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DG2016 - CK 2 > Perio > Flashcards

Perio Flashcards

1
Q

What BPE score is the following?
- pockets < 3.5mm
- no calculus/overhangs, no bleeding on probing (black band entirely visible)

A

grade 0

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2
Q

What BPE score is the following?
- pockets < 3.5mm
- no calculus/overhangs, bleeding on probing (black band entirely visible)

A

grade 1

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3
Q

What BPE score is the following?
- pockets < 3.5mm
- supra or sub gingival calculus/overhangs (black band entirely visible)

A

grade 2

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4
Q

What BPE score is the following?
- probing depth 3.5-5.5mm
- black band partially visible, indicating pocket of 4-5mm)

A

grade 3

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5
Q

What BPE score is the following?
- probing depth >5.5mm
- black band disappears, indicating pocket of 6mm or more

A

grade 4

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6
Q

What BPE score is the following?
- furcation involvement

A

*

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7
Q

What is the BPE score indicating the following treatment?
- no need for periodontal treatment

A

grade 0

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8
Q

What is the BPE score indicating the following treatment?
- oral hygiene instruction

A

grade 1

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9
Q

What is the BPE score indicating the following treatment?
- as for code 1, plus removal of PRFs, including all supra and sub gingival calculus

A

grade 2

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10
Q

What is the BPE score indicating the following treatment?
- as for code 2 and RSD if required and review in 3 months with localised 6ppc in involved sextants
- radiographs

A

grade 3

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11
Q

What is the BPE score indicating the following treatment?
- OHI, RSD, assess the need for complex treatment, referral to a specialist may be indicated
- rads and 6ppc

A

grade 4

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12
Q

What is the BPE score indicating the following treatment?
- treat according to BPE code (0-4)
- assess the need for more complex treatment, referral to a specialist may be indicated

A

*

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13
Q

What would be the diagnosis for BPE code 0/1/2 and < 10% bleeding on probing?

A

clinical gingival health

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14
Q

What would be the diagnosis for BPE code 0/1/2 and 10-30% bleeding on probing?

A

localised gingivitis

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15
Q

What would be the diagnosis for BPE code 0/1/2 and > 30% bleeding on probing?

A

generalised gingivitis

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16
Q

What would be the diagnosis for BPE code 4 and pocketing molar-incisor pattern?

A

periodontitis molar-incisor pattern

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17
Q

What would be the diagnosis for BPE code 4 and pocketing < 30% of teeth?

A

localised periodontitis

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18
Q

What would be the diagnosis for BPE code 4 and pocketing > 30% of teeth?

A

generalised periodontitis

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19
Q

What is meant by intact periodontium?

A

no bone loss

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20
Q

What is meant by reduced periodontium?

A

bone loss not caused by periodontitis

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21
Q

What is meant by staging?

A

severity of disease

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22
Q

What is meant by grading?

A

rate of disease progression

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23
Q

How is the staging of periodontal disease measured?

A

interproximal bone loss (using worst site of bone loss due to perio)

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24
Q

What staging is given to <15% bone loss (or <2mm attachment loss from CEJ)?

A

stage 1 (early/mild)

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25
Q

What staging is given to bone loss to coronal third of root?

A

stage 2 (moderate)

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26
Q

What staging is given to bone loss to mid third of root?

A

stage 3 (severe)

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27
Q

What staging is given to bone loss to apical third of root?

A

stage 4 (very severe)

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28
Q

How is grading calculated?

A

% bone loss divided by patient age

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29
Q

What is meant by grading of < 0.5?

A

grade A (slow rate of progression)

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30
Q

What is meant by grading of 0.5-1.0?

A

grade B (moderate rate of progression)

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31
Q

What is meant by grading of > 1.0?

