3rd year Flashcards
(179 cards)
1
Q
aims of supportive PD care (maintenance)
A
maintain PD health
detect and tx recurrence
maintain accepted level of disease
manage tooth loss
2
Q
supportive PD care (maintenance) - who
A
pts who have had PD tx
3
Q
supportive PD care (maintenance) - consequence of not returning
A
txed pts who do not return for regular recall are x5.6 greater risk for tooth loss than compliant pts
4
Q
what does supportive PD care (maintenance) involve?
A
exam
tx
report and scheduling
5
Q
other causes for recurrence other than inadequate OH/compliance?
A
- 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
6
Q
how long are pts at risk of disease recurrence for?
A
the rest of their lives
7
Q
PD tx in pregnancy
A
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
8
Q
2017 PDDs classification - main overall groups
A
health, gingival diseases and conditions
periodontitis
other conditions
9
Q
2017 PDDs classification - parts
A
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
10
Q
2017 PDDs classification - mneumonic
A
Please Give Greg Nine Percy Pigs Straight Past Meal Time Tonight
11
Q
2017 PDDs classification - PD health subcategories
A
intact periodontium
reduced periodontium
12
Q
2017 PDDs classification - gingivitis dental-biofilm induced subcategories
A
intact periodontium
reduced periodontium
13
Q
2017 PDDs classification - periodontitis subcategories
A
localised ≤30%
generalised >30%
MI pattern
14
Q
problems with 1999 system
A
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?
15
Q
2017 classification aims
A
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
16
Q
extent
A
captures distribution localised <30% teeth generalised >30% teeth MI pattern - tends to occur in younger pts
17
Q
what does grading tell you?
A
disease susceptibility
18
Q
what does staging tell you?
A
severity
19
Q
what stage is a pt if they are known to have lost teeth due to perio?
A
stage 4
20
Q
potential consequence of stage 3
A
potential for additional tooth loss
21
Q
potential consequence of stage 4
A
potential for loss of dentition
22
Q
what does currently in remission mean?
A
pt who had periodontitis who now has gingivitis
23
Q
what does BPE guide?
A
need for further diagnostic measures prior to establishing a definitive PD diagnosis and appropriate tx planning
24
Q
4mm threshold
A
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
25
health
intact periodontium
reduced periodontium due to causes other than periodontitis
reduced periodontium due to periodontitis
- but pt will always be a perio pt
26
plaque-induced gingivitis
associated w dental biofilm alone
mediated by systemic/local risk factors
drug influenced gingival enlargement
27
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
```
28
gingival health measurements
for an **intact** periodontium and a **reduced** and stable periodontium, gingival health is **<10% bleeding** sites with **probing depths ≤3mm**
29
plaque-induced gingivitis: **intact** periodontium
```
no ID recession - papilla intact
no probing AL
pocket depths ≤3mm
BOP ≥10%
no radiological bone loss
```
30
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
```
31
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
```
32
plaque-induced gingivitis - modifying factors
A - associated with bacterial dental biofilm only
B - potential modifying factors
C - drug-induced gingival enlargements
33
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
```
34
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
35
pregnancy epulis
```
considered a mucogingival deformity
may decide to biopsy
often resolve after baby born
no radiological bone loss
no ID recession
```
36
Rx margins 1/2 mm into sulcus
pt needs to be aware of risk of recession
| - 80% have recession after 5yrs
37
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
38
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
```
39
Necrotiotising stomatitis
serious, unlikely in UK
bone denudation extended through the alveolar mucosa
larger areas of **osteitis** and **bone sequestrum**
40
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
41
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
42
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
```
43
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
44
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: nifedipine
```
45
perio-endo lesions classification
```
with root damage
- root fracture/cracking
- RC or pulp chamber perforation
- external RR
without root damage
- perio pts
- non-perio pts
```
46
mucogingival deformities and conditions
gingival recession
```
- lack of keratinised gingiva
- aberrant frenal attachment
- pregnancy epulis
```
47
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
48
RT2
loss of IP attachment
some papilla left
amount of IP LOA ≤ buccal LOA
may??? be able to graft surgery
49
IP LOA
measured from IP CEJ to depth of IP sulcus/pocket
50
buccal LOA
measured from buccal CEJ to apical end of buccal sulcus/pocket
51
RT3
loss of IP attachment
amount of IP LOA > buccal LOA
papilla destroyed
can't graft with surgery
52
gingival abscess
localised to gingival margin
| - often caused by trauma
53
periodontal abscess
usually related to **pre-existing deep pocket** also associated with **food packing** and **tightening** of the gingival margin post-HPT
54
pericoronal abscess
associated with PE tooth most commonly 8s
55
perioendo lesions
tooth is suffering from various degrees of endo and perio disease
56
most prevalent infection demanding emergency tx
- dentoalveolar abscess
- pericoronitis
- periodontal abscess
57
SDCEP definition of PD abscess
infection in a **PD pocket** which can be acute or chronic and asymptomatic if freely draining
58
periapical infection in perioendo lesions
infection via carious cavity or traumatised crown
| infection via PDL
59
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）
60
dentinal tubules as a communication
dentine porous so pathogens can pass down
61
lateral canals as a communication
up whole length of tooth but most common in **apical** 1/3
62
furcal canals as a communication
between roots and furcation area
63
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**
64
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
65
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
66
what may the radiographic appearance of combined endo perio disease be similar to?
