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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
what is BPE useful for?
screening
26
BPE sextants
7-4 3-3 need at least 2 teeth
27
BPE probe
WHO BPE/CPITN probe
28
BPE force
20-25g 'walk'
29
should BPE be done around implants?
no
30
BPE 0
no PD tx
31
BPE 1
OHI and PGI
32
BPE 2
OHI and PGI | removal of plaque-retentive factors
33
BPE 3
OHI and PGI removal of plaque-retentive factors + RSD if required
34
BPE 4
OHI and PGI removal of plaque-retentive factors + RSD if required + assess need for more complex tx/specialist?
35
BPE *
tx according to BPE code | complex/referral?
36
SDCEP BPE3
6PPC for sextants with BPE 3 before tx and at reevaluation
37
BSP BPE3
6PPC only at reevaluation
38
limitations of BPE
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
39
BPE for U18s
``` 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)
40
instruments to sharpen curettes and scalers
test stick (acrylic) sharpening oil - lubricates and carries away metal debris. Reduces frictional heat sharpening/Arkansas stone magnifying lens
41
sharpening stone
flat smooth man-made
42
Arkansas stone
wedge-shaped natural fine abrasiveness Al2O3
43
sharpening instruments technique
need to preserve blade shape inc angles pen/palm grip make 3 strokes then check
44
instrument grip - modified pen grasp
middle finger - rest lightly on shank ring finger - oral structure (often a tooth) lower terminal shank parallel to LA of tooth
45
periodontal chart stages
``` PCP12 probe score out missing teeth position of gingival margin probing depths calculate LOA BOP mobility furcation involvement ```
46
position of gingival margin
6 points for each tooth relate to ACJ visual and tactile
47
uses of 6PPC
educate inform tx choice monitor tx outcomes medicolegal
48
polishing
smooth surfaces less likely to accumulate plaque remove any stains after scaling avoid heat production rubber cup pumice and water slurry for heavy staining
49
healing after RSD
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
50
what is healing after RSD dependent on?
RSD and effective supra gingival plaque control
51
reduction in pocket depth after RSD
reduced oedema increase in clinical attachment - form long JE - increase in 'tissue tone' produces resistance to probing
52
re-evaluation after RSD
6-8 wks after
53
probe placement
adaptation | parallelism
54
adaptation
side of probe tip should be kept in contact with tooth surface
55
parallelism
as parallel as possible to LA of tooth
56
assessing tooth mobility
try to move buccolingually with index finger and handle | apply gentle pressure on crown with handle in vertical direction
57
tooth mobility definition
amplitude of movement of crown tip from its most extreme buccal/mesial position to its most extreme lingual/distal position
58
Grade 0 mobility
'physiological' | 0.1-0.2mm horizontal
59
Grade 1 mobility
<1mm horizontal
60
Grade 2 mobility
exceeding 1mm horizontal | visually
61
Grade 3 mobility
vertical/rotation/depression/horizontal | impinges on fct
62
what can you use to assess furcation involvement?
furcation probe e.g. Nabers
63
Grade 1 furcation
<1/3
64
Grade 2 furcation
>1/3 but not though and through
65
Grade 3 furcation
through and through lesion
66
difficulty with assessing furcations
not always possible to probe | - located IP and/or significantly subgingival
67
gingival margin position
normal at CEJ young pt/inflammation - coronal recession - apical
68
probing depth
distance from gingival margin to base of pocket
69
does probing depth indicate severity?
not always
70
why can the probing depth change?
swelling or recession
71
what does probing depth indicate?
difficulty of tx and likelihood of recurrence
72
CAL
CEJ to base of pocket
73
what is CAL the best measure of?
``` tissue destruction (pre-tx) extent of repair (post-tx) ```
74
locating ACJ
probing | visual if recession
75
contraindications to US
pacemaker pregnancy swallowing difficulties Covid - AGP
76
manufacturers with US
Dentsply - number of bends in tip laminated efficiency indicator cards thinner insert = lower power
77
US aim with water
mist with some droplets
78
speed of US
25000 small strokes / second
79
US amplitude of vibratory movement in LA of tip
approx 0.006 - 0.1mm
80
why is water necessary in US?
heat
81
mechanisms of action of US
vibrational energy cavitation effect - vacuum bubbles - implode creating microcosms of energy cleansing/flushing effect of H2O spray
82
pros and cons of US
poorer tactile sensation may allow better furcation access faster may leave rougher surface
83
which power should you use with US?
lowest power
84
use of US
supra gingival and a little subgingival - can't get in deep pockets - won't cut granulose tissue - lack of tactile sensation
85
oral sulcular epithelium
parakeratinised | lines gingival sulcus
86
JE
non-keratinised most apical point CEJ in health wider coronally hemidesmosomes
87
gingival CT
``` LP gingival fibres - collagen fibre bundles ground substance fibroblasts blood and lymph vessels neural tissues ```
88
cementum and remodelling
no physiological remodelling but continuously deposited throughout life
89
Sharpey's fibres
mineralised within the cementum
90
where does cellular cementum lie?
over acellular
91
where are cementocytes?
in lacunae
92
where is cementum thicker?
in apical region of root
93
is cementum mineralised?
yes
94
gingival health - clinical
``` knife-edge, scalloped gingival margin 30% stippling pink no BOP still bacteria present in health intact barrier provided by JE ```
95
gingival health - microbiological level
``` bacteria shedding of oral epithelial cells flow of GCF antibodies in GCF phagocyte fct and lymphocyte infiltrate complement activity ```
96
gingivitis - microbiological level
bacteria altered microbial colonisation increased GCF flow influx of neutrophils, increased lymphocytes and monocytes plasma cell infiltrate proliferation and ulceration of epithelium
97
amplification of bacteria
bacteria need to be disrupted regularly and removed or they accumulate and change in quantity and type
98
is the amount of plaque predictive of progression?