A

grade C (rapid rate of progression)

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32
Q

What assessment would be given of current periodontitis status?
- BoP < 10%
- PPD 4mm or less
- no BoP at 4mm sites

A

currently stable

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33
Q

What assessment would be given of current periodontitis status?
- BoP 10% or more
- PPD 4mm or less
- no BoP at 4mm sites

A

currently in remission

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34
Q

What assessment would be given of current periodontitis status?
- PPD 5mm or more or PPD 4mm or more and BoP

A

currently unstable

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35
Q

What grade for mobility is the following?
- normal movement (up to 0.2mm)

A

grade 0

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36
Q

What grade for mobility is the following?
- < 1mm horizontal

A

grade 1

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37
Q

What grade for mobility is the following?
- > 1mm horizontal

A

grade 2

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38
Q

What grade for mobility is the following?
- horizontal and vertical

A

grade 3

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39
Q

What grade for furcation is the following?
- 1/3 of the furcation width

A

grade 1

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40
Q

What grade for furcation is the following?
- 1/3 of the furcation width but not through and through

A

grade 2

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41
Q

What grade for furcation is the following?
- through and through

A

grade 3

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42
Q

What is the difference between marginal bleeding and bleeding on probing?

A

marginal bleeding is where you sweep the probe along the gingival sulcus no more than 3mm
BoP is bleeding from base of the pocket

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43
Q

What are 2 aims of PMPR?

A
  • reduce bacterial load
  • removal of plaque retentive factors
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44
Q

What is the definition of risk factors?

A

a factor that increases the probability of a disease developing in a given individual

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45
Q

What are the 2 main categories of types of risk factors?

A
  • local risk factors
  • systemic risk factors
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46
Q

Which type of risk factors is the following?
- those which are confined to the oral cavity
- can be divided into 2 parts: acquired and anatomical/development

A

local risk factors

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47
Q

What are 5 examples of acquired local risk factors?

A
  • plaque/calculus
  • bleeding on marginal probing
  • probing pocket depth - pockets 5mm or more are at an increased risk of attachment loss
  • poorly controlled/defective restorations
  • poor prosthesis
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48
Q

Explain how plaque is an acquired local risk factor for periodontal diseases?

A
  • instigator of periodontal disease
  • biofilm creates environment which can initiate change in health
  • soft - easily removed by patient with OH measures
  • removal of plaque retentive factors can help with plaque control
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49
Q

Explain 6 reasons restorations or prosthetic are an acquired local risk factor for periodontal disease?

A
  • overhangs and deficiencies
  • partial dentures can trap plaque
  • restorations with bulbous emergence profile
  • restorations which impinge on the biological width
  • inadequate contact points
  • subgingival margins
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50
Q

What are 8 examples of anatomical risk factors for periodontal disease?

A
  • dental crowding
  • furcations
  • bone defects (presence of a dehiscence and/or fenestration)
  • mucosal defects (a high frenal attachment)
  • root grooves/concavities
  • cervical enamel projections
  • enamel pearls
  • canine fossa
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51
Q

What type of root anomaly is the following?
- located apically to the CEJ
- often found in furcation areas
- triangular, tapering apically and flat

A

cervical enamel projections

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52
Q

Which type of root anomaly is the following?
- usually larger than enamel projections and more spherical
- often found apical to the CEJ
- care must be taken when removing or sub-scaling as often contain extension of the pulp

A

enamel pearls

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53
Q

What are 5 examples of modifiable systemic risk factors for perio?

A
  • smoking
  • diabetes
  • medications
  • stress
  • nutrition
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54
Q

What are 5 examples of non-modifiable systemic risk factors for perio?

A
  • genetic predispositions (family history of perio)
  • pregnancy
  • hormonal changes
  • immunodeficiency states
  • age
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55
Q

Mutations of which genotype contribute to the immune inflammatory response for periodontal disease?

A

IL-1 genotype

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56
Q

Which condition has the following underlying defect of periodontal relevance?
- defects of PMNL chemotaxis, killing and phagocytosis
- depressed T-cell antigen induced killing

A

down syndrome

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57
Q

Which condition has the following underlying defect of periodontal relevance?
- failure of the ‘respiratory burst’ in phagocytes
- oxygen radicals are not produced and bacteria survive

A

chronic granulomatous disease

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58
Q

Which condition has the following underlying defect of periodontal relevance?
- hyperglycaemic state reduces PMNL function
- monocytes are hyper-reactive and excess IL-1B, PGE2, TNFa and oxygen radicals are produced
- effects also on collagen and vascularity reduce healing

A

insulin-dependent juvenile diabetes

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59
Q

Which condition has the following underlying defect of periodontal relevance?
- low levels of the enzyme alkaline phosphatase (ALP) result in poor mineralisation/formation of cementum and teeth exfoliate

