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BDS 2 > Disease of teeth and Periodontal tissues and TSL > Flashcards

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

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2
Q

What is a BPE score of 1?

A

Bleeding on probing, no plaque retentive factors, pockets < 3.5mm

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3
Q

What is a BPE score of 2?

A

Plaque retentive factor, not necessarily BOP, pockets <3.5mm

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4
Q

What is a BPE score of 3?

A

Probing depth 3.5mm-5.5mm, not necessarily BOP or plaque retentive factors.

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5
Q

What is a BPE score of 4?

A

Probing score of >5.5mm, not necessarily BOP or plaque retentive factors

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6
Q

What is a BPE score of *

A

Furcation involvement

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7
Q

What is the protocol for BPE of 0 or 1?

A

Give OHE and congradulate patient on good OH

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8
Q

What is the protocol for BPE score 2?

A

Give OHE and bring back for another appointment to remove plaque retentive factors

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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
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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

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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

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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

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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)
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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

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15
Q

is biofilm induced gingivitis reversible?

A

yes

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16
Q

what do we class as localised and generalised gingivitis

A

10% BoP = normal gingival health
10%-30%= localized
>30% BoP = generalised

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17
Q

what are some localised and systemic risk factors of gingivitis

A

local:

  • plaque retentive factors
  • calculus

systemic:

  • smoking
  • diabetes (type 2)
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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

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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

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20
Q

if plaque is removed and OHI is good but gingivitis remains, what is its classification?

A

gingivitis: non-biofilm induced

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21
Q

if inflammation crosses the mucogingival junction, is it more likely to be plaque or non-biofilm induced gingivitis

A

non-biofilm induced

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22
Q

what can cause non-biofilm induced gingivitis

A

burns (white patches) cause inflammation therefor gingivitis

herpes simplex causes gingivitis

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23
Q

what are manifestations of herpes simplex

A

large red swollen gingiva
Acute herpatic gingivostomatis
Coldsores

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24
Q

what sub-classifications can we find within ‘periodontitis’

A

necrotising periodontal disease
periodontitis
periodontitis as a manifestation of systemic disease

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25
Q

explain the difference between necrotising gingivits, necrotising periodontitis and necrotisisng stomatis

A

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

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26
Q

after RSD/PMPR what should we make the patient aware of and why

A

their gums may seem to recede
removing the irritation factor leads to reduced inflammation
reduced swelling so seems to receed

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27
Q

what are some diseases/syndromes that would be classified as ‘periodontal disease as a result of systemic disease’

A

downs syndrome
Papillon-Lefèvre syndrome
Ehlers-Danlos syndrome types IV and VIII

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28
Q

what are some symptoms of Ehlers-Danlos syndrome types IV and VIII

A

Periodontal disease as a result of systemic disease
hyperflexibility of joints/skin
Increased bleeding and bruising
Hyperextensible skin
Underlying molecular abnormality of collagen

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29
Q

what are some manifestations of Papillon-Lefèvre syndrome

A

Palmoplantar hyperkeratosis
Affects primary and secondary dentition
Normal dental development until hyperkeratosis of palms and soles appears
Mechanism poorly understood

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30
Q

what term replaces excessive occlusal force? and what does this include

A

traumatic occlusal force

any traumatic force leading to tooth loss/fracture

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31
Q

what is classes as ‘peri-implant health’

A

no swollen or bleeding gums

no erythema

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32
Q

for peri-implant health, can a patient have large pocket depths?

A

yes as long as they are no larger than previous examinations and aslong as the gingiva have no bleeding or erythmia

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33
Q

what is and what causes peri-implant mucositis

A

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

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34
Q

what is peri-implantitis

A

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

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35
Q

what are risk factors of peri-implantitis

A

poor oral hygiene control
past history of periodontitis
osteoporosis
smoking

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36
Q

how does smoking affect the gingiva

A

decreases inflammatory reaction (allowing infection)
dysplasia
reduced bleeding

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37
Q

if a patient scores 3’s on BPE what do we do?

A

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

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38
Q

if a patient has a 4 on BPE what do we do?

A

take radiographs

perform 6PPC in all sextants

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39
Q

which BPE scores do we take radiographs for and why

A

3 or above

diagnose caries and to grade/stage periodontitis

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40
Q

what is the procedure after 6PPC

A

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

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41
Q

if a 6PPC is done, what classifications of periodontitis can be found and what do we do after this

A

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

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42
Q

which tooth is most likely to get caries

A

maxillary first molar, U6

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43
Q

how do we grade and stage teeth

A

take periapical and look at bone % loss

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44
Q

what does the stage of periodontitis tell us

A

how much bone loss a patient has had - severity of disease

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45
Q

what does the grade of periodontitis tell us and how do we find it

A

progression rate of disease

divide ~%bone loss by age using worst site of bone loss

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46
Q

what is stage I periodontitis

A

less than 2mm bone loss or <15%

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47
Q

what is stage II periodontitis

A

bone loss entered coronal 1/3 of root

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48
Q

what is stage III periodontitis

A

bone loss entered mid third of root

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49
Q

what is stage IV periodontitis

A

bone loss entered apical 1/3 of root

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50
Q

what is grade A periodontitis

A

~% bone loss / age < 0.5 slow

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51
Q

what is grade B periodontitis

A

~% bone loss / age = 0.5-1

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52
Q

what is grade C periodontitis?

A

~% bone loss / age > 1

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53
Q

what is ‘currently stable’ periodontitis

A

<10% BoP
pockets <= 4mm
no bleeding at 4mm sites

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54
Q

what is ‘currently in remission’ periodontitis

A

BoP > =10% BoP
pockets <=4mm
no BoP at 4mm sites

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55
Q

what is ‘currently unstable’ periodontitis

A

pockets >= 5mm
OR
pockets >4mm AND BoP

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56
Q

what must we write in a periodontal diagnosis

A

type of periodontitis, stage, grade, current state of stability, risk factors

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57
Q

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

A 
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
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58
Q

why does stress affect the oral cavity

A

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

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59
Q

What is periodontal treatment? and what are the 4 stages

A

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
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60
Q

what are clinical goals of periodontal disease treatment

A 
No progression
Reduction in probing depths
No probing depths > 5mm
No BoP
No smoking
Plaque score < 20% of surfaces
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61
Q

what is the most important factor controlling prognosis of periodontal treatment

A

stopping smoking

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62
Q

how does stress alter gingival heath

A

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

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63
Q

what are risk factors of periodontal disease

A 
smoking
stress
previous periodontal disease
diet
systemic diseases e.g. diabetes mellitus
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64
Q

what mineral other than fluoride can aid gingival health and calculus formation?

