3rd year Flashcards
aims of supportive PD care (maintenance)
maintain PD health
detect and tx recurrence
maintain accepted level of disease
manage tooth loss
supportive PD care (maintenance) - who
pts who have had PD tx
supportive PD care (maintenance) - consequence of not returning
txed pts who do not return for regular recall are x5.6 greater risk for tooth loss than compliant pts
what does supportive PD care (maintenance) involve?
exam
tx
report and scheduling
other causes for recurrence other than inadequate OH/compliance?
- inadequate/insufficient tx that has failed to remove all of the potential factors favouring plaque accumulation
- incomplete calculus removal in areas of difficult access
- inadequate Rxs placed after PD tx was completed
- failure of pt to return for check-ups
- health changes - systemic disease that may affect host resistance to prev acceptable levels of plaque
how long are pts at risk of disease recurrence for?
the rest of their lives
PD tx in pregnancy
tx before if possible
provide non-surgical tx in 2nd trimester
- 1st trimester - Premature labour
- 3rd trimester – difficulty lying down
avoid ‘traumatic’ procedures
- PD surgery
- full mouth debridement??
discuss w pt
as a minimum provide supportive care
- supra gingival without LA and regular OHI
2017 PDDs classification - main overall groups
health, gingival diseases and conditions
periodontitis
other conditions
2017 PDDs classification - parts
PD health
Gingivitis - dental-biofilm induced
Gingival diseases and conditions: non-dental-biofilm induced
Necrotising periodontal diseases
Periodontitis
Periodontitis as a manifestation of systemic disease
Systemic diseases/conditions affecting the periodontal tissues
Periodontal abscesses and perio-eondo lesions
Mucogingival deformities and conditions
Traumatic occlusal forces
Tooth and prostheses related factors
2017 PDDs classification - mneumonic
Please Give Greg Nine Percy Pigs Straight Past Meal Time Tonight
2017 PDDs classification - PD health subcategories
intact periodontium
reduced periodontium
2017 PDDs classification - gingivitis dental-biofilm induced subcategories
intact periodontium
reduced periodontium
2017 PDDs classification - periodontitis subcategories
localised ≤30%
generalised >30%
MI pattern
problems with 1999 system
aggressive vs chronic
- more likely to be genetic
- often in young pts
- “usually affecting persons <30yrs but pts may be older”
- v woolly - room for interpretation
diagnosis of gingival health
- if pt has one bleeding site - gingivitis
- diagnosing everyone with a disease whether or not they have one
diagnosis of prev periodontitis?
2017 classification aims
capture extent and severity
- amount of PD tissue loss
pt susceptibility
- estimated by historical rate of progression
current PD state
- pocket depths/BOP
a system that can be future-proofed for update with new biomarker info e.g. if start to get salivary biomarkers
extent
captures distribution localised <30% teeth generalised >30% teeth MI pattern - tends to occur in younger pts
what does grading tell you?
disease susceptibility
what does staging tell you?
severity
what stage is a pt if they are known to have lost teeth due to perio?
stage 4
potential consequence of stage 3
potential for additional tooth loss
potential consequence of stage 4
potential for loss of dentition
what does currently in remission mean?
pt who had periodontitis who now has gingivitis
what does BPE guide?