A

hypophosphatasia

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60
Q

Which condition has the following underlying defect of periodontal relevance?
- defects of PMNL chemotaxis and phagocytosis
- gene mapped to PMNL enzyme (Cathepsin-C) gene locus on chromosome 11

A

papillion-lefevre syndrome

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61
Q

Which condition has the following underlying defect of periodontal relevance?
- defects of collagen synthesis -type VIII is associated with severe periodontal destruction

A

Ehlers danlos syndrome

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62
Q

Which condition has the following underlying defect of periodontal relevance?
- defects of the phagocyte chemotaxis, degranulation and membrane fusion leads to total loss of the adult dentition

A

chediak-higashi syndrome

63
Q

Which condition has the following underlying defect of periodontal relevance?
- excessive IgE and histamine release by mast cells and IgE immune complex formation

A

jobs syndrome

64
Q

What are 5 effects of smoking on the periodontium?

A
  • poorer healing response
  • more teeth with furcation involvement
  • reduction in gingival vessels
  • greater attachment loss
  • more sites with deeper pockets
65
Q

What are the effects of smoking on gingival tissues?

A
  • links between smoking and necrotising periodontal diseases are well established
  • decreased gingival bleeding
  • decreased gingival redness and GCF volume in smokers suggests decreased inflammation response to plaque
66
Q

What are 4 roles of neutrophils in the inflammatory immune response and healing response of smokers?

A
  • increase in the number of neutrophils in the systemic circulation
  • impaired neutrophil function
  • increased proteolytic activity
  • smoking affects the respiratory burst of neutrophils
67
Q

What are 5 roles of fibroblasts in the inflammatory immune response and healing response of smokers?

A
  • nicotine inhibits gingival fibroblast proliferation
  • decreased production of type 1 collagen and fibronectin
  • increased collagenase activity
  • PDL fibroblast attachment is significant decreased on root surfaces from heavy smokers
  • poor wound healing
68
Q

Which 3 drug groups are known to cause gingival overgrowth?

A
  • calcium channel blockers eg. amlodipine, nifedipine, felodipine
  • anti-rejection immunosuppressants eg. ciclosporin
  • anti-epileptic drugs eg. phenytoin
69
Q

Medication induced gingival overgrowth usually affects the anterior region with onset usually less than?

A

3 months

70
Q

What is the first bacteria to colonise a clean tooth surface?
- supragingivally
- some of them secrete endotoxins
- does not trigger an immune response

A

streptococci (gram positive)

71
Q

What is the next stage of plaque formation following initial colonisers?

A
  • if not removed within 2 days, gram negative bacteria appear in the biofilm subgingivally
  • gram negative have both exotoxins and endotoxins
  • the gingiva will become inflamed
72
Q

What are the 4 stages of periodontal disease?

A
  • the initial lesion
  • the early lesion
  • the established lesion
  • the advanced lesion
73
Q

Which stage of periodontal disease is the following?
- develops 2-4 days after plaque accumulation
- vasculitis of vessels below junctional epithelium
- increased leukocyte migration into junctional epithelium
- extravascular presence of serum proteins
- localised collagen destruction
- mainly gram positive bacteria - streptococci dominate
- stable condition - not visible clinically

A

initial lesion (healthy gingiva)

74
Q

Which stage of periodontal disease is the following?
- develops 7-10 days after plaque accumulation
- increased fluid exudate
- increase in PMNLs
- swelling and redness visible
- proliferation of basal cells at the junctional epithelium
- anaerobic filamentous bacteria dominate

A

early lesion (early gingivitis)

75
Q

Which stage of periodontal disease is the following?
- develops 21-28 days after plaque accumulation
- further proliferation of the junctional epithelium
- gingival crevice deepens
- increased neutrophils
- continuing loss of collagen
- T cells > B cells
- breakdown of connective tissue but no bone loss

A

established lesion (established gingivitis)

76
Q

Which stage of periodontal disease is the following?
- epithelium migrates apically forming a pocket
- plaque and endotoxins permeate the surface layer of the cementum
- loss of collagen and bone
- B cells > T cells
- only develops in 10-15% of patients and not always in all sites
- the lesion is unstable

A

advanced lesion (periodontitis)

77
Q

What are the 2 types of responses from the immune system?

A
  • the innate response
  • the adaptive/acquired response
78
Q

What are 4 roles of the junctional epithelium?

