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COPY BDS3 University of Adelaide Dentistry > Periodontology > Flashcards

Periodontology Flashcards

1
Q

What is the decoy molecule that will provent Osteoclastic differentiation?

A

Osteoprotegerin (OPG)

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2
Q

What is the antagonist to MMP?

A

TIMP: tissue inhibitor of MMP

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3
Q

List the pro-inflammatory cytokines involved with Perio

A

IL-1b, TNFa, IFN-g, PGE2, MMP

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4
Q

List the anti-inflammatory cytokines involved with perio

A

IL-1ra, IL-10, TGFb, TIMPs

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5
Q

Large numbers of RANKL require what to progress to bone loss

A
  1. Low levels of OPG from Osteoblasts

2. Large numbers of pre-osteoclasts expressing RANK receptors

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6
Q

What can be given to block MMPs to prevent bone loss

A

Low dose of 20mg doxycycline antibiotic for 2 weeks

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7
Q

How do Biphosphonates affect bone loss

A

Reduces bone loss by inhibiting osteoclast activity

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8
Q

What are the grades of mobility?

A

Grade 1 – mobility up to 1mm
Grade 2 - mobility up to 2mm
Grade 3 – mobility more than 3mm and vertical

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9
Q

What are the grades of furcation?

A

I: Horizontal loss of supporting tissue not exceeding 1/3 the width of the tooth
II: Horizontal loss of supporting tissue exceeding 1/3 the width of the tooth, but not encompassing the entire furcation area (can not stick probe straight through the tooth
III: “Through and through” destruction of supporting tissues in furcation (sticking probe through gap will result in it going right through to the other side)

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10
Q

What are the available tests to detect periodontal disease?

6 examples given, probably reasonable to list 4?

A
  • Medical history (predisposing/modifying systemic diseases, medications, blood tests)
  • Social history: (smoker, stress, alcohol, diet)
  • Intra-oral exam (including perio exam/probing/mobility/furcation + searching for features that pre-dispose attachment loss (vertical root fracture, enamel pearls, overhanging restorations)
  • Vitality test (for perio-endo lesions)
  • Subjective assessment of calculus
  • Radiographs (BW, OPG, Full mouth survey/FMS)
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11
Q

What are the 3 irritating factors in gingivitis

A

Gram Negative Endotoxins
Proprionic Acid
Butyric Acid

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12
Q

How is the Junctional Epithelium anchored to the basement membrane?

A

Hemidesmosomes

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13
Q

Remodelling of transseptal PDL in the early stages of periodontitis results in what?

A

Development of deeper pocket depths

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14
Q

Why is LPS destructive for the periodontal apperatus?

A

Elicits a host immune response that promotes destruction of the gingiva and PDL

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15
Q

On what bacteria can LPS be found?

A

Gram Negative

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16
Q

What stimulates the release of Matrix Metallo-Preteinase (MMP)

A

Presence of LPS in the JE. JE epithelial cells stimulate inflammatory cytokines including MMP

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17
Q

In periodontitis, during the upregulation of inflammation , what do fibroblasts produce instead of collagen?

A

MMP and TIMP

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18
Q

What influences macrophage activity during gingivitis/periodontitis?

A

1) Genetics - hyper responsive phenotype
2) Smoking
3) NSAIDS suppress PGE2 production

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19
Q

What is the role of plasma cells in periodontitis?

A

Effective plasma cells can make an individual less susceptible to periodontitis. Plasma Cells do this by

1) Agglutinate Microbes
2) Prevent epithelial adhesion
3) Work with complement to kill microbes
4) Allow effective phagocytosis by PMNs

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20
Q

Define Clinical Attachment Loss

A

CAL = Pocket Depth + Recession

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21
Q

How long can Biphosphonates be biologically active in the body

A

18 months to 10 years

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22
Q

Which has a worse prognosis? 1 walled or 3 walled bony defect?

A

1 Walled Bony Defect , only 1 side of bone left. Surgical / Regeneration impossible

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23
Q

What are Suprabony pockets?

A

Suprabony pockets are formed when bone loss occurs in a horizontal pattern

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24
Q

What are Infrabony pockets?

A

Infrabony pockets occurs when bone loss occurs in a vertical/angular direction

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25
Q

What are 3 ways to splint mobile teeth?

A

Wire Splint
Composite Resin Splint
Removable Acrylic Splint

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26
Q

Clinically, when would you do a splint?

A
  • Mobile teeth where mobility is getting worse: eg occlusal trauma
  • After removal of extensive calculus with a patient with severe perio and CAL
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27
Q

When would expect to see more physiological tooth movement?

A

In the evenings after eating, talking

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28
Q

What is Naber’s Probe used for?

A

Measuring furcations

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29
Q

What class furcation is it when you can probe to a depth of more than 2mm with periodontal probe

A

Furcation Class II

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30
Q

What are the 3 sites of furcation on an maxillary molar?

A

Buccal, Distal Palatal, Mesial Palatal

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31
Q

What congenital tooth defect would make a furcation less likely?

A

Taurodontism

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32
Q

What is the root trunk?

A

Distance from the CEJ to the roof bifurcation

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33
Q

How do you manage Class I Furcation?

A

Debridement and Maintenance

Interdental Brush for patient to clean under tooth

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34
Q

What is a furcation plasty used for?

A

For Class II Furcation, use a bur to smooth the area around the furcation to make it easier to clean.

