periodontology Flashcards
step 1 of perio treatment
explain disease - risks and benefits of treatment/no treatment
OHI
risk factor control
PMPR
extract hopeless teeth - grade 3 mobility
step 2 perio treatment
assess engagement - if non-engaging return to step 1
reinforce risk factor, OHI and behaviour change
sub gingival PMPR for >4mm pockets
revaluate 3 months
step 3 of perio treatment
skip if stable
management of non-responding sites
repeat sub gingival instrumentation on pockets >4mm
may need surgery >6mm pockets
referral
step 4 perio treatment
supportive periodontal therapy
reinforce OHI risk factor control and behaviour change
regular targeted PMPR - individually tailored intervals 3-12 months
what is involved in revaluation at each step of perio treatment
OHI
BOP
attachment levels
tooth mobility
risk factor control and behaviour change
signs of successful perio treatment
no BOP or <10%
no pockets >4mm
plaque score <20%
no increased tooth mobility
aim of SPT supportive periodontal therapy
maintain periodontal health
detect and treat recurrence
maintain accepted level of disease
manage tooth loss
treatment given for SPT
OHI
supra gingival scaling - careful at 1-3mm pockets as can cause loss of attachment
RSD
polishing
reasons for recurrence of periodontitis
inadequate plaque control
failure to comply with SPT
inadequate treatment to remove all plaque retentive factors
failure to return to check ups
presence of systemic disease - host plaque resistance affected
how many teeth are affected in localised periodontal disease
<30%
how many teeth are affected in generalised periodontal disease
> 30% teeth
3 classifications of periodontal disease
localised
generalised
Molar incisor pattern
why classify disease
to properly diagnose and treat
for scientists to investigate aetiology, pathogenesis
capture severity and current state
what are the 10 2017 periodontal disease classifications
gingival health
plaque induced gingivitis
non-plaque induced gingivitis
periodontitis
necrotising periodontal disease
periodontitis as manifestation of systemic disease
systemic diseases affecting periodontal tissues
periodontal abscess
perio-endo lesions
mucogingival deformities and conditions
what is gingival health according to 2017 classification of perio disease - 4
absence of BOP or <10% for intact peridontium and reduced and stable peridontium
no erythema or oedema
physiological bone levels 1-3mm of ECJ
probing depth less than or equal to 3mm
Patients with an intact periodontium
Patients with a reduced periodontium due to causes other than periodontitis
Patients with reduced periodontium due to periodontitis
what is plaque induced gingivitis according to 2017 classification of perio disease - 4
associated with biofilm alone
BOP <30% localised or >30% generalised
no bone loss
BPE2
modifying factors of plaque induced gingivitis
smoking
pregnancy
drugs causing gingival enlargement
puberty
causes of non plaque induced gingivitis
hereditary gingival fibromatosis
herpetic gingival stomatitis
lichen Planus
nutrition deficiency - vit C
what does perio stage measure
severity
what does perio grade measure
susceptibility
how do you stage periodontitis
use bone loss at worst site
<15% early
coronal third of root - moderate
mid third - severe
apical third - very severe
how do you grade periodontitis
percentage bone loss at worst site/age
A - slow rate of progression <0.5
B - moderate 0.5-1
C - rapid >1
when is periodontitis stable - 3
BOP <10%
PPD </=4mm
no BOP at 4mm sites
when us periodontitis in remission
BOP<10%
PPD </= 4 mm
no BOP at 4mm sites
when is periodontitis unstable
PPD >/=5mm
OR
>/=4mm with BOP
what is included in diagnostic statement of periodontitis
extent
stage
grade
stability
risk factors
BSP BPE 3 sextant guidelines
review after initial treatment and 6PPC completed for this sextant only and only after treatment
what are the characteristics of NG
necrosis and ulcer of interdental papilla
punched out appearance
pseudo membrane formation along gingival margin
halitosis
gingival bleeding - readily
severe pain
fever and lymphadenopathy
3 necrotising periodontal diseases
necrotising gingivitis
necrotising periodontitis
necrotising stomatitis
how does NP differ to NG
same signs and symptoms as NG, additionally there is periodontal attachment loss and bone destruction
what is necrotising stomatitis
progression of NP - necrosis progressed to deeper tissues beyond mucogingival line - lip, cheek mucosa, tongue etc
can lead to denudation of bone - osteitis and OAF
what exacerbates NPD
immunocompromised patients
HIV
malnourishment
stress
smokers
who is susceptible to NS
compromised patients
HIV
stress
smokers
NP
NG
which diseases and condition can lead to early presentation of severe periodontitis
papillon lefevre syndrome