need for further diagnostic measures prior to establishing a definitive PD diagnosis and appropriate tx planning
4mm threshold
critical as determines PDD stability at non-bleeding sites following successful PD therapy
5/6mm in absence of bleeding may not always represent active disease - in particular soon after PD tx
- need clinical judgement
health
intact periodontium
reduced periodontium due to causes other than periodontitis
reduced periodontium due to periodontitis
- but pt will always be a perio pt
plaque-induced gingivitis
associated w dental biofilm alone
mediated by systemic/local risk factors
drug influenced gingival enlargement
gingival health on an intact periodontium signs
no BOP no erythema and oedema no pt symptoms no attachment and bone loss physiological bone levels range from 1-3mm apical to CEJ
gingival health measurements
for an intact periodontium and a reduced and stable periodontium, gingival health is <10% bleeding sites with probing depths ≤3mm
plaque-induced gingivitis: intact periodontium
no ID recession - papilla intact no probing AL pocket depths ≤3mm BOP ≥10% no radiological bone loss
plaque-induced gingivitis: reduced periodontium (non-perio pt)
e.g. on distal of 7 where 8 has been extracted may be a bony defect probing AL pocket depths ≤3mm BOP ≥10% radiological bone loss possible
plaque-induced gingivitis: successfully txed perio pt (gingival inflammation in pt with history of perio - remission)
probing AL pocket depths ≤4mm - no site ≥4mm with BOP BOP ≥10% radiological bone loss
plaque-induced gingivitis - modifying factors
A - associated with bacterial dental biofilm only
B - potential modifying factors
C - drug-induced gingival enlargements
plaque-induced gingivitis: potential modifying factors
1 - systemic conditions - sex steroid hormones: puberty, menstrual cycle, pregnancy, OCP - hyperglycaemia - leukaemia - smoking - malnutrition 2 - oral factors enhancing plaque accumulation - prominent subgingival Rx margins - hyposalivation
plaque-induced gingivitis: drug-induced gingival enlargements
anticonvulsants - phenytoin
Ca channel blockers - Nifedipine
immunosuppressants - cyclosporin
action - gingival hyperplasia by
- interact with fibroblast - increase con tis deposition in gums
pregnancy epulis
considered a mucogingival deformity may decide to biopsy often resolve after baby born no radiological bone loss no ID recession
Rx margins 1/2 mm into sulcus
pt needs to be aware of risk of recession
- 80% have recession after 5yrs
non-plaque induced gingival diseases and conditions
- genetic/developmental disorders
- e.g. hereditary gingival fibromatosis - if you resect it often it resolves and doesn’t recur - specific infections e.g. herpetic gingival stomatitis, c albicans
- inflammatory and immune conditions e.g. LP, pemphigoid
- reactive processes
- neoplasms
- endocrine, nutritional and metabolic diseases - vit C
- traumatic lesions
- gingival pigmentation
necrotising PDDs in chronically severely compromised pts
adults - HIV+/AIDS with CD4 <200 - other severe systemic conditions (immunosuppression) children - severely malnourished - extreme living conditions - severe (viral) infections clinical conditions - NG, NP, NS, Norma possible progression
Necrotiotising stomatitis
serious, unlikely in UK
bone denudation extended through the alveolar mucosa
larger areas of osteitis and bone sequestrum
systemic diseases/conditions affecting the periodontal tissues
- Squamous cell carcinoma - Langerhans cell histocytosis
- mainly rare conditions affecting the PD tissues independently of dental-biofilm induced inflammation
- disease process itself is destroying the tissues
- A more heterogeneous group of conditions which result in breakdown of PD tissues and some of which may mimic the clinical presentation of periodontitis
cancer cell tissues can invade and destroy PD attachment
PD abscesses in non-perio pts
impaction: floss, ortho elastic, dam, popcorn hulls
harmful habits: nail biting and clenching
ortho factors: forces or a X bite
gingival overgrowth
alteration of root surface
= need to understand why they have the abscess
periodontitis as a manifestation of systemic disease
classification based on primary systemic disease
mainly rare diseases that affect the course of periodontitis resulting in the early presentation of severe perio
- much more pronounced than e.g. diabetes
Papillon Lefevre Syndrome - defect in immune system LAD - leucocyte adhesion deficiency hypophosphatasia (Down syndrome) EDS
risk factors
e.g. diabetes - variable effects that modify the course of periodontitis
- part of multifactorial
in clinical classification
e.g. diabetes could be well-controlled and not really affect perio
PD abscesses in a perio pt (in a pre-existing pocket)
acute exacerbation
- un-txed perio
