Disease of teeth and Periodontal tissues and TSL Flashcards
1
Q
What does a BPE score of 0?
A
Sound gums, no bleeding, no plaque retentive factors, pockets < 3.5mm
2
Q
What is a BPE score of 1?
A
Bleeding on probing, no plaque retentive factors, pockets < 3.5mm
3
Q
What is a BPE score of 2?
A
Plaque retentive factor, not necessarily BOP, pockets <3.5mm
4
Q
What is a BPE score of 3?
A
Probing depth 3.5mm-5.5mm, not necessarily BOP or plaque retentive factors.
5
Q
What is a BPE score of 4?
A
Probing score of >5.5mm, not necessarily BOP or plaque retentive factors
6
Q
What is a BPE score of *
A
Furcation involvement
7
Q
What is the protocol for BPE of 0 or 1?
A
Give OHE and congradulate patient on good OH
8
Q
What is the protocol for BPE score 2?
A
Give OHE and bring back for another appointment to remove plaque retentive factors
9
Q
why would a pulpal disease lead to a periapical disease
A
- no barrier between pulp and periapical tissues
- usual balance between bacteria/toxins and inflammatory cells
- if bacteria/toxins outweigh the inflammatory response and cells, the infection spreads
10
Q
If a child under 3 has any sign of smooth surface caries, what is this class of caries?
A
severe early childhood caries
11
Q
why is the 2017 periodontitis classification useful and how has it been updated
A
helps us diagnose the stage and grade of peritonitis and allows us to monitor the disease as well as have a tailored approach to treatment
had little evidence for the difference between chronic and aggressive periodontitis
now includes peri-implantitis classifications
12
Q
outline the 2017 classification of periodontal disease
A
splits periodontal health into:
periodontal health, gingival diseases and conditions
periodontitis
other conditions affecting periodontal tissues
also section on peri-implantitis
13
Q
what is ‘periodontal health and gingival health’
A
Defined as absence of clinically detectable inflammation Healthy gingiva (stippled, pale pink, sharp papilla, no bleeding) Healthy periodontium (1-3mm pockets, CEJ attached epithelium, no bone loss)
14
Q
what is biofilm induced gingivitis and hwere does this affect
A
‘an inflammatory lesion resulting from interactions between plaque and the host’s immune inflammatory response’
confined to gingival, does not pass mucogingival junction
15
Q
is biofilm induced gingivitis reversible?
A
yes
16
Q
what do we class as localised and generalised gingivitis
A
10% BoP = normal gingival health
10%-30%= localized
>30% BoP = generalised
17
Q
what are some localised and systemic risk factors of gingivitis
A
local:
- plaque retentive factors
- calculus
systemic:
- smoking
- diabetes (type 2)
18
Q
how can type 2 diabetes cause worse gingival health
A
constant high blood sugar leads to more sugar in saliva
constantly coating teeth with sugary saliva provides constant substrate for bacteria
high blood glucose levels damages blood vessels, increasing likelihood of infection
19
Q
what is the difference between gingival enlargement and gingival hyperplasia
A
gingival hyperplasia can only be seen under microscope/histologically as it is to do with cell number
gingival enlargement is diagnosable clinically
20
Q
if plaque is removed and OHI is good but gingivitis remains, what is its classification?
A
gingivitis: non-biofilm induced
21
Q
if inflammation crosses the mucogingival junction, is it more likely to be plaque or non-biofilm induced gingivitis
A
non-biofilm induced
22
Q
what can cause non-biofilm induced gingivitis
A
burns (white patches) cause inflammation therefor gingivitis
herpes simplex causes gingivitis
23
Q
what are manifestations of herpes simplex
A
large red swollen gingiva
Acute herpatic gingivostomatis
Coldsores
24
Q
what sub-classifications can we find within ‘periodontitis’
A
necrotising periodontal disease
periodontitis
periodontitis as a manifestation of systemic disease
25
explain the difference between necrotising gingivits, necrotising periodontitis and necrotisisng stomatis
NG: death of papilla and gingiva but no bone loss, pain, necrosis
NP: loss of supporting bone and supporting structures
NS: flesh eating/through cheek
26
after RSD/PMPR what should we make the patient aware of and why
their gums may seem to recede
removing the irritation factor leads to reduced inflammation
reduced swelling so seems to receed
27
what are some diseases/syndromes that would be classified as 'periodontal disease as a result of systemic disease'
downs syndrome
Papillon-Lefèvre syndrome
Ehlers-Danlos syndrome types IV and VIII
28
what are some symptoms of Ehlers-Danlos syndrome types IV and VIII
Periodontal disease as a result of systemic disease
hyperflexibility of joints/skin
Increased bleeding and bruising
Hyperextensible skin
Underlying molecular abnormality of collagen
29
what are some manifestations of Papillon-Lefèvre syndrome
Palmoplantar hyperkeratosis
Affects primary and secondary dentition
Normal dental development until hyperkeratosis of palms and soles appears
Mechanism poorly understood
30
what term replaces excessive occlusal force? and what does this include
traumatic occlusal force
| any traumatic force leading to tooth loss/fracture
31
what is classes as 'peri-implant health'
no swollen or bleeding gums
| no erythema
32
for peri-implant health, can a patient have large pocket depths?
yes as long as they are no larger than previous examinations and aslong as the gingiva have no bleeding or erythmia
33
what is and what causes peri-implant mucositis
basically gingivitis around implants
it is characterised by bleeding on gentle probing, erythema, swelling and/or suppuration may be present with no bone loss
thought to be caused by plaque biofilm
34
what is peri-implantitis
Plaque associated pathological condition occurring in tissues around dental implants, characterised by inflammation in the peri-implant mucosa and subsequent progressive loss of supporting bone
35
what are risk factors of peri-implantitis
poor oral hygiene control
past history of periodontitis
osteoporosis
smoking
36
how does smoking affect the gingiva
decreases inflammatory reaction (allowing infection)
dysplasia
reduced bleeding
37
if a patient scores 3's on BPE what do we do?
take radiographs
perform PMPR, give OHI and review in 3 months
if no improvement or worsened BPE, we do 6PPC in sextants with BPE=>3
38
if a patient has a 4 on BPE what do we do?
take radiographs
| perform 6PPC in all sextants
39
which BPE scores do we take radiographs for and why
3 or above
| diagnose caries and to grade/stage periodontitis
40
what is the procedure after 6PPC
if we have any pockets over 4mm or evidence of radiographic bone loss = periodontitis --> grade and stage
if not, carry on the BPE 0,1,2 pathway and provide OHI and review
41
if a 6PPC is done, what classifications of periodontitis can be found and what do we do after this
Molar-incisor Periodontitis = pockets >4mm on molars and incisors
Localised Periodontitis = pockets >4mm in <30% of areas
Generalised Periodontitis = pockets >4mm in >=30% of areas
after this, stage and grade
42
which tooth is most likely to get caries
maxillary first molar, U6
43
how do we grade and stage teeth
take periapical and look at bone % loss
44
what does the stage of periodontitis tell us
how much bone loss a patient has had - severity of disease
45
what does the grade of periodontitis tell us and how do we find it
progression rate of disease
| divide ~%bone loss by age using worst site of bone loss
46
what is stage I periodontitis
less than 2mm bone loss or <15%
47
what is stage II periodontitis
bone loss entered coronal 1/3 of root
48
what is stage III periodontitis
bone loss entered mid third of root
49
what is stage IV periodontitis
bone loss entered apical 1/3 of root
50
what is grade A periodontitis
~% bone loss / age < 0.5 slow
51
what is grade B periodontitis
~% bone loss / age = 0.5-1
52
what is grade C periodontitis?
