2nd year Flashcards
1 o’clock seating position
U palatals
U buccal anteriors
U buccal left
L lingual right
L buccal left
3 o’clock seating position
U buccal right
L buccal right
L lingual left
5 o’clock seating position
L anteriors
broad risk factor categories
genetic
epigenetic
env
behavioural
minisickle features
double ended triangular cross section point scaler curved blade 2 cutting edges - converge to a sharp point face at 90 degrees to lower shank
minisickle uses
supra gingival calculus from buccal and lingual embrasures
X deep subgingival - sharp point would groove root surface/lacerate pocket wall
Columbia/universal features
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
Columbia/universal uses
supra/subgingival anywhere
but only limited access to deep pockets
use of Hoe scalers
gross calculus supra and subgingivally
restricted access in v narrow pockets
hoe scalers features
blade set at 100 degree angle to shank
cutting edge bevelled at 4 degrees
set of 4 - double-ended
yellow hoe scaler
buccal and lingual
red hoe scaler
mesial and distal
Gracey curette uses
subgingival
Gracey curette features
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
grey gracey
anteriors
orange gracey
mesial of posteriors
green gracey
buccal and lingual of posteriors
blue gracey
distal of posteriors
checking for remaining calculus
root surface - CPITN probe
supra gingival - air dry
gingivitis
inflammation confined to gingiva
increase in probing depth - false pocketing
- no permanent destruction of CT attachment to root surface
bleeding
periodontitis
apical extension of inflammation destruction of CT attachment apical migration of JE lose alveolar bone true pocket microbial plaque main etiological factor
peri-implant mucositis
inflammation in mucosa no loss of bone may resolve with plaque removal and improved OH BOP redness swelling
peri-implantitis
inflammation in mucosa with loss of supporting bone
increased probing depths, BOP, (suppuration, implant mobility)
cause of peri-implant disease
likely microbial plaque and immune response
excess cement
poorly fitting superstructures
poorly positioned implants
what is BPE useful for?
screening
BPE sextants
7-4
3-3
need at least 2 teeth
BPE probe
WHO BPE/CPITN probe
BPE force
20-25g ‘walk’
should BPE be done around implants?
no
BPE 0
no PD tx
BPE 1
OHI and PGI
BPE 2
OHI and PGI
removal of plaque-retentive factors
BPE 3
OHI and PGI
removal of plaque-retentive factors
+ RSD if required
BPE 4
OHI and PGI
removal of plaque-retentive factors
+ RSD if required
+ assess need for more complex tx/specialist?
BPE *
tx according to BPE code
complex/referral?
SDCEP BPE3
6PPC for sextants with BPE 3 before tx and at reevaluation
BSP BPE3
6PPC only at reevaluation
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
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)
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
sharpening stone
flat
smooth
man-made
Arkansas stone
wedge-shaped
natural
fine abrasiveness
Al2O3
sharpening instruments technique
need to preserve blade shape inc angles
pen/palm grip
make 3 strokes then check
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
periodontal chart stages
PCP12 probe score out missing teeth position of gingival margin probing depths calculate LOA BOP mobility furcation involvement
position of gingival margin
6 points for each tooth
relate to ACJ
visual and tactile
uses of 6PPC
educate
inform tx choice
monitor tx outcomes
medicolegal
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
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
what is healing after RSD dependent on?
RSD and effective supra gingival plaque control
reduction in pocket depth after RSD
reduced oedema
increase in clinical attachment
- form long JE
- increase in ‘tissue tone’ produces resistance to probing
re-evaluation after RSD
6-8 wks after
probe placement
adaptation
parallelism
adaptation
side of probe tip should be kept in contact with tooth surface
parallelism
as parallel as possible to LA of tooth
assessing tooth mobility
try to move buccolingually with index finger and handle
apply gentle pressure on crown with handle in vertical direction
tooth mobility definition
amplitude of movement of crown tip from its most extreme buccal/mesial position to its most extreme lingual/distal position
Grade 0 mobility
‘physiological’
0.1-0.2mm horizontal
Grade 1 mobility
<1mm horizontal
Grade 2 mobility
exceeding 1mm horizontal
visually
Grade 3 mobility
vertical/rotation/depression/horizontal
impinges on fct
what can you use to assess furcation involvement?
furcation probe e.g. Nabers
Grade 1 furcation
<1/3
Grade 2 furcation
> 1/3 but not though and through
Grade 3 furcation
through and through lesion
difficulty with assessing furcations
not always possible to probe
- located IP and/or significantly subgingival
gingival margin position
normal at CEJ
young pt/inflammation - coronal
recession - apical
probing depth
distance from gingival margin to base of pocket
does probing depth indicate severity?
not always
why can the probing depth change?
swelling or recession
what does probing depth indicate?
difficulty of tx and likelihood of recurrence
CAL
CEJ to base of pocket
what is CAL the best measure of?
tissue destruction (pre-tx) extent of repair (post-tx)
locating ACJ
probing
visual if recession
contraindications to US
pacemaker
pregnancy
swallowing difficulties
Covid - AGP
manufacturers with US
Dentsply - number of bends in tip
laminated efficiency indicator cards
thinner insert = lower power
US aim with water
mist with some droplets
speed of US
25000 small strokes / second
US amplitude of vibratory movement in LA of tip
approx 0.006 - 0.1mm
why is water necessary in US?
heat
mechanisms of action of US
vibrational energy
cavitation effect - vacuum bubbles - implode creating microcosms of energy
cleansing/flushing effect of H2O spray
pros and cons of US
poorer tactile sensation
may allow better furcation access
faster
may leave rougher surface
which power should you use with US?