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35
Q

In stage 1 of periodontitis, describe the pathogenesis of periodontitis in terms of molecular biology

A
  1. Initial reaction to plaque: Presence of LPS and other irritants stimulates JE to produce proinflammatory mediators eg: IL8, TNFa, PGE2 and MMP.
    Perivascular mast cells release histamin causing endothelium releasing IL8 to attract PMN (which palisade over the biofilm and phagocytose bacteria)
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36
Q

In stage 2 of periodontitis, describe the pathogenesis of periodontitis in terms of molecular biology

A
  1. Activation of macrophage: Vascular reaction cause complement protein to enter and activates the inflammatory reaction
    Leukocytes and monocytes are then recruited
    Monocytes then differentiated into macrophage which is responsible for phagocytosis and releasing inflammatory mediators (IL1, PGE2, TNFa, MMP, IFN) and chemotaxins (MCP, RANTES, MIP)
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37
Q

In stage 3 of periodontitis, describe the pathogenesis of periodontitis in terms of molecular biology

A
  1. Upregulation of Inflammatory cell activity: Activated T-cells coordinate response via cytokines (IL2-6 10-13, TNFa, TGFb, IFNg)
    Plasma cells produces Igs and cytokines
    Activated PMN synthesise cytokines, leukotrienes and MMP
    Activated fibroblast produce MMP and TIMP instead of collagen and infiltrate expands
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38
Q

In stage 4 of periodontitis, describe the pathogenesis of periodontitis in terms of molecular biology

A
  1. Initial Attachment Loss: Immunocompetent cells produce cytokines MMP and TIMP leading to tissue destruction and bone resorption
    Plasma cells becomes dominant in the ilfiltrate
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39
Q

What bacteria are involved with the Red Complex for periodontitis?

A

P. gingivalis, B. forsythus, T. denticola

  • A. actinomycetemcomitans now part of Yellow Complex
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40
Q

What is the significance of the Red Complex in periodontitis?

A

They are the bacteria found in plaque that are pathogenic through the adaptative to the gingival environment and release of endotoxins that elicit a host response. They are found in cases of severe periodontitis.

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41
Q

What is the difference between a predisposing vs a modifying factor in Periodontitis?

A

Predisposing Factor: something that interferes with patient’s ability to reduce plaque

Modifying Factor: modifies

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42
Q

Why are restoration overhangs a periodontal risk?

A

Overhangs harbour increased number of gram-negative anaerobes that initiate perio at these sites

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43
Q

Which gender has a higher predisposition to periodontitis?

A

Females

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44
Q

What congenital aspects of tooth anatomy are predisposing risk factors for Periodontitis?

A 
Cervical Enamel Projections
Palatal Invaginations
Accessory Root Canals
Close Roots / Root Proximity
Root Concavities
Enamel Pearls
Tooth Malposition (Crowding/Rotation)
Gingival Contours
Age
Gender
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45
Q

What modifying dental factors increase risk of periodontitis?

A 
Furcation Involvement
Dental Restorations
Overhanging Margins
Poor Maintained Dental Prostheses
Oral Hygiene (Plaque Levels)
Presence of Calculus
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46
Q

A “Cup” bone loss indicates what?

A

There has been bone loss around all aspects of the tooth. Prognosis is poor, usually involving extraction.

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47
Q

What are 5 ways that furcation involvements can develop?

A
  1. Chronic and aggressive forms of periodontitis
  2. Cervical enamel projections (rare)
  3. Perforations in floor of pulp chamber during endo will cause periodontal inflammation and loss of attachment with pocket formation
  4. Accessory/furcation canals can create pockets
  5. Fenestrations, dehiscence
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48
Q

What are some invasive treatment options for Furcation Involvement?

A
  1. Root Resection (removing a root to eliminate furcation)
  2. Hemisectioning (split the tooth into half, recrown, to eliminate the plaque trap)
  3. Guided Tissue Regeneration
  4. Implants
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49
Q

What is the indication for root resectioning?

A
  1. Severe bone loss on only one root of multi-rooted teeth

2. Root Fracture

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50
Q

Is continuous eruption part of periodontitis?

A

No

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51
Q

What are the 5 main etiological causes of Periodontitis?

A
  1. Pathogenic Anaerobic Gram Negative Bacteria
  2. Host (Genetics, Systemic Disease, Heightened Immune Response, Nutrition)
  3. Habits (Smoking, Alcohol, Diet)
  4. Social Factors (SES, Education, Upbringing)
  5. Psychological Factors/Stress
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52
Q

What are environmental factors needed for Perio?

A 
Plaque
Calculus
Rough Tooth Surfaces
Defective Restorations/Appliances
Tooth Anatomy
Crowding/Rotation
Traumatic Occlusion
Smoking
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53
Q

Define periodontitis

A

Inflammation of gums, resorption of alveolar bone and degeneration of periodontal membrane

It is a complex reaction initiated when subgingival plaque bacteria are in close contact with epithelium of gingival sulcus.

Injury arises from toxins and enzymes produced by bacteria and host-mediated defense responses.

Results in apical movement of junctional epithelium indicating attachment loss and alveolar bone loss

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54
Q

What are Socransky’s Postulates?

A
  1. Improvement of disease after elimination of pathogen by therapy
  2. Activation of host immune response to specific infection
  3. Detection of putative virulence factors e.g. endotoxin (LPS), exotoxin, enzymes, antigens
  4. Elicitation of similar periodontal disease symptoms in animal experiments
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55
Q

What is the primary risk factor for Periodontitis?

A

Specific pathogens from plaque associated with severe periodontitis such as the red complex

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56
Q

What are 5 non-alterable secondary risk factors for Periodontitis?

A 
Genetics
IL-1 Gene Polymorphism 
Ethnic Origin
Gender
Age (ANUP more common in young people)
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57
Q

What is the role of host response in periodontitis?

A

Influences the clinical presentation and rate of progression of the disease

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58
Q

How can high frenal attachment affect gingival health?

A

Excessive tension on gingival margin makes brushing very sensitive. People stop brushing this area and it becomes a site for plaque attachment

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59
Q

4 types of bacteria responsible for causing periodontitis

A

P. gingivalis, B. forsythus, T. denticola, A. actinomycetemcomitans

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60
Q

List 2 main secondary risk factors that are alterable in periodontitis

A

Smoking and stress

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61
Q

In what situation will the palatal wall be resorbed first in a 3walled defect

A

Anatomical variation ie: enamel pearls, palato-radicular grooves and cervical enamel projection

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62
Q

When assessing an individual tooth for periodontal prognosis, what are factors to bear in mind?

