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PER > PER02-2005 Plaque & calculus > Flashcards

PER02-2005 Plaque & calculus Flashcards

1
Q

What are the two types of oral bacteria?

A

Planktonic and sessile

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2
Q

What is planktonic bacteria?

A

Bacteria that floats in the saliva

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3
Q

What is sessile bacteria?

A

Sessile bacteria is attached to surfaces of the mouth and grows in the biofilm

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4
Q

What is dental plaque?

A

Dental plaque is a complex microbial community that develops on the tooth surface, embedded in a matrix of polymers of bacterial and salivary origin

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5
Q

What is plaque that becomes calcified referred to as?

A

Calculus or tartar

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6
Q

What are the 4 stages of plaque formation?

A

Acquired pellicle formation
Adhesion of pioneer microbial colonisers to the pellicle
Coaggregation of microbial species present in the plaque
Maturation of plaque

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7
Q

How does the acquired pellicle form?

A

An acquired pellicle forms a few minutes after brushing on the clean tooth surface
It is a layer of saliva composed of mainly glycoproteins, phosphoproteins and lipids

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8
Q

What feature of the enamel surface makes it easier for molecules in the saliva to adhere to it?

A

Enamel surface is negatively charged due to negative phosphate groups

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9
Q

What forces attract bacteria to the acquired pellicle?

A

Van der Waals bring bacteria closer to the surface however this adhesion is reversible and can be washed away

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10
Q

Which part of the tooth do bacteria attach to?

A

Acquired pellicle only to the clean enamel surface

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11
Q

How do pioneer microbial colonisers produce extracellular polysaccharides?

A

Pioneer microbial colonisers have different receptors that can attach to the surface of the acquired pellicle
This adhesion is much tighter and specific and resistant to removal by saliva and chewing
The pioneer microbial colonisers begin to divide and produce extracellular polysaccharides

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12
Q

How do bacteria store carbohydrates?

A

Oral bacteria survive from nutrients, because we dont constantly eat EPS they are used by bacteria to store carbohydrates

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13
Q

How do pioneer species change to environment?

A

Pioneer species begin to ferment glucose and other metabolites
Consume O2
Produce CO2
So succession occurs

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14
Q

Which species acts as a bridging species between early and later colonisers in coaggregation?

A

Fusobacterium nucleatum

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15
Q

How does fusobacterium nucleatum act as a bridging species?

A

Once fusobacterium nucleatum has attached to the early species, late colonisers then attach to the fusobacterium nucleatum

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16
Q

What occurs during maturation of plaque?

A

The growth rate slows down, however there is a continuous production of EPS, which leads to structural integrity, tolerance to environmental factors and microbial

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17
Q

What forces limit the further expansion of the dental biofilm?

A

Forces of mastication

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18
Q

What is material alba?

A

The soft accumulation of bacteria, tissue cells and food particles that lack the organised structure of dental plaque (no EPS)
Material alba is loosely attached to the tooth surface and can be displaced by rinsing, unlike dental plaque

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19
Q

What is calculus?

A

Mineralised plaque with calcium phosphate crystals

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20
Q

Why is calculus not causative of periodontitis?

A

It is covered by a layer of biofilm

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21
Q

How does calculus form?

A

The plaque is mineralised
There is a precipitation of ca2+ and Po4- in saliva
Bacteria initiates crystal growth and a high pH is needed to promote mineralisation

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22
Q

What is the high pH due to in the mouth for calculus formation?

A

Presence of carbonic acid, which is formed because of a reaction between CO2 we breathe and saliva

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23
Q

How does supragingival plaque form?

A

Due to the presence of mineral salts in the saliva

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24
Q

Where is supragingival plaque found?

A

Near sites of saliva pooling and is easy to remove by the dentist
Lingual to the lower anterior teeth
Buccal to the upper posterior teeth

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25
Q

How does subgingival plaque form?

A

Due to the presence of mineral salts in the inflammatory exudate

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26
Q

How does subgingival plaque differ from supragingival plaque?

A

Subgingival plaque has a high pH and more difficult to remove

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27
Q

What is the non-specific plaque hypothesis of periodontal disease?

A

The total amount of plaque present in a person’s mouth determines the pathogenicity of the disease, and to the number of bacterial species present
But as plaque matures, microbial succession occurs

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28
Q

What is the specific plaque hypothesis of periodontal disease?

A

Periodontitis is caused by a single species of bacteria in plaque
But research shows there is no ‘single’ pathogen present in every individual with periodontitis

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29
Q

What is the ecological plaque hypothesis of periodontal disease?

A

The more accumulation of bacteria, the more inflammation, the deeper the crevice therefore more anaerobic bacteria
This changes the availability of nutrients
These changes enable the succession of different species

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30
Q

What is the keystone plaque hypothesis of periodontal disease?

A

Certain low-abundance pathogens can orchestrate inflammatory diseases by remodelling a normally benign microbiota into a dysbiotic state

31
Q

What is inflammation?

A

A protective tissue response to irritation, injury or infection, which serves to destroy or dilute both the injurious agent and injured tissues

32
Q

What are the classic signs of inflammation?

A 
Pain
heat
redness
swelling
loss of function
33
Q

What are the clinical signs of inflammation in gingivitis?

A

Stable attachment level
No bone loss
The JE is at the level of the cement-enamel junction

34
Q

What is the primary etiological factor of periodontitis?

A

Plaque

35
Q

What are the local contributing factors on periodontitis?

A

Calculus
Faulty restorations
Developmental anomalies
Patient habits

36
Q

What are systemic factors of periodontitis?

A

Diabetes
Smoking
Immunodeficiencies

37
Q

What are the stages of gingivitis?

