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perio > 2nd year > Flashcards

2nd year Flashcards

1
Q

1 o’clock seating position

A

U palatals
U buccal anteriors
U buccal left

L lingual right
L buccal left

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2
Q

3 o’clock seating position

A

U buccal right

L buccal right
L lingual left

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3
Q

5 o’clock seating position

A

L anteriors

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4
Q

broad risk factor categories

A

genetic
epigenetic
env
behavioural

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5
Q

minisickle features

A 
double ended
triangular cross section
point scaler
curved blade
2 cutting edges - converge to a sharp point
face at 90 degrees to lower shank
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6
Q

minisickle uses

A

supra gingival calculus from buccal and lingual embrasures

X deep subgingival - sharp point would groove root surface/lacerate pocket wall

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7
Q

Columbia/universal features

A

double ended
2 cutting edges on each blade - converge to form rounded toe
back of instrument rounded
face at 90 degrees to lower shank
no sharp edges/points
blade at working angulation of about 70 degrees

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8
Q

Columbia/universal uses

A

supra/subgingival anywhere

but only limited access to deep pockets

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9
Q

use of Hoe scalers

A

gross calculus supra and subgingivally

restricted access in v narrow pockets

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10
Q

hoe scalers features

A

blade set at 100 degree angle to shank
cutting edge bevelled at 4 degrees
set of 4 - double-ended

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11
Q

yellow hoe scaler

A

buccal and lingual

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12
Q

red hoe scaler

A

mesial and distal

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13
Q

Gracey curette uses

A

subgingival

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14
Q

Gracey curette features

A

double ended mirror image pairs
area-specific
single cutting edge - larger outer curve
offset blade at angle to lower shank
- 110 degrees between L shank and face of blade
- 70 degrees between face of blade and tooth
only lower 1/3 of blade in contact with tooth. Blade curves in 2 planes

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15
Q

grey gracey

A

anteriors

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16
Q

orange gracey

A

mesial of posteriors

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17
Q

green gracey

A

buccal and lingual of posteriors

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18
Q

blue gracey

A

distal of posteriors

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19
Q

checking for remaining calculus

A

root surface - CPITN probe

supra gingival - air dry

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20
Q

gingivitis

A

inflammation confined to gingiva
increase in probing depth - false pocketing
- no permanent destruction of CT attachment to root surface
bleeding

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21
Q

periodontitis

A 
apical extension of inflammation
destruction of CT attachment
apical migration of JE
lose alveolar bone
true pocket
microbial plaque main etiological factor
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22
Q

peri-implant mucositis

A 
inflammation in mucosa
no loss of bone
may resolve with plaque removal and improved OH
BOP
redness 
swelling
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23
Q

peri-implantitis

A

inflammation in mucosa with loss of supporting bone

increased probing depths, BOP, (suppuration, implant mobility)

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24
Q

cause of peri-implant disease

A

likely microbial plaque and immune response
excess cement
poorly fitting superstructures
poorly positioned implants

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25
Q

what is BPE useful for?

A

screening

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26
Q

BPE sextants

A

7-4
3-3
need at least 2 teeth

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27
Q

BPE probe

A

WHO BPE/CPITN probe

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28
Q

BPE force

A

20-25g ‘walk’

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29
Q

should BPE be done around implants?

A

no

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30
Q

BPE 0

A

no PD tx

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31
Q

BPE 1

A

OHI and PGI

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32
Q

BPE 2

A

OHI and PGI

removal of plaque-retentive factors

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33
Q

BPE 3

A

OHI and PGI
removal of plaque-retentive factors
+ RSD if required

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34
Q

BPE 4

A

OHI and PGI
removal of plaque-retentive factors
+ RSD if required
+ assess need for more complex tx/specialist?

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35
Q

BPE *

A

tx according to BPE code

complex/referral?

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36
Q

SDCEP BPE3

A

6PPC for sextants with BPE 3 before tx and at reevaluation

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37
Q

BSP BPE3

A

6PPC only at reevaluation

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38
Q

limitations of BPE

A

pocket depth misleading - gingival enlargement/incomplete eruption
recession/furcation but little pocketing - underestimate LOA
doesn’t indicate extent of disease - sextants
can’t use to monitor response

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39
Q

BPE for U18s

A 
6 index teeth
6   1      6
6      1   6
codes 0-2 in 7-11yrs (mixed dentition)
 - false pockets in newly erupting teeth
 - unusual pockets - investigate

all codes 12-17 years (permanent teeth)

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40
Q

instruments to sharpen curettes and scalers

A

test stick (acrylic)
sharpening oil - lubricates and carries away metal debris. Reduces frictional heat
sharpening/Arkansas stone
magnifying lens