lowest power
use of US
supra gingival and a little subgingival
- can’t get in deep pockets
- won’t cut granulose tissue
- lack of tactile sensation
oral sulcular epithelium
parakeratinised
lines gingival sulcus
JE
non-keratinised
most apical point CEJ in health
wider coronally
hemidesmosomes
gingival CT
LP gingival fibres - collagen fibre bundles ground substance fibroblasts blood and lymph vessels neural tissues
cementum and remodelling
no physiological remodelling but continuously deposited throughout life
Sharpey’s fibres
mineralised within the cementum
where does cellular cementum lie?
over acellular
where are cementocytes?
in lacunae
where is cementum thicker?
in apical region of root
is cementum mineralised?
yes
gingival health - clinical
knife-edge, scalloped gingival margin 30% stippling pink no BOP still bacteria present in health intact barrier provided by JE
gingival health - microbiological level
bacteria shedding of oral epithelial cells flow of GCF antibodies in GCF phagocyte fct and lymphocyte infiltrate complement activity
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
amplification of bacteria
bacteria need to be disrupted regularly and removed or they accumulate and change in quantity and type
is the amount of plaque predictive of progression?
no
microbial challenge (plaque): factors that affect progression to gingivitis
local PRFs
systemic modifying factors
what does no BOP mean?
health (except smokers)
BOP at gingival margin
gingivitis
BOP at base of pocket
periodontitis
open Qs
bleed on brushing? loose teeth? can you chew everything? bad taste/smell? pain/swelling? smoke?
describing bone loss
distribution
shape
severity
distribution of bone loss
localised <30%
generalised >30%
shape of bone loss
horizontal
vertical (angular)
severity of bone loss
mild <30% of root length
mod 30-50%
severe >50%
what is tx planing for PDD based on?
history
exam
diagnosis
aim of PDD tx
preserve fct dentition for as long as possible
why can’t the outcome of PDD tx be predicted at the start?
severity
motivation
tissue response
why is it good to stage PDD tx?
assess success before moving on
stages of tx planning
immediate infection control reevaluation reconstructive tx maintenance
infection control tx planning stage
extract hopeless teeth HPT tx caries endo provisional prostheses (manage any contributing systemic condition)
cause-related PD therapy
DHE and motivation - inc smoking cessation/risk factor modification OHI scaling and RSD remove PRFs
TIPPS
Talk Instruct Practice Plan Support
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
re-evaluation
OH inadequate with persistent inflammation
OH good - no inflammation
OH good but persistent deep pockets with evidence of inflammation
how is PD therapy success measured?
inflammation
reduction in probing depths
gain in probing attachment level
success
plaque <15% BOP <10% no pockets >4mm no increasing tooth mobility a fct and comfortable dentition
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
aims of PD therapy
arrest disease process
ideally regenerate lost tissue
maintain PD health long-term
control inflammation - keep tooth
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)
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
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
scaling
removal of plaque and calculus from tooth surfaces
debridement
removing dead, contaminated or adherent tissue, or foreign material
root planing
the removal of contaminated cementum, leaving the root smooth and hard
- don’t do anymore
RSD
scaling and removal of supra gingival calculus
what is decision making at re-evaluation based on?
OH BOP pocket depth attachment levels tooth mobility
options at decision making stage
maintenance
repeat NST
surgical access
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
effects of debridement
reduces microbial challenge - decreased inflammation
inoculation with plaque microorganisms - boosts immune response
organisation of the tx
quadrant approach
full mouth disinfection
- prevent txed pockets being re-colonised by IO translocation of bacteria
limitations of NST
root morphology furcation involvement deep pockets skill level time
selective pressure
prevent overt pathogenicity
why does tx fail?
poor compliance
inadequate debridement
host factors (mainly smoking)
MMPs
collagenases
secreted by local inflammatory cells
progression of AL
varies
may be episodic/continuous
PDL fibre groups
alveolar crest
horizontal
oblique
apical
gingival fibre groups
dentogingival
alveologingival
circular
transseptal
pathogenicity
ability of microbe to cause disease
virulence factors
overcome immune response
protective functions of ABs
inhibiton of adhesion/invasion
complement activation
neutralisation of toxins
opsonisation and phagocytosis
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
what do activated lymphocytes express?
RANKL
what effect do pro-inflammatory cytokines have on bone formation?
they inhibit it
what is the result of elevated and dysregulated MMP activation?
CT destruction
what immune cells are found in early lesions?
T and B cells
what immune cells are found in advanced lesions?
B/plasma cells
how does OPG inhibit RANK?
it binds RANKL
virulence factors of p gingivalis
immune evasion and subversion inflammophillic asaccharolytic gingipains - degrade host proteins, activate MMPs atypical LPS-TLR-4 antagonist
fusobacterium nucleatum
adheres commensals then gram - anaerobes
role of neutrophils in PD destruction
excessive infiltration in chronic inflammation
immune under-reaction problem
immune over-reaction
red complex
but can be found in healthy sites (in lower numbers) p gingivalis t forsythia t denticola don't meet Koch's postulates
what is necessary but not sufficient for PDD?
bacterial biofilm
which is the main Ig in GCF?
IgG
role of lymphocytes in health
present but not active - surveillance
what does TLR stimulation induce the epithelium to secrete?
chemo/cytokines
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
keystone pathogen
the pathogen that disrupts harmony and causes dysfunction in the group - changes the fct of that group of bacteria
role of epithelium
physical barrier
cell shedding
produce inflammatory mediators
biofilm
one or more communities of MOs, embedded in a glycocalyx, attached to a solid surface
properties of biofilms
protection
facilitate uptake of nutrients and removal of metabolic products
develop appropriate physiochemical env
communication between bacteria
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