A

Phosphates
Calcium
zinc systems

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65
Q

what is the evidence behind floss and interdental brushes and what should be advised

A

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

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66
Q

what are the effects of PMPR (with good OHI) after 6 months

A

reduced BoP
reduced pocket depth
reduced plaque score

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67
Q

after PMPR what must be done

A

review oral health at 1 month

review periodontal health (6PPC) at 3 months and 6 months

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68
Q

what are some side effects of PMPR which must be explained to patient

A 
possible recession (of swollen gums)
sensitivity due to root becoming exposed
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69
Q

can periodontal disease be cured

A

no, it can be stopped but OH is needed to prevent further loss

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70
Q

what may affect BoP score

A

smoking due to vasoconstriction

recently quit smoking leads to bleeding gums

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71
Q

what are limitations doing a 6PPC

A

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

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72
Q

are antibiotics needed for periodontal treatment

A

rarely

treatment involves removal of stimulus of inflammation can be done via good OHI and PMPR

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73
Q

when do we use antibiotics in periodontal treatment and who recommends this

A

BSP - British society of periodontology recommends

severe rapidly progressing forms of the disease e.g. necrotising forms of periodontal disease or abscesses.

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74
Q

what systemic and topical antimicrobials can be used to treat rapidly progressing severe periodontitis/gingivitis and what considerations must we make

A

topical chlorhexidine mouthwash - stains teeth over time

amoxicillin 500mg TDS for 7 days - check interactions in BNF

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75
Q

what forms of chlorhexidine are there

A

solution mouthwash

CHX chips placed between teeth

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76
Q

when do we use CHX chips

A

Localized periodontitis with few sites
if there is a poor response to debridement
deep sites on maintenance patients or under repeat applications.

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77
Q

what is periodontal surgery and when is it undertaken

A

done when unresponsive to PMPR and any other treatment

flap surgery/gingivectomy to create accessibility for instrumentation of teeth

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78
Q

what should be involved with periodontal treatment reviews?

A 
OHI reinforcement
PMPR supragingival
localised subgingival PMPR
medical history and smoking update
full peiro charting and review
assessment of prosthodontics
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79
Q

what grade of mobility do we extract teeth and when do we try to avoid extraction

A

grade III
avoid if risk of MRONJ (bisphosphonates for cancer or + cortisteroids) or if high risk of bleed with blood thinners, haemophilia or warfarin

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80
Q

if the patient is not engaging with OHI what do we do

A

go back to step 1 of OHI - do not give further treatment until they are cooperating

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81
Q

how do we differentiate an engaging and non-engaging patient

A

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
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82
Q

what is step 2 of the BSP flowchart and what do we do after this

A

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

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83
Q

if patient is unstable after step 2 of BSP flowchart, what do we do

A

step 3
re-iterate OHI instruction, behavioural change
re-preform PMPR subgingival
pockets >6
possible referral to periodontal surgeon or regenerative surgeon

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84
Q

if patient is stable after step 2 on BSP flowchart, what do we do

A 
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
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85
Q

is PMPR or self plaque removal more important

A

self removal

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86
Q

How can we prevent pulp treatment (3)

A
  • maintenance of crown and pulpal health, preventing caries
  • wear mouth guards to prevent trauma and fractures
  • minimise impact of therapeutic interventions e.g. fillings
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87
Q

why is it better to preserve a tooth than let it rot?

A
  • 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
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88
Q

if a tooth becomes necrotic, what can this lead to?

A
  • no sensibility means no proprioception so excess force on tooth leads to fracture
  • pulpitis
  • periapical pathology like granuloma
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89
Q

even with the most optimistic studies, what is the highest rate of compliance with recommended tooth brushing technique

A

50%

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90
Q

what factors affect compliance

A 
Patient factors - disability
Disease - increased difficulty may feel hopeless
Treatment - bad treatment
Operator - bad communication
Support System
Facilities
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91
Q

what three types of patient can we have relating to motivation

A

already motivated
latent motivator - need trigger
unmotivated

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92
Q

what are the barriers to communication

A 
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
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93
Q

what is the correct tooth brushing technique

A

modified bass technique

small circular motions on each tooth surface applying moderate pressure, going into the gum line

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94
Q

what brush should be o the end of a manual toothrbush

A

medium nylon brush

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95
Q

is manual or electric toothbrushing better in the long/short term? how do we know

A

electric

2014 Cochrane review level 1 evidence

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96
Q

what should we consider when giving advise on OH with a difficult patient

A

give few instructions at a time (just toothbrushing to start)
explain reasoning
don’t repeatedly state it as this an reduce motivation

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97
Q

how wide is healthy periodontal ligament space around the apex?

A

0.2-0.3mm

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98
Q

what is the difference in outcome of chronic and acute periapical periodontitis

A

chronic: periapical granuloma –> periapical cyst
acute: periapical abscess

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99
Q

what is an abscess and when does it occur within periodontal disease

A

acute inflammation
accumulation of pus - neutrophils, dead necrotic tissue and liquified bacteria
can occur at any point

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100
Q

what is a periapical granuloma

A

main chronic inflammatory lesion that develops in the periapical tissues after necrotic pulp
fibrovascular tissue that accumulates at apex
<1cm diameter, not corticated

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101
Q

when will a periapical cyst form

A

if there is a periapical granuloma and epithelium is present, the epithelium will surround the granuloma and possibly corticate - more than 1cm diameter

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102
Q

what are the 3 consequences of long standing apical periodontitis

A

radicular cyst (after granuloma)
osteomyelitis
root resorption

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103
Q

what is plaque and what is its general composition

A

bacterial biofilm that forms on soft/hard tissue surface
30% ECM - enzymes, epithelial cells, immune cells, LPS, lipids, carbohydrates
70% microbes

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104
Q

what is the acquired pellicle

A

colorless acellular bacteria-free film composed of salivary glycoproteins, deposited on the teeth within minutes after eruption or cleaning.

