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Dentistry Year 2 - Perio > Plaque and Calculus > Flashcards

Plaque and Calculus Flashcards

1
Q

What is the most significant aetiological factor of periodontal disease?

A

Plaque

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2
Q

What are the two types of bacteria in the biofilm?

A

Planktonic bacteria that float and sessile ones that sit on hard surfaces.

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3
Q

Once bacteria in the biofilm enter cells, what are they called?

A

Intracellular colonisation

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4
Q

Grouping the microflora in 3 groups:

  1. Indigenous species
  2. Supplemental species
  3. Transcient flora
A

1 = almost always present in a stable relationship with the host and dont compromise the host survival

2 = present in small numbers but if the environment changes they can become more abundant

3 = pass through but do not become established

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5
Q

What is the definition of dental biofilm?

A

Complex microbial community that develops on the tooth surface (and other hard, non-shedding materials), embedded in a matrix of polymers of bacterial and salivary origin

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6
Q

What are the 4 stages in plaque formation and explain these?

A
  1. Acquired pellicle formation
  2. Adherence of the pioneer microbial colonisers to the pellicle
  3. Co-aggregation (enrichment of the microbial present)
  4. Maturation of plaque
  5. Bacteria cannot attach to clean enamel surface. Saliva is rich in glycoproteins, phosphoproteins and lipids that can attach. Enamel surface is negatively charged due to phosphate groups. Attachment of positively charged glycoproteins and the other molecules onto enamel surface. First molecules attached are low molecular size. Bacteria do not take part in this first stage
  6. Some of the first bacterial colonisers can now attach to the pellicle. This is because some biofilm bacteria have the receptors to recognise the proteins on the pellicle and attach to those proteins. Oral bacteria go through ‘feast and famine’. Once the bacteria are firmly attached, the colonisers produce extracellular polysaccharide as food storage. The EPS produced are glucan and fructan, both produced from sucrose. Pioneer species produce products that other bacteria need to survive. Conc of oxygen decreases.
  7. The plaque microflora becomes more diverse. Alteration of local environment by initial colonisers (receptors, nutrients, CO2). Bridging species provide lots of adhesions to bridge early and late colonisers.
  8. After 7-10 days, the growth rate slows down. Continuous production of EPS (for structural integrity and protection). Co-ordination of activities. Shear forces from masticator limit further expansion.
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7
Q

What can some bacteria do which is not beneficial to the host?

A

Produce toxins, produce organic acid to lower pH

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8
Q

What is materia alba?

A

Soft accumulation of bacteria, tissue cells and food particles that lack organisation. They are loosely attached to the tooth surface and soft oral tissues. No extracellular polysaccharide.

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9
Q

Give the main details on calculus

A
  • Creamy white colour that can turn yellow-brown
  • Mineralised plaque
  • Can take 2-14 days to form
  • Matures over time
  • Not a causative for periodontitis as calculus is covered by a layer of biofilm
  • Acts as a plaque trap
  • Professional removal needed
  • Supra and sub gingival
  • Plaque retentive factor
  • Mineralisation relies on bacterial presence
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10
Q

How does the calculus form from plaque?

A

Need a saturated solution of Ca2+ and PO4-. Bacteria needed to initiate crystal growth. A suitably high pH needed to promote mineralisation.

(Microbes provide the matrix and drives precipitation of the mineral salts from saliva (calcium and phosphate). Bacteria initiate the crystal growth and a high pH is needed which is found in saliva.)

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11
Q

What causes supra gingival calculus and what causes sub gingival calculus?

A

Supra = due to precipitation of mineral salts in the saliva

  • Found in sites of saliva pooling
  • Easier to remove

Sub = due to presence of mineral salts in inflammatory exclude

  • High pH in pockets
  • More tenacious and difficult to remove
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12
Q

What are the local and systemic factors leading to periodontitis?

A

Local - promote accumulation of dental plaque (calculus, restoration with overhanging margins)

Systemic - modify the host-bacteria interaction (puberty, pregnancy, immunodeficiency, age, race, gene polymorphism, smoking, medication)

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13
Q

Periodontal tooth destruction:

What two things cause this and what % of the destruction do they cause?

A
  1. Direct action of the micro-organims (20%)

2. De-regulated inflammatory response to dental plaque, disruption of protective innate immunity (80%)

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14
Q

What factors make a bacteria perio-pathogenic?