~% bone loss / age > 1
53
what is 'currently stable' periodontitis
<10% BoP
pockets <= 4mm
no bleeding at 4mm sites
54
what is 'currently in remission' periodontitis
BoP > =10% BoP
pockets <=4mm
no BoP at 4mm sites
55
what is 'currently unstable' periodontitis
pockets >= 5mm
OR
pockets >4mm AND BoP
56
what must we write in a periodontal diagnosis
type of periodontitis, stage, grade, current state of stability, risk factors
57
A 80 year old patient has 40% BoP (non of which at deep pocket sites) and at the worst pocket depth which is 4mm deep, there is ~60% bone loss radiographically. 20% of pockets in the mouth have pockets above 4mm. What is the diagnosis. 65% plaque score
```
plaque induced generalised gingivitis (>30% BoP)
localised periodontitis ( 30%< pockets over 4mm), stage III (~2/3 root), grade B (60/80 = 0.75), currently in remission (no BoP at 4mm), no risk factors
```
58
why does stress affect the oral cavity
stress increases cortisol which activates inflammation of gingival tissues
stress causes sympathetic innervation
chronic sympathetic leads to
-reduced digestion therefore reduced salivary flow = caries
-increased beta oxidation = ketosis = ketone bodies = halitosis
59
What is periodontal treatment? and what are the 4 stages
OHI, PMPR, surgical treatment, review, monitoring
1. intitial treatment e.g. emergency, removal of plaque retentive factors, extraction of low prognosis
2. cause related therapy : OHI
3. non-surgical treatment PMPR
4. maintenance and monitoring
60
what are clinical goals of periodontal disease treatment
```
No progression
Reduction in probing depths
No probing depths > 5mm
No BoP
No smoking
Plaque score < 20% of surfaces
```
61
what is the most important factor controlling prognosis of periodontal treatment
stopping smoking
62
how does stress alter gingival heath
decreases salivary flow increasing caries/periodontal disease
alters salivary secretions to be more acidic
crevicular fluid has more cortisol increasing inflammation and progression of disease
63
what are risk factors of periodontal disease
```
smoking
stress
previous periodontal disease
diet
systemic diseases e.g. diabetes mellitus
```
64
what mineral other than fluoride can aid gingival health and calculus formation?
Phosphates
Calcium
zinc systems
65
what is the evidence behind floss and interdental brushes and what should be advised
cochrane reviews found plaque accumulation is lower when using interdental brushing along side brushing
cochrane review found interdental brushes to be more effective at plaque removal than floss
use interdental brushes over floss
66
what are the effects of PMPR (with good OHI) after 6 months
reduced BoP
reduced pocket depth
reduced plaque score
67
after PMPR what must be done
review oral health at 1 month
| review periodontal health (6PPC) at 3 months and 6 months
68
what are some side effects of PMPR which must be explained to patient
```
possible recession (of swollen gums)
sensitivity due to root becoming exposed
```
69
can periodontal disease be cured
no, it can be stopped but OH is needed to prevent further loss
70
what may affect BoP score
smoking due to vasoconstriction
| recently quit smoking leads to bleeding gums
71
what are limitations doing a 6PPC
false pocketing
pockets being subjective based on how hard we press
BI and PI subjective based on 'what counts' as blue for plaque
sensitivity prevents proper pocketing
smoking affects BI
72
are antibiotics needed for periodontal treatment
rarely
| treatment involves removal of stimulus of inflammation can be done via good OHI and PMPR
73
when do we use antibiotics in periodontal treatment and who recommends this
BSP - British society of periodontology recommends
| severe rapidly progressing forms of the disease e.g. necrotising forms of periodontal disease or abscesses.
74
what systemic and topical antimicrobials can be used to treat rapidly progressing severe periodontitis/gingivitis and what considerations must we make
topical chlorhexidine mouthwash - stains teeth over time
| amoxicillin 500mg TDS for 7 days - check interactions in BNF
75
what forms of chlorhexidine are there
solution mouthwash
| CHX chips placed between teeth
76
when do we use CHX chips
Localized periodontitis with few sites
if there is a poor response to debridement
deep sites on maintenance patients or under repeat applications.
77
what is periodontal surgery and when is it undertaken
done when unresponsive to PMPR and any other treatment
| flap surgery/gingivectomy to create accessibility for instrumentation of teeth
78
what should be involved with periodontal treatment reviews?
```
OHI reinforcement
PMPR supragingival
localised subgingival PMPR
medical history and smoking update
full peiro charting and review
assessment of prosthodontics
```
79
what grade of mobility do we extract teeth and when do we try to avoid extraction
grade III
avoid if risk of MRONJ (bisphosphonates for cancer or + cortisteroids) or if high risk of bleed with blood thinners, haemophilia or warfarin
80
if the patient is not engaging with OHI what do we do
go back to step 1 of OHI - do not give further treatment until they are cooperating
81
how do we differentiate an engaging and non-engaging patient
engaging patient will have:
- favourable improvement in OH
- >50% improvement in PI and BI
- or <20% BI and <30% PI
- or patient has met targets set by dental professional
82
what is step 2 of the BSP flowchart and what do we do after this
if patient is engaging - we provide PMPR
review OHI after 1 month for complications e.g. sensitivity and check OHI
3 month and review 6PPC to decide if unstable or stable
83
if patient is unstable after step 2 of BSP flowchart, what do we do
step 3
re-iterate OHI instruction, behavioural change
re-preform PMPR subgingival
pockets >6
possible referral to periodontal surgeon or regenerative surgeon
84
if patient is stable after step 2 on BSP flowchart, what do we do
```
step 4
supportive periodontal care
OHI
re-PMPR
review depending on compliance
make pt aware of high risk of getting periodontal disease again
congratulate patient on progression
re-infection = retreatment
```
85
is PMPR or self plaque removal more important
self removal
86
How can we prevent pulp treatment (3)
- maintenance of crown and pulpal health, preventing caries
- wear mouth guards to prevent trauma and fractures
- minimise impact of therapeutic interventions e.g. fillings
87
why is it better to preserve a tooth than let it rot?
- save NHS time and money
- save the tooth decreases bone resorption
- pain and risk of socket not healing when tooth falls out
- decreases need for complete dentures
- 0keep proprioception of the teeth
- real tooth is much better than any restoration
- if crown is needed this damaged adjacent teeth
88
if a tooth becomes necrotic, what can this lead to?
- no sensibility means no proprioception so excess force on tooth leads to fracture
- pulpitis
- periapical pathology like granuloma
89
even with the most optimistic studies, what is the highest rate of compliance with recommended tooth brushing technique
50%
90
what factors affect compliance
```
Patient factors - disability
Disease - increased difficulty may feel hopeless
Treatment - bad treatment
Operator - bad communication
Support System
Facilities
```
91
what three types of patient can we have relating to motivation
already motivated
latent motivator - need trigger
unmotivated
92
what are the barriers to communication
```
Social status: class, age, gender, socio-economic group
Cultural/ ethnic
Environment
Patient
Pain
Anxiety
Embarrassment
Cognitive level
Clinician
Lack of interpersonal skills/ training
Lack of sensitivity/ empathy
Lack of active listening
Time pressures
Jargon
```
93
what is the correct tooth brushing technique
modified bass technique
| small circular motions on each tooth surface applying moderate pressure, going into the gum line
94
what brush should be o the end of a manual toothrbush
medium nylon brush
95
is manual or electric toothbrushing better in the long/short term? how do we know
electric
| 2014 Cochrane review level 1 evidence
96
what should we consider when giving advise on OH with a difficult patient
give few instructions at a time (just toothbrushing to start)
explain reasoning
don't repeatedly state it as this an reduce motivation
97
how wide is healthy periodontal ligament space around the apex?
0.2-0.3mm
98
what is the difference in outcome of chronic and acute periapical periodontitis
chronic: periapical granuloma --> periapical cyst
acute: periapical abscess
99
what is an abscess and when does it occur within periodontal disease
acute inflammation
accumulation of pus - neutrophils, dead necrotic tissue and liquified bacteria
can occur at any point
100
what is a periapical granuloma
main chronic inflammatory lesion that develops in the periapical tissues after necrotic pulp
fibrovascular tissue that accumulates at apex
<1cm diameter, not corticated
101
when will a periapical cyst form
if there is a periapical granuloma and epithelium is present, the epithelium will surround the granuloma and possibly corticate - more than 1cm diameter
102
what are the 3 consequences of long standing apical periodontitis
radicular cyst (after granuloma)
osteomyelitis
root resorption
103
what is plaque and what is its general composition
bacterial biofilm that forms on soft/hard tissue surface
30% ECM - enzymes, epithelial cells, immune cells, LPS, lipids, carbohydrates
70% microbes
104
what is the acquired pellicle
colorless acellular bacteria-free film composed of salivary glycoproteins, deposited on the teeth within minutes after eruption or cleaning.