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41
Q

sharpening stone

A

flat
smooth
man-made

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42
Q

Arkansas stone

A

wedge-shaped
natural
fine abrasiveness
Al2O3

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43
Q

sharpening instruments technique

A

need to preserve blade shape inc angles
pen/palm grip
make 3 strokes then check

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44
Q

instrument grip - modified pen grasp

A

middle finger - rest lightly on shank
ring finger - oral structure (often a tooth)
lower terminal shank parallel to LA of tooth

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45
Q

periodontal chart stages

A 
PCP12 probe
score out missing teeth
position of gingival margin
probing depths
calculate LOA
BOP
mobility
furcation involvement
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46
Q

position of gingival margin

A

6 points for each tooth
relate to ACJ
visual and tactile

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47
Q

uses of 6PPC

A

educate
inform tx choice
monitor tx outcomes
medicolegal

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48
Q

polishing

A

smooth surfaces less likely to accumulate plaque
remove any stains after scaling
avoid heat production
rubber cup
pumice and water slurry for heavy staining

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49
Q

healing after RSD

A

bacterial remnants washed out of pocket by blood and gingival fluid
acute inflammatory reaction
remnants of pocket epithelium proliferate, pocket wall fully epithelialised within 2 days
- involution of pocket epithelium - new JE
epithelial reattachment starts apically
- 5th-14th day
new gingival sulcus
collagen forms to replace GT
- immature collagen appears after 3wks

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50
Q

what is healing after RSD dependent on?

A

RSD and effective supra gingival plaque control

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51
Q

reduction in pocket depth after RSD

A

reduced oedema
increase in clinical attachment
- form long JE
- increase in ‘tissue tone’ produces resistance to probing

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52
Q

re-evaluation after RSD

A

6-8 wks after

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53
Q

probe placement

A

adaptation

parallelism

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54
Q

adaptation

A

side of probe tip should be kept in contact with tooth surface

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55
Q

parallelism

A

as parallel as possible to LA of tooth

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56
Q

assessing tooth mobility

A

try to move buccolingually with index finger and handle

apply gentle pressure on crown with handle in vertical direction

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57
Q

tooth mobility definition

A

amplitude of movement of crown tip from its most extreme buccal/mesial position to its most extreme lingual/distal position

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58
Q

Grade 0 mobility

A

‘physiological’

0.1-0.2mm horizontal

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59
Q

Grade 1 mobility

A

<1mm horizontal

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60
Q

Grade 2 mobility

A

exceeding 1mm horizontal

visually

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61
Q

Grade 3 mobility

A

vertical/rotation/depression/horizontal

impinges on fct

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62
Q

what can you use to assess furcation involvement?

A

furcation probe e.g. Nabers

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63
Q

Grade 1 furcation

A

<1/3

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64
Q

Grade 2 furcation

A

> 1/3 but not though and through

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65
Q

Grade 3 furcation

A

through and through lesion

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66
Q

difficulty with assessing furcations

A

not always possible to probe

- located IP and/or significantly subgingival

67
Q

gingival margin position

A

normal at CEJ
young pt/inflammation - coronal
recession - apical

68
Q

probing depth

A

distance from gingival margin to base of pocket

69
Q

does probing depth indicate severity?

A

not always

70
Q

why can the probing depth change?

A

swelling or recession

71
Q

what does probing depth indicate?

A

difficulty of tx and likelihood of recurrence

72
Q

CAL

A

CEJ to base of pocket

73
Q

what is CAL the best measure of?

A 
tissue destruction (pre-tx)
extent of repair (post-tx)
74
Q

locating ACJ

A

probing

visual if recession

75
Q

contraindications to US

A

pacemaker
pregnancy
swallowing difficulties
Covid - AGP

76
Q

manufacturers with US

A

Dentsply - number of bends in tip
laminated efficiency indicator cards
thinner insert = lower power

77
Q

US aim with water

A

mist with some droplets

78
Q

speed of US

A

25000 small strokes / second

79
Q

US amplitude of vibratory movement in LA of tip

A

approx 0.006 - 0.1mm

80
Q

why is water necessary in US?

A

heat

81
Q

mechanisms of action of US

A

vibrational energy
cavitation effect - vacuum bubbles - implode creating microcosms of energy
cleansing/flushing effect of H2O spray

82
Q

pros and cons of US

A

poorer tactile sensation
may allow better furcation access
faster
may leave rougher surface

83
Q

which power should you use with US?