A

1) Strategic Value

2) Perio Value
- % Bone Loss
- Probing Depth
- Distribution / Type of Bone Loss
- Mobility
- Crown to Root Ratio
- Presence/Severity of Furcation
- Root Form

3) Tooth Factors
- Caries
- Pulpal Involvement
- Tooth Position / Occlusal Relationship

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63
Q

What are 9 factors to take into account when doing an overall periodontal prognosis

A 
Age
Medical Status
Individual Tooth Prognosis
Rate of Progression
Patient Cooperation
Economic Considerations
Knowledge and Ability of Dentist
Risk Factors
Oral Habits
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64
Q

What would define a questionable periodontal prognosis?

A

1) When local + systemic factors are not controllable

2) Clinical signs include:
- Severe Attachment Loss
- Poor Crown / Root Ratio
- Class II-III Furcation with difficult access
- Class II-III Mobility
- Root Proximity

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65
Q

What would define a poor periodontal prognosis?

A

1) When local + systemic factors might not be controllable

2) Clinical signs include:
- Moderate Attachment Loss
- Class I-II Furcation with difficult access

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66
Q

What is the main aspect of patient acceptance for a periodontal plan?

A

The patient takes responsibility for the treatment option selected.

In order to do so:

1) Understanding the risk factors,
2) Role of plaque in gingivitis 3) Steps they need to do improve the local/systemic factors

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67
Q

What are steps in treatment planning for advanced generalised chronic periodontitis?

A

1) Risk Factor Management
2) Detailed Oral Hygiene Instruction
3) Changing Microflora
4) Systematic Subgingival Debridement
5) Removal of irritating factors
6) Periodontal Surgery
7) Periodontal Maintenance

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68
Q

In some very seriously medically compromised patients, what are something to do whilst address the systemic phase of periodontal care?

A

1) Address medical history
2) Need for antibiotic cover
3) Address hemostatic issues
4) Interaction with GP/Haematologist/Specialists
5) Assess the presence and severity of risk factors

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69
Q

If a patient has a blood clotting issue, what are some considerations before periodontal treatment?

A

1) Check with their GP/Haematologist
2) Cessation of warfarin
3) INR check (Blood Clotting Measure)
4) Tranexamic Acid Mouthwash (Prevents excessive bleeding)

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70
Q

What are the 5 periodontal treatment goals?

A
  1. Control of Infection
  2. Removal of predisposing factors
  3. Regulate/Control any modifying factor
  4. Regenerate to original form/function
  5. Maintain lifespan/function/aesthetics of remaining dentition
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71
Q

Can you have gingivitis and periodontitis at the same time?

A

No, periodontitis infers that the microbial composition subgingivally has changed. You can have gingival inflammation (that clinically appears the same as gingivitis) coming from the specific periodontitis microbes

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72
Q

What is supportive periodontal therapy?

A

SPT is the cleaning procedure performed to thoroughly clean the teeth.

It is an important therapy for halting the progression of periodontal disease and gingivitis by keeping the oral cavity in good health and also halt the progression of gum disease

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73
Q

What are important patient factors to take into consideration for perio diagnosis?

A 
Age
Smoking
Medical Conditions: Uncontrolled Diabetes
Medications
Stress
Compliance / Motivation
Initial Diagnosis: Aggressive Perio + Advanced Chronic Perio
Genetics: IL-1 Polymorphism
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74
Q

What are important oral factors to take into consideration for perio diagnosis?

A 
Oral Hygiene
Parafunctional Habits
Previous Tooth Loss History
Bone Loss
Gingival Biotype
Mucocutaneous Disorders
Prosthesis: Dentures + Bridge
Access
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75
Q

What are important tooth factors to take into consideration for perio diagnosis?

A 
Levels of Calculus
CAL = Probing Depth + Recession
BOP
Furcation: using Naber’s Probe
Bone Loss (if > 75%)
Suppuration
Mobility
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76
Q

What groups are high risk for IL-1 Polymorphism that affects susceptibility to perio?

A

Caucasian people

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77
Q

What are important predisposing factors to take into consideration for perio diagnosis?

A 
Enamel Projections
Grooves + Fissures on Root Surfaces
Carious Lesions, Resorptive Defects
Subgingival Restorations, Overhang Restorations
Vertical Root Fractures
Endodontic Considerations
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78
Q

What 6 factors can be measures to determiner periodontal risk assessment?

A 
Smoking
Genetic / Systemic
BOP
Bone Loss divided by Age
Tooth Loss
Number of sites PD > 5mm
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79
Q

How would differentiate between buccal and palatal bone loss?

A
  1. Check clinically - with perio probe

2. Horizontal Shift with Radiographs

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80
Q

You have two patients of differing ages - one in their 30s and another in the 60s with the exact same perio symptoms. Are their diagnosis the same?

A

No, older patient’s damage is cumulative and could be indicative of past aggressive perio which is now stabilised and considered chronic rather than acute.

An individual with perio in their 30s is more likely to facing aggressive forms of perio that is not indicative of plaque levels. This would then be considered more likely to be acute aggressive forms of the disease

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81
Q

T/F: Smoking is the main cause of periodontitis

A

False. Bacteria are the main causative factor for periodontitis but smoking is the main modifying risk factor.

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82
Q

What are the main modifying risk factors for periodontitis?

A
  1. Smoking
  2. Systemic diseases (diabetes)
  3. Genetics
  4. Stress
  5. Neutrophil Dysfunction
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83
Q

What are some clinical signs of a patient with periodontitis if they are a smoker

A
  1. Pale Pink Gingiva
  2. Reduced BOP for the amount of calculus present
  3. Smoker’s Breath
  4. Extrinsic staining of teeth
  5. Pale complexion in peripheries (eg fingers)
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84
Q

T/F: In Australia, more than half of severe cases of periodontitis would have been prevented if smoking could be eliminated in the population

A

True

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85
Q

For smokers where is the likely area of greater periodontal attachment loss?

A

Areas where nicotine has more contact with the mucosa eg Maxillary palatal aspects

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86
Q

What symptoms of gingivitis are you likely to see in a heavy smoking patient with perio?

A

Less gingivits and less bleeding on probing

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87
Q

Why is there more severe alveolar bone loss in smokers?

A

Vasoconstriction of nicotine decreases nutrient supply to bone, increase resorption rates

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88
Q

What effect does smoking have to bacterial flora?