105
what is the first stage of plaque formation
bacteria, macromolecules (amino acids, carbohydrates) and salivary products stick to the acquired pellicle via van der Waals forces in reversible reactions and attachments
106
within the first 4 hours of plaque what is the percentage of gram positive bacteria
90%
| cocci and rods
107
when does plaque become clinically visible and what will its initial percentage of streptococci and anaerobes be
24 hours after initial attachment
~45% strep
~ 90% anaerobes
108
give an example of a secondary colonizer and what type of adhesion is this
fusobacterium
| irreversible adherence
109
what are the steps of plaque formation
Reversible attachment of primary colonisers to acquired pellicle
Colonisation forming the matrix
Co-adhesion of secondary and tertiary colonisers
Multiplication of bacteria
Detachment and recolonization
110
as plaque matures, what happens to the bacterial colony
number of anaerobic gram negative bacteria increase
ECM matures and becomes protective
possibly calcify to form calculus
virulent factors released
111
where does subgingival plaque get nutrients from and why
crevicular fluid
no oxygen
anaerobic bacteria
112
how does plaque cause pathology
protects bacteria
release of endotoxins (LPS) increase bone resorption and tooth resorption and inflammation (periodontitis)
release of acid demineralizes enamel and dentine (caries)
release of collagenases (periodontitis)
113
how do we detect calculus
with a WHO probe, curette or bitewings
114
what is the composition of calculus
80% inorganic mineralized tissue
| 20% organic material e.g. lipids, proteins, carbs
115
how is calculus attached to the tooth
via pellicle
ionic attractions between crystals of calculus and dentine/enamel/cementum
micromechanical interactions
116
what is the CO2 hypothesis of calculus formation
high levels of CO2 in saliva as it exits glands
CO2 leaves saliva increasing its pH
Ca and PO4 ions come out of solution
precipitation onto plaque
117
which inflammatory factors cause bone resorption and so can be inhibited in periodontal medication
IL-1a and IL-6
PGE2 fibroblasts
RANKL
118
how do we advise use of TP brush
use for large interproximal area
get correct size
dip in toothpaste and burhs within gap in and out 3 times
119
which areas of the tooth have 1,2,3 place in caries prelevence
1: pits and fissures of posterior teeth
2: under contact point of incisors
3: cervical area
120
what bacteria are common in caries
Strep. Mutans
| Lactobacilli
121
what salivary rate is included as a risk factor for caries
<1ml/min
122
what allergern is in many flouride varnishes/toothpastes and who does this affect
colophony
| asthmatics or people with allergens to plasters
123
what dental varnish can be used on someone with asthma
flourimax
| not duraphat as this has colophony
124
how do we clinically find caries
good lighting
dry surfaces with 3 in 1
blunt ended probe - do not apply pressure, just see if rough/shiny surface
125
what is the difference between infected and affected areas
infected contains demineralization, bacteria, acid and non-repairable collgen damage
affected area contains demineralization and acid - no bacteria, partial collagen damage
126
what are affects of caries on daily life
```
bad breath
pain
loss of teeth
time off work/school
loss of sleep
reduced confidence
```
127
how do we know something is wrong with our childhood caries prevention system
25% increase in caries in children in the past 10 years
128
what is ICDAS
International caries detection and assessment system
129
what extra tools can we use to find caries
Foti - transillumination
| Laser fluorescence detects fluorescence off of bacteria
130
how can we score a tooth's carious lesion and give the scores
```
ICDAS 0-6
0 = sound
1 = inital markings of carious lesion
2= distinct changes in enamel
3 = enamel breakdown, no dentine
4 = enamel breakdown with shadow of enamel
5 = moderate cavitation with dentine showing
6 = excessive cavitation with dentine
```
131
are carious lesions always removed
```
no
not necessarily active (can be arrested)
Not for hall technique
Not for low.prognosis
Not for near exfoliation
```
132
how do we test if a lesion is arrested or active
use probe to test if it is smooth or not smooth
| take into account past history, diet and habits
133
how much tooth paste do we provide for children
smear for 0-3 up to 1000ppm flouride
| pea sized amount for 3+over 1000ppm flouride
134
what is xylitol
stops metabolism of strep. Mutans - major carious bacteria
found in sugar free chewing gum
natural sweetner
135
why is sugar free chewing gum good for prevention
increases salivation
| contains xylitol which inhibits metabolism of Strep. Mutans
136
what product turns carious lesions black and arrests them
Riva star
| Silver Diamine flouride
137
what is Keye's Triad
Venn diagram of 3 things necessary for tooth decay:
- cariogenic food - carbohydrates, diet
- bacteria
- tooth
138
when do white spot lesions go dark
when they reach dentine which scleroses and turns black
or when stained e.g. coffee/smoking
Remineralized
Riva star silver diamine fluoride placement
139
describe infected tooth tissue
```
high mineral loss
necortic tissue
bacteria present
collagen matrix breakdown
soft tissue
```
140
describe affected tooth tissue
collagen matrix still not damaged enough to remove
less bacteria
mineral loss and demineralization
141
what is CPP-APC
milk product containing calcium and phosphates increasing mineralization for people with low calcium phosphate saliva levels
142
what are the 3 aims of caries removal
remove plaque and bacteria
protect pulp and vitality of tooth and arrest the caries
restore function
143
when and what is step wise caries removal used
caries removal over 2 appointments when the caries is very close to the pulp
partially remove (infected) caries and add temporary restoration
leave for up to 6 months for pulp to lay down reactionary dentine
remove temp restoration and place difinitive
still complete caries removal
144
in all methods of caries removal, what is constant in aims
all infected tooth tissue removed
| clear, un-infected ADJ
145
what is class I caries
caries in occlusal/fissure pattern of cingulum cusp
146
what is class II caries
proximal caries of posterior teeth
147
what is Class III caries
proximal caries of anterior teeth
148
what is class IV caries
incisal edge caries
149
what is class V caries
smooth surface caries, can be near gingival margin
150
What is the structure of a carious lesion involving zones
Surface zone - pellicle
Body of lesion - infected, bacteria
Dark zone - active bacterial invasion
Translucent zone - demineralization affected
151
What is the translucent zone
Advanced surface of lesion
| Not infected but affected
152
What is the dark zone
Where demineralization is in progress in between the body of lesion and translucent zone
153
What is the body of the carious lesion
Where the dead necrotic tissue lies with bacteria, bulk of cavity
154
What percentage of plaque is bacteria
70%
| Rest is bacterial ECM and proteins
155
how do we use transillumination
use mirror to reflect light
| carious areas absorb more light and appear shadowed
156
what can we use instead of transillumination in posterior teeth
FOTI fibre optic transillumination
157
how does resistance/impedence change in carious tooth
sound enamel is very resistant (DC) and very impendent (AC)
| carious enamel is less resistant and less impedent
158
how do we use DC to detect caries and what are its flaws
Electronic Conductance Monitor uses single AC current to detect caries
technique sensative
depends on ions in saliva
159
how can we compare large populations on caries (2 methods of gradoing caries)
ICDAS or DMFT
| international caries detection and assessment system and decay missing filled teeth
160
why is DMFT less useful in older age
DMFT is cumulative
| less representative of oral health
161
why is DMFT not the best way of assessing oral hygeine
cumulative so past bad oral hygiene doesn't mean bad oral hygiene now
missing teeth aren't necessarily due to poor OHI e.g. trauma, congenital, never had the teeth
no severity record so a small carious lesion = grossly carious lesion
162
why is DMFT useful
finding trends between OH and other factors e.g. fluoridated water, socioeconomic status etc
163
which caries assessment is better for population studied and individual assessments
DMFT for population
| ICDAS for personal assessment
164
how do we take a DMFT score
score 1 point for a tooth that is either decayed, missing or filled teeth