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105
Q

what is the first stage of plaque formation

A

bacteria, macromolecules (amino acids, carbohydrates) and salivary products stick to the acquired pellicle via van der Waals forces in reversible reactions and attachments

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106
Q

within the first 4 hours of plaque what is the percentage of gram positive bacteria

A

90%

cocci and rods

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107
Q

when does plaque become clinically visible and what will its initial percentage of streptococci and anaerobes be

A

24 hours after initial attachment
~45% strep
~ 90% anaerobes

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108
Q

give an example of a secondary colonizer and what type of adhesion is this

A

fusobacterium

irreversible adherence

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109
Q

what are the steps of plaque formation

A

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

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110
Q

as plaque matures, what happens to the bacterial colony

A

number of anaerobic gram negative bacteria increase
ECM matures and becomes protective
possibly calcify to form calculus
virulent factors released

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111
Q

where does subgingival plaque get nutrients from and why

A

crevicular fluid
no oxygen
anaerobic bacteria

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112
Q

how does plaque cause pathology

A

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)

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113
Q

how do we detect calculus

A

with a WHO probe, curette or bitewings

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114
Q

what is the composition of calculus

A

80% inorganic mineralized tissue

20% organic material e.g. lipids, proteins, carbs

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115
Q

how is calculus attached to the tooth

A

via pellicle
ionic attractions between crystals of calculus and dentine/enamel/cementum
micromechanical interactions

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116
Q

what is the CO2 hypothesis of calculus formation

A

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

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117
Q

which inflammatory factors cause bone resorption and so can be inhibited in periodontal medication

A

IL-1a and IL-6
PGE2 fibroblasts
RANKL

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118
Q

how do we advise use of TP brush

A

use for large interproximal area
get correct size
dip in toothpaste and burhs within gap in and out 3 times

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119
Q

which areas of the tooth have 1,2,3 place in caries prelevence

A

1: pits and fissures of posterior teeth
2: under contact point of incisors
3: cervical area

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120
Q

what bacteria are common in caries

A

Strep. Mutans

Lactobacilli

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121
Q

what salivary rate is included as a risk factor for caries

A

<1ml/min

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122
Q

what allergern is in many flouride varnishes/toothpastes and who does this affect

A

colophony

asthmatics or people with allergens to plasters

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123
Q

what dental varnish can be used on someone with asthma

A

flourimax

not duraphat as this has colophony

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124
Q

how do we clinically find caries

A

good lighting
dry surfaces with 3 in 1
blunt ended probe - do not apply pressure, just see if rough/shiny surface

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125
Q

what is the difference between infected and affected areas

A

infected contains demineralization, bacteria, acid and non-repairable collgen damage
affected area contains demineralization and acid - no bacteria, partial collagen damage

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126
Q

what are affects of caries on daily life

A 
bad breath
pain
loss of teeth
time off work/school
loss of sleep
reduced confidence
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127
Q

how do we know something is wrong with our childhood caries prevention system

A

25% increase in caries in children in the past 10 years

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128
Q

what is ICDAS

A

International caries detection and assessment system

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129
Q

what extra tools can we use to find caries

A

Foti - transillumination

Laser fluorescence detects fluorescence off of bacteria

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130
Q

how can we score a tooth’s carious lesion and give the scores

A 
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
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131
Q

are carious lesions always removed

A 
no
not necessarily active (can be arrested)
Not for hall technique 
Not for low.prognosis 
Not for near exfoliation
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132
Q

how do we test if a lesion is arrested or active

A

use probe to test if it is smooth or not smooth

take into account past history, diet and habits

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133
Q

how much tooth paste do we provide for children

A

smear for 0-3 up to 1000ppm flouride

pea sized amount for 3+over 1000ppm flouride

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134
Q

what is xylitol

A

stops metabolism of strep. Mutans - major carious bacteria
found in sugar free chewing gum
natural sweetner

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135
Q

why is sugar free chewing gum good for prevention

A

increases salivation

contains xylitol which inhibits metabolism of Strep. Mutans

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136
Q

what product turns carious lesions black and arrests them

A

Riva star

Silver Diamine flouride

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137
Q

what is Keye’s Triad

A

Venn diagram of 3 things necessary for tooth decay:

  • cariogenic food - carbohydrates, diet
  • bacteria
  • tooth
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138
Q

when do white spot lesions go dark

A

when they reach dentine which scleroses and turns black
or when stained e.g. coffee/smoking
Remineralized
Riva star silver diamine fluoride placement

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139
Q

describe infected tooth tissue

A 
high mineral loss
necortic tissue
bacteria present
collagen matrix breakdown
soft tissue
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140
Q

describe affected tooth tissue

A

collagen matrix still not damaged enough to remove
less bacteria
mineral loss and demineralization

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141
Q

what is CPP-APC

A

milk product containing calcium and phosphates increasing mineralization for people with low calcium phosphate saliva levels

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142
Q

what are the 3 aims of caries removal

A

remove plaque and bacteria
protect pulp and vitality of tooth and arrest the caries
restore function

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143
Q

when and what is step wise caries removal used

A

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

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144
Q

in all methods of caries removal, what is constant in aims

A

all infected tooth tissue removed

clear, un-infected ADJ

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145
Q

what is class I caries

A

caries in occlusal/fissure pattern of cingulum cusp

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146
Q

what is class II caries

A

proximal caries of posterior teeth

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147
Q

what is Class III caries

A

proximal caries of anterior teeth

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148
Q

what is class IV caries

A

incisal edge caries

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149
Q

what is class V caries

A

smooth surface caries, can be near gingival margin

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150
Q

What is the structure of a carious lesion involving zones

A

Surface zone - pellicle
Body of lesion - infected, bacteria
Dark zone - active bacterial invasion
Translucent zone - demineralization affected

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151
Q

What is the translucent zone

A

Advanced surface of lesion

Not infected but affected

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152
Q

What is the dark zone

A

Where demineralization is in progress in between the body of lesion and translucent zone