A

Smokers have more plaque and virulent (red complex) periodontal bacteria

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89
Q

What effect does smoking have to host response?

A
  1. Impeded ability to combat bacterial egress due to vasoconstriction
  2. Decreased PMNs in JE
  3. Increase in pro-inflammatory cytokines (PGE2, IL-4, IL-8, TNF-α in GCF)
  4. Decrease in anti-inflammatory cytokines (IL-6)
  5. Decreased IgG antibodies to A. actinomycetemcomitans
  6. Poor B Cell Function
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90
Q

What effect does smoking have epithelial cells?

A

Smoking increases proliferation of gingival keratinocytes

Increases the levels of keratin in the epithelium

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91
Q

What effect does smoking have on fibroblasts

A

Poor periodontal regeneration due to:

1) Altered Cell Morphology
2) Poor Adhesion to root surfaces
3) Reduced soft tissue/PDL healing

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92
Q

How would you gauge if your diabetic patient is at risk for perio?

A

1) Ask about their resting blood glucose levels

2) Is their diabetes controlled via medications or diet

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93
Q

What constitutes controlled diabetes?

A

HbA1c-glycated haemoglobin measure over a 3 month period reading 4-8 mmol/L

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94
Q

Is controlled blood glucose levels a risk factor for gingivitis?

A

No

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95
Q

What are the clinical signs of gingivitis in an uncontrolled diabetic?

A

Increased gingival bleeding and gingivitis irrespective of plaque levels

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96
Q

T/F: A patient with long term Type 2 Diabetes is at high risk of periodontal disease

A

False - diabetes is only a risk modifier and the risk factors only increase if it is not well controlled

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97
Q

The production of advanced glycation end products (AGEs) in the periodontal apparatus occurs under what conditions?

A

Non enzymatic glycosylation occurs under chronic hyperglycaemia with uncontrolled diabetes (Type I/II)

98
Q

Advanced glycation end products (AGEs) does what to collagen?

A

Alters the structure and turnover rate of collagen.

99
Q

What are the long term immunological implications of AGEs build up in the periodontal apparatus?

A
  1. AGEs alter the structure and turnover rate of collagen.
  2. In the Junctional Epithelium, there is too much collagen forming and the basement membrane becomes too thick. This results in:
  • Impairs oxygen diffusion
  • Waste elimination
  • Leukocyte migration
  • May contribute to pathogenesis of periodontitis
  1. AGEs modify the phenotype expression of macrophages and interfere with macrophage ability to help repair
100
Q

What does hyperglycemia do to PMNs?

A

Increased glucose concentration inhibits:

  • PMN migration/chemotaxis
  • Phagocytosis of pathogens
  • Respiratory burst
101
Q

What does hyperglycemia do to Macrophages?

A

1) Phenotype of macrophages altered due to cell surface interactions with AGEs
2) Prevent the development of macrophages associated with repair

102
Q

What interactions does Hyperlipidemia have with macrophages?

A

Upregulates pro-inflammatory cytokines (IL-1, PGE2 and TNFα )

103
Q

How does hyperglycaemia result in poor wound healing

A

1) Impaired host response leading to infection
2) Decreased cellular proliferation and fibroblast numbers
3) Defective remodelling and rapid degradation of newly synthesized, poorly linked collage
4) Upregulation of inflammation

104
Q

What interactions does HIV have on periodontitis?

A

More severe and extensive chronic periodontitis related attachment loss, particularly with CD4 positive T cell counts below 200

105
Q

What medications can result in gingival enlargement?

A

Phenytoin, calcium channel blockers and cyclosporine

106
Q

Why can stress play a role in periodontitis?

A
  • Cortisol released HPA axis upregulates proinflammatory cytokines
  • Sympathetic nervous innervation releases adrenaline and noradrenaline is indirectly immunosuppressive => provoking periodontal tissue breakdown
107
Q

What are the 3 ways genetics can influence periodontitis?

A

Different expression for innate immunity, adaptive immunity and nonspecific inflammatory mediators

108
Q

What effects can puberty have on gum health?

A

High prevalence of gingivitis due to spikes in sex hormones

109
Q

What effects can menstruation have on gum health?

A

Swollen gingiva + bleeding due to:

Increase in progesterone
Increase in vascularisation
Increased collagen production in gingiva
Increased prostaglandins and chemotaxis of PMNs

110
Q

What effects can pregnancy have on gum health?

A

Increases risk of perio

Pregnancy Gingivitis

111
Q

How can Osteoporosis affect periodontitis?

A

Decreased bone mineralisation + density means resorption (if present) occurs at a faster rate

112
Q

How can Menopause affect periodontitis?

A

Production of pro-inflammatory cytokines in response to oestrogen withdrawal at menopause is responsible for characteristic loss of bone density through effects on osteoclast activity

113
Q

What is an example of a neutrophil dysfunction that affects gingival health?

A

Cyclic Neutropenia - very fiery red gums due to low PMN count

114
Q

What are the 4 ways to control Periodontal Disease

A

1) Control host response modifying factors (diabetes, smoking)
2) Elimination of plaque retentive factors (fissures, overhangs)
3) Disruption and reduction of plaque biofilm (Supportive Periodontal Therapy)
4) Shift of microbial flora composition (Antibacterials)

115
Q

What sort of antibiotics would be more appropriate for Periodontal bacteria?

A

Metronidazole (Flagyl) - narrow spectrum for anaerobes

116
Q

Are penicillin based antibiotics appropriate for Periodontal therapy?

A

No, Prevotella in periodontal pockets contains beta-lactamase.

117
Q

Is tetracycline appropriate for periodontal therapy?

A

No due to increased antibiotic resistance to tetracycline

118
Q

How as dentists can we prevent antibiotic resistance in perio treatment?

A
  1. Prescribe antibiotics carefully
  2. Must select appropriately and use the appropriate agent in each clinical scenario
  3. Salivary/Exudate swab to identify species (expensive)
119
Q

When is metronidazole contraindicated for AB treatment for perio?

A

If patient is currently on Warfarin - increases bleeding time
Alcohol - overtaxes liver

120
Q

What opportunistic infections can occur during AB treatment for perio?