- non-responsive to therapy perio
- supportive PD therapy
after tx
- post-scaling
- post-surgery
- post-medication
- systemic antimicrobials
- other drugs: nifedipineperio-endo lesions classification
with root damage - root fracture/cracking - RC or pulp chamber perforation - external RR without root damage - perio pts - non-perio pts
mucogingival deformities and conditions
gingival recession
- lack of keratinised gingiva - aberrant frenal attachment - pregnancy epulis
RT1
no loss of IP attachment
IP CEJ not clinically detectable at both M+D aspects of the tooth
might be amenable to grafting surgery
RT2
loss of IP attachment
some papilla left
amount of IP LOA ≤ buccal LOA
may??? be able to graft surgery
IP LOA
measured from IP CEJ to depth of IP sulcus/pocket
buccal LOA
measured from buccal CEJ to apical end of buccal sulcus/pocket
RT3
loss of IP attachment
amount of IP LOA > buccal LOA
papilla destroyed
can’t graft with surgery
gingival abscess
localised to gingival margin
- often caused by trauma
periodontal abscess
usually related to pre-existing deep pocket also associated with food packing and tightening of the gingival margin post-HPT
pericoronal abscess
associated with PE tooth most commonly 8s
perioendo lesions
tooth is suffering from various degrees of endo and perio disease
most prevalent infection demanding emergency tx
- dentoalveolar abscess
- pericoronitis
- periodontal abscess
SDCEP definition of PD abscess
infection in a PD pocket which can be acute or chronic and asymptomatic if freely draining
periapical infection in perioendo lesions
infection via carious cavity or traumatised crown
infection via PDL
Communication btw pulp and periodontium
- apical foramen - main route
- exposed dentinal tubules
- lateral & accessory canals
- furcal canals
- perforation
- extensive caries
- resorption
- iatrogenic
- developmental groove (infrabony pocket）
dentinal tubules as a communication
dentine porous so pathogens can pass down
lateral canals as a communication
up whole length of tooth but most common in apical 1/3
furcal canals as a communication
between roots and furcation area
necrotic pulp can lead to perio endo lesions
- pulpal inflammatory by-products out apex, lateral, accessory canals and dentinal tubules - trigger inflammatory response in periodontium
primary perio with secondary endo mechanism
- infection entering via lateral canals/apical foramen - accessory canal exposed to oral micro biofilm
- if blood supply circulating through the apex is intact - pulp good prospects for survival
perio endo lesions - when does PDD usually directly affect the pulp?
when recession has opened up an accessory canal to the oral env
- cementum has a protective effect
what may the radiographic appearance of combined endo perio disease be similar to?
a vertically fractured tooth
if what remains intact will the pulp maintain vitality?
if the microvasculature of the apical foramen remains intact
effect of PD tx on the pulp
similar during scaling and RSI or PD surgery if accessory canals are severed/opened to oral env
microbial invasion and secondary pulp necrosis can occur
primary endo lesion characteristics
non-vital
local perio only
primary perio lesion characteristics
generalised perio
minimally/unrestored tooth
non-vital, possibly vital if apex has managed to remain intact
what does combined lesions prognosis depend on?
primarily upon severity of PDD and PD tissues response to tx, and PA tissues
PDDs
group of diseases affecting the periodontal tissues, representing an immune reaction (innate and adaptive) to adjacent microbial plaque
- gingivitis - inflammation of STs of gingiva
- doesn’t always progress…
- periodontitis - disease of entire periodontium inc bone
what is PD health the outcome of?
the balance between bacteria of the dental plaque and the host immune system
primordial prevention
prevention in whole of society without particular risk factors, prevent development of risk factors
primary prevention
identify groups with risk factors and prevent development of disease
what does the development of risk factors appear to be dependent on?
specific inherited, behavioural and env factors
risk determinants
genes
gender - M
systemic diseases which are genetic disorders and syndromes (periodontitis as manifestation of systemic diseases)
SE status
multifactorial disease - complex aetiopathogenesis
microbial biofilm - type of bacteria present fct of the immune system (genetics) genetics general health - stress - fatigue - smoking - diet - medications - hygienic habits additional pathological conditions - viral/bacterial infections - diabetes mellitus - hypoxia - liver diseases
risk/modifying factors - broad groups
can change them
1 - general
2 - local risk factors
general risk/modifying factors
smoking