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153
Q

What is the body of the carious lesion

A

Where the dead necrotic tissue lies with bacteria, bulk of cavity

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154
Q

What percentage of plaque is bacteria

A

70%

Rest is bacterial ECM and proteins

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155
Q

how do we use transillumination

A

use mirror to reflect light

carious areas absorb more light and appear shadowed

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156
Q

what can we use instead of transillumination in posterior teeth

A

FOTI fibre optic transillumination

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157
Q

how does resistance/impedence change in carious tooth

A

sound enamel is very resistant (DC) and very impendent (AC)

carious enamel is less resistant and less impedent

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158
Q

how do we use DC to detect caries and what are its flaws

A

Electronic Conductance Monitor uses single AC current to detect caries
technique sensative
depends on ions in saliva

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159
Q

how can we compare large populations on caries (2 methods of gradoing caries)

A

ICDAS or DMFT

international caries detection and assessment system and decay missing filled teeth

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160
Q

why is DMFT less useful in older age

A

DMFT is cumulative

less representative of oral health

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161
Q

why is DMFT not the best way of assessing oral hygeine

A

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

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162
Q

why is DMFT useful

A

finding trends between OH and other factors e.g. fluoridated water, socioeconomic status etc

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163
Q

which caries assessment is better for population studied and individual assessments

A

DMFT for population

ICDAS for personal assessment

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164
Q

how do we take a DMFT score

A

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
Q

what is gingivitis split into (phases)

A

early stage gingivitis (1st week)

chronic marginal gingivitis (3rd week) can stay in this stage for a long time

166
Q

what is ‘early gingivitis’ and what occurs

A

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
Q

what is GCF and what does it contain

A

gingival crevicular fluid
exudate released from periodontal tissues to counteract bacterial plaque
inflammatory mediators, antibodies and neutrophils

168
Q

how does a pseudo pocket form

A

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
Q

what occurs in the second week of early gingivitis

A

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
Q

what are symptoms of early gingivits

A

swollen gums that bleed on probing
loss of stippling and loss of knife edge margins
red due to vasodilation

171
Q

compare early gingivitis to chronic marginal gingivitis

A

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
Q

give 1 clinical and 1 biological disadvantage of swollen pockets

A 
clinical = pseudo pockets may be mistaken for real pockets leading to incorrect diagnosis
biological = create habitat for plaque and bacteria to further infection
173
Q

what follows chronic marginal gingivitis nd describe its characteristics

A

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
Q

what is the regularity of destructive periodontitis

A

occurs in bursts

175
Q

compare early gingivitis to destructive periodontitis

A

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
Q

how do we treat early and chronic gingivitis

A

PMPR, good OHI, possible mouthwash, fluoride,

177
Q

what differentiates RSD from PMPR

A

root surface debridement removes plaque and biofilm form root surface subgingival
PMPR is mostly supragingival on the crown enamel surface

178
Q

what is the purpose of RSD

A

removal of the stimulus of inflammation from the root surface in treatment for periodontitis

179
Q

what occurs after successful RSD with good OHI

A

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
Q

what is the leading cause for loss of teeth and why

A

age
cumulative disease and failed restorations
medications

181
Q

after RSD, what happens to pocket depth and why

A

reduces
mainly reduced swelling and oedema
re-attachment of 15-20% of PDL to cementum but NOT sharpeys fibres reattachment

182
Q

why do we only get 15-20% long epithelial growth post RSD

A

oral mucosal tissue grows much faster than JE tissue
proliferates down the sulcus to meet JE
contact epithelium stops growth

183
Q

at what age do children have most plaque and why

A

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
Q

whhy might a child with amelogenesis imperfecta have a lot of calculus

A

acts as an insulator on very soft, sensitive enamel and dentine

185
Q

if a child has extreme calculus build up, why might this be

A

amelogenesis imperfecta to insulate teeth

fed via gastronomy so reduced saliva and scared to brush teeth as no cough reflex

186
Q

which side of the mouth usually has more caries and why

A

RHS

most people right handed so brush left hand side better

187
Q

at what ages to we start BPE and modified BPE

A

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
Q

what is the most common dental problem with childrens teeth and why

A 
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
Q

what can we provide for autistic/downs syndrome children

A

Oro-Nurse

tooth paste with no taste as the sensation is sometimes not liked by children with learning difficulties

190
Q

what is localised gingival recession and what is its incidence in children

A

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
Q

what is gingival hyperplasia and what commonly causes it

A

overgrowth (too many cells) of gingiva

mainly drug induced - cyclosporins (immunosupressant), Phenytoin (anti-epeleptic)

192
Q

what affect does OH have on drug induced hyperplasia

A

good oral hygeine keeps it the same, no reduction

poor oral hygeine makes it grow larger

193
Q

how do we reduce drug induced gingival hyperplasia

A

change drugs

194
Q

what percent of patients on ciclosporins get gingival hyperplasia

A

30%

195
Q

what types of disease can cause systematic disease gingival hyperplasia (2)

A 
sarcoid (simialr to TB affecting whole body)
cyclic neutropenia (comprimised white blood cells)
196
Q

what types of gingival hyperplasia are there and what are there causes

A

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
Q

is drug induced or systematic disease induced gingival hyperplasia usually more severe

A

drug induced

198
Q

what types of self inflicted gingival trauma are there

A

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
Q

if a patient bites fingernails and causes gingival dmaaged, what is this diagnosis

A

type B self inflicted trauma

200
Q

if a patient pokes their gums with a pencil what is this diagnosed as

A

Type C self inflicted gingival trauma

201
Q

what is acute herpatic gingivostomatitis

A

herpatic (viral) gingvo (gingival tissue) stomatitis (mouth and lips)
oral manifestation of Herpes simplex virus I

202
Q

what are some oral manifestations of acute herpetic gingivostomatitis

A 
high temperature
high salivation
small ulcerations tongue
sore throat, lips, tongue, gingiva 
wanting to eat
203
Q

how long will acute herpetic gingivostomatitis last

A

roughly 10 days unless immunocompromised where antivirals are needed

204
Q

how do we treat acute herpetic gingivostomatitis (6)

A 
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
Q

what is necrotizing ulcerative gingivitis, what is the cause and who is more prone to this disease