A
  • innate response starts with the junctional epithelium, epithelial cells release cell signalling molecules which initiate inflammation
  • allow bacterial products to go in
  • allow GCF and neutrophils to go out
  • becomes more permeable in disease
79
Q

Which fluid is the following?
- washes and dilutes
- allows vehicle for swallowing bacteria
- contains antibacterial enzymes

A

saliva

80
Q

Which 2 bacterial enzymes does saliva contain?

A
  • lysozyme
  • immunoglobulins (IgA and IgG)
81
Q

Which fluid is the following?
- carries all components of serum including complement and immunoglobulins
- increased flow during inflammation

A

GCF

82
Q

Which type of molecule does the following?
- stimulate cells to release other molecules

A

cytokines
- cytokines and lymphokines can stimulate cells to perform other functions

83
Q

Which type of molecule does the following?
- attract cells to areas of infection

A

chemokines

84
Q

What is the most important cell signalling molecule as it is a powerful pro-inflammatory and causes bone resorption?

A

IL-1

85
Q

Which cytokine has the following effects?
- activates osteoclasts
- increases PMNL margination
- increases PGE2 production
- increases TNF-alpha production
- causes bone resorption

A

IL-1

86
Q

Which cytokine has the following effects?
- increases IL-1 production
- increases PGE2 production

A

TNF-a (tumour necrosis factor alpha)

87
Q

Which cytokine has the following effects?
- stimulates bone resorption

A

PGE2 (prostaglandin E2)

88
Q

What are 4 cells of origin of IL-1?

A
  • macrophages
  • fibroblasts
  • monocytes stimulated by endo/exotoxins
  • epithelial cells
89
Q

What are 3 cells of origin of TNF-a?

A
  • activated macrophages
  • monocytes
  • epithelial cells
90
Q

What are 5 cells of origin of PGE2?

A
  • activates macrophages
  • monocytes
  • PMNLs
  • mast cells
  • epithelial cells
91
Q

Histamine (vasoactive peptide) is stimulated by which complements of the complement cascade?

A

C3a and C5a

92
Q

Which cell type is histamine released?

A

mast cells

93
Q

What is the role of adhesion molecules and what is the most important one?

A
  • used to stick to each other or to components of intercellular matrix
  • ICAM-1
94
Q

What are 2 roles of vasoactive peptides?

A
  • vasodilation, more blood cells and plasma proteins, slows blood flow allowing PMNLs to touch vessel walls
  • increases vessel permeability
95
Q

What are the 4 main components of PMNLs?

A
  • receptors - pathogen recognition, opsonisation
  • cytoskeleton - movement, actin muscle fibres
  • lysosomes - destroy bacterial strictures
  • oxygen radicals - super-oxides, destroy bacterial structures
96
Q

Which cell type is the following?
- develop from monocytes in the blood
- emigrate to inflamed gingival tissue
- scavengers of dead cells
- bridge between innate and acquired immunity

A

macrophages

97
Q

Which macrophage allow recognition between host and foreign tissue?

A

MHC-class II

98
Q

What are the 3 main roles of the complement cascade?

A
  • recruit phagocytes
  • aid phagocytosis - opsonisation
  • kill bacteria - formation of membrane attack complex leading to cell lysis
99
Q

What are the 2 pathways for complement activation?

A
  • alternative pathway - activated by bacterial endotoxin (LPS) mainly
  • classical pathway - only activated by the antigen-antibody complexes (the adaptive/acquired response)
100
Q

Alternative and classical pathways of the complement cascade activate which complement component?

A

C3

101
Q

Summarise the complement cascade?

A
  • classical and alternative activate C3
  • C3 activates C5
  • cascade amplifies
  • MAC formed (membrane attack complex)
  • cell lysis occurs
  • bacteria dies
102
Q

What does the membrane attack complex lead to?

A

cell lysis

103
Q

What effect does C3a of the complement cascade have?

A

chemotaxis of phagocytes

104
Q

What 3 effects does C3b of the complement cascade have?

A
  • cytokine production
  • macrophage secretion
  • opsonisation
105
Q

What effect does C5a of the complement cascade have?

A
  • leukocytes stick to vessel walls
  • neutrophils release enzymes and oxygen radicals (degranulation)
106
Q

What effect does C3a and C5a of the complement cascade have?