A

Pseudomembranous colitis

Oral Candidiasis

121
Q

When is AB prophylaxis indicated before perio therapy?

A

To high risk patients 1 hour before treatment.

  1. Immunocompromised patients
  2. Infective Endocarditis + Heart Valve implants
  3. ANUG
  4. Aggressive Refractive Perio

Low benefit for prevention of post-operative infection or regenerative outcomes. Only considered for very invasive procedures

122
Q

Why is there a barrier to diffusion for systemic AB treatment of perio?

A

Mature biofilm prevents diffusion of AB from GCF. High concentrations need.

AB will work better after debridement/disturbing biofilm with SPT.

123
Q

Which AB is appropriate for very aggressive perio bacteria?

A

Azithromycin (500 mg once daily for 3 days (a tablet)

124
Q

What is Refractory perio and what are treatment options

A

When perio does not respond to treatment. Antibiotic therapy is indicated as well as addressing major risk factors (diabetes/smoking)

125
Q

Is Tetracycline effective for generalised aggressive perio

A

No

126
Q

What type of antibiotic is Azithromycin?

A

Macrolide - a protein synthesis inhibitor

127
Q

How often can you prescribe Azithromycin for perio?

A

Once every 6 months. High AB resistance - particularly against pneumonia

128
Q

When is Azithromycin contraindicated?

A

Patients with CVD

129
Q

2nd Generation chemical control agents have what type of substantivity

A

High substantivity = can bond to the surface so several hours

130
Q

What are the 3 main ingredients in mouthrinses?

A

1) Alcohol
2) Surfactant
3) Flavouring Agents

131
Q

What are the main group of chemical agents to control plaque / gingivitis?

A
  1. Bisbiguanide antiseptics
  2. Quaternary ammonium compounds
  3. Essential oils (EO)
  4. Natural products
  5. Oxygenating agents
  6. Amine alcohols
  7. Other
132
Q

T/F: Chlorhexidine removes/kills existing plaque bacteria

A

False, it is a surfactant that prevents recolonisation of surfaces after plaque removal

133
Q

How long is the action of surfactant in Chlorhexidine?

A

48 hours

134
Q

Why should Chlorhexidine not be taken straight after brushing?

A

Fluoride binds to the positivity charged CHx, rendering it useless

135
Q

What are short term indications for Chlorhexidine use?

A
  • After periodontal/oral surgery
  • Acute periodontal conditions: ANUG, periodontal abscess (1-2 weeks)
  • Apthous ulcers
  • Severe chronic gingivitis (1-4 weeks)
  • Rampant caries
136
Q

What are long term indications for Chlorhexidine use?

A
  • Patient with physical/mental handicap
  • Medically compromised
  • Patients with jaw fixation
137
Q

What are side effects of Chlorhexidine?

A
  • Bitter, unpleasant taste
  • Interfere with sense of taste
  • Staining of teeth/restorations
  • Enhanced supraginginval calculus formation
  • Allergy/sensitivity, possible anaphylaxis
  • Uni/bilateral parotid swelling (very rare)
138
Q

Cetylpyridinium Chloride (CPC) is what type of chemical agent and what product can you find this in?

A

Quaternary Ammonium

Colgate Plax

139
Q

T/F: Quaternary Ammonium are high substantivity chemical agents

A

False, low substantivity

140
Q

What is the mode of action of essential oils on microbes?

A
  • Microorganisms killed by disrupting their cell walls and inhibiting enzyme activity
  • Prevents bacteria from aggregating hence slowing bacterial proliferation
  • Reduces bacterial load
141
Q

What are the concerns of long term essential oil usage for plaque control?

A

Listerine contains alcohol which can dehydrate mucosa. Long term use can cause metaplasia - alter cell architecture / histology.

No definitive link to cancer

142
Q

What is considered gold standard for chemical plaque control?

A

Chlorhexidine, as adjunct to daily mechanical oral hygiene

143
Q

What are indications for use of mouthrinses as an adjunct?

A
  • After surgical procedures: as toothbrushing may be difficult
  • In medically compromised patients
144
Q

What are the only 2 systemic diseases that have bi-directional aetiology with periodontitis?

A
  • Diabetes

- Rheumatoid Arthritis

145
Q

How does a focal periodontal infection affect the body on a systemic level?

A

Chronic Inflammation places a burden at the systemic level due to increased circulation of pro-inflammatory cytokines

146
Q

What is the Periodontal medicine hypothesis?

A

That focal periodontal infection presents a chronic inflammatory burden at the systemic level

147
Q

How might periodontal pockets influence systemic conditions

A
  1. Bacteria and their products may pass through periodontal pockets systemically into the bloodstream (eg for infective endocarditis)
  2. Chronic perio inflammation: pro-inflammatory mediators released systemically
148
Q

What is a focal infection?

A

Where a bacterial infection limited to a specific organ or region causing symptoms elsewhere in the body:

1) Perio => Infective Endocarditis
2) Systemic infections: Gangrene, TB, Meningitis, Septicaemia, Pneumonia

149
Q

How could perio bacteria enter the bloodstream

A 
Toothbrushing/flossing (can cause bleeding)
Mastication
Scaling
Subgingival irrigation
Endodontic treatment
Tooth extraction
150
Q

How does diabetes influence perio?

A

Worse symptoms

Increase likelihood of abscesses

151
Q

What are the current links between CVD and Perio?

A
  1. 44% of carotoid atheromas contain perio pathogens
  2. CVD patients have elevated C-reactive protein: a marker for bacterial infections
  3. Perio pathogens are linked to platelet aggregation: increase chance of stroke

Overall: elevated risks/poorer outcomes for CVD for patients with perio

152
Q

What are indirect effects that perio bacteria might have on modifying CVD symptoms?

A

Release of bacterial LPS:

  • May affect liver
  • Inflammatory Factors: C-reactive protein
  • CRP Fibrinogen: increased heart attack risk
  • Lipid abnormalities
  • Coagulation factors
153
Q

What are direct effects that perio bacteria might have on modifying CVD symptoms?