A

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
Q

what is the treatment necrotizing ulcerative gingivitis

A

good oral hygiene and antibiotics

207
Q

what happens to untreated necrotizing ulcerative gingivitis

A

can spread to oral tissues like the lips and cheek

208
Q

what is herpangina, symptoms and cause

A

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
Q

what is hand foot and mouth disease

A

combination of herpangina (sores in back of mouth) and also on palms of feet and hands

210
Q

how do we treat herpangina and hand, foot and mouth disease

A 
drink lots of water
isolate as very contagious
possible antivirals if immunocompromised
pain relief
healthy, soft diet e.g. yogurt, Weetabix, milk
211
Q

a pt has itchy feet, loose teeth and poor prognosis. what are they likely to have and what is likely treatment

A

Papillion- Lefever syndrome
hyperkeratinisation of palms of hands and soles of feet
likely need to remove all teeth

212
Q

a child has sores on the back of their throat, what are some differential diagnosis and what investigations should we do

A 
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
Q

young pt has loss of gingival tissue, seemingly dead tissue. what is the diagnosis and how do we treat

A

necrotising ulcerative gingivitis
attack the causes e.g. smoking, poor OH
provide antibiotics

214
Q

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

A

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
Q

what are the ways of classifying pulpal disease

A 
acute
chronic
reversible
irreversible
open 
closed
symptomatic
asymptomatic
216
Q

what causes acute open pulpitis

A

fracture into pulp

217
Q

what causes acute closed pulpitis

A

trauma

218
Q

what causes chronic closed pulpitis

A

caries

219
Q

what causes chronic open pulpitis

A

grossly cavitated caries

220
Q

which teeth are most likely to get pulpitis due to caries

A

upper lateral incisors

infolding of enamel organ near cingulum is very plaque retentive for caries

221
Q

what is a bacteremia and how is this relevent to dentistry

A

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
Q

what type of trauma can cause acute pulpitis (5)

A

heat -physcial
direct blow - physical
filling materials can irritate pulp chamber - chemical
cavity prep can enter pulp - mechanical

223
Q

what are general symptoms of pulpitis

A

‘toothe ache’
radiating pain, localised sharp pain
radiates across jaw

224
Q

what must we classify pulpitis as when diagnosing

A

reversible symptomatic
irreversible symptomatic
irreversible asymptomatic

225
Q

with an established dentine lesion, what occurs in the pulp

A

odontoblasts die preventing laying down of reactionary dentine
vasodilation
recruitment of neutrophils
inflammatory exudate near site

226
Q

why does pulpitis lead to necrosis

A

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
Q

what is the effect of pulpal necrosis

A

more inflammatory cells and exudate and chronic inflammatory cells
pulpal abscess - exudate, dead cells, neutrophils, bacteria

228
Q

what may happen to a pulpal abscess

A

may drain into oral cavity

if closed, will build pressure and pain and spread around tooth and to periapex –> periapical pathology

229
Q

what is and what causes chronic hyperplastic pulpitis

A

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
Q

what are pulp stones and what types can we get

A

small parts of mineralized tooth tissue, sometimes dentine that grow with age
true pulp stones - dentine
false pulp stones - amorphous calcified material

231
Q

what would be found in a pulpal abscess

A 
dead tissue including odontoblasts and tooth tissue
bacteria
neutrophils and other inflammatory cells
exudate 
'pus'
232
Q

what salivary components help defend against bacteria

A

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
Q

what is the epitheliums role in protecting the oral cavity from microbes (3)

A

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
Q

how can bacteria use GCF for themself

A

metabolize some components

235
Q

what are the antimicrobial components of GCF

A

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
Q

what are neutrophils function in GCF

A

phagocytose free bacteria near gingiva
release hydrogen peroxide and NETs to destroy attached bacteria
release cytokines to get a greater inflammatory response

237
Q

what are some affects of cyclic neutropenia (2)

A

increased risk of periodontitis and destruction

increased risk of systemic disease causing gingival hyperplasia

238
Q

what are the functions of macrophages

A

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
Q

what is the role of dendritic cells and where are they found

A

found in epithelium

detect, phagocytose and antigen present to lymphatic system for humoral response

240
Q

what are some functions of antibodies

A

act as opsins to increase phagocytosis
neutralize toxins
prevent bacterial attachment
activate complement for inflammatory response and MAC

241
Q

what cause most destruction during infection

A

host cells reducing inflammation

242
Q

what are some negative effects of IL-1b and TNFa and what secretes them

A

they stimulate soft tissue and bone loss leading to periodontitis
macrophages

243
Q

which inflammatory mediators mainly lead to tissue loss and what secretes them

A

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
Q

what do neutrophils release that cause soft tissue loss and what stimulates this

A

MMP8 stimulated by IL-1b and TNFa secreted by macrophages

245
Q

what do fibroblasts release that leads to bone loss and what causes this

A

PGE2 stimulated by IL-1b and TNFa secreted by macrophages

246
Q

what are some inflammatory mediators that lead to soft tissue loss

A

neutrophils - MMP-8

macrophages - IL1b and TNFa

247
Q

how do macrophages lead to soft tissue loss

A

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
Q

how do macrophages lead to bone loss

A

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
Q

what negative affect does RNAKL have on the body and what causes its secreton

A

stimulates osteoclasogenesis
bone resorption
triggered by IL-1b
IL-1b and RANKL secreted by macrophages during inflammation

250
Q

how do we get bone and tissue loss during infecton

A

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
Q

what causes necrotising gingivitis

A

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
Q

what is leukoplakia and why are they relevent

A

white lesion in mouth

keep under strong watch - premalignancy

253
Q

what is erthyroplakia and why are they relevent

A

red lesion in mouth

keep under watch –> premalignnacy

254
Q

what is a sign and symptom

A

sign is something found by the clinician

symptom is something that the patient relays to the clinician

255
Q

what are some unfavourable characteristics of the pulp chamber

A

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
Q

what steps do we go through when trying to diagnose pulpal disease

A 
patient complaint
history of complaint
clinical investigations
special investigations for vitality, sensibility, periapical pathology 
radiographs
257
Q

what is a healthy response to a cold test

A

uncomfortable for a few seconds and wears off near to immediately

258
Q

what is pulpitis

A

inflammation of pulpal tissue

259
Q

why does pulpal inflammation hurt more with cold test

A

pulpal inflammation lowers nerve threshold due to inflammatory response + prostaglandins
nerves need less stimulus to cause action potential response

