Microbiology Of Periodontal Disease Flashcards

1
Q

What anaerobes are involved in periodontal diseases?

A

Gram negative anaerobes- spirochaetes, Porphyromonas gingivalis, Tannerlla forsythia, Aggregibacter actinomycetemcomitans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the definition of dental plaque?

A

Structured, resilient yellow/grey substance that adheres tenaciously to intraoral hard surfaces, including removable and fixed appliances and restorations, it is a biofilm community of microorganisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does biofilm form and mature?

A

As plaque matures gram positive bacteria are gradually replaced by gram negative species. This causes the formation of gram negative filamentous forms such as fusiforms (spindle shaped bacteria) and spirochaetes (cork screw shaped bacteria) appear in the later stages of plaque maturation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is dental plaque composed of?

A

80-90% water with 70% of the dry weight being made up of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is calculus?

A

Calcified dental plaque and is 70-80% inorganic salts (hydroxyapatite)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is supra-gingival plaque composed of?

A

It is 50% matrix, mostly gram positive, aerobic bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is sub-gingival plaque composed of?

A

Contains little or not matrix, mostly gram negative rods and spirochetes, less oxygenated so favours the growth of anaerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In what areas does dental plaque form quicker?

A

Lower jaw, molar areas, buccal tooth surfaces, interdental regions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name two out-dated periodontal disease hypotheses.

A

Specific plaque hypothesis and the non-specific hypothesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does the specific plaque hypothesis of periodontal disease propose?

A

Only a few specific species out of the diverse collections of microorganisms in plaque are actively involved in disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does the non-specific plaque hypothesis of periodontal disease propose?

A

The disease is considered to be of the outcome of the overall activity of the total plaque microflora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the main hypothesis for the development of periodontal disease?

A

The ecological plaque hypothesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does the ecological plaque hypothesis for periodontal disease propose?

A

The organisms associated with disease may be found at healthy sights but at levels that are too low to be clinically relevant. Disease occurs as a result of a shift in the balance of the resident microflora due to a change in the local environmental conditions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ecological plaque hypothesis

A

Total amount of dental plaque and specific microbial composition of plaque contribute to the transitions from health to disease. The health-associated plaque is said to be relatively stable and in a state of equilibrium or microbial homeostasis. Then chemical and physical changes happen to the habitat e.g. increased GCF flow which then changes the nutrient status in the periodontal pocket.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a consequence of the ecological plaque hypothesis?

A

Periodontal disease can be prevented, not only by targeting the putative pathogens, but also by interfering with the environmental factors that drive the changes in the balance of the microflora.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name the bacterial species in the red complex of periodontal disease.

A

Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the aetiology of gingivitis?

A

Accumulation of dental plaque -> gingival inflammation, can be reversed by plaque removal or worsened by systemic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the aetiology of periodontitis?

A

Colonisation of sub-gingival regions by specific groups of micro-organisms -> expression of virulence factors e.g. proteases, leukotoxin -> destructive immune responses -> loss of periodontal tissue including gingiva, periodontal ligament and alveolar bone

19
Q

How do plaque bacteria cause disease?

A

Majority of plaque Bactria are commensal in nature and can be removed easily from teeth and tissues with good oral hygiene technique. Red and orange complex organisers produce a variety of virulence factors that initiate periodontal disease and allow its progression. Bacteria do not need to invade tissues and colonise periodontal tissues in order to causes disease. The immune states of the host and effectiveness of the host response are key determinants of disease susceptibility.

20
Q

What is virulence?

A

Virulence is a measure of the damage induced by the micro-organism.

21
Q

What are virulence factors?

A

These are microbial determinants that mediate host damage in the context of microbial pathogenicity. They help the bacteria colonise the host at the cellular level.

22
Q

Name some virulence factors.

A

Surface associated factors- adhesion pili, capsule, adhesins, LPS flagella, surface proteins
Secreted factors- exotoxin, enzymes, iron binding proteins

23
Q

How do bacteria acquire virulence genes?

A

Bacteria can acquire virulence genes by phages (via transduction) and other mobile genetic elements such as plasmids (via conjugation)

24
Q

What virulence factors have direct toxic effects?

