Plaque and Calculus Flashcards

1
Q

When the colonization of the oral cavity starts?

A

Day 1 - Starts at birth with facultative and aerobic bacteria

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2
Q

When the anaerobic bacteria can be detected?

A

Day 2

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3
Q

When mature microbiota is established in gut of newborn?

A

Day 14 (by 2 weeks)

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4
Q

What are 6 Major Ecosystems in Oral Cavity?

A
• Intraoral, supragingival, hard surfaces
• Periodontal/peri-implant pocket
• Buccal epithelium, palatal
epithelium and floor of mouth
• Dorsum of tongue
• Tonsils
• Saliva
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5
Q

What is the dental plaque?

A

A structured, resilient, yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restorations

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6
Q

Name two categories of plaques:

A
  • Supragingivalplaque

* Subgingivalplaque

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7
Q

True or False: Plaque is differentiated from materia alba and calculus

A

True

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8
Q

Name three major phases of plaque formation:

A
  1. Formation of pellicle on the tooth surface
  2. Initial adhesion and attachment of bacteria
  3. Colonization and plaque maturation
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9
Q

True or False: All surfaces of oral cavity are coated with a pellicle

A

True

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10
Q

When Dental pellicle are obvious?

A

Within nanoseconds after polishing teeth they are covered with saliva-derived layer = derived pellicle

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11
Q

What pellicle consists of:

A
Pellicle consists of glycoproteins, 
proline-rich proteins, 
phosphoprotein, 
histidine-rich proteins, 
enzymes . . . 

Adhesion sites for bacteria

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12
Q

What are the mechanisms of Dental pellicle formation (The molecule bonds):

A

Mechanism of formation electrostatic, van derWaals, hydrophobic forces

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13
Q

Name the 3 phases of Initial Adhesion and Attachment of Bacteria:

A
  • Phase 1: transport to surface/random contact.
  • Phase 2: initial adhesion – reversible
  • Phase 3: attachment – firm anchorage
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14
Q

Which phases of Initial Adhesion and Attachment of Bacteria are non-specific and which one is specific?

A
  • Phase 1 and 2 are non-specific

* Phase 3 depends on specific interactions between microbial cell adhesin molecules and receptors in pellicle

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15
Q

The action of teeth and implants in the formation of calculus and entry of bacteria:

A

• Provide hard, non-shedding surface that allows development of extensive structured bacterial deposits
• Unique ectodermal interruption
• Teeth are “port of entry” for
periopathogens
• Key periodontal pathogens will disappear after full mouth extractions

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16
Q

Define supragingival plaque: (What is supragingival?)

Which bacteria are prominent at the tooth surface and which bacteria predominate at the outer surface?

A
  • Defined as marginal plaque when in contact with gingival margin
  • Gram positive cocci and short rods predominate at the tooth surface
  • Gram negative rods and filaments, spirochetes predominate at outer surface
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17
Q

Topography of supragingival plaque. (Explain initial growth and further extension)

A
  • Initial growth along gingival margin and from interdental space
  • Further extension in coronal direction • Changes with surface irregularities
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18
Q

Factors Affecting Supragingival Dental Plaque Formation

A
  • Rough surfaces* accumulate and retain more plaque
  • Thicker plaque has more pathogenicity, more motile organisms, spirochetes, denser packing
  • Smoothing surface decreases rate of formation
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19
Q

In which jaw the plaque forms faster?

A

Forms faster in lower jaw versus upper

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20
Q

In which areas plauqe formation is faster?

A
Forms faster in lower jaw versus upper
• Forms faster in molar areas
• Forms faster on buccal surfaces
of teeth
• Forms faster interproximaly compared to strict buccal or lingual
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21
Q

Individual Variables Influencing Plaque Formation

A
  • Rate of formation differs significantly between subjects
  • Saliva-induced aggregation and relative salivary flow conditions explain 90% of variation
  • Other factors include diet, chewing fibrous foods, smoking, tongue and palate brushing antimicrobial factors in saliva . .
  • Age does NOT influence de novo plaque formation

• Plaque in older people led to more gingivitis • Plaque forms faster adjacent to inflamed vs
healthy gingiva

• Plaque is NOT removed spontaneously during eating

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22
Q

What is subgingival plaque?

A
  • Subgingival plaque differs due to the availability of blood products and anaerobic environment
  • Are specific microorganisms the cause of the consequence of disease?
  • Periodontal pathogens that are strict anaerobes may contribute little to the initiation of disease
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23
Q
Explain De Novo subgingival plaque formation 
(Is it easy to remove?) 
(Effect of remaining bacteria)
(pathogens action)
(Growth after pre-treatment)
A

• Difficult to completely remove
• Remaining bacteria are source for re-
colonization
• Some pathogens penetrate soft tissue and dentinal tubules
• Fast re-growth to pre-treatment level within 7 days

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24
Q

Does age influence de novo plaque formation?