260
Q

what classes as reversible pulpitis and how do we treat

A

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
Q

what are key symptoms of irreversible pulpitis and how do we treat

A

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
Q

if we have bad pain that lingers and keeps us awake but cannot tell where the pain is coming from what is this

A

irreversible symptomatic pulpitis

has not yet reached apex so no periapical pathology

263
Q

why may irreversible pulpitis be asymptomatic

A

if nerve innervation ha been disrupted or no longer has blood supply, the tooth will not cause pain until preapical pathology occurs

264
Q

how might we diagnose asymptomatic irreversible pulpitis

A

clinical investigation of very large caries definitely in pulp
radiographic evidence of necrosis

265
Q

can closed pulpitis cause periapical pathology

A

no - as no bacteria are in the pulp

bacteria must be near the apex to cause periapical pathology

266
Q

how does pulp necrosis occur

A

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
Q

how do we diagnose necrosis of pulp and what are differential diagnosis of this

A

negative sensibility test

may also be down to thick enamel, calcification and tertiary dentine - especially in elderly

268
Q

how does periapical pathology occur

A

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
Q

what would it be called if bacteria formed a colony in the periapex and is this common

A

extra radicular infection

very uncommon as bacteria rarely leave the periapex as they would be killed

270
Q

how does bone loss occur from periapical pathology

A

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
Q

differentiate periapical, apical and peri radicular periodontitis

A 
periapical = around the apex
apical = at apex
peri-radicular = around root
272
Q

in periapical periodontal disease what does chronic and acute mean

A 
chronic = asymptomatic
acute = symptomatic
273
Q

how do we diagnose symptomatic acute periapical periodontitis

A

pt can LOCALISE pain on percussion test
tenderness to pressure
radiographic changes may or may not be visible

274
Q

how do we diagnose chronic asymptomatic periapical periodontitis

A

periapical radiolucency

low grade inflammation causing no pain

275
Q

how do we diagnose an acute periapical abscess and what is it (3)

A

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
Q

how do we diagnose a chronic periapical abscess

A

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
Q

how do we diagnose condensing osteitis and how likely is it

A

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
Q

when diagnosing periapical/pulpal disease what must we always include

A

state of both pulp and periapical, even if one is healthy e.g.
necrotic pulp, healthy periapical tissue

279
Q

what is the disease pathway of chronic and acute periapical inflammaiton

A

acute: abscess –> bacteraemia (fever, lymphadenopathy)
chronic: granuloma –> cyst

280
Q

where are some common dentoalveolar infection sites

A 
palatal abscess
vestibular abscess
periapical abscess
periodontal abscess
all around infected tooth
281
Q

why are abscesses dangerous

A

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
Q

what is osteomalacia and relate to dentistry

A

reduced bone remineralization

leads to pseudo fractures held together by bone matrix

283
Q

with a BPE of 3 and radiographs showing some bone loss, what can we put in the diagnosis

A

periodontal disease

cannot determine grade, stage, severity and rate until 6PPC is done at 3 month review

284
Q

what are the 4 prognosis levels

A

good
fair
guarded
poor

285
Q

what questions do we ask to investigate periapical diagnosis

A

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
Q

when investigating a pain, what system do we go thorugh

A 
SOCRATES
site of pain
onset of pain
character of pain
radiation of pain
alleviating factors
time scale
exacerbating factors
scale of 1-10
287
Q

if we see a draining sinus (from an abscess) how do we determine its origin

A

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
Q

why do we investigate occlusion with toothache

A

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
Q

if there is an isolated pocket and radiographic evidence of a J shaped lesion surrounding root, what is the diagnosis and prognosis

A

vertical root fracture

poor prognosis, remove tooth

290
Q

what does mobility indicate

A

periodontal tissue loss and possibly bone loss

periapical pathology with fremitus raising out of socket OR periodontitis

291
Q

what different types of discolouration can teeth have

A

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
Q

why will a cold test only cause pain and no other sensaiton

A

only pain A delta fibres go near dentinal tubules

293
Q

what is the difference in disease progression between sharp and dull pain, explain

A

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
Q

define specificity and sensitivity of a test

A

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
Q

which sensibility tests have good sensitivity and specificity

A

cold test: good both
hot test : bad specify
EPT is good but cold test has higher sensitivity

296
Q

which tests test the pulp and which tests test the periapex

A

pulp : vitality and sensibility = cold, hot, EPT

periapical : percussion, pressure, palpation, tooth sloth,

297
Q

how do we test for a fracture (2)

A

tooth slooth - pressure on each cusp until pain

Transillumination can find cracks in teeth (with tooth slooth).

298
Q

how can we determine the symptomatic tooth (4)

A

anaesthetise individual teeth to see if pain remains
x-rays
GP if draining sinus
special tests

299
Q

when do we take an x-ray for diagnosis of periapical pathology

A

after all over tests have been done

300
Q

A patient has a painful, inflamed 3rd molar. What is procedure for this

A

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
Q

what occurs to dentine after it is infected histologically

A

forms liquefaction foci which join to form transverse clefts 90 degrees to dentinal tubules
bacteria, necrotic dentine and toxins

302
Q

why might a pulp chamber appear white histologically

A

necrotic pulp

no tissue - drained out either of sinus, open cavity or through apex into periapical tissue

303
Q

if we perforated the pulpal horn roof what would happen in healthy and inflamed scenario

A 
healthy = slight bleeding, very little
inflamed= heavy bleeding due to vasodilation
304
Q

what are neutrophils negative affect during pulpitis

A

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
Q

how can we treat dentinal sensativity (4)

A

restore over exposed dentine
alter ionic state of dentinal tubules
reduce permeability of tubules
demineralizing/desensitising toothpastes

306
Q

why do we get spontaneous pain in irreversible pulpitis

A

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
Q

what are symptoms of dry socket (4)

A

severe pain
Foul taste and smell
Localised inflammation and tenderness
partial/total loss of blood clot