do not score more than 1 point for 1 tooth
165
what is gingivitis split into (phases)
early stage gingivitis (1st week)
| chronic marginal gingivitis (3rd week) can stay in this stage for a long time
166
what is 'early gingivitis' and what occurs
first stage of gingivitis
initial inflammatory reaction to plaque
vasodilation, oedema, swelling, neutrophils and crevicular fluid
loss of collagen fibres is first sign of gingivitis
167
what is GCF and what does it contain
gingival crevicular fluid
exudate released from periodontal tissues to counteract bacterial plaque
inflammatory mediators, antibodies and neutrophils
168
how does a pseudo pocket form
early gingivitis leads to vasodilation and oedema accumulation
swells the gingival tissue, making it seem as though there is a pocket but the CEJ has not migrated
169
what occurs in the second week of early gingivitis
JE proliferates and becomes undulated and no longer flat with rete ridges, still attached to CEJ and tooth
more GCF is released with increased neutrophils
chronic inflammatory cells like macrophages and lymphocytes recruited
fibroblasts damaged but collagen still inserting into cementum
170
what are symptoms of early gingivits
swollen gums that bleed on probing
loss of stippling and loss of knife edge margins
red due to vasodilation
171
compare early gingivitis to chronic marginal gingivitis
early gingivitis = JE attached to CEJ and enamel, less GCF, les damaged collagen, less inflammatory cells
chronic marginal gingivitis = JE attached to CEJ but not tooth and rete ridges, more GCF, more damaged collagen, more inflammatory cells
172
give 1 clinical and 1 biological disadvantage of swollen pockets
```
clinical = pseudo pockets may be mistaken for real pockets leading to incorrect diagnosis
biological = create habitat for plaque and bacteria to further infection
```
173
what follows chronic marginal gingivitis nd describe its characteristics
destructive periodontitis
loss of collagen attachments into cementum
JE no longer attached to CEJ and discontinuation in fragments of JE
exposed cementum
leads to bone loss
174
what is the regularity of destructive periodontitis
occurs in bursts
175
compare early gingivitis to destructive periodontitis
EG : collagen inserts cementum, JE to CEJ, less GCF, less destruction to collagen, neutrophils, no bone loss, possible undulating JE
DP : collgen no longer attaches to cementum, JE migrated down cementum, More GCF, more destruction of collagen, macrophages and lymphocytes, possible bone loss, definite rete ridges on JE
176
how do we treat early and chronic gingivitis
PMPR, good OHI, possible mouthwash, fluoride,
177
what differentiates RSD from PMPR
root surface debridement removes plaque and biofilm form root surface subgingival
PMPR is mostly supragingival on the crown enamel surface
178
what is the purpose of RSD
removal of the stimulus of inflammation from the root surface in treatment for periodontitis
179
what occurs after successful RSD with good OHI
subsided inflammation, swelling and bleeding
reduced pockets by proliferation and re-attachment of JE to cementum by long epithelial attachment - NOT inserting into cementum
no bone regeneration
JE will never reattach at CEJ
180
what is the leading cause for loss of teeth and why
age
cumulative disease and failed restorations
medications
181
after RSD, what happens to pocket depth and why
reduces
mainly reduced swelling and oedema
re-attachment of 15-20% of PDL to cementum but NOT sharpeys fibres reattachment
182
why do we only get 15-20% long epithelial growth post RSD
oral mucosal tissue grows much faster than JE tissue
proliferates down the sulcus to meet JE
contact epithelium stops growth
183
at what age do children have most plaque and why
8 years
just after parents probably stop helping brush teeth and eating more sweets
mixed dentition where it may hurt to brush teeth or be hard to brush teeth
orthodontic appliances may make it difficult for oral hygiene
184
whhy might a child with amelogenesis imperfecta have a lot of calculus
acts as an insulator on very soft, sensitive enamel and dentine
185
if a child has extreme calculus build up, why might this be
amelogenesis imperfecta to insulate teeth
| fed via gastronomy so reduced saliva and scared to brush teeth as no cough reflex
186
which side of the mouth usually has more caries and why
RHS
| most people right handed so brush left hand side better
187
at what ages to we start BPE and modified BPE
no BPE from 0-7
7-11 modified BPE from 0-2 as false pocketing due to exfoliation would give false positives
12-18 normal BPE
188
what is the most common dental problem with childrens teeth and why
```
chronic gingivits
doesnt hurt but bleeds
scared to brush because of bleeding
eat a lot of sweets
parents stop brushing for them
orthodontic appliances
inflammation due to exfoliation
crowding
```
189
what can we provide for autistic/downs syndrome children
Oro-Nurse
| tooth paste with no taste as the sensation is sometimes not liked by children with learning difficulties
190
what is localised gingival recession and what is its incidence in children
tooth recession on a single tooth cuased by labially positioned teeth, lip tightening and overbruhsing
10% of children under 10
mainly affecting lower incisors
191
what is gingival hyperplasia and what commonly causes it
overgrowth (too many cells) of gingiva
| mainly drug induced - cyclosporins (immunosupressant), Phenytoin (anti-epeleptic)
192
what affect does OH have on drug induced hyperplasia
good oral hygeine keeps it the same, no reduction
| poor oral hygeine makes it grow larger
193
how do we reduce drug induced gingival hyperplasia
change drugs
194
what percent of patients on ciclosporins get gingival hyperplasia
30%
195
what types of disease can cause systematic disease gingival hyperplasia (2)
```
sarcoid (simialr to TB affecting whole body)
cyclic neutropenia (comprimised white blood cells)
```
196
what types of gingival hyperplasia are there and what are there causes
drug induced GH : cyclosporins (immunosuppressant) or phenytoin (anti-epeleptic) or calcium channels blockers
disease induced GH : cylic neutropenia (supressed WBC) or sarcoid ( similar to TB)
197
is drug induced or systematic disease induced gingival hyperplasia usually more severe
drug induced
198
what types of self inflicted gingival trauma are there
A: injuries are superimposed upon a pre-existing source of irritation
B: secondary to habits e.g. biting fingernails
C: complex aetiology and are a physical manifestation of an underlying emotional disturbance - self harm, poking gums with pencil
199
if a patient bites fingernails and causes gingival dmaaged, what is this diagnosis
type B self inflicted trauma
200
if a patient pokes their gums with a pencil what is this diagnosed as
Type C self inflicted gingival trauma
201
what is acute herpatic gingivostomatitis
herpatic (viral) gingvo (gingival tissue) stomatitis (mouth and lips)
oral manifestation of Herpes simplex virus I
202
what are some oral manifestations of acute herpetic gingivostomatitis
```
high temperature
high salivation
small ulcerations tongue
sore throat, lips, tongue, gingiva
wanting to eat
```
203
how long will acute herpetic gingivostomatitis last
roughly 10 days unless immunocompromised where antivirals are needed
204
how do we treat acute herpetic gingivostomatitis (6)
```
keep hydrated
eat soft foods
antivirals if immunocompromised
use soft toothbrush
wipe mouth with CHX
isolate saliva and bodily fluids from anyone else as very contagious
```
205
what is necrotizing ulcerative gingivitis, what is the cause and who is more prone to this disease
common non-contagious necrosis of gingival tissue
necrotising bacteria - fuso spirocheatal complex
common in third world countries, stress, smokers, not removing dentures and HIV patients, poor OHI
206
what is the treatment necrotizing ulcerative gingivitis
good oral hygiene and antibiotics
207
what happens to untreated necrotizing ulcerative gingivitis
can spread to oral tissues like the lips and cheek
208
what is herpangina, symptoms and cause
very common contagious disease effecting 3-10 year olds
viral infection in immunocompromised patients (pregnant, young)
small white ulcers in back of mouth, tongue and throat
209
what is hand foot and mouth disease
combination of herpangina (sores in back of mouth) and also on palms of feet and hands
210
how do we treat herpangina and hand, foot and mouth disease
```
drink lots of water
isolate as very contagious
possible antivirals if immunocompromised