a vertically fractured tooth
67
if what remains intact will the pulp maintain vitality?
if the **microvasculature** of the apical foramen remains intact
68
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
69
primary endo lesion characteristics
non-vital
| local perio only
70
primary perio lesion characteristics
generalised perio
minimally/unrestored tooth
non-vital, possibly vital if apex has managed to remain intact
71
what does combined lesions prognosis depend on?
primarily upon severity of PDD and PD tissues response to tx, and PA tissues
72
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
73
what is PD health the outcome of?
the **balance** between bacteria of the dental plaque and the host immune system
74
primordial prevention
prevention in whole of society without particular risk factors, prevent development of risk factors
75
primary prevention
identify groups with risk factors and prevent development of disease
76
what does the development of risk factors appear to be dependent on?
specific inherited, behavioural and env factors
77
risk determinants
genes
gender - M
systemic diseases which are genetic disorders and syndromes (periodontitis as manifestation of systemic diseases)
SE status
78
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
```
79
risk/modifying factors - broad groups
can change them
1 - general
2 - local risk factors
80
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
81
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
82
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
83
nutrition
severe vit C deficiency - scurvy - **scorbutic gingivitis**
| lack of nutrients decreases function of the immune system
84
obesity
contributes to systemic inflammation - **pro inflammatory effect**
**adipose tissue** produces lots of inflammatory **cytokines**
adipokines secreted by adipocytes
85
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
86
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
87
**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**
88
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
89
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
90
drugs that can lead to gingival enlargement
```
anticonvulsant - phenytoin
immunosuppressant - cyclosporin
= rarer
Ca channel blockers - nifedipine, amlodipine
= common
```
91
why can drugs lead to gingival enlargement?
interaction between the drug and **host fibroblasts** - increased **deposition of CT** supporting a hyperproliferative epithelium
92
gingival enlargement / hyperplasia
more fibroblasts
| often have inflammation also as enlargement is making OH difficult
93
gingival swelling
* more intercellular fluid,
* increased permeabilisation of the vessels
| softer as full of water - press with probe
94
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
95
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
96
acquired systemic diseases and syndromes - HIV
increased risk of **necrotising** conditions but no evidence of increased progression of periodontitis
97
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
98
acquired systemic diseases and syndromes - scurvy
vit C deficiency causing **abnormal collagen turnover**
| increased risk of PD attachment loss
99
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
100
osteoporosis and osteopenia
* low bone mineral density in max and mand
* oestrogen
* RANKL/ OPG ratio dysregulaiton
101
psychological stress
increased **cortisol** - stimulates immune system
| ANS stimulated - catecholamine and substance P - regulates immune response, affect bacterial adhesion and growth
102
what is the most severe inflammatory PDD disorder caused by plaque bacteria?