A

No

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25
Q

Does saliva influence de novo plaque formation?

A

Yes

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26
Q

What is Tooth-associated Subgingival Plaque?
(looks like which calculus?)
(what happens to deep pocket and apical portion?)

A
  • Tooth-associated cervical plaque similar to supragingival plaque
  • Deeper parts of pocket less filamentous
  • Apical portion dominated by smaller organisms without particular orientation
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27
Q

Which bacteria are involved with Tissue associated Subgingival Plaque?

A

• Contain primarily gram(-) rods and cocci, as well as large numbers of filaments, flagellated rods, and spirochetes

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28
Q

explain Plaque as a Biofilm. (the lower layers are bound by which material?)
(where do the nutrients run?)
How do the bacterial cells communicate?)

A

• Biofilms have organized structure
• In lower layers: bound together by polysaccharide
matrix and organic and inorganic materials
• Nutrients run through fluid channels in plaque mass
• Bacterial cells communicate with each other (quorum sensing)

29
Q

Explain Bacterial transmission and translocation:
(are Periodontal pathogens and cariogenic bacteria transmissible?)
vertical vs horizontal
The path of translocation

A
  • Periodontal pathogens and cariogenic bacteria are transmissible
  • Vertical transmission more frequent than horizontal in families
  • Translocation occurs from 1 niche to another, ie by oral hygiene device
30
Q

Name Nonbacterial inhabitants of the oral cavity:

A
  • Viruses
  • Fungi
  • Protozoa
  • Archaea
31
Q

Explain Non-specific plaque hypothesis:

A

• Mid1900s, accumulation of plaque over time, diminished host response, and host susceptibility with age.

. Plaque control is key to disease control.

• This hypothesis has been discarded, yet most therapy is still based on this principle

32
Q

Explain Specific plaque hypothesis:

A
  • 1960’s. only certain plaque is pathogenic and this depends on specific microorganisms
  • Majoradvancesin techniques used to isolate, identify and sample increased the power of association studies
  • Unknown whether specific bacteria cause or correlate
33
Q

What is Ecologic plaque hypothesis:

A

Attempt to unify theories on plaque and disease. Both total amount of plaque and specific microbes may contribute to disease. Site may impact microbiome. Host response may be affected by excessive plaque or host factors (ie smoking, diabetes, diet)

34
Q

What is Keystone pathogen hypothesis?

A

A specific pathogen present in low abundance (P.gingivalis) that is able to disrupt the periodontal microbiota and lead to dysbiosis. (Darveau, 2009)
May provide basis for targeted treatment

35
Q

What is Experimental gingivitis model?

A
  • Early undisturbed plaque formation follows exponential growth rate
  • Duringfirst24hours,plaque growth is negligible (<3% of vestibular surface)
  • Next 3 days follow rapid rate
  • After 4 days growth slows but composition shifts toward anaerobic and gram -
36
Q

What are Microorganisms associated gingivitis?

A

• Initial bacteria are gram positive rods, gram positive cocci and gram-negative cocci.

FYI:
• Gram + species include
Streptoccus, Actinomyces, Eubacterium and Parvimonas

• Gram – species include
Capnocytophaga, Fusobacterium, Prevotella, Campylobacter gracilis, C. concisus, B. parbula, E. corrodens.

37
Q

Name Microorganisms associated with chronic periodontitis:

A

• Spirochetes, anaerobic (90%) and gram – bacteria (75%)

FYI:
• Bacteria most often cultivated: P. gingivalis, T. forsythia, P. intermedia, C. rectus, E. corrodens, F. nucleatum, A. actinomycetemcomitans, T. denticola . . . . .

38
Q

Name Microorganisms associated with severe periodontitis occurring at an early age:

A
  • Almost all localized aggressive harbor A. actinomycetemcomitans
  • A.a. may comprise as much as 90% of microbiota
  • A.a is primary etiologic agent

FYI:
• Generalized aggressive periodontitis is dominated by P. gingivalis, P. intermedia, T. forsythia, treponema spp. And less A.a.

39
Q

True or False: Bone destruction is extensive in relation to patient’s age.

A

True.

40
Q

Name the Microorganisms associated with necrotizing periodontal diseases:

A
  • Associated with stress of HIV infection

* High levels of P. intermedia and spirochetes

41
Q

What is the treatment of Microorganisms associated with necrotizing periodontal diseases?