systemic diseases: diabetes mellitus, leukaemia, HIV, osteoporosis, osteopenia
stress
drugs: Ca channel blockers, immunosuppressants, anticonvulsant, OCP (in past)
nutrition
obesity
pregnancy
local risk factors
PRFs (dentists can contribute to development of PDD in pts)
- calculus, Rxs, carious cavities, RPDs, ortho appliances, malpositioned teeth
others
- trauma from occlusion
- insufficient OH - microbial factor
smoking
- effect on palque microbiome more anaerobic
- increases activation of immune system
- vasoconstrictor of gingival vessel - recue healing and mask severity of disease
risky if >10 cig a day
nutrition
severe vit C deficiency - scurvy - scorbutic gingivitis
lack of nutrients decreases function of the immune system
obesity
contributes to systemic inflammation - pro inflammatory effect
adipose tissue produces lots of inflammatory cytokines
adipokines secreted by adipocytes
genes
genetic polymorphism can affect expression levels of genetic products
IL-1 most important
possible polymorphisms of genes encoding TNF-a, IL-1, vit D receptor, IgG receptor
occlusal trauma
may lead to production of IL-1 and bone loss but doesn’t cause periodontitis
may be a co-factor in destructive PDD - enhance rate
suboptimally controlled diabetes mellitus
hyperglycaemia
- may modulate RANKL/OPG ratio and so contribute to alveolar bone destruction
- production of AGE (advanced glycation end products) increases inflammation
- production of pro-inflammatory cytokines and destructive MMPs
diabetic control and questions to ask
For diabetic pt - good control (no more than)
- HbA1c test
- 48-58mmol/mol
- 6.5-7.5%
should do blood test every 3 months
- RBC turnover every 3 months
* degree of control
* age of onset
* duration of disease
systemic genetic conditions/diseases where periodontitis is one of the symptoms
Papillon-Lefevre syndrome
Chediak-Higashi syndrome
Lazy leukocyte syndrome
Luekocyte adhesion deficiency LAD syndrome
EDS
chronic granulomatous disease
Down Syndrome
hypohosphatasia
drugs that can lead to gingival enlargement
anticonvulsant - phenytoin immunosuppressant - cyclosporin = rarer Ca channel blockers - nifedipine, amlodipine = common
why can drugs lead to gingival enlargement?
interaction between the drug and host fibroblasts - increased deposition of CT supporting a hyperproliferative epithelium
gingival enlargement / hyperplasia
more fibroblasts
often have inflammation also as enlargement is making OH difficult
gingival swelling
- more intercellular fluid,
- increased permeabilisation of the vessels
softer as full of water - press with probe
managing drug related gingival enlargement
need professional scaling
v intensive pt training - plaque control at v high level
surgical tx to remove excess - but need some plaque control before you go down surgical route
change meds? speak to doc
PDD as a risk factor for systemic diseases
systemic activation of the immune system
- RA
- diabetes
- pre-eclampsia and adverse pregnancy outcomes
- atherosclerosis and hypertension
- Alzheimers disease
- neoplasms
acquired systemic diseases and syndromes - HIV
increased risk of necrotising conditions but no evidence of increased progression of periodontitis
acquired systemic diseases and syndromes - blood dyscrasias e.g. neutropenia, agranulocytosis, leukaemia
reduced numbers/fct of neutrophils and macrophages
increased risk of NG and progressive periodontitis
acquired systemic diseases and syndromes - scurvy
vit C deficiency causing abnormal collagen turnover
increased risk of PD attachment loss
acquired systemic diseases and syndromes - pregnancy
- increased risk of pregnancy gingivitis
- immune system in pregnancy is reduced
- risk of adverse pregnancy
- oral bacteria entering feto-placental unit
osteoporosis and osteopenia
- low bone mineral density in max and mand
- oestrogen
- RANKL/ OPG ratio dysregulaiton
psychological stress
increased cortisol - stimulates immune system
ANS stimulated - catecholamine and substance P - regulates immune response, affect bacterial adhesion and growth
what is the most severe inflammatory PDD disorder caused by plaque bacteria?
NPDs
why are NPDs known to occur in epidemic-like patterns?
due to shared predisposing factors in a pop (e.g. students during exams, armed forces recruits)
not contagious
main features of NPDs
- painful bleeding gums
- ulceration and necrosis of the ID papilla
- gingival margin “punched out” appearance,
- craters
- sloughing - yellow/white/grey
- lesions develop quickly
- 1st lesions often seen IP in mandibular anteriors
- halitosis
- sequestrum formation necrosis of parts of alv bone
- lymphadenopathy
what type of infection is NPDs?
opportunistic - caused by bacteria inhabiting healthy oral cavity
epidemiology of NPDs
more common in developing countries
what may happen if NG is improperly txed?
