exam notes (big doc) Flashcards
clinical and lab investigations
thorough history (inc FH) pocket chart microbial analysis of sample (swab of crevicular fluid)
deciding prognosis of individual teeth
loss of attachment
mobility
furcation involvement
Why would mechanical root surface debridement not be successful in eliminating pocket bacteria?
difficulty with access esp furcation
pt not adhering to OH requirements
inadequate RSD/lack of operator experience
pt immunocompromised
may not be able to remove pathogens as sites inaccessible to instruments e.g. invaded dentinal tubules
failure to disrupt biofilm
why may ABs not be effective?
may be resisted by biofilms
may have inadequate drug concentration and retention (not in therapeutic range)
may not reach site of disease activity
clinical signs of improved health
reduced probing depths <4mm
BOP <10%
requirements for implant placement
space (7mm)
bone levels
periodontal health
bacteria in NG
p intermedia
fusobacterium
spirochetes e.g. treponema
NG S+S
blunting papillae halitosis grey slough wipes off to reveal ulcerated tissue crater like ulcers reverse gingival architecture
OFD information to give to pt
risks - gingival recession, infection (+ post-op ones)
benefits - effectively debride area with direct vision
outcomes - possible reduction of pocket depth
other options - NSPT
risks if don’t get tx - increase in pocket depth, increase in mobility, increased likelihood of losing teeth
reviewing pt after OFD
at least 8 weeks to allow time frame for healing
OFD clinical findings indicating successful tx
<4mm probing depths
plaque scores <15%
BOP <10%
why might antibiotics not work for chronic periodontal disease?
biofilm resistance to antibiotics
inactivated by first pass metabolism
poor pt adherence to regimen
antibiotic resistance
SIRS
any 2 or more of :
- temp <36 or >38 degrees
- resp rate >20/min
- WBC <4000 or >12000 cells/mm3
- hr >90bpm
what is a periodontal abscess?
acute exacerbation of an existing periodontal pocket e.g. trauma or obstruction
caused by food packing or inadequate RSD
S+S of PD abscess
pain on biting/spontaneous TTP swelling pus pocketing at swelling mobility
differentiating PD abscess from PA abscess
sensibility test non-vital vs vital
also consider perio condition in rest of mouth
how do you manage occlusal trauma in a pt with periodontal disease?
address cause (remove high Rxs, parafct)
bite raising appliance nighttime wear
HPT
what factors can influence localised mobility?
existing PDD occlusal trauma causing widening of PDL morphology and length of roots alveolar bone loss resorption/trauma
when might splinting be advised?
mobility due to advanced LOA
causing discomfort or difficulty in chewing
to facilitate RSD
why is there a decrease in mobility after tx?
increased tissue tone and long junctional epithelium attachment
what can you do if the PDL is still widened after successful Rx?
reduce contact in occlusion
what are the findings for aggressive periodontitis?
severe periodontal destruction not consistent with oral hygiene
familial aggregation
pt otherwise clinically fit
localised aggressive periodontitis
localised LOA
6s, incisors
circumpubertal onset
robust antibody response
generalised aggressive periodontitis
generalised LOA 6s, incisors and 3+ other teeth usually onset under 30years poor serum antibody response episodic nature
bacteria in aggressive periodontitis
aggregatibacter actinomtcetemcomitans (AA) porphyromonas gingivalis
why does mobility indicate poor prognosis?
reduced bone support
why does furcation involvement indicate poor prognosis?
more difficult to keep clean for pt
why does LOA indicate poor prognosis?
less supporting structures for tooth
factors which indicate poor prognosis for a tooth
mobility
furcation involvement
LOA
non-vitality
further info needed from pt before determining poor prognosis teeth
smoking
drug history
systemic disease
how is localised angular periodontitis caused?
when pathway of inflammation travels directly into PDL space, localised PRFs
classifying localised angular periodontitis
mild <30%
moderate 30-50%
severe >50%
3 clinical/radiographic signs of healing
gingival recession - black triangles
clinical reattachment - reduced probing depth
reduced BOP
difference between horizontal and angular bone loss
radius of destruction of plaque is approximately 2mm
horizontal bone loss found where plaque destroys bone completely between 2 roots, angular is where the radius is still bone on one side
how does a healthy periodontium react to traumatic occlusion?