A
  • increased vascular permeability due to histamine release from mast cell degranulation
107
Q

What effect does C3b and C5a of the complement cascade have?

A

production of oxygen radicals

108
Q

What effect does C5a and C567 complex of the complement cascade have?

A

leukocyte chemotaxis

109
Q

What effect does C5b, C6, C7, C8 and C9 of the complement cascade have?

A

bacterial cell lysis

110
Q

Which 3 things does the acquired response involve?

A
  • T lymphocytes - cell mediated response
  • B lymphocytes - humoral response
  • immunoglobulins
111
Q

Which immunoglobulin is the first one produced?

A

IgM

112
Q

Which immunoglobulin are the most important in periodontal disease?

A

IgG and IgA

113
Q

Which immunoglobulin is the following?
- from GCF
- small molecular weight
- originates from blood plasma

A

IgG

114
Q

Which immunoglobulin is the following?
- from saliva
- dimer

A

IgA

115
Q

Which cells are the first to arrive in gingivitis?

A

T-lymphocytes

116
Q

Which immune response is the following?
- constantly in function
- rapid response
- usually involved in early gingival inflammation
- T cells > B cells

A

innate response

117
Q

Which immune response is the following?
- specific cell-cell interactions
- slower response
- usually involved in moderate gingivitis and periodontitis
- B cells > T cells

A

adaptive response

118
Q

What are bacterial factors contributing to perio?

A
  • increased number
  • specific pathogens
  • direct tissue invasion
119
Q

What are host factors contributing to perio?

A
  • reduced effectiveness of host defences
  • increased damage in response to microbial changes
120
Q

What are 3 conditions with a strong evidence base link to periodontal disease?

A
  • cardiovascular disease
  • diabetes
  • adverse pregnancy outcomes
121
Q

Explain why pregnancy has a strong link to periodontal disease?

A
  • hormonal changes during pregnancy, elevated oestrogen and progesterone increase vascular permeability
  • plaque alongside this will promote inflammation, worse in women with existing periodontitis
122
Q

What are 5 risk factors for pregnancy complications?

A
  • young mothers <18 years old
  • drug or alcohol use
  • maternal stress
  • genetics
  • periodontal disease
123
Q

What are 3 complications which can be seen in pregnancy associated with periodontitis?

A
  • low birth weight
  • preterm birth
  • pre-eclampsia
124
Q

What are 5 disease processes associated with chronic hyperglycaemia?

A
  • retinopathy
  • nephropathy
  • neuropathy
  • micro and macrovascular disease
  • periodontal disease
125
Q

Explain how PMNL function contribute to perio risk in diabetic patients?

A
  • impaired chemotaxis, phagocytosis and adherence
  • PMNL defects may be inherited or secondary to hyperglycaemia
126
Q

Explain how collagen metabolism contribute to perio risk in diabetic patients?

A
  • diabetic synthesise less collagen
  • diabetics have higher levels of PMNL collagenase
127
Q

Explain how advanced glycation end-products (AGE) contribute to perio risk in diabetic patients?

A
  • hyperglycaemic environment = AGE formation increased
  • AGE products cause increased collagen cross-linking and so reduced turnover/stability
  • monocytes/macrophages have AGE receptors (RAGE) which when bound by AGE products, cause release of pro inflammatory cytokines
128
Q

Perio patients have a higher chance of developing which?

A
  • pre diabetes
  • type 2 diabetes
129
Q

What is the mechanism of the link between perio and cardiovascular diseases?

A
  • perio leads to entry of bacteria (or their products) into the blood stream
  • bacteria activate the host inflammatory response by multiple mechanisms
  • the host immune response favours atheroma formation, maturation and exacerbation
130
Q

How should patients who have had recent adverse CVD event diagnosed with perio be managed?

A
  • treatment should be staggered
  • multiple visits advised as periodontal treatment associated with transient impairment of endothelial function for a week after
  • patient with perio and other known risk factors (smoking, obesity, hypertension) who have not seen their GP for over a year should be advised to have a cardiac review
  • focus on preventative advice
  • CVD patients should have thorough periodontal assessment- - regular periodontal monitoring for those with CVD but no perio - at least every 12 months
131
Q

Improved oral hygiene has an important role in the prevention of what?