become chronic and/or recurrent
NS
progression of NP into tissue beyond the mucogingival jct
mostly malnutrition and HIV
may result in denudation of the bone - osteitis and OAFs
NG and bone loss
no bone loss or attachment loss
inflammation confined to STs
NP and bone loss
attachment loss
NS and bone loss
more extensive mucosal and bone loss beyond gums
Vincent’s angina
different disease - of the throat not the periodontium
mixed spirochetal microbiota in necrotic areas in tonsils during sore throat infections
NPDs and VA occur independently of each other
NP
where the infection leads to AL
may be an extension of NG into the PDL but not completely proven
cancrum oris (noma)
necrotising and destructive infection of the mouth and face
not a PDD
usually in malnourished children in developing countries
may be disfiguring, often fatal
been suggested that all cases develop from pre-existing NG - not confirmed
- most NPDs won’t progress to the more severe forms, even without tx
what is the diagnosis of NPDs based on?
symptoms
why is the diagnosis of NPDs not based on any test?
biopsy - histopathology is not pathognomic (characteristic) for NPD
microbiology - not characteristic
- constant flora: treponema sp, selenomonas sp, fusobacterium sp, prevotella intermedia
- variable flora: heterogeneous array of bacterial types
spirochetes and fusobacterias are isolated from large numbers of necrotic lesions, their presence is not evidence of a primary etiologic importance (they are not always found in the primary lesion)
risk factors
developed countries - mostly young adults - stress - sleep deprivation - poor OH - smoking - immunosuppression (HIV and leukaemia) - malnutrition developing countries - malnourishes children
NPD vs PHG
NPD
- bacteria
- age freq 15-30yrs
- site: ID papilla, rarely outside gingiva
- symptoms: ulceration and necrotic tissue, yellowish plaque, bad breath, may have mod fever
- lasts 1-2 days if tx
- not contagious - no immunity
- healing: destruction of PD tissue remains
PHG
- HSV
- freq children
- site: gingiva and entire oral mucosa
- symptoms: multiple vesicles which disrupt - small round fibrin covered ulcerations, bad breath, fever
- lasts 1-2 weeks
- contagious, get partial immunity
- no permanent destruction
NPDs tx
US debridement
if pain preventing pt from brushing - 0.2% CHX MW x2 daily
only ABs if indicated
recall for review
smoking cessation, OH, vit supplementation, dietary advice
- prevent recurrence
NPDs indications for ABs
- pts with malaise, fever, lassitude,
- lack of response to mechanical therapy,
- impaired immunity
- unable to complete local measures upon initial presentation
NPDs antibiotics
400mg metronidazole x3 daily for 3 days
adjuncts to tx of periodontitis - tx strategies
mechanical disruption - reducing the bacterial challenge - scaling and RSD systemic ABs or local antimicrobials host modulation therapy
PD tx with use of systemic ABs
not first line tx, if used in selected cases are only allowed once combined with mechanical disruption of biofilm
cases to consider
- aggressive perio
- young pts with grade C
amoxicillin contraindication
allergies
metronidazole contraindications
alcohol intake
increases anticoagulant effect of warfarin
pregnancy
doxycycline contraindications
pregnancy
(tetracycline shown staining of teeth)
biofilm formation
pedicle - proteins and glycoproteins of saliva - a few mins to form
association adhesion - trailblazing bacteria - streptococcus, actinomyces - poses adhesion molecules
growth - micro colonies - production of polysaccharides matrix
mature biofilm - microcolonies transition into metabolic complexes
aerobic to anaerobic bacteria
advantages of local antimicrobials
reduce systemic dose -
reduce GI upset ( intestinal microbiome)
high local conc
superinfection e.g. c dificile unlikely
drug interactions unlikely
site specific
pt compliance not an issue as applied by HCP
can utilise agents which can’t be utilised systemically e.g. CHX
disadvantages of local antimicrobials
£££
still require RSD or biofilm disruption
limited indications
Periochip
local antimicrobial/antiseptic
bovine origin gelatine based
evidence shows benefits
only good for certain clinical conditions
use during HPT or maintenance or both? - wait until pockets heal after instrumentation and use it in persisting pockets only during review visit and maintenance recalls
Piscean
fish collagen based
local antimicrobial/antiseptic
Chlosite
CHX gel
local antimicrobial/antiseptic
local antimicrobials - antibiotics
Arestin - 1mg minocycline HCl microspheres
Atridox - doxycycline hyelate 10%
Elyzol - 25% metronidazole
Periostat dosage
20mg doxycycline x2 daily for 3m systemically, as an adjunct to supra/subgingival instrumentation
Periostat mechanism of action
dose sub-antimicrobial - insufficient to inhibit the growth of bacteria