A
  • Have to be able to attach to the host tissue or biofilm (via adhesions on early colonisers)
  • Multiplication at a susceptible site (producing proteases to get nutrients and inhibiting other bacterial growth)
  • Evading host defence - inhibiting the host immune response e.g. supressor T cell induction. leukotoxin
  • Damage host tissues via enzymes (collagenase), bone resorbing factors (LPS), cytotoxins (ammonia)
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15
Q

Give some direct and indirect ways of tissue damage

A
  • Cytotoxins
  • LPS (bone resorption)
  • Prostaglandins (humoral immunity, bone resorption)
  • Antigens
  • Proteases (evasion of host defences)
  • Lysosomal enzymes and free radicals (tissue damage)
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16
Q

Outline some of the key parts of the model of periodontal diseases

A

Need to start with specific bacteria producing antigens and LPS. This activates the host immuno-inflammatory response. Host produced cytokines and enzymes leading to connective tissue and bone metabolism. This leads to clinical expression of the diease.

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17
Q

Give a few cytokines that the biofilm can produce and their function

A

IL1 - osteoclast activation, inhibiting neutrophils

IL6 - increases bone resorption, activates T cells

IL8 - chemotaxis of neutrophils

IL10 - anti inflammatory suppression

PGE2 - vascular permeability, vasodilation, bone resorption

TNF - increases IL1 production and phagocytosis

TGF - anti inflammatory repair potential

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18
Q

What happens if we have more bacteria or more host?

A

If there is more bacteria - lead to direct tissue damage.

Most host response - indirect affect to the tissue damage.

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19
Q

Give a few details on the non-specific plaque theory

A
  • Caused by non-specific overgrowth of all bacteria in dental plaque
  • All bacteria in dental plaque can lead to periodontal disease
  • Doesn’t distinguish between different bacteria, its due to quantity of the plaque
  • Host has a threshold capacity to detoxify and disease would only occur if this threshold was passed
  • However not all patients get periodontal diseases from gingivitis - downside to the theory as this cannot be explained
  • Current treatment is non-surgical and we remove the plaque (remove all the plaque non-specifically). We base our current treatment on this theory
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20
Q

Give some details on the specific plaque theory

A
  • Cultivation of the aerobic species
  • This theory explains periodontal disease occurring due to the presence of specific pathogenic microbes causing inflammation
  • If these pathogens are present, periodontal disease will occur

Uses the diagram with the different bacteria in the colours. Yellow are gram positive bacteria (non perio-pathogenic).
Red are obligated periodontal pathogens. They are gram negative.

21
Q

Explain the difference between gram negative and gram positive

A

Positive = have a cytoplasm membrane on the surface and a thick cell wall of peptioglycan. No outer membrane.

Negative - inner cytoplasms membrane and thinner cell wall of peptidoglycan. Outer membrane present. High amount of lipopolysaccharide (can cause bone resorption directly and can activate the host immune response to cause inflammation).

Negative ones are more protected due to outer membrane so are much more resistance to antibiotics or host immune responses.

22
Q

Explain the ecological plaque theory

A

Periodontal disease is due to the imbalance in microflora. Even in the healthy mouth you can have the pathogenic bacteria but changes in the local environment, these pathogens start to grow faster and can lead to periodontal disease if numbers increase.

This can be due to the change in nutrients or if essential cofactors become presence, low oxygen and change in pH.

The bacteria can affect the environment in order to survive.

23
Q

What is the keystone pathogen theory?

A

Explains the pathogenesis of periodontal disease by organisms that have an effect on their environment that is disproportional compared to abundance.

Low abundance microorganisms can increase the quantity of normal microbes to cause inflammation. Highlights the importance of the whole microbe as the keystone pathogens cannot cause the disease on their own.

Healthy sites = have symbiotic bacteria living in harmony
Introducing the key pathogens, these can change the environment and impair host immunity. This leads to inflammation which will lead to changes to sub-gingival microbiota. More pathogen microbes and can lead to periodontitis.

24
Q

Explain the Inflammation-Medicated polymicrobial emergence and dysbiotic exacerbation theory

A

Highlighting the importance of inflammation.

Healthy mouth and plaque, more gram positive can lead to gingivitis. This inflammation can lead to growth of the periodontal pathogens due toe environment changes.
If this is controlled, gingivitis will be sustained and will not progress.
If the inflammatory response is not effective, there is further inflammation and tissue damage leading to periodontal pockets.

