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paeds Flashcards

1
Q

what are Piaget’s four stages of cognitive development?

A

<2yo sensorimotor
2-7yo preoperational
7-11yo concrete operational
≥12yo formal operational

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2
Q

why is it recommended that toothbrushing is done by parents until at least 7yo?

A

≤6yo = likely to miss areas and swallow large amounts of toothpastes

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3
Q

what percentage of school children are afraid of the dentist and what consequences does this have?

A

16%
avoid attending = deterioration of oral health
often need more complicated and traumatic treatment

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4
Q

what are the three most significant risk factors in the development of dental anxiety in children?

A
  • new carious lesions
  • toothache
  • extractions
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5
Q

give some of the manifestations of dental anxiety in children (~6)

A
  • thumb sucking, nail biting, nose picking
  • clumsiness, stuttering
  • needing to go to the toilet, stomach pain
  • headache, dizziness
  • fidgeting, clinging to parent, hiding
  • silence
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6
Q

what is behaviour contagion and how could this affect a child’s dental anxiety?

A
  • “tendency of a person to copy certain behaviours of others around them”
  • enhances a child’s anxiety (copying parents/family)
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7
Q

when does a parent’s presence help the child in a dental appointment?

A

<5yo behave better with parent present (separation anxiety)

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8
Q

when would you exclude the parent from a dental appointment?

A
  • competing with dentist for child’s attention
  • unintentionally conveying their own anxieties to the child (verbal or non-verbal)
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9
Q

what are the different components of communication and their relative importance?

A
  • verbal communication 5% - language used
  • paralinguistic communication 30% - tone, loudness, pitch
  • non-verbal communication 65% - behaviour and environment
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10
Q

how might you adjust your verbal communication when speaking to a child?

A
  • avoid jargon and specific terms that the pt may not understand
  • avoid emotive language
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11
Q

how might you adjust your paralinguistic communication when speaking to a child?

A

commands given in a loud voice are better received by children

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12
Q

describe the epidemiology of dental trauma in children (demographic, type)

A
  • males
  • peaks at 2-4yo (walking) and 8-10yo (sports)
  • more in primary teeth than permanent, especially maxillary central incisors
  • crown fractures most commonly
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13
Q

risk factors for dental trauma in children (6)

A
  • activities and environment more important than gender or age
  • hyperactivity
  • poor motor coordination
  • increased OJ (>5mm) and incompetent lips
  • anterior open bite
  • epilepsy
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14
Q

what needs to be included when taking the history of dental trauma in a child? (6)

A
  • where, when and how?
  • attending with?
  • loss of consciousness (A&E)
  • previous TDIs
  • all tooth fragments accounted for?
  • NAI - any other injuries, does story match between adult and child, any delays?
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15
Q

describe the EO examination for paediatric dental trauma (3)

A
  • clean face and oral cavity with saline/water
  • looking for lacerations, tooth fragments
  • exclude facial fractures by palpating facial skeleton and mandible, step deformities, difficulties opening/closing
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16
Q

what is a degloving injury?

A

traumatic injury where the entire gingiva/alveolar mucosa is separated from the underlying bone

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17
Q

what radiographs may you take following paediatric dental trauma and why? (5)

A
  • PA = open/closed apex, detect root fracture
  • USO = parallax with PA, detect root fracture
  • DPT = developing dentition, facial fractures
  • soft tissue radiograph (30-50% exposure) = tooth fragments
  • lateral skull = relationship of teeth to successors
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18
Q

what things may be included in the trauma stamp? (up to 7)

A
  • colour
  • mobility
  • sinus
  • TTP
  • percussion
  • ethyl chloride (unreliable in primary teeth)
  • EPT (unreliable in primary teeth)
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19
Q

how many clinical and radiographic signs do you need before starting endo tx following trauma?

A

at least 3

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20
Q

define a splint (tooth)

A

rigid or flexible device/compound used to support, protect or immobilise teeth that have been loosened/replanted/fractured/subjected to certain endodontic/surgical procedures

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21
Q

what are the different materials that can be used for splinting teeth? (5)

A
  • composite/wire
  • acrylic ProTemp splint
  • soft mouthguard (eg if no teeth to place splint)
  • brackets/orthodontic wire (lengthy splinting)
  • titanium trauma splint (TTS)
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22
Q

what is the difference between rigid and flexible splinting and which is preferred?

