Cariology Lecture 4

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51 Terms

1
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What is the Non-Specific Plaque Hypothesis?

The idea that all plaque bacteria collectively contribute to caries through acid production rather than any single species.

2
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What were the findings of Orland's germ-free rat study?

Conventional rats developed caries, germ-free rats did not, proving bacteria are essential for decay.

3
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What is the critical pH for enamel demineralization?

Approximately pH 5.4.

4
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What did Kligler propose about cariogenic species?

That bacteria both acidogenic and aciduric are key etiologic agents in caries.

5
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What is the Specific Plaque Hypothesis?

The idea that specific bacterial species, such as S. mutans, are primarily responsible for dental caries.

6
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What were the main findings supporting S. mutans' role?

It caused smooth surface caries in animals, produced acid rapidly, and formed adherent biofilms in sucrose presence.

7
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Why is S. mutans' role debated?

It is found in low proportions even in caries, absent in some lesions, and caries can develop without detectable S. mutans.

8
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What is the Ecological Plaque Hypothesis?

A theory proposing that caries results from a shift in the overall plaque community toward acidogenic and aciduric species due to environmental changes like frequent sugar intake.

9
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How do Specific and Ecological Plaque Hypotheses differ in treatment approach?

Specific Plaque Hypothesis targets the pathogen; Ecological Plaque Hypothesis targets the dysbiosis.

10
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What is the significance of sucrose in caries development?

Sucrose uniquely promotes extracellular polysaccharide (glucan) production, bacterial adhesion, and acid formation, leading to high caries rates.

11
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What historical change increased caries prevalence?

Introduction of sucrose into human diets during agricultural and industrial eras.

12
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What does "plaque ecology" refer to?

The overall balance of microbial species and their metabolic activities in dental biofilms.

13
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Why is there still debate about caries etiology?

Because caries can occur with or without S. mutans, and many species can contribute through acid metabolism and ecological imbalance.

14
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When does S. mutans usually colonize the mouth?

During the "window of infectivity" between 19-31 months after tooth eruption.

15
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Why is the window of infectivity important?

Early colonization by S. mutans may prime teeth for future decay and influence long-term plaque ecology.

16
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Why is frequent snacking harmful for oral ecology?

Repeated sugar intake maintains low pH and selects for aciduric species like S. mutans and lactobacilli.

17
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What are the three main virulence traits of S. mutans?

Adherence mechanisms, acidogenicity, and aciduricity.

18
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What are the two types of adhesion used by S. mutans?

Sucrose-independent and sucrose-dependent adhesion.

19
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What mediates sucrose-independent adhesion in S. mutans?

The AgI/II surface protein (also called SpaP, P1, or PAc) that binds to salivary pellicle proteins.

20
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Why is sucrose-independent adhesion relatively inefficient?

S. mutans cannot strongly adhere without extracellular glucans, so its early colonization is limited.

21
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What enzyme enables sucrose-dependent adhesion?

Glucosyltransferases (GTFs), which synthesize glucans from sucrose.

22
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How does glucan promote adhesion?

Large glucan polymers create multiple weak-force interactions, forming a strong, sticky matrix for bacterial accumulation.

23
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What types of glucan does S. mutans produce?

Water-soluble glucans (α-1,6-linked) and water-insoluble glucans (α-1,3-linked, also called mutan).

24
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Why is S. mutans considered highly acidogenic?

It ferments many carbohydrates, rapidly producing lactic acid as a major product, especially under sugar-rich or low-pH conditions.

25
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What does aciduricity mean?

The ability to survive and continue metabolizing in acidic conditions.

26
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What is the Acid Tolerance Response (ATR)?

A global physiological adaptation that allows S. mutans to survive lower pH by altering gene expression and protein synthesis.

27
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How does S. mutans maintain intracellular pH under acid stress?

By using the F-ATPase (H+-ATPase) proton pump to expel protons and adjusting membrane composition to reduce permeability.

28
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What changes occur in acid-adapted bacteria?

Increased F-ATPase activity, altered fatty acids, production of stress and metabolic proteins, and improved energy conservation for pH regulation.

29
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What are keystone pathogens?

Species that drive dysbiosis by altering the microbial environment and host response.

30
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What are pathobionts?

Normally harmless species that become pathogenic in dysbiotic conditions.

31
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What host factors can influence caries risk independent of microbiota?

Genetic variation (MMPs, enamel genes), low saliva flow, tooth anatomy, and immune differences.

32
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What role do MMPs play in caries?

They contribute to dentin collagen breakdown; some genetic variants may reduce caries risk.

33
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Why does sucrose play a unique role compared to other sugars?

It serves as a substrate for glucan production and is highly fermentable, driving both adhesion and acid production.

34
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what is the equation for cavities

carbs (sugars) + saliva (bacteria) + tooth

35
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what is necessary for decay to occur

bacteria

  • an experiment was done where germ free and normal mice were given the same diet, and only the normal mice had caries due to the germ free mice not having any bacteria

36
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Specific Plaque Hypothesis

specific species in dental plaque were more responsible than others for promoting the caries process

37
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Ecological Plaque Hypothesis

allows for the role of specific cariogenic species (such as strep mutans) but puts greater emphasis on the global composition of plaque

38
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why was the ecological plaque hypothesis formed?

Some investigators found that that simplifying it down to one or a few bacterial species as the cause for caries was too simplistic

39
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overall what did the ecological plaque hypothesis state was the cause of cavities

dysbiosis

a change in homeostatic balance of the resident microbiota is responsible for conditions that promote the growth of pathogens. (does not HAVE to include strep mutans)

40
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The specific plaque hypothesis targets the _____

pathogen

41
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The ecological plaque hypothesis targets the _____

dysbiosis

42
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what is the most common site for caries

fissures

43
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why are smooth surface caries less common

requires strong adhesion factors from the bacteria

44
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Dietary carbohydrates are correlated with caries rates but _____ consumption has been linked to very high rates of caries development

sucrose

45
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There is accumulating evidence that host ______ _______ play a role in the development or severity of dental decay

matrix metalloproteases (MMPs)

46
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MMPs are involved in

proper tooth formation

47
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MMP_ and MMP_ have been shown to be involved in dentin collagen breakdown in caries lesions

2, 9

48
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what does snacking have to do with caries risk

frequent snacking leads to greater drops in the oral pH, meaning the mouth spends more time demineralizing than remineralizing

49
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What are the 3 cariogenic properties of S. mutans

  1. adherance mechanisms (sucrose-dependent)

  2. acidogenicity (produces acid)

  3. acid tolerance (still metabolizing carbs and churning out more acid at low pH)

50
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sucrose-dependent adhesion

glucan synthesus catalyzed by glucotransferases (GTFs)

GTFs can be found associated with the surface of the bacterium or in the plaque (VERY STICKY)

51
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Why is glucan effective in promoting adhesion and accumulation?

It is likely that the -OH groups of glucan have the opportunity for extensive hydrogen bonding that help it stick tenacioulsy to tooth surfaces