pain relief
healthy, soft diet e.g. yogurt, Weetabix, milk
```
211
a pt has itchy feet, loose teeth and poor prognosis. what are they likely to have and what is likely treatment
Papillion- Lefever syndrome
hyperkeratinisation of palms of hands and soles of feet
likely need to remove all teeth
212
a child has sores on the back of their throat, what are some differential diagnosis and what investigations should we do
```
herpangina (if white)
hand food and mouth disease
check for white lesions on palms of hands and soles of feet
pt will have fever and soreness too
Acute herpatic gingivostomatis (red)
Antibody test
```
213
young pt has loss of gingival tissue, seemingly dead tissue. what is the diagnosis and how do we treat
necrotising ulcerative gingivitis
attack the causes e.g. smoking, poor OH
provide antibiotics
214
young pt has high salivation, fever and small red spots on tongue and red marks on lips. what is this and what do we tell the patient to do
acute herpetic gingivostomatitis from herpes simplex I
isolate from other children and prevent contamination with eyes/saliva
very hydrated, soft healthy foods e.g. yogurt, milk
antivirals if immunocomprimised
should go within 10 days but consult with GP
215
what are the ways of classifying pulpal disease
```
acute
chronic
reversible
irreversible
open
closed
symptomatic
asymptomatic
```
216
what causes acute open pulpitis
fracture into pulp
217
what causes acute closed pulpitis
trauma
218
what causes chronic closed pulpitis
caries
219
what causes chronic open pulpitis
grossly cavitated caries
220
which teeth are most likely to get pulpitis due to caries
upper lateral incisors
| infolding of enamel organ near cingulum is very plaque retentive for caries
221
what is a bacteremia and how is this relevent to dentistry
where there is bacteria in the blood stream
bacteria can get to pulp via bloodstream
bacteria can get from tooth to heart valves --> infective endocarditis
222
what type of trauma can cause acute pulpitis (5)
heat -physcial
direct blow - physical
filling materials can irritate pulp chamber - chemical
cavity prep can enter pulp - mechanical
223
what are general symptoms of pulpitis
'toothe ache'
radiating pain, localised sharp pain
radiates across jaw
224
what must we classify pulpitis as when diagnosing
reversible symptomatic
irreversible symptomatic
irreversible asymptomatic
225
with an established dentine lesion, what occurs in the pulp
odontoblasts die preventing laying down of reactionary dentine
vasodilation
recruitment of neutrophils
inflammatory exudate near site
226
why does pulpitis lead to necrosis
acute inflammation leads to vasodilation and exudate
apex is very small, increased tissue pressure leads to increased pressure in blood vessels causing collapse
hypoxia
cells die in necrosis
227
what is the effect of pulpal necrosis
more inflammatory cells and exudate and chronic inflammatory cells
pulpal abscess - exudate, dead cells, neutrophils, bacteria
228
what may happen to a pulpal abscess
may drain into oral cavity
| if closed, will build pressure and pain and spread around tooth and to periapex --> periapical pathology
229
what is and what causes chronic hyperplastic pulpitis
pulpitis that is exposed to the oral cavity with a thin epithelial/fibrin layer covering
pulpitis in a open cavity or where crown is fractured
230
what are pulp stones and what types can we get
small parts of mineralized tooth tissue, sometimes dentine that grow with age
true pulp stones - dentine
false pulp stones - amorphous calcified material
231
what would be found in a pulpal abscess
```
dead tissue including odontoblasts and tooth tissue
bacteria
neutrophils and other inflammatory cells
exudate
'pus'
```
232
what salivary components help defend against bacteria
secretory IgA can opsonise bacteria and neutralise toxins
Lactoferrin is antifungal and antiviral. Binds to iron which is needed by P.Gingivalis
Definsins and small proteins that help lysis of bacteria
233
what is the epitheliums role in protecting the oral cavity from microbes (3)
desquamation (shedding of cells) removes bacteria attached
acts as a permeability barrier (excluding JE)
release cytokines like IL-2 to stimulate inflammation
Impermeable barrier
234
how can bacteria use GCF for themself
metabolize some components
235
what are the antimicrobial components of GCF
complement - MAC
IgA and IgG heling opsonisation
inflammatory cells like neutrophils that attack free bacteria and release NETS and hydrogen peroxide attacking plaque bacteria
fibrin heals wounds and protects blood
236
what are neutrophils function in GCF
phagocytose free bacteria near gingiva
release hydrogen peroxide and NETs to destroy attached bacteria
release cytokines to get a greater inflammatory response
237
what are some affects of cyclic neutropenia (2)
increased risk of periodontitis and destruction
| increased risk of systemic disease causing gingival hyperplasia
238
what are the functions of macrophages
stimulate inflammation by releasing cytokines for attracting inflammatory cells
M" release growth factors to stimulate fibroblast and angiogenesis (granulation tissue for healing)
phagocytosis of pathogens
antigen presentation to get humoral response
239
what is the role of dendritic cells and where are they found
found in epithelium
| detect, phagocytose and antigen present to lymphatic system for humoral response
240
what are some functions of antibodies
act as opsins to increase phagocytosis
neutralize toxins
prevent bacterial attachment
activate complement for inflammatory response and MAC
241
what cause most destruction during infection
host cells reducing inflammation
242
what are some negative effects of IL-1b and TNFa and what secretes them
they stimulate soft tissue and bone loss leading to periodontitis
macrophages
243
which inflammatory mediators mainly lead to tissue loss and what secretes them
IL-1b and TNFa secreted by macrophages
| lead to activation of pathways e.g. MMP8 and RANKL that lead to soft tissue and bone loss
244
what do neutrophils release that cause soft tissue loss and what stimulates this
MMP8 stimulated by IL-1b and TNFa secreted by macrophages
245
what do fibroblasts release that leads to bone loss and what causes this
PGE2 stimulated by IL-1b and TNFa secreted by macrophages
246
what are some inflammatory mediators that lead to soft tissue loss
neutrophils - MMP-8
| macrophages - IL1b and TNFa
247
how do macrophages lead to soft tissue loss
secrete IL-1b and TNFa that directly cause soft tissue loss
| IL-1b and TNFa also intitate neutrophils to release MMP8 which directly causes soft tissue damage
248
how do macrophages lead to bone loss
they secrete IL-1b and TNFa which stimulate:
fibroblasts to secret PGE2 which directly causes bone lopss
other inflammatory cells (including macrophages) to release RANKL which acts on osteoclasts to bone loss
249
what negative affect does RNAKL have on the body and what causes its secreton
stimulates osteoclasogenesis
bone resorption
triggered by IL-1b
IL-1b and RANKL secreted by macrophages during inflammation
250
how do we get bone and tissue loss during infecton
bacterial factors:
- proteases cause tissue and bone breakdown
- Endotoxins damage fibroblasts and CT
- collagenases break down CT
host response:
- macophages release TNF, IL-1b and RANKL causing bone and soft tissue loss
- neutrophils release MMP-8 causing soft tissue loss
- fibroblasts release PGE2 causing bone loss
251
what causes necrotising gingivitis
Deep invasion of fuso-spirochaetal complex bacteria
depression of host response from smoking, malnutrition, stress
depression of peripheral blood supply to teeth and soft tissues causing hypoxia and necrosis
252
what is leukoplakia and why are they relevent
white lesion in mouth
| keep under strong watch - premalignancy
253
what is erthyroplakia and why are they relevent
red lesion in mouth
| keep under watch --> premalignnacy
254
what is a sign and symptom
sign is something found by the clinician
| symptom is something that the patient relays to the clinician
255
what are some unfavourable characteristics of the pulp chamber
tight apical constriction : blood and lymph flow limited and easily disrupted, intrapulpal pressure
unyielding walls : limiting volume to accommodate pulp swelling = pain
surrounded by bone = infection often leads to bone loss
256
what steps do we go through when trying to diagnose pulpal disease
```
patient complaint
history of complaint
clinical investigations
special investigations for vitality, sensibility, periapical pathology
radiographs