A
  • rigid splint = completely immobilises tooth (≥2 teeth either side, thicker wire), increased risk of ankylosis
  • flexible splint preferred = allows some functional movement of teeth (usually 1 tooth either side)
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23
Q

give some features of an ideal splint (5)

A
  • easy to place, remove and maintain (often buccal)
  • cleansable
  • discourages plaque retention
  • does not impinge on gingival tissues
  • no occlusal interference
  • enables endodontic treatment and sensibility testing
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24
Q

when would you place a splint, what type and for how long? (paeds)

A
  • permanent teeth usually
  • 2 weeks flexible = most traumatic dental injuries
  • 4 weeks flexible = associated alveolar bone fractures, apical/mid-1/3 root fractures
  • 4 months rigid = cervical 1/3 root fractures
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25
Q

describe the procedure to splint a tooth flexibly

A

1 reposition tooth (usually with LA)
2 use small piece of floss to measure length of splint required, trim wire to length and bend/curve
3 spot-etch in middle of crowns, wash, dry
4 apply bond, dry, cure
5 place small ball of composite on tooth and place wire gently on top, ensuring it runs across the centre of adjacent teeth, cure
6 sandwich the wire with composite, cure
7 place composite balls over ends to ensure no sharp edges, cure

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26
Q

give some generic post-op advice following dental trauma (5)

A
  • 2 weeks = avoid contact sports, soft diet, avoid eating on traumatised teeth
  • careful OH +/- soft toothbrush
  • topical CHX 0.1% alcohol-free MW/gel BD 7/7
  • appropriate analgesia
  • if splint debonds, reattend before next review for reattachment
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27
Q

factors affecting prognosis of dental trauma (5)

A
  • age (maturity of roots)
  • type and severity of injury
  • associated injuries (displacements, fractures)
  • time between injury and treatment
  • presence of infection
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28
Q

give some possible complications following dental trauma in children (7)

A
  • loss of pulp vitality
  • arrest of root development in immature teeth
  • root resorption (inflammatory or replacement)
  • loss of tooth before adulthood
  • delayed exfoliation
  • delayed eruption of permanent tooth
  • injury to permanent successor
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29
Q

what possible effects on the permanent successor may be caused by primary tooth trauma? (6)

A
  • delayed eruption
  • hypomineralisation
  • hypoplasia
  • dilaceration (crown or root)
  • arrest of development
  • odontoma formation
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30
Q

define dilaceration of a tooth (2)

A
  • abrupt deviation of the long axis of the crown/root portion of the tooth
  • due to disturbance between the unmineralised and mineralised portions of the developing tooth germ (trauma or developmental)
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31
Q

what s/s may indicate non-vital pulp? (8)

A
  • discolouration
  • TTP+
  • buccal tenderness
  • negative sensibility testing
  • sharp pain on thermal stimulus
  • sinus tract
  • spontaneous pain or pain on biting
  • radiograph - PA RL, PDL widening
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32
Q

how soon will signs of loss of pulp vitality appear radiographically following dental trauma?

A

within 6 weeks (resorption, arrested root development)

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33
Q

how does arrest of root development appear radiographically? (3)

A
  • appears shorter than adjacent uninjured teeth
  • failure of pulp canal to mature/reduce in size
  • may see calcific barrier across apical area (residual vitality)
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34
Q

give the three types of root resorption that may occur following dental trauma

A
  • transient
  • inflammatory (infection-related)
  • replacement (ankylosis-related)
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35
Q

describe inflammatory/infection-related root resorption following dental trauma (cause, process, radiograph, tx)

A
  • usually immature teeth, occurs very quickly
  • caused by non-vital pulp with severe traumatic injuries and PDL injury
  • commonly external RR
  • necrosed pulp, damaged cementum –> osteoclast activity on root surface
  • seen radiographically from 3 weeks = punched out resorption
  • propagated by necrotic pulp so early extirpation and calcium hydroxide dressing helps
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36
Q

describe replacement root resorption/ankylosis following dental trauma (process, clinical, radiograph, management)

A
  • aetiology poorly understood
  • damage to root surface –> replacement with bone
  • tooth may be lost in 3-7 years in younger patients (fast bone turnover)
  • high “metallic” note when tapped, no physiological movement
  • loss of radiographic PDL space from 2-12months
  • often decoronated to maintain alveolar bone whilst preventing gingival margin discrepancy
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37
Q

how do open and closed apices differ in prognosis following trauma?