prescribed for role as collagenase inhibitor
- breaks down collagen, implicated in PD tissue damage
- produced by bacterial and human cells
dose unlikely to exert a significant evolutionary pressure so less likely to accelerate the development of drug resistant bacteria
indications for local antiseptics
only persisting pockets >5mm (review visit, maintenance visit)
always with RSD
not many of them as if a lot of persisting pockets in the quadrant OFD is more beneficial or systemic antibiotics with RSD within 24hrs from starting ABs
in cases of PD abscesses
- after evacuation of pus and RSD
Periowave - photodisinfection
irrigate
- photosensitising solution topically applied to the gums at the tx site
- preferentially attaches to the harmful bacteria and toxins associated with PDD
illuminate
- thin plastic light diffusing tip is painlessly placed at the tx site
- specifically calibrated laser light, activating the photosensitising solution and destroying the harmful bacteria and toxins
host modulation therapy
corticosteroids
- suppress immune response they don’t modulate it
NSAIDs
anti-cytokine and biological therapies
biological-disease-modifying anti-rheumatic drug
- e.g. infliximab, TNF-a
lipid mediators of resolution of inflammation
- derived from omega-3 fatty acids resolvins, protectins, maresins
small molecule compounds
- target specific cytokine-mediated processes - inhibition of RANKL - induced OC
bisphosphonates
- disrupt OC activity and inhibit bone resorption
function of the periodontium
- attach the teeth to the jaws
- dissipate occlusal forces
dissipating occlusal forces - periodontium
living tissue - viscoelastic fct
interradicular tissues filled with a fluid which absorbs forces
tension, compression, viscous forces
horizontal forces
constant - ortho
intermittent - occlusal (jiggling) e.g. denture clasp too tight
tipping movement
selective deposition and resorption of bone due to horizontal forces
areas of pressure result in bone resorption
areas of tension - bone deposition
tooth tips due to bone remodelling
protective occlusion
ideal
posterior teeth meet first
anterior teeth just touch in ICP
when mandible slides forward anterior teeth take all of the load - posteriors disocclude
lateral excursion - all molars disocclude, canines guide
occlusal interferences
often no effects
but eccentric occlusal contacts can mean some teeth are taking excessive loading - jiggling
- discomfort
- excessive mobility
the effect of “abnormal” occlusal forces on:
the healthy periodontium
the healthy but reduced periodontium
- previous PDD, shortened teeth, surgery
the diseased periodontium
- presence of plaque-induced inflammation
effect on healthy periodontium
non-axial occlusal load - PDL well-designed to take axial vertical loading
areas of intermittent pressure and tension
- needs more shock absorber so excessive load is dissipated
areas of widened PDL
hyper-mobile tooth - attachment unaffected
gingival margin remains normal and intact - no LOA
gingival inflammation is not initiated by occlusal forces - in the absence of bacteria occlusal trauma doesn’t cause perio disease - need a biofilm
effect on a reduced but healthy PDL
less PDL to dissipate load - higher forces per mm2 of ligament
same will happen but to a greater extent
excessive mobility
widening of PDL
no further LOA in absence of biofilm inducing inflammatory action
response of the healthy periodontium: physiological
PDL width increases until forces can be adequately dissipated, the PDL width should then stabilise
increased tooth mobility
successful adaptation to increased demand - physiological
if demand is subsequently reduced (e.g. remove high spot, stop Bruxism etc) PDL width should return to normal
response of the healthy periodontium: pathological
if demand of occlusal forces is too great or the adaptive capacity of the PDL reduced, PDL width may continue to increase
PDL width and tooth mobility fail to reach a stable phase
failure of adaptation - pathological
occlusal trauma
tooth mobility which is progressively increasing and/or tooth mobility associated with symptoms
with radiographic evidence of increased PDL width
occlusion and periodontitis
an association with vertical bone defects? NO
increased rate of disease progression? MAYBE
vertical bone defects
for a given amount of biofilm you get a certain amount of bone loss - 2mm
narrow bone spicule - all within circle so all lost - horizontal bone loss
wider alveolar bone spicule - same circle of destruction but because bone is wider you retain the medial aspect of the bone
not directly related to occlusal trauma - vertical bony defect are a factor of how wide bone is at beginning - zone of destruction the same regardless of the cause of periodontitits
occlusal trauma and periodontitis - increased rate of disease progression - maybe?