308
Q

what are some differential diagnosis of dry socket

A

spetic socket - infection but no loss of blood clot
osteonecrosis - loss of jaw bone
osteomyelitis - infection of cancellous bone marrow

309
Q

what is osteomyelitis and how does it present and what can it lead to

A

infection of cancellous bone marrow
radiolucency’s in jaw, pain, swelling, altered sensation, pus
can lead to loss of portions of the jaw

310
Q

what is infection of the jaw causing necrosis

A

osteonecrosis of the jaw

311
Q

what is septic socket and how is this treated

A

infection of an extraction socket

treated with antibiotics (never used for dry socket)

312
Q

what is the main cause of dry socket and what can cause this

A 
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
Q

how can oestrogens affect the wound healing of a extraction socket

A

oestrogens lead to fibrinolysis breaking down fibrins in the blood clot leading to dry socket

314
Q

what is the incidence of dry socket and which teeth are more prone to dry socket

A

0.5-5% incidence
wisdom teeth have 1/5 or 1/6 incidence
lower wisdoms most prone being 25% prone to dry socket

315
Q

why are the lower molars more prone to dry socket (3)

A

denser bone
more traumatic extraction
more likely to get infected

316
Q

what patient factors lead to dry socket (4)

A

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
Q

how can we prevent dry socket

A

OHI to stop smoking and dont over use mouthwash

can pack with pre-emptive alvogyl

318
Q

what therapeutic management of dry socket is there

A

smoking cessation - preventative
appropriate mouth bathing in saline solution and pack with
alvogyl - antiseptic, analgesic, LA
analgesia

319
Q

what is alvogyl

A

therapeutic agent used to pack sockets (especially bleeding a lot) that acts as an antiseptic, analgesic and LA

320
Q

what are the symptoms of septic socket (3)

A

dry socket symptoms - pain, fowel smell,
Extraoral swelling
Lymphadenopathy
Formation of pus

321
Q

if a patient had granulation tissue covering a socket for over a week, what would we do? differential diagnosis?

A

take an x-ray to rule out residual bone

possibly delayed healing or squamous cell caricnoma

322
Q

who is likely to get osteomyelitis

A

immunocompromised or people on medications leading to infection after extraction

323
Q

which jaw is more likely to get osteomyelitis

A

mandible due to being more dense and having reduced vascularity and healing

324
Q

what can osteomyelitis be divided into

A

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
Q

what bacteria cause osteomyelitis

A

mainly Staphylococcus aureus found on skin and respiratory tract

326
Q

what are the histological presentations of ostemyelitis (4)

A

dead bone - necrotic bone (chronic)
neutrophil infiltration
lacunae without osteocytes
scalloping of bone where it has been lost

327
Q

what is osteoradionecrosis

A

necrosis of the jaw caused by radiation therapy before an extraction
destruction of bone cells reducing its vascularity and vitality

328
Q

what is the threshold of radiation grays between low and high risk of radio necrosis

A

65 grays

329
Q

how do we manage someone who has osteonecrosis

A

removal of parts of jaw until bone bleeds

330
Q

how do we prevent osteoradionecrosis

A

prevent need for extraction with good OH

remove teeth with poor prognosis before radiotherapy

331
Q

what is MRONJ and what was it formally know as, why has its name changed?

A

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
Q

what drugs lead to MRONJ

A

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
Q

what are the three criteria for MRONJ

A

no radiotherapy since extraction (as this can be osteoradionecrosis)
MRONJ related drug
bone exposed for 8 weeks or more

334
Q

what does MRONJ display as

A

green/yellow slough covering bone of extracted pocket
Loss of mucosa over bone
8 weeks after extraction
radiolucencies

335
Q

what stages of MRONJ do we have

A 
at risk
stage 0
stage 1
stage 2
stage 3
336
Q

what is stage 0 MRONJ and how do we manage

A

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
Q

what is stage 1 MRONJ and how do we manage it

A

at risk, exposed/necrotic bone, pain, no infection or inflammation.
treat with antibacterial mouthwash, monitor

338
Q

what is stage 2 MRONJ and how do we manage

A

exposed necrotic bone, pain, pus, inflammation, erythema

antibacterial mouthwash, antibiotics, pt management, pain control, debridement of necrotic bone?

339
Q

what is stage 3 MRONJ and how do we manage

A

exposed/necrotic bone, bone loss radiographically, extends below alveolar socket into mandible, pain, inflammation, pus, FRACTURE
manage with surgical removal of bone

340
Q

how does MRONJ occur because of bisphosphonates (3)

A

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
Q

How do we treat ORN and what would happen if we did this to an MRONJ patient

A

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
Q

at what MRONJ stage should we provide antibiotics? what should we provide before this

A

stage 2

CHX mouthwash weekly

343
Q

how do we prevent MRONJ

A

Avoid bisphosphonates
prevent need to extract teeth
12 month drug holiday

344
Q

which drugs cause dry socket to increase incidence (4)

A 
(anti-inflammatory drugs or vasoconstrictors)
Steroids 
Ciclosporins 
Methotrexate 
OCP oral contraceptive pill - osteogren
bisphosphonates
nicatine
345
Q

should we provide antibiotics for dry socket, septic socket or MRONJ?

A

dry socket = no
septic socket = yes
MRONJ = only if over stage 2

346
Q

what is the treatment for dry socket

A

gentle rinse with saline solution to remove debirs or bacteria and then dress socket with alvogyl - LA, anti-inflammatory and antiseptic

347
Q

why does smoking increase risk of dry socket

A

sucking on cigarette increases likelihood of blood clot dislodging

348
Q

what causes pneumatization of the MAS

A

movement of the air sinus lining down

ageing and lack of teeth

349
Q

what is exudate

A

fluid that passes out of blood vessels into tissues full of oxygen, proteins and other molecules - tissue fluid

350
Q

What bacteria would be found in the blood of a pt with infective endocarditis due to poor oral hygeiene AND IV drug use

A

IV drug use - staph. aureus

OH - strep. viridans

351
Q

what are the 2 likely paths of least resistance for an abscess of a maxillary molar