A
  • open apex = more likely to survive trauma, harder to RCT (thin dentine walls, poor crown:root)
  • closed apex = more likely to lose vitality +/- root resorption, more easily treated endodontically
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38
Q

define luxation injury

A

displacement injury involving teeth moving in or out of the socket, often requiring splinting

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39
Q

define concussion injury

A
  • mild luxation injury to tooth-supporting structures
  • with no mobility or displacement but tender to percussion
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40
Q

concussion clinical and radiographic presentation

A
  • TTP+
  • no mobility/displacement
  • normal radiograph
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41
Q

concussion management (3)

A
  • no tx
  • soft diet 1 week and good OH
  • f/u at 1 month, 1 year
    (95% pulp survival)
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42
Q

describe concussion presentation and management

A
  • TTP+
  • no mobility/displacement
  • normal radiograph
  • no tx
  • soft diet 1 week and good OH
  • f/u at 1 month, 1 year
    (95% pulp survival)
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43
Q

define subluxation injury

A
  • minor injury to tooth-supporting structures
  • bleeding around gingival margin, may be mobile but not displaced, tender to touch
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44
Q

subluxation clinical and radiographic presentation

A
  • gingival bleeding
  • mobile but not displaced
  • tender to touch
  • normal radiograph
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45
Q

permanent tooth subluxation management (3)

A
  • no tx unless discomfort then flexible splint 2 weeks
  • 1 week soft diet with good OH
  • f/u 2 weeks (splint), 3/6/12 months
    (85% closed apex survival)
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46
Q

permanent tooth subluxation presentation and management

A
  • gingival bleeding
  • mobile but not displaced
  • tender to touch
  • normal radiograph
  • no tx unless discomfort then flexible splint 2 weeks
  • 1 week soft diet with good OH
  • f/u 2 weeks (splint), 3/6/12 months
    (85% closed apex survival)
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47
Q

define lateral luxation injury

A

displacement of tooth other than axially (usually palatal)

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48
Q

lateral luxation clinical and radiographic presentation

A
  • displacement +/- communication fracture of alveolar bone
  • +/- occlusal interference
  • may be non-mobile (locked in)
  • radiograph shows fracture, shortened or elongated root
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49
Q

permanent tooth lateral luxation management (3)

A
  • LA and reposition, with flexible splint for 4 weeks
  • extirpate if signs of non-vitality
  • f/u 2 weeks, 1/2/3/6/12 months then annually until 5 years
    (95% open apex, 85% closed apex)
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50
Q

primary tooth lateral luxation management (3)

A
  • allow to reposition spontaneously if no occlusal interference (at least 6 months)
  • reposition if minor displacement and occlusal interference
  • extraction otherwise
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51
Q

permanent tooth lateral luxation presentation and management

A
  • displacement +/- communication fracture of alveolar bone
  • +/- occlusal interference
  • may be non-mobile (locked in)
  • radiograph shows fracture, shortened or elongated root
  • LA and reposition with flexible splint for 4 weeks
  • extirpate if signs of non-vitality
  • f/u 2 weeks, 1/2/3/6/12 months then annually until 5 years
    (95% open apex, 85% closed apex)
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52
Q

define extrusion injury

A

partial displacement of tooth in the axial direction out of its socket

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53
Q

extrusion clinical and radiographic presentation

A
  • extruded (elongated)
  • gingival bleeding
  • +/- occlusal interfence
  • mobile
  • radiograph = increased PDL space apically and laterally
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54
Q

permanent tooth extrusion management

A
  • digital repositioning +/- LA and flexible splint 2 weeks
  • antibiotics if severe injury
  • corsodyl MW/gel, soft diet
  • extirpate if signs of non-vitality
  • f/u 2 weeks, 1/2/3/6/12 months and annually until 5 years
    (guarded prognosis, 40% open apex, 0% closed apex with RR likely)
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55
Q