two processes
- pathological resorption due to inflammation
- physiological resorption (remodelling) due to excessive occlusal forces
happening at same time
if coalesce - additive effect - zone of co-destruction - see more PDL and attachment loss than if you had only one process
1 - plaque-induced inflammation
2 - trauma-induced inflammation
occlusal forces and periodontitis
alone cannot initiate or exacerbate gingival inflammation
alone cannot initiate or sustain loss of CT attachment
can result in widening of PDL and increasing tooth mobility
in combination with plaque-induced inflammation may exacerbate LOA
what does tooth mobility depend on?
width of PDL
height of PDL
inflammation - flaccid tissue tone due to inflammatory infiltrate
number, shape and length of roots
why can tooth mobility be improved by NSHPT?
long JE
general maturation of tissue, improved tissue tone
why doesn’t tooth mobility necessarily show pathology?
may indicate successful adaptation of the periodontium to functional demands
and/or
may reflect the nature of the remaining attachment
when can’t tooth mobility be accepted?
it is progressively increasing
it is causing symptoms
it creates difficulty with restorative tx
therapy to reduce tooth mobility
control plaque-induced inflammation
correction of occlusal relations
splinting
correcting occlusal relations
don't adjust very often occlusal adjustment (selective grinding) restorations orthodontics
= occlusal therapy may be indicated for the management of tooth mobility and migration
BUT it isn’t a tx for periodontitis
management of tooth migration
tx the periodontitis
correct occlusal relations
either
- accept position of teeth and stabilise
- move the teeth orthodontically and stabilise
what splint is most commonly used?
composite and wire
indications for splinting
mobility due to advanced LOA
mobility causing discomfort or difficulty in chewing
teeth need to be stabilised for debridement
disadvantages of splinting
doesn’t influence the rate of periodontal destruction
may create hygiene difficulties - PRF
“last resort” - palliation tx
- won’t save the tooth will just save the fct
deep traumatic overbite
trauma from the bite - not occlusal trauma it is trauma from the occlusion
treat plaque-related inflammation
relieve trauma
- occlusal slint - palliative
- orthodontic/orthognathic tx
- restorative - must inc occlusal stops for anterior teeth
PD therapy as an aid to Rx dentistry
improves soft tissue management
- impressions, placing restorations, moisture control
establishes stable gingival margin position
contributes to aesthetics
reduces tooth mobility
informs prognosis
signs of an inflamed gingival margin
linear band of inflammation lost stippling abundant soft plaque bleeds during operative procedures unstable in its apico-coronal location
why can poor margins cause recession?
gingivae will recede away from the irritant e.g. cement
overhangs and bone loss
larger the overhang = greater bone loss
- development of pathogenic flora
contour
contour - shape of Rxs same shape as teeth
inadequate tooth prep = over contoured crowns
keys to periodontally successful indirect Rxs
start with healthy tissue adequate tooth prep precise margin location excellent provisional Rxs careful tissue handling and impression technique - prevent damage to tissues
biological width
base of sulcus to alveolar bone approx 2mm
JE 1mm, CT 1mm
biological width and Rxs
if you place a crown margin in this space you will cause inflammation
Rx margins need to be within the gingival sulcus - don’t place >0.5mm subgingivally
in non-aesthetic areas - supra gingival as more cleansable
margins need to follow the interdental col - otherwise will be way too subgingival interproximally
need to be at least 3mm from alveolar crest
if margin enroaches on BW: possible outcomes
persistent inflammation
LOA
- pocketing or recession
later - exposure of Rx margin
gingival veneer/masks/flange prostheses/removable gingival prostheses
restore gingival contour and improve aesthetics even after successful PDD tx
acrylic/silicone
can be removed for OH
indications for gingival veneer
post-PD therapy
- aesthetics
- speech (spitting when talking - IP bone loss)
- foaming of saliva
- interference of lip and tongue
- dentine hypersensitivity (cover exposed roots)
- lack of lip support
local drug administration
- could apply a topical steroid underneath it
gingival veneer contraindications
poor OH uncontrolled PDD incomplete PD therapy allergy to acrylic/silicone high caries susceptibility poor manual dexterity risk of inhalation (epilepsy) prominent labial frenum - may be too weak in midline
Ante’s law
combined PD area of the abutment teeth should be equal to or greater than the PD area of the tooth/teeth to be replaced
what prostheses are usually preferable from a PD perspective?
fixed - in a compliant pt with good OH