```
257
what is a healthy response to a cold test
uncomfortable for a few seconds and wears off near to immediately
258
what is pulpitis
inflammation of pulpal tissue
259
why does pulpal inflammation hurt more with cold test
pulpal inflammation lowers nerve threshold due to inflammatory response + prostaglandins
nerves need less stimulus to cause action potential response
260
what classes as reversible pulpitis and how do we treat
probable trauma or large carious lesion
inflamed pulpitis
cold test leads to pain and pain after but does not linger
removal of stimulus (removal of caries) should settle the pulp
261
what are key symptoms of irreversible pulpitis and how do we treat
painful cold test that lingers
spontaneous pain that can keep awake at night
referred pain if it has not reached the apex where mechanoreceptors can localise pain
necrosis will occur and periapical pathology will follow so RCT needed
262
if we have bad pain that lingers and keeps us awake but cannot tell where the pain is coming from what is this
irreversible symptomatic pulpitis
| has not yet reached apex so no periapical pathology
263
why may irreversible pulpitis be asymptomatic
if nerve innervation ha been disrupted or no longer has blood supply, the tooth will not cause pain until preapical pathology occurs
264
how might we diagnose asymptomatic irreversible pulpitis
clinical investigation of very large caries definitely in pulp
radiographic evidence of necrosis
265
can closed pulpitis cause periapical pathology
no - as no bacteria are in the pulp
| bacteria must be near the apex to cause periapical pathology
266
how does pulp necrosis occur
endotoxins inflame the pulp which leads to death of odontoblasts
inflammatory response can kill soft tissues by release of MMP-8 and IL-1b and TNFa
blood supply cut off due to increased interpupil pressure = hypoxia = necrosis
267
how do we diagnose necrosis of pulp and what are differential diagnosis of this
negative sensibility test
| may also be down to thick enamel, calcification and tertiary dentine - especially in elderly
268
how does periapical pathology occur
bacteria enter necrotic pulp
form biofilm on inside of pulpal walls and inside dentinal tubules
feed on necrotic tissue to release endotoxin and enzymes into periapical tissues
periapical inflammation = periapical pathology
269
what would it be called if bacteria formed a colony in the periapex and is this common
extra radicular infection
| very uncommon as bacteria rarely leave the periapex as they would be killed
270
how does bone loss occur from periapical pathology
increased pressure due to inflammatory response
mediators released such as IL-1b trigger RANKL repose leading to bone resorption
inflamed fibroblasts released PGE-2 which leads to bone resorption
271
differentiate periapical, apical and peri radicular periodontitis
```
periapical = around the apex
apical = at apex
peri-radicular = around root
```
272
in periapical periodontal disease what does chronic and acute mean
```
chronic = asymptomatic
acute = symptomatic
```
273
how do we diagnose symptomatic acute periapical periodontitis
pt can LOCALISE pain on percussion test
tenderness to pressure
radiographic changes may or may not be visible
274
how do we diagnose chronic asymptomatic periapical periodontitis
periapical radiolucency
| low grade inflammation causing no pain
275
how do we diagnose an acute periapical abscess and what is it (3)
Inflammation of the periapical tissues with pus (necrotic tissue, bacteria and WBC) formation and swelling
rapid onset with spontaneous extreme pain due to pressure build up
may also have fever and lymphadenopathy
possible radiographic change
276
how do we diagnose a chronic periapical abscess
Inflammation of the periapical tissues with intermittent discharge of pus through an associated sinus tract.
Usually associated with little or no discomfort due to a release of pressure.
Radiographic changes usually appear as a periapical radiolucency
277
how do we diagnose condensing osteitis and how likely is it
Diffuse radiopaque lesion
representing a localised bony reaction to a low-grade inflammatory stimulus usually seen at the apex of the tooth
occurs in 5% of periapical pathology
278
when diagnosing periapical/pulpal disease what must we always include
state of both pulp and periapical, even if one is healthy e.g.
necrotic pulp, healthy periapical tissue
279
what is the disease pathway of chronic and acute periapical inflammaiton
acute: abscess --> bacteraemia (fever, lymphadenopathy)
chronic: granuloma --> cyst
280
where are some common dentoalveolar infection sites
```
palatal abscess
vestibular abscess
periapical abscess
periodontal abscess
all around infected tooth
```
281
why are abscesses dangerous
bacteria can travel through path of least resistance
maxillary abscesses can enter nasal cavity, MAS and even to the brain
cause bacteraemia which can affect immunocompromised patients and lead to endocarditis
lead to osteomyelitis if bacteria gets t bone
282
what is osteomalacia and relate to dentistry
reduced bone remineralization
| leads to pseudo fractures held together by bone matrix
283
with a BPE of 3 and radiographs showing some bone loss, what can we put in the diagnosis
periodontal disease
| cannot determine grade, stage, severity and rate until 6PPC is done at 3 month review
284
what are the 4 prognosis levels
good
fair
guarded
poor
285
what questions do we ask to investigate periapical diagnosis
When did you first notice the problem?
Is it continuous or intermittent?If intermittent, how often does it occur?
Are there any initiating or relieving factors?
Is it getting worse, better or staying the same?
Where is the problem?
History of the complaint (specific to pain)
Location - specific to tooth or generalised?
Initiating or relieving factors eg hot/cold, biting, sweet stimuli, bending forwards?
Character – dull, sharp, throbbing, shooting?
Duration – short or long lasting?
Severity – causing sleep loss, pain scale (1-10)?
Spread/radiation – to adjacent structures, referred pain?
286
when investigating a pain, what system do we go thorugh
```
SOCRATES
site of pain
onset of pain
character of pain
radiation of pain
alleviating factors
time scale
exacerbating factors
scale of 1-10
```
287
if we see a draining sinus (from an abscess) how do we determine its origin
place a thin gutta percha point down the sinus
take a radiograph
gutta percha is thin and radiopaque
follow to apex of tooth to find periapical abscess
288
why do we investigate occlusion with toothache
if all occlusion is on a few sites, this puts lots of pressure and causes inflammation on these teeth
if there is fremitus, movement on pressure, this may be evident of inflammation raising a tooth out of the socket
289
if there is an isolated pocket and radiographic evidence of a J shaped lesion surrounding root, what is the diagnosis and prognosis
vertical root fracture
| poor prognosis, remove tooth
290
what does mobility indicate
periodontal tissue loss and possibly bone loss
| periapical pathology with fremitus raising out of socket OR periodontitis
291
what different types of discolouration can teeth have
white lesions - early caries
brown lesions- stained, remineralised lesion or base/GP above ADJ
yellow shadowing = less translucent tertiary dentine laid down due to pulpal inflammation - caries, still vital
black staining = result of pulp necrosis, blood clot, non-vital, pulpitis
292
why will a cold test only cause pain and no other sensaiton
only pain A delta fibres go near dentinal tubules
293
what is the difference in disease progression between sharp and dull pain, explain
sharp pain is due to peripheral A delta fibres in the pulp
dull pain is due to C fibres central of the pulp
if inflammation is reaching C fibres and pain is dull, this inflammation is more advanced
294
define specificity and sensitivity of a test
sensitivity measures amount of true positives: %of positives that actually have nerve supply
specificity measures amount of true negatives: %of negatives that actually have no nerve supply
295
which sensibility tests have good sensitivity and specificity
cold test: good both
hot test : bad specify
EPT is good but cold test has higher sensitivity
296
which tests test the pulp and which tests test the periapex
pulp : vitality and sensibility = cold, hot, EPT
| periapical : percussion, pressure, palpation, tooth sloth,
297
how do we test for a fracture (2)
tooth slooth - pressure on each cusp until pain
| Transillumination can find cracks in teeth (with tooth slooth).
