease
  • causes systemic disease like endocarditis
40
Q

Virulence factors in A. actinomycetemcomitans

A
  • adhesins/invasins
  • LPS
  • leukotoxins
  • cytolethal distending toxin
  • proteases
41
Q

How do
- adhesins/invasins
in A.actinomycetemcomitans act as virulence factors?

A
  • tight adherence to surfaces mediated by fimbriae and assoicated gene products
  • fimbriae bind epithelial cells and enhance receptor-mediated endocytosis
42
Q

How do
- leukotoxin
in A.actinomycetemcomitans act as virulence factors?

A
  • 116 kDa pore-forming toxin
  • anchored to cell wall
  • targets immune cells expressing beta-2 integrin
43
Q

How do
- proteases
in A.actinomycetemcomitans act as virulence factors?

A
  • trysin-like proteases produced by some strains
44
Q

Explain the JP2 strain of A.actinomycetemcomitans

A
  • clone of serotype b associated with aggressive periodontitis in adolescents of West African descent
  • clone emerged in population and spread worldwide
  • strongly haemolytic
  • strong leukotoxin activity
45
Q

How does leuokotoxin regulation occur in A. actinomycetemcomitans?

A
  • JP2 clone has a mutant upstream of operon encoding for leukotoxin
  • results in excessive amounts produced
46
Q

Periodontium is very/not very vascular?
What does this mean?

A
  • very
  • subgingival bacteria and proinflammatory molecules can enter circulatory system and affect sites/systems in body
47
Q

Explain how bacteria in periodontium can get into circulation

A
  • barrier breach occurs
  • viable bacteria, LPS, pro-inflammatory mediators enter circulation
  • then systemic spread occurs with these going to the liver and causing atherosclerosis, obesity, rheumatoid arthritis, pregnancy complications
48
Q

Association of periodontal disease and diabetes mellitus?

A
  • increased periodontal disease in those with poorly controlled diabetes
  • periodontal disease can lead to increased issues with it (but treatment could improve metabolic control)
  • some evidence that severity of periodontal disease may affect glycaemic control
49
Q

Link of periodontal disease to adverse pregnancy outcomes

A
  • linked to preterm birth and low birth weight but inconclusive
  • periodontal therapy doesn’t improve birth outcomes
  • association with F. nucleatum and P. gingivalis - the former is the most prevalent species in amniotic fluid from pregnancies complicated by preterm birth
50
Q

Link of periodontal disease with cardiovascular disease

A
  • contributes to increased infectious/inflammatory burden and linked to cardiovascular events
  • associated with atherosclerosis
  • P.gingivalis, F.nucleatum and A.actinomycetemcomitans detected with atheromatous plaques
51
Q

Link of periodontal disease to rheumatoid arthritis?

A
  • less strong evidence
  • both conditions show similarities in host-mediated chronic inflammatory response

Microbiology for Dentists (37 decks)

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