PDL widening so mobility
no LOA or inflammation
will resolve once occlusion sorted
how does a healthy but reduced periodontium react to traumatic occlusion?
same but due to less PDL mobility is increased
how does a periodontitis periodontium react to traumatic occlusion?
plaque still primary etiological factor but may make rate of LOA faster
widened PDL and mobility same
what is CHX?
biguanide antiseptic
CHX mode of action
dicationic >1 cation adheres to pellicle and 1 cation disrupts bacterial membrane
antibacterial and antiseptic so bacteriostatic and bacteriolytic
works against gram + and - bacteria, fungi and viruses
CHX substantivity
12 hours
give 2 common doses of CHX
- 2% 10ml/20mg 2x daily
0. 12% 15ml/18mg 2x daily
side effects of CHX
staining taste disturbance salivary gland enlargement anaphylaxis interacts with SLS
uses of CHX
surgical pre-op rinse post IO surgery OHI pts with jaw fixation NG recurrent oral ulceration denture stomatitis tx of dry socket endo irrigant medically compromised high caries risk
how is HPT provided?
non-surgical periodontal therapy - scaling and RSI
remove PRFs
OHI
HPT success
pockets <4mm
plaque scores <15%
bleeding scores <10%
TIPPS
OHI Talk Instruct Practise Plan Support
things recorded on a PD pocket chart
teeth missing gingival margin pocket depth LOA mobility furcation BOP
give 2 disadvantages of a pocket chart
assumes all pts have same root length so may appear worse than they are
probing depths are subjective/variation between operators
local factors for gingival recession
periodontal disease habits traumatic tooth brushing abrasive toothpaste high frenal attachment traumatic overbite orthodontics poor marginal fit restorations
how can you measure recession?
photos
study models
pocket chart
how is localised recession managed?
atraumatic tooth brushing technique minimise other risk factors monitor treat sensitivity free/pedicle ST graft (from palate) coronal advancement flap
what would you look for in a pt who wants an implant?
bone quantity and quality pt motivation OH smoking MH e.g. bisphosphonates restorative options
intervention for inadequate bone levels
GTR
bone graft
biological mediator = Emdogain (enamel matrix derivative)
sinus lift
mechanism of a vertical bone defect
radius of destruction of plaque determines this
approx 1.5-2mm and if the IP bone loss is greater than this then the pattern is vertical/angular
how are vertical defects classified?
by number of walls: 1,2 or 3 wall defects
- 2 and 3 wall defects heal better
indications for regenerative periodontal surgery
2 and 3 walled defects
grade 2 furcation in mandibular teeth
grade 2 buccal furcation in maxillary molars
why might NST for PDD be unsuccessful?
inadequate RSI furcation/angular defects that are difficult to effectively clean motile anaerobes moving into tissues pt not adhering to OHI pt immunocompromised smoking
why is diabetes a risk factor in PDD?
WIPA
1 - poor wound healing
2 - both pro-inflammatory diseases
3 - immunosuppression: impaired PMN neutrophil fct
4 - advanced glycation end (AGE) products causing increased tissue destruction
give 2 tests to test for diabetes
RPG - random plasma glucose
FPG - fasting plasma glucose
RPG values
normal <11.1 mol/L
diabetes >11.1mmol/L on 2 separate occasions
FPG values
normal <7mmol/L
diabetes >7mmol/L on 2 separate occasions
test for diabetic control
Hb1AC - gylcated haemoglobin
normal Hb1AC value
<7%
how does smoking affect the periodontal tissues?
CCEB 1 - impaired chemotaxis and phagocytosis 2 - affects cytokine production 3 - affects enzyme catalases 4 - blood flow restricted
what is IL-1?
a pro-inflammatory cytokine
stimulates the release of enzymes and osteoclasts causing increased tissue destruction
desquamative gingivitis
inflamed gingiva extending beyond the mucogingival jct
conditions associated with desquamative gingivitis
lichen planus
pemphigoid
pemphigus
local factors that may exacerbate desquamative gingivitis
SLS
plaque
smoking
topical txs for desquamative gingivitis
topical steroids e.g. betamethasone or beclomethasone
tacrolimus MW
medications associated with gingival hyperplasia
phenytoin
cyclosporine
nifedipine
managing medication associated gingival hyperplasia
plaque is still the primary aetiological factor so OHI and RSI first
if no improvement and pt still has good OH then consider surgery and liase w/GP to discuss changing meds
Grade 0 mobility
physiological movement (<0.2mm)
Grade 1 mobility
<1mm horizontal
Grade 2 mobility
1-2mm horizontal
Grade 3 mobility
> 2mm and vertical movement (rotations and depressions)
Grade 1 furcation
<3mm horizontal
Grade 2 furcation
> 3mm horizontal but not through and through
Grade 3 furcation
through and through
how is gingival recession graded?
Miller’s classification
how would you decide the prognosis of individual teeth?
symptoms level of bone loss furcation involvement mobility angular defects making RSI more difficult difficult for pt to maintain short tapered roots