A

Release of bacterial LPS:

  • Increase mobilisation of macrophages
  • Pro inflammatory Mediators:
    Il-1, Il-6, TNF-alpha, PGE-2
154
Q

Why might perio symptoms be worse in uncontrolled diabetic?

A

Higher BGL in blood and GCF provide ample nutrition for bacteria to proliferate

155
Q

How might symptoms in a perio patient with uncontrolled diabetes be different?

A
  • Higher prevalence of exudate
  • Abnormally high response to LPS: exaggerated monocyte response, inflammatory cytokines
  • Impaired Wound Healing
156
Q

Is there a link between obesity and perio?

A

Possibly, but most likely because of undiagnosed Type II diabetes

157
Q

What defines low birthweight / preterm birth and what are the long terms health implications?

A

Low birthweight = < 2500g
Preterm = delivery before 37 weeks gestation

Birthweight considered an important determinant for infant’s chances to survive, grow and mature

158
Q

What is the epidemiology of low birth weight in SA?

A

4.5% births in SA

11% indigenous births

159
Q

What are the links between periodontitis and low birth weight?

A

2 Hypothesis:

  • Indirect mechanism via inflammatory mediators
  • Direct bacterial assault on the amnion

However no proof yet that treating maternal perio will result in better birth outcomes

160
Q

What is the link between respiratory illnesses and perio?

A

Perio is typically an indicator of poor oral hygiene.

Higher bacterial load in the mouth can spread into the oropharynx

Improving oral hygiene can reduce rate of pneumonia in high risk patients

161
Q

Why is there a likely link between rheumatoid arthritis and periodontitis?

A

They have same risk factors therefore assumed to have a relationship:

  • Chronic inflammation
  • Immunoregulation imbalance
  • Initiating bacterial peptides/antigens
  • Macrophage presence
  • Release of multitude of cytokines
  • Genetic/environmental
162
Q

Why might Rheumatoid Arthritis patients have more perio?

A

Arthritis limits manual dexterity and the ability to brush well

163
Q

Why might Perio patients have worse Rheumatoid Arthritis symptoms

A

Elevated serum CRP levels and additional inflammatory burden

164
Q

What is the link between osteopenia (pre-osteoarthritis) and periodontitis?

A

Higher rates of progressive alveolar bone loss when compared to normal bone density patients

165
Q

How can innate immune cells in the periodontium detect the presence of microbes in the JE?

A

Sampling microbes by detecting MAMPS/PAMPS via Protein Recognition Receptors (PRRs) such as Toll Like Receptors, C-type Lectin Receptors (CLR) and Mannose Receptors found on the membrane of innate cells such as Macrophages and Dendritic Cells

166
Q

T/F: The presence of High Endothelial-Like Venules (HEVs) is always pathological

A

False

Normal: Found near lymphatic tissue (Lymphatic organs, tonsils, peyer’s patches)

Pathological: during chronic inflammation HEVs are created. Being slightly larger than capillaries and creating turbulence in endothelial flow, they encourage innate defense cells to migrate to the site of inflammation.

167
Q

When are PMNs found during perio related disease

A
  1. Initial inflammation of the pocket as first responders

2. Migration in large numbers during chronic inflammation

168
Q

Low Neutrophil count with normal function would be found in what sort of perio?

A

Chronic Aggressive Periodontitis

169
Q

Normal Neutrophil count with compromised function would be found in what sort of perio?

A

Chronic Aggressive Periodontitis

170
Q

High Neutrophil count with normal function would be found in what sort of perio?

A

Acute Periodontitis

171
Q

What factors would determine the amount of collateral damage could be caused by Neutrophils in periodontitis?

A
  1. Duration of chronic inflammation
  2. Elevated Numbers
  3. Hyperactivity
172
Q

How are neutrophils involved with either tissue health in perio?

A
  1. Collateral damage during chronic inflammation
  2. Role in Osteoclast Differentiation
  3. Role in Tissue Repair
173
Q

What two chemical mediators add in osteoclastic differentiation and activation that leads to alveolar bone loss?

A
  1. Macrophage Colony Stimulating Factor (M-CSF)

2. RANKL / Lack of OPG

174
Q

What immune cell is involved with down-regulating inflammation response including:

  • Blocking CD4
  • Blocking Dendritic Cell proliferation
  • Signal defence cell apoptosis
A

T Regulatory Cells

175
Q

What are the 2 main innate immunity actions that lead to connective tissue breakdown and bone resorption in perio?

A

Upregulation of pro-inflammatory cytokines leading to:

1: PMN activation/migration via vascular changes (HEVs)
2. Osteoclast differentiation + activation

176
Q

What are the 2 main adaptive immunity actions that lead to connective tissue breakdown and bone resorption in perio?

A

Maturation of naive T cells leading to:

1) B-Cell Responses via TH2
2) Cell Mediated Immunity via TH1
3) Lack of Immune Suppression via T-reg
4) Up regulation of pro-inflammatory cytokines via TH17

177
Q

What are the 6 major PDL fibre types when viewing from a sagittal view?

A

Transeptal: lie above the alveolar bone in the gingiva
Crestal: lie equal to the crest of the alveolar bone
Horizontal
Oblique: mainly absorbs forces
Apical
Interradicular: between bone in furcations for multi-rooted teeth

178
Q

What gingival fibres are mostly affected due to heavy occlusal loads

A

A physiological change occurs to alter the alignment of Transseptal and Alveolar Crest Fibres

179
Q

What changes in the periodontium can occur due to heavy occlusal load?

A

Increased Tooth Mobility
Widening of PDL
No attachment loss (without perio)

180
Q

T/F: Heavy Occlusion is a co-factor in the aetiology of localised perio

A

Possibly, there is currently limited evidence for this in human studies.

In animal studies heavy occlusion results in physiological remodelling of transseptal and alveolar crest fibres provide a more direct pathway for inflammation to reach the PDL. But does not induce perio.

With existing perio, it can increase the rate of angular bone loss

181
Q

T/F: Splinting is still required if Class II mobility has been stable for 12 months

A

False: Splinting is only required if mobility prognosis is getting worse

182
Q

What are the 3 common types of splints?