25
Q

Give the names of the type of gingiva going from oral cavity downwards along the tooth

A

Free gingiva, attached gingiva, alveolar mucosa

26
Q

How shows clinically healythy gingiva?

A

Coral pink, firm gum with uniform colour. No swelling. Knife-edged and intact margins. Flat, intact papillae. Absence of bleeding on probing. Probing depth of healthy gingival sulcus < 3mm. Surface texture (gingival stippling).

27
Q

What is the definition of inflammtion?

A

A protective tissue response to irritation, injury or infection, which serves to destroy, dilute or wall of both the pathogenic agent and the injured tissues.
Classical signs are pain, heat, redness, swelling and loss of function.

Types are acute and chronic.

28
Q

Give some details on dental plaque induced gingivitis

A
  • Signs and symptoms that are confined to the free gingiva (this is where dental plaque forms along this margin)
  • The presence of dental plaque to initiate the lesion (along the gingival margin)
  • Clinical signs of inflammation
  • Stable attachment level (junctional epithelium), no bone loss (only in the initial stage)
  • Reversibility of the disease be removing the aetiology
  • Possible role as a precursor to periodontitis
29
Q

Give some examples of primary, local and systemic factors leading to periodontal disease

A

Primary - dental plaque

Local - calculus, habits, development abnormalities

Systemic - diabetes, smoking, immunodeficiency

30
Q

What are the 4 stages of gingivitis and explain each?

A
  1. Initial Lesion
    - Occurs 1-2 days of plaque accumulation
    - Gram + anaerobes provoke immune response
    - Vasodilation with increase in neutrophils and gingival crevicular fluid
    - Infiltrate confined to small area of connective tissue under junctional epithelium
    - Minimal tissue damage
  2. Early Lesion:
    - Occurs 4-7 days of plaque accumulation
    - Increase of inflammatory infiltrate (mainly polymorphonuclear cells (PMN) and lymphocytes)
    - Loss of fibroblasts and collagen in infiltrated area to accommodate for inflammatory infiltrate
    - Proliferation and increases rete peg formation in JE
    - Increases gingival crevicular fluid
    - PMNs accumulate in gingival crevice
    - May get bleeding on probing
  3. Established Lesion:
    - Gingival connective tissue largely replaced by inflammatory infiltrate
    - Large and increasing numbers of neutrophils, lymphocytes and plasma cells
    - Blood stasis
    - Epithelial ulcerations (due to epithelial cells not getting enough nutrients)
  4. Advanced Lesion:
    - Progression to periodontitis
    - Inflammatory infiltrate affects the alveolar bone to be lost.
    - Usually 2-3 weeks of dental plaque.
31
Q

Give the details on probing the gingival sulcus, the gingival pocket and the junctional epithelium

A

Gingival sulcus: up to 3mm and no bleeding

Gingival pocket: greater than 3mm due to inflammatory infiltrate and bleeding due to vasodilation

Junctional epithelium - apical to the level of cementum-enamel junction and there is bleeding on probing

32
Q

What are the treatment options for gingivitis?

A
  • Oral hygiene and plaque removal
  • Address local factors involved
  • Be aware of the systemic factors
33
Q

Give the differences clinically between gingivitis and periodontitis:

A

Gingivitis = periodontal pocket larger than 3mm, bleeding occurring on probing, junctional epithelium at the level of the cement-enamel junction and intact alveolar bone.
No destruction of deeper periodontal tissues. Reversible.

Periodontitis - irreversible, cannot regenerate all the lost periodontal tissues, resorption of the alveolar bone (more apical >3mm), junctional epithelium id apical to the cement-enamel junction, probing pocket > 3mm and bleeding one probing.

34
Q

Explain what the critical pathway model is

A

We start with normal dental plaque that can be removed by tooth brushing. This is non-pathogenic commensal bacteria and lives in harmony with immune system.
If dental biofilm accumulates, we get an increase in pathogenic bacteria.

The innate immune reponses start to control the bacteria. If this is successful, we get gingivitis and if not, we get increased bacterial load and the bacteria penetrates into the periodontal tissues to get adaptive immune response.
If this is successful, we get gingivitis and if not, the infection gets out of control.

Constant presence of the bacteria and increase in GCF (gingival crevicular fluid) and decrease in oxygen conc.

Co-operation of bacteria will commensal bacteria. Leads to further inflammation that spreads to periodontal tissue. This leads to tissue destruction. Areas are hard to clean and rich in proteins, low in oxygen which enhance the growth of the perio-pathogenic bacteria.