A

lowest power

84
Q

use of US

A

supra gingival and a little subgingival

  • can’t get in deep pockets
  • won’t cut granulose tissue
  • lack of tactile sensation
85
Q

oral sulcular epithelium

A

parakeratinised

lines gingival sulcus

86
Q

JE

A

non-keratinised
most apical point CEJ in health
wider coronally
hemidesmosomes

87
Q

gingival CT

A 
LP
gingival fibres - collagen fibre bundles
ground substance
fibroblasts
blood and lymph vessels
neural tissues
88
Q

cementum and remodelling

A

no physiological remodelling but continuously deposited throughout life

89
Q

Sharpey’s fibres

A

mineralised within the cementum

90
Q

where does cellular cementum lie?

A

over acellular

91
Q

where are cementocytes?

A

in lacunae

92
Q

where is cementum thicker?

A

in apical region of root

93
Q

is cementum mineralised?

A

yes

94
Q

gingival health - clinical

A 
knife-edge, scalloped gingival margin
30% stippling
pink
no BOP
still bacteria present in health
intact barrier provided by JE
95
Q

gingival health - microbiological level

A 
bacteria
shedding of oral epithelial cells
flow of GCF
antibodies in GCF
phagocyte fct and lymphocyte infiltrate
complement activity
96
Q

gingivitis - microbiological level

A

bacteria
altered microbial colonisation
increased GCF flow
influx of neutrophils, increased lymphocytes and monocytes
plasma cell infiltrate
proliferation and ulceration of epithelium

97
Q

amplification of bacteria

A

bacteria need to be disrupted regularly and removed or they accumulate and change in quantity and type

98
Q

is the amount of plaque predictive of progression?

A

no

99
Q

microbial challenge (plaque): factors that affect progression to gingivitis

A

local PRFs

systemic modifying factors

100
Q

what does no BOP mean?

A

health (except smokers)

101
Q

BOP at gingival margin

A

gingivitis

102
Q

BOP at base of pocket

A

periodontitis

103
Q

open Qs

A 
bleed on brushing?
loose teeth?
can you chew everything?
bad taste/smell?
pain/swelling?
smoke?
104
Q

describing bone loss

A

distribution
shape
severity

105
Q

distribution of bone loss

A

localised <30%

generalised >30%

106
Q

shape of bone loss

A

horizontal

vertical (angular)

107
Q

severity of bone loss

A

mild <30% of root length
mod 30-50%
severe >50%

108
Q

what is tx planing for PDD based on?

A

history
exam
diagnosis

109
Q

aim of PDD tx

A

preserve fct dentition for as long as possible

110
Q

why can’t the outcome of PDD tx be predicted at the start?

A

severity
motivation
tissue response

111
Q

why is it good to stage PDD tx?

A

assess success before moving on

112
Q

stages of tx planning

A 
immediate
infection control
reevaluation
reconstructive tx
maintenance
113
Q

infection control tx planning stage

A 
extract hopeless teeth 
HPT
tx caries
endo
provisional prostheses
(manage any contributing systemic condition)
114
Q

cause-related PD therapy

A 
DHE and motivation
 - inc smoking cessation/risk factor modification 
OHI
scaling and RSD
remove PRFs
115
Q

TIPPS

A 
Talk
Instruct
Practice
Plan
Support
116
Q

DHE and OHI

A 
ask pt first
discuss exam findings
explain disease process
 - plaque irritates gums - sticky film of sugars and bacteria on teeth
brushing
 - modified bass
ID cleaning
demonstrate and get them to try
117
Q

re-evaluation

A

OH inadequate with persistent inflammation
OH good - no inflammation
OH good but persistent deep pockets with evidence of inflammation

118
Q

how is PD therapy success measured?

A

inflammation
reduction in probing depths
gain in probing attachment level

119
Q

success

A 
plaque <15%
BOP <10%
no pockets >4mm
no increasing tooth mobility
a fct and comfortable dentition
120
Q

maintenance

A

maintain PD health obtained during tx phase - so objective varies
interval varies - most every 3m
at each visit assess and reinforce OH
scaling, RSD and any other tx as necessary

121
Q

aims of PD therapy

A

arrest disease process
ideally regenerate lost tissue
maintain PD health long-term
control inflammation - keep tooth

122
Q

effects of supra gingival plaque control alone

A

reduction in gingival inflammation
limited effect on probing depth
no change in ALs
no alteration in subgingival microflora in deep pockets (>6mm)

123
Q

factors that influence manual probing measurements

A 
resistance of tissues
size, shape, tip diameter of probe
site and angle of probe insertion
pressure applied
presence of obstructions e.g. calculus
pt discomfort
124
Q

effects of RSD without supra gingival plaque control

A

initial reduction in inflammation and pocket depth
pockets recolonised by bacteria from supra gingival plaque
disease recurs

125
Q

scaling

A

removal of plaque and calculus from tooth surfaces

126
Q

debridement

A

removing dead, contaminated or adherent tissue, or foreign material

127
Q

root planing

A

the removal of contaminated cementum, leaving the root smooth and hard
- don’t do anymore

128
Q

RSD

A

scaling and removal of supra gingival calculus

129
Q

what is decision making at re-evaluation based on?