downs syndrome
leucocyte adhesion deficiency
systemic diseases or conditions that affect periodontal tissues
squamous cell carcinoma
uncontrolled diabetes mellitus
causes of periodontal abscess in non-perio patients
impaction
harmful habits
gingival overgrowth
causes of periodontal abscess in perio patient
acute exacerbation - untreated periodontitis, SPT
post scaling
medication e.g. nifedipine
3 examples of mucogingival deformities and conditions
lack of keratinised gingiva
abnormal renal attachment
recession
describe type 1 recession
no loss of inter proximal attachment
CEJ not detectable at distal and mesial
describe type 2 recession
loss of inter proximal attachment
inter proximal attachment loss less than or equal to buccal attachment loss
gums look normal but more apical
describe type 3 recession
low of inter proximal attachment
inter proximal attachment loss greater than buccal attachment loss
gums look straight across
where is attachment loss measured from and to
from CEJ to apical depth of pocket
two subdivisions of perio endo lesions
with or without root damage
In developed countries, NPD occurs mostly in young adults with predisposing factors. what are these predisposing factors
stress
sleep deprivation
poor OH
smoking
immunosuppression (HIV)
malnutrition
In cases that show unsatisfactory response to debridement or show systemic effects, what should you consider prescribing
400mg metronidazole TID
aesthetic consequence of NP
gingival creators
2 genetic conditions associated with periodontitis due to impairment of immune system
papillon lefevre syndrome
downs syndrome
3 diseases/conditions that lead to impairment of immune system and therefore periodontitis
leukaemia
neutropenia
HIV infection
give 3 local acquired risk factors of perio
overhangs
calculus
ortho appliance
give 3 local anatomical risk factors of periodontitis
malpositioned teeth
root grooves
enamel pearls
3 modifiable systemic risk factors of periodontitis
smoking
poor controlled diabetes
stress
3 non-modifiable systemic risk factors of periodontitis
age
genetic disorders
gender - males higher risk
why is smoking a risk factor of periodontitis
poor healing capacity - reduced blood flow
chemicals in smoke activate immune cells
what effect does suboptimal diabetes control have on periodontitis development - 3
in hyperglycaemia production of advanced glycation end products (AGE) increases
leads to exacerbation of inflammation - production of pro inflammatory cytokines and destructive metalloproteinases
RANKL:OPG ratio is altered leading to alveolar bone destruction
cause of scorbutic gingivitis
severe vit C deficiency - scurvy
2 drugs that are a risk factor for periodontitis
phenytoin - anticonvulsant
cyclosporin - immunosuppressant
what is neutropenia
reduced number and function of neutrophils
and macrophages
increasing risk of NUG and periodontitis
what is leukaemia
reduced number and function of neutrophils and macrophages
increasing risk of NUG and periodontitis
modifiable systemic risk factors of periodontitis
smoking
poor controlled diabetes
stress
osteoporosis
HIV
why is stress a risk factor for periodontal disease
secretion of cortisol stimulates immune system and ANS
leading to secretion of catecholamine and substance P
regulates immune inflammatory response
affects bacterial adherence and growth
can cause suppression of the immune system which tips
host-bacterial interaction in favour of bacteria
what health issues is periodontitis a risk factor of
CV disease - atherosclerosis and hypertension
preeclampsia
how does diabetes contribute to increased inflammation in periodontitis
increased production of AGEs (advanced glycation end products) which leads to activation of local immune and inflammatory responses
results in periodontal tissue damage and resorption of bone
how does periodontitis impact diabetes
circulating bacteria causes inflammatory state and elevates HbA1c and causes impaired insulin signalling and resistance
what step of perio is controlling risk factors part of
step 1
function of periodontum
to attach teeth to jaws
to dissipate occlusal forces
define excessive occlusal force
occlusal force that exceeds reparative capacity of periodontal attachment apparatus -> occlusal trauma and tooth wear
tooth mobility can be accepted unless - 3
progressively increasing
gives rise to symptoms
creates difficulty with restorative treatment
how can you correct occlusal relations
adjust occlusal surfaces - grinfing
restorations
orthodontics
how can you reduce tooth mobility
splint
correct occlusal relations
control plaque induced inflammation
what is primary occlusal trauma
Injury resulting in tissue changes from excessive occlusal forces appliedto a tooth or teeth with normal periodontal support.