permanent tooth extrusion presentation and management

A
  • extruded (elongated)
  • gingival bleeding
  • +/- occlusal interfence
  • mobile
  • radiograph = increased PDL space apically and laterally
  • firm digital repositioning +/- LA and flexible splint 2 weeks
  • antibiotics if severe injury
  • corsodyl MW/gel, soft diet
  • extirpate if signs of non-vitality
  • f/u 2 weeks, 1/2/3/6/12 months and annually until 5 years
    (guarded prognosis, 40% open apex, 0% closed apex with RR likely)
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56
Q

primary tooth extrusion management (2)

A
  • allow to reposition spontaneously
  • extract if excessively mobile or >3mm extruded
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57
Q

define avulsion injury

A

complete displacement of tooth out of socket

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58
Q

should you replant primary avulsed teeth?

A

NO

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59
Q

what factors may you consider before replanting an avulsed tooth? (5)

A
  • permanent teeth only
  • MH (5) - tetanus, immunosuppressed, haematology, cardiac defects, allergy
  • state of tooth (caries, fractured)
  • very immature teeth with prolonged EADT may not survive
  • need for immediate medical treatment (takes priority)
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60
Q

what solutions may you keep an avulsed tooth in?

A

fresh cold MILK > saline > saliva

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61
Q

describe how a permanent tooth may be immediately replanted with LA

A

1 gently rinse in milk/saline if visible debris
2 remove any bony fragments, flush clots
3 replant with firm digital pressure
4 suture any gingival lacerations
5 check occlusion, check radiograph
6 flexible splint 2 weeks

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62
Q

what antibiotics may be prescribed following avulsion?

A

(limited evidence, up to clinician)
- penicillin first line
- doxycycline if penicillin allergy (but caution <12yo due to intrinsic discolouration)
(may help prevent IRR)

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63
Q

what immunisation must be checked following avulsion?

A

tetanus (refer to GP within 48hrs)

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64
Q

what other clinical procedure might you do following replantation of an avulsed tooth?

A

extirpation within 2 weeks and non-setting calcium hydroxide placed if CLOSED apex

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65
Q

in what scenario may a replanted avulsed permanent tooth survive?

A
  • open apex only
  • <60mins EADT
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66
Q

primary tooth avulsion management (3)

A
  • confirm with radiograph
  • do not replant primary avulsed tooth
  • monitor for permanent tooth eruption carefully
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67
Q

define intrusion injury

A

displacement of tooth apically into alveolar bone, often accompanied with fracture of alveolar socket

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68
Q

intrusion clinical and radiographic presentation and severity score

A
  • “short” firm tooth or even not visible
  • high metallic sound on percussion
  • severity = <3mm mild, 3-7mm moderate, >7mm severe
  • radiograph = loss of PDL space, more apical CEj
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69
Q

permanent tooth intrusion management

A

1 allow spontaneous eruption:
- mild with closed apex
- moderate with open apex
- may take up to a year
2 orthodontic repositioning (needs permanent teeth to bond to)
- mild and not spontaneously resolved
- moderate with closed apex
- severe with open apex
3 surgical repositioning and 4 week flexible splint
- severe with open apex
- moderate/severe with closed apex

  • extirpate if signs of non-vitality (within 3-4 weeks if closed apex)
  • f/u 2 weeks, 1/2/3/6/12 months, annually until 5 years
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70
Q

primary tooth intrusion management (3)

A
  • take USO or PA to ascertain position (elongated = apex towards palatal and may affect permanent tooth germ)
  • allow to reposition spontaneously irrespective of direction of displacement (6 months - 1 year)
  • warn parent of risk to permanent tooth
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71
Q

define enamel infraction

A

incomplete fracture/crack of enamel without loss of tooth tissue

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72
Q

enamel infraction management

A

monitor if no issues

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73
Q

define enamel fracture

A

fracture confined to enamel with loss of tooth structure

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74
Q

define uncomplicated fracture

A

fracture confined to enamel and dentine with loss of tooth structure, NOT involving pulp