no
99
microbial challenge (plaque): factors that affect progression to gingivitis
local PRFs | systemic modifying factors
100
what does no BOP mean?
health (except smokers)
101
BOP at gingival margin
gingivitis
102
BOP at base of pocket
periodontitis
103
open Qs
``` bleed on brushing? loose teeth? can you chew everything? bad taste/smell? pain/swelling? smoke? ```
104
describing bone loss
distribution shape severity
105
distribution of bone loss
localised <30% | generalised >30%
106
shape of bone loss
horizontal | vertical (angular)
107
severity of bone loss
mild <30% of root length mod 30-50% severe >50%
108
what is tx planing for PDD based on?
history exam diagnosis
109
aim of PDD tx
preserve fct dentition for as long as possible
110
why can't the outcome of PDD tx be predicted at the start?
severity motivation tissue response
111
why is it good to stage PDD tx?
assess success before moving on
112
stages of tx planning
``` immediate infection control reevaluation reconstructive tx maintenance ```
113
infection control tx planning stage
``` extract hopeless teeth HPT tx caries endo provisional prostheses (manage any contributing systemic condition) ```
114
cause-related PD therapy
``` DHE and motivation - inc smoking cessation/risk factor modification OHI scaling and RSD remove PRFs ```
115
TIPPS
``` Talk Instruct Practice Plan Support ```
116
DHE and OHI
``` 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
re-evaluation
OH inadequate with persistent inflammation OH good - no inflammation OH good but persistent deep pockets with evidence of inflammation
118
how is PD therapy success measured?
inflammation reduction in probing depths gain in probing attachment level
119
success
``` plaque <15% BOP <10% no pockets >4mm no increasing tooth mobility a fct and comfortable dentition ```
120
maintenance
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
aims of PD therapy
arrest disease process ideally regenerate lost tissue maintain PD health long-term control inflammation - keep tooth
122
effects of supra gingival plaque control alone
reduction in gingival inflammation limited effect on probing depth no change in ALs no alteration in subgingival microflora in deep pockets (>6mm)
123
factors that influence manual probing measurements
``` 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
effects of RSD without supra gingival plaque control
initial reduction in inflammation and pocket depth pockets recolonised by bacteria from supra gingival plaque disease recurs
125
scaling
removal of plaque and calculus from tooth surfaces
126
debridement
removing dead, contaminated or adherent tissue, or foreign material
127
root planing
the removal of contaminated cementum, leaving the root smooth and hard - don't do anymore
128
RSD
scaling and removal of supra gingival calculus
129
what is decision making at re-evaluation based on?
``` OH BOP pocket depth attachment levels tooth mobility ```
130
options at decision making stage
maintenance repeat NST surgical access
131
effects of RSD with supra gingival plaque control
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
effects of debridement
reduces microbial challenge - decreased inflammation | inoculation with plaque microorganisms - boosts immune response
133
organisation of the tx
quadrant approach full mouth disinfection - prevent txed pockets being re-colonised by IO translocation of bacteria
134
limitations of NST
``` root morphology furcation involvement deep pockets skill level time ```
135
selective pressure
prevent overt pathogenicity
136
why does tx fail?
poor compliance inadequate debridement host factors (mainly smoking)
137
MMPs
collagenases | secreted by local inflammatory cells
138
progression of AL
varies | may be episodic/continuous
139
PDL fibre groups
alveolar crest horizontal oblique apical
140
gingival fibre groups
dentogingival alveologingival circular transseptal
141
pathogenicity
ability of microbe to cause disease virulence factors overcome immune response
142
protective functions of ABs
inhibiton of adhesion/invasion complement activation neutralisation of toxins opsonisation and phagocytosis
143
smoking
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
what do activated lymphocytes express?
RANKL
145
what effect do pro-inflammatory cytokines have on bone formation?
they inhibit it
146
what is the result of elevated and dysregulated MMP activation?
CT destruction
147
what immune cells are found in early lesions?
T and B cells
148
what immune cells are found in advanced lesions?
B/plasma cells
149
how does OPG inhibit RANK?
it binds RANKL
150
virulence factors of p gingivalis
``` immune evasion and subversion inflammophillic asaccharolytic gingipains - degrade host proteins, activate MMPs atypical LPS-TLR-4 antagonist ```
151
fusobacterium nucleatum
adheres commensals then gram - anaerobes
152
role of neutrophils in PD destruction
excessive infiltration in chronic inflammation immune under-reaction problem immune over-reaction
153
red complex
``` but can be found in healthy sites (in lower numbers) p gingivalis t forsythia t denticola don't meet Koch's postulates ```
154
what is necessary but not sufficient for PDD?
bacterial biofilm
155
which is the main Ig in GCF?
IgG
156
role of lymphocytes in health
present but not active - surveillance
157
what does TLR stimulation induce the epithelium to secrete?
chemo/cytokines
158
evidence for specific bacterial causation
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
keystone pathogen
the pathogen that disrupts harmony and causes dysfunction in the group - changes the fct of that group of bacteria
160
role of epithelium
physical barrier cell shedding produce inflammatory mediators
161
biofilm
one or more communities of MOs, embedded in a glycocalyx, attached to a solid surface
162
properties of biofilms
protection facilitate uptake of nutrients and removal of metabolic products develop appropriate physiochemical env communication between bacteria
163
bacterial virulence
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

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