A

hospital acquired pneumonia (especially patients on ventilators)

132
Q

What are 3 aims of supportive periodontal therapy?

A
  • prevent or minimise periodontal disease recurrence or progression
  • prevent or reduce incidence of tooth loss
  • increase the likelihood of detecting and treating other oral conditions
133
Q

Which study aimed to look at periodontal disease in Sri Lankan tea workers?

A

loe et al 1986

134
Q

What did the Loe et al study 1986 conclude?

A
  • all had similar high plaque and calculus levels
  • a small group showed rapidly progressing disease, some showed no progression
  • this suggests a possible genetic component influencing disease progression
135
Q

How is the supportive therapy phase utilised for patients with stable disease, good compliance, good response to treatment and prognosis?

A
  • phase is vital to ensure stability
  • implementing regular clinical assessment
  • retreatment of certain sites
  • patient motivation
136
Q

How is the supportive therapy phase utilised for patients with unstable disease, rapidly progressing disease, uncompliant patient, poor prognosis and tooth loss expected?

A
  • regular clinical assessment
  • retreatment of certain sites
  • motivation
  • modify risk factors: smoking cessation
  • discuss progression
137
Q

In what circumstances is supportive periodontal therapy likely to be effective?

A
  • good OH (reinforce)
  • healthy looking gingiva
  • shallow pockets
  • stable attachment levels
  • intact dentition (no tooth loss or increasing mobility)
  • removal of deposits
138
Q

In what circumstances is supportive periodontal therapy likely to be ineffective?

A
  • marked gingivitis
  • deepening pocket depths
  • loss of attachment
  • tooth loss
  • evidence of ineffective debridement
139
Q

What are the 9 stages of supportive therapy?

A
  1. review history: medical, dental, social
  2. review OH
  3. clinical assessment and periodontal review
  4. radiographic assessment (if indicated)
  5. diagnosis
  6. discuss findings
  7. treatment
  8. reinforce advice
  9. arrange recall/review
140
Q

Radiographs can be justified when what 3 deteriorations are suspected?

A
  • deepening pockets
  • increased attachment loss/mobility/furcation involvement
  • suppuration or abscess
141
Q

When discussing findings, what should the patient be informed of?

A
  • their current condition
  • any non-responsive sites
  • reasons why sites have not responded (if known)
  • any sites being missed during plaque control
  • changes in prognosis
  • recommended options (risks and benefits)
142
Q

What are 5 potential reasons for non-responding sites?

A
  • incorrect diagnosis
  • inadequate plaque control
  • inadequate sub-gingival debridement
  • smoking
  • other (systemic, bacterial)
143
Q

What are 5 potential reasons for non-compliance?

A
  • time
  • cost
  • personal views of disease (don’t think its an issue/part of ageing process)
  • social issues
  • treatment complexity
144
Q

What is the treatment for responding sites 4mm and no bleeding?

A

maintenance: reinforce OH, regular targeted PMPR

145
Q

What is the treatment for residual sites 4mm or more +/- bleeding?

A

sub gingival PMPR

146
Q

What is the treatment for residual sites 6mm or more?

A

refer to specialist for possible surgical options

147
Q

What are 5 indications of when frequent recalls are indicated?

A
  • unstable disease, risk factors
  • grade C disease (rapidly progressing)
  • poor plaque control
  • deep pockets
  • poor response to treatment
148
Q

What are 5 indications of when less frequent recalls are indicated?

A
  • stable disease
  • grade A disease
  • good plaque control
  • shallow pockets
  • good response to treatment
149
Q

Evidence base shows microbial plaque tend to grow back to pre-cleaning levels during what time period post debridement?

A

3-4 months

150
Q

Professional support is recommended to prevent the initial onset of periodontitis every?

A

3-4 months

151
Q

What is the healing phase of the long junctional epithelium?

A

3+ months
avoid probing for this period as to not disrupt healing process

152
Q

What is the healing phase of the surrounding gingival and connective tissues?

A

6-9 months

153
Q

What are 5 reasons why recall periods are important?

A
  • helps to review the clinical condition to maintain stability
  • assess changes which may affect stability
  • identify problems early and manage them appropriately
  • keep the patient informed about their disease status
  • avoid medico-legal issues

DG2016 - CK 2 (10 decks)

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