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75
Q

define complicated fracture

A

fracture involving enamel and dentine with loss of tooth structure, exposing the pulp

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76
Q

define root fracture (2)

A
  • uncommon fracture involving cementum, dentine and pulp
  • apical, middle or cervical third of root
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77
Q

define complicated crown-root fracture

A

fracture involving enamel, dentine and cementum with loss of tooth structure, involving the pulp

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78
Q

enamel fracture management (4)

A
  • possible reattachment of fragment with flowable composite under LA
  • composite restoration
  • selective grinding if primary tooth to smooth
  • f/u 6-8 weeks and 1 year
    (excellent prognosis)
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79
Q

uncomplicated fracture management (4)

A
  • possible reattachment of fragment with flowable composite
  • composite restoration
  • GIC bandage if poor cooperation
  • f/u 6-8 weeks and 1 year
    (good prognosis)
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80
Q

complicated fracture management (5)

A
  • direct pulp cap (CaOH, GIC, composite) for pinpoint exposures within 24 hours and not grossly contaminated
  • Cvek pulpotomy for small exposures with asymptomatic tooth with non-inflamed pulp - within 9 days
  • coronal pulpotomy
  • pulpectomy
  • extraction if poor compliance
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81
Q

what two factors affect prognosis of a complicated crown fracture?

A

size and duration of pulp exposure

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82
Q

describe how a Cvek pulpotomy is carried out

A

1 LA, rubber dam (212 clamp)
2 remove 2-4mm pulp until bright red
3 haemostasis with sterile cotton pledget and saline
4 non-setting CaOH powder/Biodentine/MTA (discolours)
5 GIC to seal
6 composite restoration

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83
Q

how may a cellulose crown form be used to help restore following a Cvek pulpotomy?

A

1 bevel cavity for retention and aesthetics
2 adjust crown form to shape of tooth with scissors
3 pierce hole in incisal corner of crown form with probe to allow release of excess composite
4 etch, wash, dry
5 bond, dry, cure
6 place composite in crown form and push onto tooth and remove excess, cure buccal and palatal
7 remove crown form and polish until margins are flush

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84
Q

root fracture management (4)

A
  • parallax radiography to visualise fracture line
  • excessively mobile and occlusal interference: LA and…
    – extract only coronal fragment
    – digital repositioning of coronal fragment +/- flexible splint 4 weeks (mid/apical 1/3) or rigid splint 4 months (cervical 1/3)
  • loss of vitality = RCT up to fracture line (CaOH dressing)
  • f/u = 4wks, 2/4/6/12 months and annually until 5 years
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85
Q

how may a root fracture heal and which is more favourable? (2)

A
  • granulation tissue = poor prognosis, difficult to RCT (tissue enters canal)
  • hard tissue union = more favourable (less severe injuries)
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86
Q

complicated crown-root fracture management (3)

A
  • extract fragment and assess remaining tooth for restoration (often leave apical portion to be resorbed)
  • RCT with MTA if restorable
  • f/u = 1 wk, 2/3/6/12 months and annually until 5 years
    (poor prognosis, difficult to restore)
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87
Q

alveolar fracture management (3)

A
  • manual/forcep repositioning of displaced segment under GA ideally
  • flexible splint 4 weeks
  • monitor teeth in fracture line
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88
Q

describe the possible types of discolouration following tooth trauma

A
  • immediate = reddish, may regress or persist (sign of root resorption), may maintain vitality
  • intermediate = brown/black due to pulp breakdown products, non-vital tooth
  • long-term = yellow/opaque due to pulp calcification
    (50% of primary incisors with post-trauma dark discolouration remain asymptomatic until exfoliation)
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89
Q

what are the general follow up intervals following traumatic dental injuries and what are you assessing?

A
  • severe injuries to permanent dentition = 2/4/6/8 weeks, 3-4 months, 12 months, annually for 5 years
  • primary dentition = 1/4/8 weeks, 6 months, annually until permanent tooth erupts
  • looking for s/s of healing, assessing pt’s perception of aesthetics, any anxiety and effects on QoL
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90
Q

define amelogenesis imperfecta (3)

A
  • group of hereditary conditions affecting the structure and appearance of enamel, often in conjunction with changes in other tissues
  • single gene mutations
  • affects all teeth in both dentitions
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91
Q

what is the difference between hypoplasia, hypomineralisation, hypomaturation?