NPDs
103
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
104
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
105
what type of infection is NPDs?
opportunistic - caused by bacteria inhabiting healthy oral cavity
106
epidemiology of NPDs
more common in developing countries
107
what may happen if NG is improperly txed?
become chronic and/or recurrent
108
NS
progression of NP into tissue **beyond the mucogingival jct**
mostly malnutrition and HIV
may result in **denudation of the bone** - **osteitis and OAFs**
109
NG and bone loss
no bone loss or attachment loss
| inflammation confined to STs
110
NP and bone loss
attachment loss
111
NS and bone loss
more extensive mucosal and bone loss beyond gums
112
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
113
NP
where the infection leads to AL
| may be an extension of NG into the PDL but not completely proven
114
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
115
what is the diagnosis of NPDs based on?
symptoms
116
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)
117
risk factors
```
developed countries - mostly young adults
- stress
- sleep deprivation
- poor OH
- smoking
- immunosuppression (HIV and leukaemia)
- malnutrition
developing countries - malnourishes children
```
118
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**
119
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
120
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
121
NPDs antibiotics
400mg metronidazole x3 daily for 3 days
122
adjuncts to tx of periodontitis - tx strategies
```
mechanical disruption
- reducing the bacterial challenge
- scaling and RSD
systemic ABs or local antimicrobials
host modulation therapy
```
123
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
124
amoxicillin contraindication
allergies
125
metronidazole contraindications
**alcohol** intake
increases anticoagulant effect of **warfarin**
**pregnancy**
126
doxycycline contraindications
**pregnancy**
(tetracycline shown **staining** of teeth)
127
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
128
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
129
disadvantages of local antimicrobials
£££
still require RSD or biofilm disruption
limited indications
130
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
131
Piscean
fish collagen based
| local antimicrobial/antiseptic
132
Chlosite
CHX gel
| local antimicrobial/antiseptic
133
local antimicrobials - antibiotics
Arestin - 1mg minocycline HCl microspheres
Atridox - doxycycline hyelate 10%
Elyzol - 25% metronidazole
134
Periostat dosage
20mg doxycycline x2 daily for 3m systemically, as an adjunct to supra/subgingival instrumentation
135
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
136
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
137
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
138
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
139
function of the periodontium
* attach the teeth to the jaws
* dissipate occlusal forces
140
dissipating occlusal forces - periodontium
living tissue - **viscoelastic** fct
interradicular tissues filled with a fluid which absorbs forces
tension, compression, viscous forces
141
horizontal forces
constant - ortho
| intermittent - occlusal (jiggling) e.g. denture clasp too tight
142
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
143
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
144
occlusal interferences
often no effects
but eccentric occlusal contacts can mean some teeth are taking excessive loading - jiggling
- discomfort
- excessive mobility
145
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
146
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 a**bsence of bacteria** occlusal trauma **doesn't cause** perio disease - need a biofilm
147
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
148
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**
149
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
150
occlusal trauma
**tooth mobility** which is progressively increasing and/or tooth mobility associated with **symptoms**
with radiographic evidence of **increased PDL width**
151
occlusion and periodontitis
an association with vertical bone defects? NO
| increased rate of disease progression? MAYBE
152
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
153
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
154
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**
155
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
156
why can tooth mobility be improved by NSHPT?
long JE
| general maturation of tissue, improved tissue tone
157
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
158
when can't tooth mobility be accepted?
it is progressively **increasing**
it is causing **symptoms**
it creates **difficulty with restorative tx**
159
therapy to reduce tooth mobility
control plaque-induced inflammation
correction of occlusal relations
splinting
160
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
161
management of tooth migration
tx the periodontitis
correct occlusal relations
either
- accept position of teeth and stabilise
- move the teeth orthodontically and stabilise
162
what splint is most commonly used?
composite and wire
163
indications for splinting
mobility due to **advanced LOA**
mobility causing **discomfort** or **difficulty in chewing**
teeth need to be **stabilised for debridement**
164
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**
165
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
166
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
167
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
```
168
why can poor margins cause recession?
gingivae will recede away from the irritant e.g. cement
169
overhangs and bone loss
larger the overhang = greater bone loss
| - development of **pathogenic flora**
170
contour
contour - shape of Rxs same shape as teeth
| inadequate tooth prep = over contoured crowns
171
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
```
172
biological width
base of sulcus to alveolar bone approx 2mm
| JE 1mm, CT 1mm
173
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
174
if margin enroaches on BW: possible outcomes
persistent **inflammation**
**LOA**
- pocketing or recession
later - exposure of Rx margin
175
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
176
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
177
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
```
178
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
179
what prostheses are usually preferable from a PD perspective?
fixed - in a compliant pt with good OH