A

if apex of root is above buccinator = side of face

if apex is within buccinator = oral cavity

352
Q

what are the 23 likely paths of least resistance for an abscess of a mandibular molar

A

apex of root above mylohyoid = oral cavity

apex of root below mylohyoid = swelling in submandibular space and possibly cause pharyngeal obstructions

353
Q

which teeth are likely to cause airway obstructions, and why, during a periapical abscess

A

mandibular molars with the apex of root below the mylohyoid muscle
swelling goes into submandibular space
into pharynx

354
Q

if a swelling as small dimples, what is likely to happen

A

discharge into oral cavity

355
Q

when do we get a periapical granuloma

A

chronic (asymptomatic) periapical periodontitis

356
Q

why might a radicular cyst form

A

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
Q

if a cyst radiographically is undefined or defined, what does this tell us

A 
defined = chronic, established, no longer as inflamed
undefinied = still very inflamed and growing
358
Q

what are the 3 characteristics of a cyst

A

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
Q

which epithelium forms the lining of a radicular cyst

A

non-keratinized stratified squamous cell epithelium

360
Q

what are the crystal shaped white patches found in a cyst histologically

A

cholesterol clefts
when cells die their cholesterol is released and forms crystals of cholesterol
when taking a histological slide, the cholesterol dissolves

361
Q

what types of osteitis can we get from inflammation

A 
condensing or focal sclerosing osteitis (5%) - increased density
rarefying osteitis (95%) - decreased density
362
Q

what are some causes of hypercementosis

A

teeth that are in little function
e.g. teeth without opposition or impacted 8’s
inflammation and mobility can contribute
pagets disease

363
Q

what would we see on the roots of a patient with pagets disease

A

hypercementosis

364
Q

what is Ankylosis

A

obliteration of PDL between cementum and bone
cementum and bone fuse
causing strong attachments between bone and tooth, complicating extractions

365
Q

which teeth and what demographic are likely to be effected by cement-osseous dysplasia

A

30-50 year old black women

lower incisors

366
Q

what is cemento-osseous dysplasia

A

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
Q

what is florid cemento-osseous dysplasia

A

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
Q

which tooth is likely to experience a cementoblastoma

A

lower 6s

369
Q

what is a cementoblastoma

A

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
Q

if a cement blastoma is removed, what happens

A

will not reccur, benign

371
Q

which 3 bacteria are the main culprits for root caries

A

Actinomyces spp. (not present a lot in coronal caries)
Mutans streptococci
Lactobacilli

372
Q

compare coronal and root caries

A

root caries do not have white spot lesion phase - straight to brown spot
root caries have Actiomyes spp. bacteria, coronal do not

373
Q

how can we tell between an arrested and not-arrested carious lesion

A

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
Q

describe the progression of root caries

A

develops at CEJ
spreads around CEJ
deepens into the dentine

375
Q

what type of caries is not shown on radiographs

A

buccal/lingual/palatal root caries

occlusal caries

376
Q

how do we manage xerostomia causes caries

A 
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
Q

what are thee aims of a carious restoration

A

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
Q

what is attrition and what causes it

A

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
Q

what is abrasion and what causes it

A 
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
Q

what is erosion and what causes it

A

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
Q

which 2 TSL components usually come paired

A

erosion and attrition

382
Q

how cna we tell if a TSL is caused by erosion

A

helix around crown exposing dentine

smooth , shiny surface

383
Q

what are 4 ways to get TSL

A

erosion
attrition
abrasion
trauma

384
Q

which demographc are most likely to get traumatic TSL

A

8-10 year old boys

385
Q

how can we diagnose what is causing TSL

A 
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
Q

explain the difference in appearance between dentinogenesis and amelogenesis imperfecta

A 
dentinogenesis = glossy, trnasparent dentine
amelogenesis = pitted, white, opaque enamel
387
Q

what are the main components of a granuloma

A 
marcophages (destruction)
fibroblasts (reconstructive)
endothelial cells (angiogenesis)
other immune cells like neutrophils
388
Q

what is an ‘engorged’ lumen

A

dilated and full e.g. the blood vessel was engorged of blood cells

389
Q

which cells are involved in acute inflammation and compare their structure

A

neutrophils and macrophages
both phagocytose
neutrophils are small trinucleated cells
macrophages are large cells with a foamy appearance

390
Q

what ae the chronic inflammatory cells and describe their function and structure

A

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
Q

give three characteristics of a plasma cell

A

eccentric nucleus
1 nucleus
clock faced shaped chromatin
lots of cytoplasm

392
Q

what are craze lines

A

fracture lines caused by bruxism, biting nails

393
Q

what type of fractures of teeth can we get

A 
complicated involving the pulp
non-complicated
enamel
enamel dentine
crown root
crwon
enamel infarction (certical not thorugh and through)
393
Q

what type of fractures of teeth can we get

A 
complicated involving the pulp
non-complicated
enamel
enamel dentine
crown root
crwon
enamel infarction (certical not thorugh and through)
394
Q

what is labial luxation

A

tooth moves up near the lips

395
Q

what is lateral luxation

A

tooth mobile side to side

396
Q

what is tooth extrusion

A

tooth can come partially out of socket

397
Q

what is tooth avulsion

A

tooth comes fully out of socket

398
Q

what is intrusion

A

tooth is pushed into alveolar socket

399
Q

recommended techniques for detecting caries

A

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
Q

what is an acute abscess

A

no sinus, swelling, very painful

401
Q

what is a symptomatic abscess

A

no sinus but painful

402
Q

what is a chronic abscess

A

with sinus and no pain

403
Q

what is an asymptomatic abscess

A

no pain., no sinus, find radiographically

404
Q

how can we prevent caries in a patient

A

stimulate salivation e.g. chewing gum
good OHI
fluoride regimes
removal of risk factors e.g. smoking, partial dentures

405
Q

what percent of healthy adults does root caries effect

A

20-40%

406
Q

Compare predisposing and precipitating factors

A 
Predisposing = increases risk 
Precepitating = increases incidence after risk is involved
407
Q

Give 5 dental characteristics of dentinogenesis imperfecta

A 
Short roots
Slender roots
Large crowns
Lacking enamel
Absence root canals and pulp chambers

BDS 2 (13 decks)

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