35
Q

How can the host immune response lead to bone loss?

A

Antigens activate the dendritic cells. These release pro-inflammatory cytokines. These activate B and T cells. Some inflammatory cytokines have a big effect on differentiation of osteoclasts. If these osteoclasts are activated, alveolar bone loss occurs.

36
Q

What is the process of tissue loss in periodontitis?

A

Migration of the junctional epithelium in health is prevented by healthy connective tissue underlying.

In periodontitis, this JE migrates into the spaces of destroyed gingival connective tissue and periodontal ligament fibres.

Breakdown of collagen fibres between the alveolar bone and cementum. Damaged fibroblasts (less ground substance). Build up of host factors and bacterial factors in connective tissue.
Necrotic cementum as it gets no nutrients from the periodontal tissue.

LPS stimulate release of cytokines to activate osteoclasts. Other inflammatory mediators are released by neutrophils and macrophages.

37
Q

What are the 6 points that are important to undergo when a periodontal condition is found?

A
  1. Prevention - what bacteria are involved and how we manage them
  2. Risk assessment - for each patient, need to know the aetiopathogenesis of periodontal diseases
  3. Diagnosis - what periodontal disease it is
  4. Communication
  5. Treatment planning
  6. Monitoring treatment
38
Q

What do we notice in the gingival pockets when they become unhealthy?

A
  • More anaerobic
  • Gingival crevicular fluid (provides nutrients for pathogenic bacteria)
  • Novel substrates for bacterial metabolism e.g. proteins
  • Asaccharolytic bacteria (cannot metabolise sugars so get nutrients from GCF)
  • pH 6.9-7.8
  • Motile bacteria
  • Gram negative
39
Q

What type of bacteria do we find in gingivits?

A

Non-specific gram positive bacteria.

40
Q

Porphyromonas gingivalis is a bacteria in the red category.. Give some factors it has for survival

A

LPS
Proteases for breaking down cytokines to stop immune response
Has a capsule to protect rom host
Anaerobic

41
Q

What do most gram-negative bacteria produce?

A

LPS to trigger immune response to cause bone loss.
Leukotoxin (toxin to monocytes)
Collagenases (destruct connective tissue)

42
Q

What is a necrotinizing periodontal disease?

A

Acute diseases

  • pain
  • bleeding
  • lymph nodes damaged
  • grey pseudomembranes - made from dental plaque and necrotic tissues

This disease is badly affected by systemic factors i.e. smoking, poor oral hygiene, immunosupression, emotional stress, diet.

43
Q

What is the main role of antibiotics in periodontal therapy and explain each

A

Local and systemic
Decreasing the amount of particular bacteria from the plaque

Penicillins - inhibition of cell wall synthesis
Tetracyclins - inhibition of protein synthesis
Metronidazole - inhibition of nucleic acid synthesis

44
Q

What can we use to detect the biofilm?

A

We use a disclosing solution to detect the biofilm. Usually along the gingival margin and inter proximal areas, it will form (no shedding movements in the oral mucosa).

45
Q

How do disclosing agents work?

A 
Substances that work by changing the colour of the dental biofilm to provide a contrast with the tooth surface 
Biofilms have the capacity to retain large amount of dye substances due to interactions with biofilm components
Electrostatic iterations (proteins) and hydrogen bonds (polysaccharides) bind the particles together
Surfaces which are biofilm free can easily be rinsed off as nothing to retain the dye
46
Q

What is good about ‘two tone’ disclosing agent?

A

Stains < 3 days biofilm with red and > 3 days with blue

47
Q

What are the advantages of a disclosing agent to a clinician and to a patient?

A

Clinician:

  • Visualise the biofilm
  • Colour helps to guide removal
  • Plaque indicies can be taken

Patient:

  • Motivation
  • Personalised patient instruction
  • Self-evaluation by patient
  • Maintenance
48
Q

What are the two ways of measuring plaque?

A

Plaque Index -
Quantitative as it measures the amount of dental plaque.
Move the probe along the gums and see if you can see any plaque. Give a score from 0 to 3.

0’Leary Plaque Score -
Qualitative - is there plaque or not
Use all surfaces of the teeth
Use disclosing agent first

0 = no plaque 
1= plaque present

Calculate the % covered by plaque. Up to 20% is considered good oral hygiene.

Dentistry Year 2 - Perio (6 decks)

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