A

Endotoxins and exotoxins

25
Q

What are endotoxins?

A

Bacterial endotoxin is produced by all gram negative bacteria, endotoxins consist principally of lipopolysaccharides (LPS), LPS is released from the bacterial cell wall during growth and after cell lysis, LPS is a potent toxin capable of activating complement and macrophages, degranulating neutrophils and stimulating bone resorption

26
Q

What are exotoxins?

A

Exotoxins are continuously released by certain live bacteria. An example is leukotoxin produced by Aggregatibacter actinomycetemocimitans which inhibits neutrophils and macrophages

27
Q

What are some surface associated virulence factors?

A

Adhesins, flagella and capsules

28
Q

What are adhesins?

A

These are microbial components that enable a microbe to attach to host tissues. They are chemically diverse molecules that include proteins, polysaccharides and bacterial cells wall components

29
Q

What are flagella?

A

These help some bacteria be mobile, they function in attachment and biofilm formation

30
Q

What are capsules?

A

They protect the microbe against host immune mechanisms, Porphyromonas gingivalis has a capsule which protects it from phagocytosis and intracellular killing

31
Q

What are some enzyme virulence factors?

A

Enzyme virulence factors include proteases, glucosidases and phospholipases

32
Q

What do enzymes do?

A

They damage cells and provide nutrients by digesting substrates into smaller components that can be assimilated by microbes.

33
Q

What does Fusobacterium nucleatum do?

A

It acts as a key bridging organisms for periodontal pathogens such as Porphyromonas gingivalis and Treponema denticola. It is an obligate anaerobe.

34
Q

What is Porphyromonas gingivalis?

A

A gram negative, strictly anaerobic bacteria which is strongly associated with adult periodontitis and rapidly aggressive periodontitis.

35
Q

What virulence factors does Porphyromonas gingivalis (red complex) produce?

A

Production of proteases which degrade complement, immunoglobulins and collagen. It also has a capsule.

36
Q

What virulence factors are produced by Tannerlla forsythia (red complex)?

A

Production of trypsin-like proteases and glycosidase enzymes

37
Q

What virulence factors are produced by Treponema denticola (red complex)?

A

Production of potent hydrologic names including collagenases and proteases

38
Q

What are some examples of Prevotella species?

A

Prevotella are strictly anaerobic. Prevotella intermedia and Prevotella nigrescens are black pigmented strains.

39
Q

What virulence factors does Prevotella intermedia include?

A

Ability to resist phagocytosis and LPS production

40
Q

What virulence factors are associated with Fusobacterium nucleatum?

A

Production of potent LPS and the production of butyric acid. It is unable to produce hydrolytic enzymes

41
Q

What is Aggregatibacter actinomycetemocomitans?

A

A facultative gram negative anaerobe. It has been implicated in a particularly aggressive form of periodontal disease in adolescents (localised aggressive periodontitis). It appears to be associated with actively progressive lesions.

42
Q

What are some of the virulence factors associated with Aggregatibacter acinitomycetemcomitans?

A

Production of collagen are and ability to resist phagocytosis

43
Q

What bacterial interactions and pathogenic synergy take place in the aetiology of periodontal disease?

A

Bacteria can signal to each other and relay information about the biofilm environment.
Bacterial gene transfer can occur readily within biofilms.
Co-adhesion between bacteria allows organisation of the biofilm architecture.
The extracellular polymeric matrix and the presence of other bacteria within the biofilm is protective.
Microorganisms may be dependent on each other for essential nutrients or bacterial interactions are required for attachment to the acquired enamel pellicle so that bacteria can adhere and resist the removal forces provided by GCF.

44
Q

How do pathogens lead to tissue destruction?

A

LPS (endotoxin) is particularly important in periodontal disease as it is a component of all gram -ve periodontal pathogens. LPS activates complement and macrophages, degranulates neutrophil and directly stimulates bone resorption.
Leukocidin,a toxin released by Aggregatibacter acitnomycetemcomitans destroys or lyses white blood cells.
Bacterial enzymes such as collagenases break down host proteins.
Bacteria elicit innate and adaptive immune response and the magnitude of these responses determine whether bacteria are eliminated successfully or whether bystander damage occurs.