normal attachment levels, normal bone levels, and excessive occlusal force(s).
how does healthy periodontium respond to occlusal trauma
PDL width increases
tooth mobility increases as result
this is regarded physiological and successful adaptation
how does healthy periodontium respond to excessive occlusal trauma
PDL width continues to increase
PDL width and tooth mobility do not stabilise
failure to adaptation - pathological
what is secondary occlusal trauma
injury resulting in tissue changes from normalor excessive occlusalforces applied to a tooth or teeth with reducedperiodontal support.
occurs in presence of attachment loss, bone loss and normal or excessive forces
what is fremitus
palpable or visible movement of a tooth when subjected to occlusal forces
what is bruxism
habit of grinding clenching or clamping teeth
force may damage tooth and attachment apparatus
what is the effect on attachment loss where there is plaque induced inflammation in addition to trauma induced inflammation
greater attachment loss
what causes tooth migration
loss of periodontal attachment
unfavourable occlusal forces and soft tissue profile
when is splinting appropriate
last resort treatment
appropriate if mobility is caused by advanced loss of attachment
causing discomfort and difficulty eating
needs stabilised for debridement
what is a gingival abscess
abscess localised to gingival margin
signs and symptoms of periodontal abscess
swelling
pain and bleeding
TTP laterally
suppuration fever
enlarged lymph nodes
what is a periodontal abscess
abscess within periodontal pocket
acute chronic or free draining (asymptomatic)
rapid destruction of periodontal tissues
associated rated with food packing and tightening of gingival margin after HPT
what is a pericoronal abscess
associated with partially erupted tooth
treatment of periodontal abscess
sub gingival instrumentation of pocket
Drain pus through pocket or incision
0.2% chlorhexadine
when would you prescribe antibiotics to a pt with periodontal abscess and what would you prescribe
signs of spread of infection
systemic effects
symptoms don’t resolve
250mg penicillin or
400mg metronidazole or
500mg amoxicillin
for 5 days
4 components of periodontium
gum or gingiva
periodontal ligament
cementum
alveolar bone
which of these is not an acute cause of periapical periodontitis
trauma
periodontitis
perforation
periodontitis
signs and symptoms of perioapical infection
deep pockets
bone resorption apical or furcation
spontaneous pain
TTP
what result would you expect from pulp vitality test on tooth with apical infection
negative or altered
how does infection spread to the apex of tooth
through PDL
through apex of root canal with necrotic pulp
through furcal
through lateral and accessory canals
role of apical foramen in periodical infection
main route of communication between pulp and periodontist
microbial and inflammatory bi products can exit apical foramen, or enter to affect pulp where there are deep pockets
what is perforation of root canal and give 3 causes
communication between root canal and either peri-radicular tissues, PDL or oral cavity
extensive caries
resorption
operator error
classification of perioendo lesion
by a carious lesion that affects the pulp and, secondarily, affects the periodontium.
by periodontal destruction that secondarily affects the root canal
grade 1, grade 2 and grade 3 endo-periodontal lesions
grade 1 - narrow deep periodontal pocket in 1 tooth surface
grade 2 - wide deep periodontal pocket in 1 tooth surface
grade 3 - deep perio pocket in more than one tooth surface
how can pathogenic invasion and secondary inflammation and necrosis of the pulp result from scaling?