A

Wire splint
Composite resin split (no tooth preparation)
Removable acrylic splint

183
Q

What are some indications for splinting to aid treatment of tooth mobility?

A
  • Post Regenerative treatment to aid healing
  • Trauma: Emergency treatment for extremely mobile teeth
  • Enhance masticatory comfort in highly mobile teeth
  • Post-orthodontic treatment
184
Q

What components of cigarette smoke are Immunomodulatory?

A

Nicotine
Carbon Monoxide
Acrolein
Reactive Oxygen Species

185
Q

How can cigarette smoke modular oral immunity?

A
  1. Activation of Epithelial and Immune Cells
  2. Subsequent recruitment of other immune cells
  3. Impairs Immune Host Defense Mechanisms to pathogens
  4. Chronic Inflammation
  5. Autoimmunity issues
186
Q

What immune suppression action may result in increased oral cancer risk?

A
  • Suppression of Natural Killer Cell function

- Disregulation of Signal Transducer (Ras) => upregulation of cell growth/division

187
Q

Why might oral tissue healing be impaired by cigarette smoke in a perio patient?

A
  • Chronic thermal/chemical trauma
  • Decreased innate/adaptive cell activation
  • Insufficient cell numbers/responsiveness to deal with excessive cellular debris and phagocytosis needed for chronic inflammation from perio
188
Q

How might smoking result in increased pro-allergic factors in a perio patient?

A

Up regulation of TH2 Helper Cells, resulting in an IgE response, resulting more progressive periodontal lesions

189
Q

What is the overall effect of smoking on perio?

A
  1. Persistent Mucosal Epithelial Activation
  2. Diminished antimicrobial functions relevant to the clearance of infection
  3. Higher likelihood of smokers to develop colonisation + subsequent perio infection
190
Q

What is the main modifiable risk factor in chronic periodontitis?

A

Smoking

191
Q

How can advanced periodontitis result in an endodontic lesion? (Class II Lesion)

A

Pulpal inflammation via the egress of bacteria through the root apices, lateral canales or furcation

192
Q

How can an advanced endodontic lesion result in periodontitis? (Class I Lesion)

A

Egress of pulpal bacterial through lateral canals or the root apices to induce a primary inflammation response in the PDL.

193
Q

What are possible reasons a combined perio + endo lesion can occur?

A
  1. Infection of one/both of the dental pulp + periodontium
  2. Iatrogenic damage: Perforation of the root apex during endodontic treatment
  3. Trauma: vertical root fracture
194
Q

What would be your treatment approach for a Class 1 Primarily Endodontic lesion that has perio involvement?

A
  • Treatment of Endodontic Lesion first and observe.
  • Redress pulp every month
  • Delay perio treatment whilst observing
  • Allow cementum + PDL to regenerate
  • If unresponsive, start perio treatment
  • If nil improvement: hemisection of affected root or extraction
195
Q

What would be your treatment approach for a Class 2 Primarily Periodontal lesion that has endo involvement?

A
  1. Endodontic Treatment first
  2. Subsequent periodontal treatment
  3. Extraction if unresponsive - typically severe perio involvement will have poor prognosis
196
Q

What would be your treatment approach for a Class 3 Combined Endo + Perio lesion?

A
  1. Extraction

2. Endodontic Treatment: if tooth is important as an abutment for fixed/removable pros work

197
Q

What is the zone of co-destruction?

A

The addition of

  • Zone of Irritation from biofilm
  • Zone of Adaptive changes resulting from heavy occlusal loads
198
Q

Combined periodontitis + heavy occlusal loading can result in what?

A
  • Stretched PDL
  • Increased CAL
  • Angular Bone Loss
  • Increased Tooth Mobility
199
Q

Do iatrogenically restoration overhangs directly cause perio?

A

No, they create a a plaque trap but perio requires a compromised host response to occur.

200
Q

What are the characteristics of the microbiome in a healthy gingival crevice?

A
  1. Relatively low microbial numbers
  2. Mainly Gram Positive
    - Cocci: Streptococcus 40%
    - Rods: Actinomyces 35%
  3. Low Redox Potential
  4. Nutrition: Mostly from GCF
201
Q

What shifts in the microbiome occur from healthy to plaque induced gingivitis?

A
  1. 10-20x mass and diversity of microbial numbers
  2. Shift to Capnophilic and Anaerobic Gram Negatives
  3. Decreased redox position (as a result of bacterial metabolism)
  4. Host Response via inflammation
202
Q

What would be the broad characteristics of bacteria involved with chronic periodontitis?

A
  • Asaccharolytic: doesn’t metabolise carbohydrate. Metabolism is via Amino Acid,
  • Bacteria prefer high pH:
    Protease-producing
    Liberation of Ammonia as by-product => increases pH
  • Anaerobic: being subgingival
203
Q

What AB prophylaxis indicated before perio therapy for a patient at risk of infective endocarditis?

A

Oral Amoxycillin 2g 1hr before appointment

If allergy/adverse reaction, past long-term penicillin treatment, then use Clindamycin 600mg

204
Q

What are causes of gingival recession?

A 
Morphology of Teeth
Abrasion
Chronic Inflammation
Frenum Pulls
Ortho extraction/movement
Bruxism
Aging
Continuous Eruption
205
Q

Does recession necessary equate to perio?

A

No. Recession can occur from non-perio related causes including

Morphology of Teeth
Abrasion
Chronic Inflammation
Frenum Pulls
Ortho extraction/movement
Bruxism
Aging
Continuous Eruption
206
Q

Which of the following sharpening stones is a natural fine grit stone?

A. Arkansas
B. India
C. Ceramic

A

Arkansas stone

207
Q

Which hand and at what angle of the clock should you be holding the perio instrument to be sharpened?

A

12 o clock with the non-dominant hand, end to be sharpened facing the floor

208
Q

What should happen with the acrylic test strip if the instrument is sharp?

A

The blade will catch against the strip and make a ping noise

209
Q

What were some limitations with the old classification of periodontitis?

A
  • Lots of overlap of categories
  • Absence of gingival disease
  • Inappropriate emphasis of age of onset
210
Q

What is the difference in microbiology between acute/chronic perio?