A

Initial lesion
Early lesion
Established lesion
Advanced lesion

38
Q

What is the initial lesion of gingivitis?

A

Due to the presence of gram-positive anaerobic species that induce inflammation in the free gingiva
Vasodilation of capillaries in the free gingiva and increase in neutrophils
The infiltrate is confined to small areas of the connective tissue under the JE

39
Q

When does the initial lesion occur?

A

24-48 hours of plaque accumulation

40
Q

When does the early lesion occur?

A

4-7 days after plaque accumulation

41
Q

What occurs during the early lesion?

A

Increased inflammatory infiltrate
Loss of fibroblasts and collagen in infiltrated areas to accommodate the increasing amount of inflammatory agents
Proliferation of JE and rete peg formation
Increased GCF production

42
Q

What are clinical signs of early lesions?

A

Bleeding on probing may occur due to increased vasodilation

43
Q

When does the established lesion occur?

A

14-21 days after plaque accumulation

44
Q

What occurs during the established lesion?

A

Gingival connective tissue largely replaced by inflammatory infiltrate
Cannot see fibroblasts or collagen in free gingiva
Increasing number of neutrophils, lymphocytes and plasma cells

45
Q

What are clinical signs of established lesion?

A

Blood stasis

Epithelial ulcerations

46
Q

What is the advanced lesion?

A

The inflammatory infiltrate affects the alveolar bone causing alveolar bone loss

47
Q

What happens when we probe the gingival sulcus?

A

The probing is upto 3mm and there is no bleeding

48
Q

What happens when we probe a gingival pocket?

A

The probing is greater than 3mm and there is bleeding on probing due to vasodilation

49
Q

What are signs of healthy periodontal tissue?

A

Has an intact alveolar bone that is located 2-3mm apically from the cementum-enamel junction
The JE is at the level of the cementum-enamel junction Probing pocket is 3mm without bleeding on probing

50
Q

What are the clinical signs of gingivitis?

A

More than 3mm probing pocket with bleeding on probing
The JE is still at the level of the cementum-enamel junction
Alveolar bone was intact

51
Q

What are the signs of periodontitis?

A

Resorption of the alveolar bone, typically 2-3mm apically from the cementum-enamel junction
Greater probing pocket

52
Q

How is periodontal tissue damage caused?

A

20% of tissue damage is caused by the direct action of microorganisms
80% of periodontal tissue damage is caused by de-regulated inflammatory response to dental plaque

53
Q

Why does the JE migrate apically in periodontitis?

A

It migrates into the space of the destroyed gingival connective tissue due tot destroyed collagen gingival fibres and periodontal ligament fibres

54
Q

How does the periodontal ligament breakdown?

A

Breakdown of collagen fibres inserting between the alveolar bone and cementum, by proliferation of inflammatory filtrate
Damaged fibroblasts as there is a reduction in fibres ad ground substance of PDL
There is a build up of host factors in connective tissue, which leads to destruction of periodontal fibres

55
Q

How does the cementum become necrotic?

A

Destroy PDL means

Cementum can now not get nutrients from blood vessels in PDL so it becomes necrotic

56
Q

How does alveolar bone get damaged?

A

LPS stimulate the release of cytokines, leukotrienes, prostaglandins which activate osteoclasts

57
Q

Why are there more anaerobic species in the gingival sulcus?

A

They are in deeper areas which have less oxygen in the gingival and periodontal pockets

58
Q

What is necrotising periodontal disease characterised by?

A

Fuso-spirochaetal complexes that invade host gingival tissues

59
Q

What antibiotics are used during periodontal therapy?

A

Pencillin
Tetracylins
Metronidazole

60
Q

What does penicillin do?

A

Inhibits cell wall synthesis

61
Q

What does tetracyclins do?

A

Inhibit protein synthsis

62
Q

What does metronidazole do?

A

Inhibits nucleic acid synthesis

63
Q

What are the stagnant areas where there are abundance of dental plaque?

A

Along the gingival margin and inter proximal areas

64
Q

How do disclosing agents work?

A

Change the colour of dental biofilm to provide a contrast with the tooth surface
Biofilms have the capacity to retain large amounts of dye substances due to interactions with biofilm components

65
Q

How does the two tones work in disclosing agents?

A

Stains early biofilm which is less than 3 days old with reddish pink and mature biofilm which is more than 3 days old with a blue colour

66
Q

What are the advantages of disclosing tablets to the dentist?

A

visualising dental biofilm
Color guides biofilm removal
Take plaque indicies

67
Q

What are the advantages of disclosing tablets to the patient?

A

Shwon where they need to brush better

Motivation and education

68
Q

What are the plaque index scores?

A

3- thick plaque visible along the gingival margin (no need to probe)
2- plaque is visible along the gingival margin, with or without air drying (no need to air probe)
1- following air drying, plaque is no visible but can be wiped using an explorer)
0- Following air drying, plaque is not visible nor can be wiped off

69
Q

What is recorded if an index tooth is missing?

A

Score the nearest tooth that is in that sextant

If there are no teeth enter X

70
Q

What is recorded if the plaque thickness varies across the gingival margin?

A

Score according to the worst situation

71
Q

What s the overall place index score?

A

Sum of the 12 surface scores

Both buccal and lingual -max of 36

72
Q

What is the O’Leary plaque score?

A

Determines if plaque is present or not on the 4 surfaces of the tooth

73
Q

What are the scores of O’Leary?

A

0 if there is no plaque and 1 if there is plaque

Score is expressed as a percentage of all surfaces

74
Q

What O’Leary score is considered appropriate oral hygiene?

A

20%

PER (3 decks)

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