accessory canals severed and opened to oral environment
treatment of perio-endo lesion
primary endo therapy
analgesia and 0.2% chlorhexadine mouth wash
periodontal therapy - supra and sub gingival instrumentation
review within 10 days
how can developmental grooves/invaginitation lead to deep pockets
if epithelial attachment is breached, groove becomes contaminated and pocket forms along its entire length
what is an S3 guideline
evidence and consensus based guideline
step one of perio treatment and when to progress to step 2
control risk factors
OHI and education of disease
PMPR
proceed when engaging and if PPD >3mm
if non engaging repeat step 1
step 2 of perio treatment and when to progress step 3 or 4
step 1 plus
sub gingival instrumentation of pockets >4mm
step 3 if residual pockets >4mm
step 4 if no residual pockets
step 3 of perio treatment and when to proceed to step 4
reinforce OHI, RFC and behaviour change
repeated sub-gingival instrumentation on >4mm pockets
consider referring for periodontal surgery in residual pockets
proceed when PPD less than or equal to 4 with no BOP
step 4 perio treatment
SPT
reinforce OHU, RFC and behaviour change
3-12 months - individually tailored
continuous monitoring
regular targeted PMPR
factors that influence the decision of periodontal surgery
smoking
compliance
OH
systemic disease
suitability of site - access, prognosis
define an engaging patient according to bop
favourable improvement of OH
50% or more improvement in plaque and marginal bleeding scores
OR
plaque levels </=20% and bleeding </=30%
OR
pt met targets in personal care plan with dentist
define non-engaging pt according to BSP
insufficient improvement in OH
less than 50% improvement in plaque
OR
plaque >20% bleeding >30%
IR pt states preference to palliative approach
indicators of successful perio treatment
good OH
no BOP or <10%
plaque scores < 20%
no pockets > 4mm
no increasing mobility
functional and comfortable dentition
what does a re-evaluation perio exam includee
OH
BOP
pocket depth
attachment levels
tooth mobility
treatment of residual pocked depths >/=6mm
surgical approach
treatment of residual pocket depths 4-5mm
repeated sub gingival instrumentation
aim of SPT
maintain perio health
detect and treat recurrence
maintain accepted level of disease
manage tooth loss
why give SPT
patients who are not recalled subsequent to active treatment show signs of recurrent periodontitis
more often patients get SPT - less likely to lose teeth
how often is patient recalled for SPT
individually assessed 3-12 months
steps of SPT
examination - look for changes since last recall
treatment - PMPR, care to avoid 1-3mm normal sites as can cause loss of attachment
why do patients experience bleeeding from gingivae when they quit smoking
smoking causes vasoconstriction so quitting increases vascularisation in gingivae as it returns to normal
how to calculate pack years
multiplying the number of packs of cigarettes smoked per day by the number of years the person has smoked
(packets are 20)
minimum teeth required for a sextant to qualify in BPE
2
probing force for BPE
20-25g
BPE 0
healthy tissues
no bleeding or calculus
BPE 1 meaning and management
bleeding
<3.5mm probing
plaque and bleeding scores
OHI
BPE 2 meaning and management
calculus or plaque retentive factor
<3.5mm probing
plaque and bleeding scores
OHI
remove plaque retentive factors
BPE 3
3.5-5.5mm probing
BPE 4
> 5.5mm probing
6 index teeth for simplified BPE - children and adolescents
UR6 UL6 LR6 LL6
UR1
LL1
best probe for BPE
BPE probe (WHO probe)
OR
WHO 621
best probe for sBPE and why
WHO 621 - second black band useful if false pocketing
BPE codes used for 7-11 year old
0-2
BPE codes for 12+
all codes
why not use BPE on implants
no PDL - les resistance to probe in healthy sites
management of BPE 3
OHI, risk factor control, RSD
6ppc after initial treatment, in code 3 sextant only
plaque and bleeding scores
radiographs to monitor alveolar bone levels
management of BPE 4
6ppc for full dentition before and after treatment
OHI, RSD, plaque and bleeding scores
radiographs to monitor alveolar bone levels
gold standard radiograph for periapical assessment
periapical using long-cone paralleling technique
what is TIPPS and what does it stand for
aim is to make patients feel more confident in their ability to perform OH and to help them plan
Talk
Instruct
Practice
Plan
Support