A

Acute: Generally Actinobacillus Actinomycetemcomitans infection, with some P gingivalis

Chronic: polymicrobial with red complex (P gingivalis + P forsythus)

211
Q

What is the terminology for chronic periodontitis that don’t respond to treatment?

A

Recurrent / Refractory Periodontitis

212
Q

What invasive treatment modalities are available for mild chronic perio?

A

Flap Debridement for Access

213
Q

What invasive treatment modalities are available for severe perio?

A

Flap Curettages
Regenerative Procedures (GTR)
Implant

214
Q

What invasive treatment modalities are available for agressive perio?

A

Comprehensive Flap Debridement

215
Q

What is a pseudopocket?

A

If the gingival margin is enlarged above the CEJ (due to inflammation) it goes a false deeper pocket depth

216
Q

Which teeth have a higher likelihood for accessory canals that can be problematic in endo-perio lesions?

A

Molars

217
Q

A Short Root Trunk is more likely to have what perio issue?

A

Furcation involvement

218
Q

What is a Hemiseptal Defect:?

A

Where the bone loss has included either/or buccal/lingual plates. Known as either a 1 or 2 wall bony defect

219
Q

What are the 6 stages of periodontitis?

A
  1. Inflammatory cells invading gingival CT, sulcular + junctional epithelium
  2. Ulceration of Pocket Epithelium
  3. Deepening of Pocket Depth
  4. Downward migration of JE
  5. Loss of connective tissue attachment
  6. Loss of Alveolar Bone
220
Q

What are the predominant microbial species and composition in periodontitis?

A

Anaerobes 80%
Gram Negative Rods 75%
Reduces Cocci, Non-Motile Rods
Increased Spirochetes: shape designed to burrow into tissue (d Denticola)

221
Q

What are clinical signs of NUG?

A 
Pain on probing
Marginal Bleeding / BOP
Fiery Red Blunted Interdental Papilla
Grey Pseudomembrane along gingival margin
Halitosis
Fever
222
Q

What bacteria are implicated in NUG?

A

40% Treponema
24% P. intermedia
3% F nucleatum

223
Q

What Antibiotic cover can be given for NUG?

A

Antibiotic Cover: Metronitazole (Flagl)

  • Targets obligate anaerobes
    Metronidazole 400mg 2x/daily for 5 days
  • If unresponsive / immunocompromised

Metronidazole 400mg 2x/daily for 5 days AND
Amoxycillin 500mg orally 3x / 5 days OR
Clindamycin 300mg orally, 3x / 5 days (if penicillin allergy)

224
Q

What are Koch’s Postulates for plaque derived diseases?

A
  1. The microbe should be present in sufficient numbers to initiate disease
  2. The microbe should generate increased levels of specific antibodies
  3. The microbe should possess relevant virulence factors
  4. The microbe should cause disease in an appropriate animal model
  5. Elimination of the microbe should result in clinical improvement
225
Q

What bacterial factors in perio contribute to attachment to host tissues?

A

Cell Surface Adhesins

226
Q

What bacterial factors in perio contribute to evasion of host defences?

A

Proteases/Haemolysin: Enzymes to obtain nutrients
Ability to compete with other flora
Production of bacteriocins

227
Q

What bacterial factors in perio contribute to bacterial evasion of defences?

A

Capsule + Slime Layer
Leukotoxin Production
Antibody specific proteases
Complement degrading proteases

228
Q

What bacterial factors in perio contribute to indirect tissue damage?

A
  1. Proteolytic Enzymes: Trypsin-like protease, Collagenase, Hyaluronidase, Chondroitin Sulphatase
  2. Bone Resorbing Factors
  3. Endotoxins: TLA, LPS, Capsule, Cytotoxins
  4. Metabolic Products: Short chain fatty acids, ammonia, volatile sulphur compounds
229
Q

What bacterial factors in perio contribute to direct tissue damage?

A

Host Inflammatory Response to plaque antigens

230
Q

What helps P. gingivalis helps attachment to epithelial cells?

A

Fimbriae

231
Q

Red complex proteases serve what function?

A
  1. Aid attachment
  2. Degrade proteins
  3. Degrade Immunoglobulins
  4. Release nutrients
  5. Activates host MMPs
232
Q

T/F: Periodontitis only has red complex bacteria present

A

False: microbial research indicates that commensal and early colonisers are all necessary to create conditions to allow red complex to be sufficient in number and virulence

233
Q

What 3 viruses are implicated in lesions of aggressive periodontal disease?

A

Herpes Simplex
Cytomegalovirus (CMV)
Epstein-Barr Virus Type 1 (EBV-1)

234
Q

During orthodontic movement what happens to areas of pressure?

A

Bone Resorption

235
Q

During orthodontic movement what happens to areas of tension?

A

Bone Deposition

236
Q

What periodontic issues can occur in periodontally healthy patients during orthodontic treatment?

A

Gingival inflammation, gingival hyperplasia, increased probing depths, loss of connective tissue attachment (between 0.2-0.3mm) and alveolar bone resorption (0.3mm)

237
Q

What periodontic issues can occur in periodontally compromised patients during orthodontic treatment?

A

Accelerated bone loss from inflammation (plaque retention) and orthodontic forces

238
Q

Elastomeric rings in ortho can present what problem in periodontal health?

A

Areas of increased plaque retention

239
Q

What microbiological changes can be seen during orthodontic treatment?

A

Shift towards an anaerobic periodontopathogens

eg. P.intermedia, spirochetes, motile rods and filaments

240
Q

What recall protocol should occur for periodontally at risk patients option for orthodontic treatment

A

4 month SPT

Orthodontic treatment terminated if OH can not be maintained or signs of disease progression

241
Q

What treatment can be done for impacted canines prior to orthodontics?

A

Apical Repositioning Flap

242
Q

What is a typical cause of a diastema and what is the treatment

A

Failure of frenal fibres from maxillary labial frenum to migrate apically.

Residual band of elastic tissue prevents I/P contact of central incisors

Frenectomy is an option after eruption of 1-6 permanent teeth

COPY BDS3 University of Adelaide Dentistry (28 decks)

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