A
  • hypoplasia = decrease in quantity of tissue
  • hypomineralisation = decrease in quality of tissue/deposition of mineral
  • hypomaturation = decrease in quality/deposition of mineral during maturation stage
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92
Q

what are the three stages of amelogenesis?

A

1 secretory phase = thickness secreted by ameloblasts, lots of organic content and water
2 transition
3 maturation = inorganic ions secreted and exchanged for water and organic material

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93
Q

in what two ways may amelogenesis imperfecta be classified?

A
  • mode of inheritance and specific mutations
  • phenotype
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94
Q

name the different phenotypes of amelogenesis imperfecta

A
  • hypoplastic type I (F>)
  • hypomature type II (M>)
  • hypocalcified type III
  • hypomaturation-hypoplastic with taurodontism type IV
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95
Q

what is the most common phenotype of amelogenesis imperfecta?

A

hypoplastic type I

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96
Q

describe type I amelogenesis imperfecta (what, presentation)

A
  • hypoplastic type I
  • decreased enamel thickness but normal colour and contrast
  • pitting, grooves
  • F>M
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97
Q

describe type II amelogenesis imperfecta (what, presentation)

A
  • hypomature type II
  • normal thickness but similar radiographic density to dentine
  • enamel tends to flake or chip away from dentine
  • multiple brown-yellow local/diffuse opacities +/- snow-capped appearance
  • M>F
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98
Q

describe type III amelogenesis imperfecta (what, presentation)

A
  • hypocalcified type III
  • extremely soft enamel, less radiopaque than dentine, may be lost soon after eruption
  • teeth rapidly worn down and stained
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99
Q

what does a taurodont tooth look like radiographically? (3)

A
  • enlarged body of tooth
  • elongated pulp chamber
  • root bifurcation displaced apically with short roots
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100
Q

what other dental features are commonly seen with amelogenesis imperfecta? (2)

A
  • delayed eruption
  • anterior open bite (esp hypocalcified type III)
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101
Q

differential diagnosis of amelogenesis imperfecta and how to differentiate (5)

A
  • dental fluorosis (chronological, history)
  • tetracycline staining (coloured banding)
  • enamel chronological hypoplasia (eg vit D dependent rickets; chronological)
  • MIH (only molars and incisors)
  • trauma (localised)
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102
Q

what are the five aims of amelogenesis imperfecta management?

A

1 early diagnosis
2 pain management
3 prevention and stabilisation, maintain vertical dimension
4 restoration of any defects, manage aesthetics
5 regular maintenance

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103
Q

what will prevention and pain management of amelogenesis imperfecta consist of? (6)

A
  • education, OHI
  • fluoride MW, TP
  • tooth mousse (CPP-ACP)
  • warm water only
  • diet analysis and advice
  • shorter recall periods
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104
Q

what are the care principles of the primary dentition with amelogenesis imperfecta? (3)

A
  • treatment should reflect degree of symptoms/wear - aim for function and maintaining arch perimeter
  • aesthetic composites for anterior teeth, helps acclimatisation
  • SS crowns, GIC for primary molar occlusal surfaces
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105
Q

what are the care principles of the mixed dentition with amelogenesis imperfecta? (3)

A
  • PMCs or gold onlays or SS crowns for first molars
  • consider GIC and fluoride on occlusal surfaces due to longer eruption time +/- operculectomy
  • composite veneers for permanent incisors (aesthetic, decrease sensitivity/wear)
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106
Q

what are the care principles of the permanent dentition with amelogenesis imperfecta? (2)

A
  • premolars with wear and sensitivity = full coronal coverage restorations (but if no s/s then no intervention)
  • canines with wear and sensitivity = composite veneers
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107
Q

options for resorbing teeth in amelogenesis imperfecta (2)

A
  • extraction
  • orthodontic extrusion before too much resorption occurs
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108
Q

management for intact but discoloured enamel in AI (2)