298
how can we determine the symptomatic tooth (4)
anaesthetise individual teeth to see if pain remains
x-rays
GP if draining sinus
special tests
299
when do we take an x-ray for diagnosis of periapical pathology
after all over tests have been done
300
A patient has a painful, inflamed 3rd molar. What is procedure for this
check if infected
if infected, provide antibiotics and salt water wash - should slow down infection
if a second or third episode then send for sectional OPT or CT of tooth and send for XLA
301
what occurs to dentine after it is infected histologically
forms liquefaction foci which join to form transverse clefts 90 degrees to dentinal tubules
bacteria, necrotic dentine and toxins
302
why might a pulp chamber appear white histologically
necrotic pulp
| no tissue - drained out either of sinus, open cavity or through apex into periapical tissue
303
if we perforated the pulpal horn roof what would happen in healthy and inflamed scenario
```
healthy = slight bleeding, very little
inflamed= heavy bleeding due to vasodilation
```
304
what are neutrophils negative affect during pulpitis
adverse stimulation leads to neutrophil recruitment
neutrophils come to inflammatory sit and release enzyme such as MMP-8 which cause soft tissue breakdown
necrosis occurs and stimulates further inflammation to remove necrotic tissue
spreads to surrounding tissues = pulpitis
305
how can we treat dentinal sensativity (4)
restore over exposed dentine
alter ionic state of dentinal tubules
reduce permeability of tubules
demineralizing/desensitising toothpastes
306
why do we get spontaneous pain in irreversible pulpitis
highly inflamed pulp
increased nerve density and neuropeptide density
High BP and tp
release of prostaglandins and other pain causing genes expressed e.g CGRN, VIP
307
what are symptoms of dry socket (4)
severe pain
Foul taste and smell
Localised inflammation and tenderness
partial/total loss of blood clot
308
what are some differential diagnosis of dry socket
spetic socket - infection but no loss of blood clot
osteonecrosis - loss of jaw bone
osteomyelitis - infection of cancellous bone marrow
309
what is osteomyelitis and how does it present and what can it lead to
infection of cancellous bone marrow
radiolucency's in jaw, pain, swelling, altered sensation, pus
can lead to loss of portions of the jaw
310
what is infection of the jaw causing necrosis
osteonecrosis of the jaw
311
what is septic socket and how is this treated
infection of an extraction socket
| treated with antibiotics (never used for dry socket)
312
what is the main cause of dry socket and what can cause this
```
loss of blood clot
caused by over- rinsing/mouth washing
poor blood supply
Fibrinolysis as a result of oestrogens, trauma and bacterial pyrogens
bacterial colonisation breaks down clot
```
313
how can oestrogens affect the wound healing of a extraction socket
oestrogens lead to fibrinolysis breaking down fibrins in the blood clot leading to dry socket
314
what is the incidence of dry socket and which teeth are more prone to dry socket
0.5-5% incidence
wisdom teeth have 1/5 or 1/6 incidence
lower wisdoms most prone being 25% prone to dry socket
315
why are the lower molars more prone to dry socket (3)
denser bone
more traumatic extraction
more likely to get infected
316
what patient factors lead to dry socket (4)
being female and menstruating/contraceptive pill - as oestrogen affects fibrinolysis
smoking
poor OHI
overuse of mouthwash
poor healing due to systemic factors like calcium deficency or steroids
317
how can we prevent dry socket
OHI to stop smoking and dont over use mouthwash
| can pack with pre-emptive alvogyl
318
what therapeutic management of dry socket is there
smoking cessation - preventative
appropriate mouth bathing in saline solution and pack with
alvogyl - antiseptic, analgesic, LA
analgesia
319
what is alvogyl
therapeutic agent used to pack sockets (especially bleeding a lot) that acts as an antiseptic, analgesic and LA
320
what are the symptoms of septic socket (3)
dry socket symptoms - pain, fowel smell,
Extraoral swelling
Lymphadenopathy
Formation of pus
321
if a patient had granulation tissue covering a socket for over a week, what would we do? differential diagnosis?
take an x-ray to rule out residual bone
| possibly delayed healing or squamous cell caricnoma
322
who is likely to get osteomyelitis
immunocompromised or people on medications leading to infection after extraction
323
which jaw is more likely to get osteomyelitis
mandible due to being more dense and having reduced vascularity and healing
324
what can osteomyelitis be divided into
acute supprative oseteomyelitis occurs up to 4 weeks after infection - no necrosis
chronic supprative osteomyelitits occurs after 4 weeks and can include bone necrosis
325
what bacteria cause osteomyelitis
mainly Staphylococcus aureus found on skin and respiratory tract
326
what are the histological presentations of ostemyelitis (4)
dead bone - necrotic bone (chronic)
neutrophil infiltration
lacunae without osteocytes
scalloping of bone where it has been lost
327
what is osteoradionecrosis
necrosis of the jaw caused by radiation therapy before an extraction
destruction of bone cells reducing its vascularity and vitality
328
what is the threshold of radiation grays between low and high risk of radio necrosis
65 grays
329
how do we manage someone who has osteonecrosis
removal of parts of jaw until bone bleeds
330
how do we prevent osteoradionecrosis
prevent need for extraction with good OH
| remove teeth with poor prognosis before radiotherapy
331
what is MRONJ and what was it formally know as, why has its name changed?
medication related osteonecrosis of the jaw
BRONJ - bisphosphonate related osteonecrosis of the jaw
changed as more medications have been identified that lead to osteonecrosis of the jaw
332
what drugs lead to MRONJ
bisphosphonates (especially IV and in combination with steroids)
Monoclonal antibodies - e.g. Denosumab
Tyrosine Kinase inhibitors - e.g. Sunitinib are all small cell receptor antagonists for cancer
333
what are the three criteria for MRONJ
no radiotherapy since extraction (as this can be osteoradionecrosis)
MRONJ related drug
bone exposed for 8 weeks or more
334
what does MRONJ display as
green/yellow slough covering bone of extracted pocket
Loss of mucosa over bone
8 weeks after extraction
radiolucencies
335
what stages of MRONJ do we have
```
at risk
stage 0
stage 1
stage 2
stage 3
```
336
what is stage 0 MRONJ and how do we manage
at risk, non-specific, pain post extraction, radiographic change, no bone loss, no bone exposure or inflammation
pain medication, monitor, treat other dental problems
337
what is stage 1 MRONJ and how do we manage it
at risk, exposed/necrotic bone, pain, no infection or inflammation.
treat with antibacterial mouthwash, monitor
338
what is stage 2 MRONJ and how do we manage
exposed necrotic bone, pain, pus, inflammation, erythema
| antibacterial mouthwash, antibiotics, pt management, pain control, debridement of necrotic bone?
339
what is stage 3 MRONJ and how do we manage
exposed/necrotic bone, bone loss radiographically, extends below alveolar socket into mandible, pain, inflammation, pus, FRACTURE
manage with surgical removal of bone
340
how does MRONJ occur because of bisphosphonates (3)
bisphosphonates:
- act as anti-angiogenesis so reduce blod flow to bone
- can kill/reduce action of bone cells
- toxic to overlying soft tissues so prevent healing over
341
How do we treat ORN and what would happen if we did this to an MRONJ patient
ORN we can strip back bone and soft tissue until it bleeds showing vitality
MRONJ this would just release more bisphosphonates into the mouth and soft tissues, causing a larger problem
342
at what MRONJ stage should we provide antibiotics? what should we provide before this
stage 2
| CHX mouthwash weekly
343
how do we prevent MRONJ
Avoid bisphosphonates
prevent need to extract teeth
12 month drug holiday
344
which drugs cause dry socket to increase incidence (4)
```
(anti-inflammatory drugs or vasoconstrictors)
Steroids
Ciclosporins
Methotrexate
OCP oral contraceptive pill - osteogren
bisphosphonates
nicatine
```
345
should we provide antibiotics for dry socket, septic socket or MRONJ?