A 
OH
BOP
pocket depth
attachment levels
tooth mobility
130
Q

options at decision making stage

A

maintenance
repeat NST
surgical access

131
Q

effects of RSD with supra gingival plaque control

A

reduction in gingival inflammation
reduced probing depth
marked changes in the subgingival microbial flora
gain in probing attachment level
- due to long JE formation and improved tissue tone (inflammatory infiltrate replaced by collagen)

gradual repair and maturation of tissues over 9-12m

132
Q

effects of debridement

A

reduces microbial challenge - decreased inflammation

inoculation with plaque microorganisms - boosts immune response

133
Q

organisation of the tx

A

quadrant approach
full mouth disinfection
- prevent txed pockets being re-colonised by IO translocation of bacteria

134
Q

limitations of NST

A 
root morphology
furcation involvement
deep pockets
skill level
time
135
Q

selective pressure

A

prevent overt pathogenicity

136
Q

why does tx fail?

A

poor compliance
inadequate debridement
host factors (mainly smoking)

137
Q

MMPs

A

collagenases

secreted by local inflammatory cells

138
Q

progression of AL

A

varies

may be episodic/continuous

139
Q

PDL fibre groups

A

alveolar crest
horizontal
oblique
apical

140
Q

gingival fibre groups

A

dentogingival
alveologingival
circular
transseptal

141
Q

pathogenicity

A

ability of microbe to cause disease
virulence factors
overcome immune response

142
Q

protective functions of ABs

A

inhibiton of adhesion/invasion
complement activation
neutralisation of toxins
opsonisation and phagocytosis

143
Q

smoking

A

effect on subgingival plaque uncertain
vasoconstriction of gingival vessels and increased gingival keratinisation
impaired antibody production
reduction in number of Th lymphocytes
impaired PMN function
increased production of pro inflammatory cytokines

144
Q

what do activated lymphocytes express?

A

RANKL

145
Q

what effect do pro-inflammatory cytokines have on bone formation?

A

they inhibit it

146
Q

what is the result of elevated and dysregulated MMP activation?

A

CT destruction

147
Q

what immune cells are found in early lesions?

A

T and B cells

148
Q

what immune cells are found in advanced lesions?

A

B/plasma cells

149
Q

how does OPG inhibit RANK?

A

it binds RANKL

150
Q

virulence factors of p gingivalis

A 
immune evasion and subversion
inflammophillic
asaccharolytic
gingipains - degrade host proteins, activate MMPs
atypical LPS-TLR-4 antagonist
151
Q

fusobacterium nucleatum

A

adheres commensals then gram - anaerobes

152
Q

role of neutrophils in PD destruction

A

excessive infiltration in chronic inflammation
immune under-reaction problem
immune over-reaction

153
Q

red complex

A 
but can be found in healthy sites (in lower numbers)
p gingivalis
t forsythia
t denticola
don't meet Koch's postulates
154
Q

what is necessary but not sufficient for PDD?

A

bacterial biofilm

155
Q

which is the main Ig in GCF?

A

IgG

156
Q

role of lymphocytes in health

A

present but not active - surveillance

157
Q

what does TLR stimulation induce the epithelium to secrete?

A

chemo/cytokines

158
Q

evidence for specific bacterial causation

A

present in elevated numbers at diseased sites
reduction in numbers following PD therapy
presence of elevated specific immune response
production of virulence factors
evidence from animal models

159
Q

keystone pathogen

A

the pathogen that disrupts harmony and causes dysfunction in the group - changes the fct of that group of bacteria

160
Q

role of epithelium

A

physical barrier
cell shedding
produce inflammatory mediators

161
Q

biofilm

A

one or more communities of MOs, embedded in a glycocalyx, attached to a solid surface

162
Q

properties of biofilms

A

protection
facilitate uptake of nutrients and removal of metabolic products
develop appropriate physiochemical env
communication between bacteria

163
Q

bacterial virulence

A

ability to colonise and compete in an ecological niche
ability to evade host defences
- degrade host immunoglobulin and complement
- leucotoxin production
- tissue invasion
- inhibition of AB synthesis

perio (8 decks)

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