A

Tx includes debridement, OHI, mouth rinse and pain medication, antibiotics as an adjunct if not responsive

42
Q

When Microorganisms associated with abscesses of the periodontium happen?

A
  • Often occur in untreated periodontitis but can also occur after SRP or during maintenance
  • May occur in absence of periodontitis (popcorn!)
43
Q

Symptoms of Microorganisms associated with abscesses of the periodontium?

A
• Pain, 
swelling, 
suppuration, 
BOP, 
mobility
44
Q

Name the Microorganisms associated with abscesses of the periodontium:

A

• Bacteria: F. nucleatum, P. intermedia, P. gingivalis, P. micros, T. forsythia

45
Q

Explain Microorganisms associated with periodontitis as a manifestations of systemic disease:

A
  • Severe destruction may be associated with mutation of Cathepsin C receptor
  • Neutrophil defects and leukocyte adhesion defects
  • NOT specific microbes
46
Q

In which microorganism categories Neutrophil defects and leukocyte adhesion defects?

A

Microorganisms associated with periodontitis as a manifestations of systemic disease

47
Q

What is the Role of Beneficial Species of Bacteria?

A

• Passively occupy niche
• Limit a pathogen’s ability to
adhere to tissue surfaces
• Adversely affect growth or vitality of pathogen
• Affectability of pathogen to produce virulence factor
• Degrade virulence factor

48
Q

True or Flase: Periodontitis is a mixed infection.

A

True

49
Q

True or False: The presence of pathogens alone is not

sufficient for disease.

A

True

50
Q

True or False: Several species have large intrastrain variations.

A

True.

51
Q

True or False: The quality of host response cannot be estimated.

A

True

52
Q

True or False: Resistance to antibiotics is greatly increased in biofilm vs. planktonic bacteria.

A

True

1000-1500 times more resistant than planktonic

53
Q

The Biofilms get antimicrobial resistance due to which factors?

A

• Due to slower growth rate, variations in nutritional status, pH, prior exposure to antibiotic, resistance to diffusion of antibiotic

54
Q

What is Claculus?

A
  • Mineralized bacterial plaque that forms on the surfaces of natural teeth and dental prostheses
  • Supragingival or subgingival
  • Documented thousands of years ago
  • Rough and porous surface covered with bacterial plaque
55
Q

Composition: mineral crystals in the organic matrix:

A
• 70-90% inorganic:
• Percent of components similar to
other calcified tissues
• 76% calcium phosphate
• 3% calcium carbonate
• 4% magnesium phosphate and other metals
• 2/3 of inorganic are crystalline:
• Hydroxyapatite
• Magnesium whitlockite
• Octocalcium phosphate
• Brushite
56
Q

When Precipitation of mineral salts starts?

A

between 1st and 14th day of plaque formation.

57
Q

When Calcification starts?

A

4-8 hours

58
Q

Where does Calcification beging?

A

Calcification begins on the inner surface of the plaque

59
Q

Name

4 modes of attachment to tooth surface:

A
  • Via organic pellicle on enamel or cementum
  • Mechanical locking into surface irregularities
  • Close adaptation of calculus undersurface depressions to cementum surface
  • Penetration of calculus bacteria into the cementum
60
Q

Explain Supragingival Calculus:

A
  • Located above gingival margin
  • Heaviest near major salivary ducts
  • Mineral source from saliva
  • White/yellowish
  • Moderately hard but easily removed • Can form in less than 24 hours
61
Q

Explain Subgingival Calculus (where, color, formation rate, shape)

A
  • Not site specific
  • Mineral source GCF and inflammatory infiltrate
  • Highest incidence on proximal surfaces
  • Brown to black
  • Dense, hard, tenacious
  • Formation rates generally slower than supra
62
Q

True or False: Distinguishing between the effect of plaque and calculus is difficult.

A

True.

63
Q

True or False: Calculus is always covered with plaque

A

True

64
Q

True or False: Positive correlation exists between calculus and gingivitis

A

True

65
Q

True or False: Removal of plaque and calculus is the cornerstone of periodontal therapy

A

True

66
Q

True or False: microbial testing can not estimate the quality of host response.

A

True.

67
Q

Why calculus is harder than bone?

A

due to habing inorganic matterial

68
Q

Why Subgingival plaque differ?

A

Subgingival plaque differs due to the availability of blood products and anaerobic environment

69
Q

Which gingiva calculus has the highest incidence on proximal surfaces?

A

Subgingiva