dry socket = no
septic socket = yes
MRONJ = only if over stage 2
346
what is the treatment for dry socket
gentle rinse with saline solution to remove debirs or bacteria and then dress socket with alvogyl - LA, anti-inflammatory and antiseptic
347
why does smoking increase risk of dry socket
sucking on cigarette increases likelihood of blood clot dislodging
348
what causes pneumatization of the MAS
movement of the air sinus lining down
| ageing and lack of teeth
349
what is exudate
fluid that passes out of blood vessels into tissues full of oxygen, proteins and other molecules - tissue fluid
350
What bacteria would be found in the blood of a pt with infective endocarditis due to poor oral hygeiene AND IV drug use
IV drug use - staph. aureus
| OH - strep. viridans
351
what are the 2 likely paths of least resistance for an abscess of a maxillary molar
if apex of root is above buccinator = side of face
| if apex is within buccinator = oral cavity
352
what are the 23 likely paths of least resistance for an abscess of a mandibular molar
apex of root above mylohyoid = oral cavity
| apex of root below mylohyoid = swelling in submandibular space and possibly cause pharyngeal obstructions
353
which teeth are likely to cause airway obstructions, and why, during a periapical abscess
mandibular molars with the apex of root below the mylohyoid muscle
swelling goes into submandibular space
into pharynx
354
if a swelling as small dimples, what is likely to happen
discharge into oral cavity
355
when do we get a periapical granuloma
chronic (asymptomatic) periapical periodontitis
356
why might a radicular cyst form
in the state of a periapical granuloma with non-vital tooth
if there is odontogenic epithelia - cell rests of molasses, present then this may proliferate and encapsulate the granuloma = cyst
357
if a cyst radiographically is undefined or defined, what does this tell us
```
defined = chronic, established, no longer as inflamed
undefinied = still very inflamed and growing
```
358
what are the 3 characteristics of a cyst
lumen - holds semifluid, dead necrotic tissue
lining - is almost always stratified squamous nonkeratinized epithelium, cell rests
wall - remanence of granulation tissue, fibroblasts, endothelial cells, neutrophils
359
which epithelium forms the lining of a radicular cyst
non-keratinized stratified squamous cell epithelium
360
what are the crystal shaped white patches found in a cyst histologically
cholesterol clefts
when cells die their cholesterol is released and forms crystals of cholesterol
when taking a histological slide, the cholesterol dissolves
361
what types of osteitis can we get from inflammation
```
condensing or focal sclerosing osteitis (5%) - increased density
rarefying osteitis (95%) - decreased density
```
362
what are some causes of hypercementosis
teeth that are in little function
e.g. teeth without opposition or impacted 8's
inflammation and mobility can contribute
pagets disease
363
what would we see on the roots of a patient with pagets disease
hypercementosis
364
what is Ankylosis
obliteration of PDL between cementum and bone
cementum and bone fuse
causing strong attachments between bone and tooth, complicating extractions
365
which teeth and what demographic are likely to be effected by cement-osseous dysplasia
30-50 year old black women
| lower incisors
366
what is cemento-osseous dysplasia
small radiolucent lesions at the apex of teeth with smaller radiopaque masses in the middle
irregular trabeculae of woven bone and cementum in fibrous stroma
367
what is florid cemento-osseous dysplasia
Often in edentulous areas we get irregular radiopacities showing masses of fused bone and cementum-like tissue. Reactive, ‘scarred bone’
irregular bone formation with connective tissue
368
which tooth is likely to experience a cementoblastoma
lower 6s
369
what is a cementoblastoma
radio-opaque lesion attached to a tooth root usually being the mandibular first molar tooth.
Histologically there are large sheets of cementum and fuses with tooth roots with lots of very active osteoblasts and cementoblasts within the tumour.
370
if a cement blastoma is removed, what happens
will not reccur, benign
371
which 3 bacteria are the main culprits for root caries
Actinomyces spp. (not present a lot in coronal caries)
Mutans streptococci
Lactobacilli
372
compare coronal and root caries
root caries do not have white spot lesion phase - straight to brown spot
root caries have Actiomyes spp. bacteria, coronal do not
373
how can we tell between an arrested and not-arrested carious lesion
arrested:
- black and shiny
- smooth surface
- not sticky
- not associated with plaque
not-arrested:
- brown and matt
- rough surface with probe
- sticky
- associated with high plauqe
374
describe the progression of root caries
develops at CEJ
spreads around CEJ
deepens into the dentine
375
what type of caries is not shown on radiographs
buccal/lingual/palatal root caries
| occlusal caries
376
how do we manage xerostomia causes caries
```
sip water throughout day
reduce sugar intake
mouthwash daily 0.05% F-
saliva stimulation (xylitol, chewing gum)
saliva replacement
review in short recall periods
```
377
what are thee aims of a carious restoration
Aid plaque control & thereby manage caries activity at this specific location.
Protect the pulp-dentine complex & arrest the lesion by sealing it.
Restore the function, form & aesthetics of the tooth
378
what is attrition and what causes it
tooth on tooth contact causing TSL
caused by bruxism, stress, anger, drugs
natural part of ageing
Skeletal patterns III puts more stress on anterior teeth
379
what is abrasion and what causes it
```
tooth on external object TSL
caused by toothbrushing
holding objects e.g. nails in mouth
biting nails
food
woodwind instruments
tongue peircings
worsened by porous enamel e.g. after eating under acid attack
```
380
what is erosion and what causes it
non-carious dissolution of mineralized tooth tissue - TSL
caused by acid reflux
acidic foods e.g. lemons, kimchi
acidic drinks e.g. fizzy pop
being sick e.g. bulimia or pregnancy
industrial gases or chlorine in swimming baths
professional wine taster
381
which 2 TSL components usually come paired
erosion and attrition
382
how cna we tell if a TSL is caused by erosion
helix around crown exposing dentine
| smooth , shiny surface
383
what are 4 ways to get TSL
erosion
attrition
abrasion
trauma
384
which demographc are most likely to get traumatic TSL
8-10 year old boys
385
how can we diagnose what is causing TSL
```
take a thorough history and diagnose by disproving alternate diagnosis
give diet diary to dislcude diet/erosion/bulimia
general health
check cheeks for keratinization
look into bruxism
look for fracutre marks
sports/injury history
fmaily history (imperfecta)
```
386
explain the difference in appearance between dentinogenesis and amelogenesis imperfecta
```
dentinogenesis = glossy, trnasparent dentine
amelogenesis = pitted, white, opaque enamel
```
387
what are the main components of a granuloma
```
marcophages (destruction)
fibroblasts (reconstructive)
endothelial cells (angiogenesis)
other immune cells like neutrophils
```
388
what is an 'engorged' lumen
dilated and full e.g. the blood vessel was engorged of blood cells
389
which cells are involved in acute inflammation and compare their structure
neutrophils and macrophages
both phagocytose
neutrophils are small trinucleated cells
macrophages are large cells with a foamy appearance
390
what ae the chronic inflammatory cells and describe their function and structure
Plasma cells: look like fried egg, lots of cytoplasm surrounding clock faced pattern chromatic and eccentrically placed nuclei. Produce specific antibodies (derived rom B cells)
Lymphocytes: cause more inflammation by producing B cells to produce antibodies or T cells that cause clonal expansion
391
give three characteristics of a plasma cell
eccentric nucleus
1 nucleus
clock faced shaped chromatin
lots of cytoplasm
392
what are craze lines
fracture lines caused by bruxism, biting nails
393
what type of fractures of teeth can we get
```
complicated involving the pulp
non-complicated
enamel
enamel dentine
crown root
crwon
enamel infarction (certical not thorugh and through)
```
393
what type of fractures of teeth can we get
```
complicated involving the pulp
non-complicated
enamel
enamel dentine
crown root
crwon
enamel infarction (certical not thorugh and through)
```
394
what is labial luxation
tooth moves up near the lips
395
what is lateral luxation
tooth mobile side to side
396
what is tooth extrusion
tooth can come partially out of socket
397
what is tooth avulsion
tooth comes fully out of socket
398
what is intrusion
tooth is pushed into alveolar socket
399
recommended techniques for detecting caries
Bitewings for interproximal
cleaning and drying the surface with 3 in 1 to view early lesions
using blunt ended probe for feeling rough surfaces (demineralized) or sticky cavitated lesions
transillumination and good lighting with magnification
400
what is an acute abscess
no sinus, swelling, very painful
401
what is a symptomatic abscess
no sinus but painful
402
what is a chronic abscess
with sinus and no pain
403
what is an asymptomatic abscess
no pain., no sinus, find radiographically
404
how can we prevent caries in a patient
stimulate salivation e.g. chewing gum
good OHI
fluoride regimes
removal of risk factors e.g. smoking, partial dentures
405
what percent of healthy adults does root caries effect
20-40%
406
Compare predisposing and precipitating factors
```
Predisposing = increases risk
Precepitating = increases incidence after risk is involved
```
407
Give 5 dental characteristics of dentinogenesis imperfecta
```
Short roots
Slender roots
Large crowns
Lacking enamel
Absence root canals and pulp chambers
```