A
  • bleaching
  • +/- microabrasion
    (aesthetic)
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109
Q

describe the morphological differences between primary and permanent dentition

A

1 primary
- thin uniform layer of enamel, thin layer of dentine, large pulp with fine root canals
- broad proximal contacts
- divergent thin roots
2 permanent
- variable enamel thickness, thicker dentine layer, proportionally smaller pulp
- deeper fissures

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110
Q

why do we restore carious lesions in children? (5)

A
  • prevention and pain relief
  • fostering positive attitude to dental health
  • general health and well-being
  • prevent damage to permanent successors
  • prevent adverse consequences of early tooth loss
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111
Q

describe fissure sealants (what, material)

A
  • material placed into pits and fissures of teeth to prevent development of dental caries
  • bis-GMA or GIC
  • must be retained and monitored to be most effective
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112
Q

fissure sealant (resin) technique

A

1 clean and dry the tooth
2 isolate
3 etch with 37% phosphoric acid
4 rinse 15s
5 dry 15s
6 bond and dry
7 deposit the resin and light cure
8 check adhesion immediately and monitor in future

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113
Q

what are the different cavity designs we may use in primary teeth? (3)

A
  • occlusal cavity = ≤1.5mm width, preserve the transverse ridge in upper molars
  • proximal cavity = isthmus 1/3-1/2 of occlusal surface width, rounded line angles
  • minimal box preparation = no occlusal extension
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114
Q

which restorative material has the best longevity in the primary dentition?

A

metal crowns (conventional technique)

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115
Q

what does the Minamata Treaty advise regarding children?

A

NO use of amalgam in treatment of deciduous teeth or in children <15yo
(except when strictly deemed necessary by practitioner by grounds of specific medical needs)

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116
Q

disadvantages of early primary tooth loss (5)

A
  • loss of space and risk of malocclusion
  • decreased masticatory function
  • impeded speech development
  • psychological disturbance
  • trauma (anaesthesia and surgery)
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117
Q

indications for pulp treatment in children (6)

A
  • good cooperation
  • promoting positive attitude to oral health care
  • MH precludes extraction (eg haematological)
  • missing permanent successor
  • maintaining a strategically important tooth
  • developmental state of tooth (usually <9yo)
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118
Q

contraindications for pulp treatment in children (6)

A
  • poor cooperation, poor dental attendance
  • MH where infection would be risky (eg cardiac defects)
  • multiple grossly carious teeth
  • advanced root resorption (>2/3) or extensive internal RR
  • severe/recurrent pain
  • cellulitis, pus in pulp chamber, gross bone loss
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119
Q

considerations with primary tooth endodontics (7)

A
  • compliance
  • restricted access
  • physiological resorption
  • root morphology
  • lack of/thin secondary dentine
  • porous pulp floor with accessory canals
  • risk to permanent successor
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120
Q

describe pulpotomy in children (when/why, procedure)

A
  • when = carious/traumatic exposure of vital pulp, caries >2/3 into dentine on radiograph
  • why = preserve radicular pulp, maintain tooth until normal exfoliation
    1 LA, isolation, access and caries removal
    2 amputation (roof of pulp chamber and coronal pulp)
    3 assess pulp status by colour and haemostasis
    4 15% ferric sulphate for 15-30s (up to 4x)
    5 ZOE base
    6 GIC core
    7 PMC
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121
Q

how far down from occlusal surface is the pulp of a primary molar?

A

3mm

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122
Q

what is odontopaste? (components, use)

A
  • clindamycin, triamcinolone, calcium hydroxide
  • for emergencies only as intracanal medicament (pt unable to tolerate procedure or failed LA)
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123
Q

describe pulpectomy in children (when/why, procedure)

A
  • when = non-vital/hyperaemic pulp, irreversible pulpitis with excellent cooperation
  • why = control or prevent infection
    1 LA, isolate, access and caries removal
    2 amputation and assess for non-vital/hyperaemic pulp
    3 remove pulp with files, preparing to 2mm short of the apex, irrigating with saline/LA/CHX
    4 obturate with creamy mix of Vitapex
    5 ZOE base
    6 GIC core
    7 PMC
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124
Q

give some s/s which may indicate irreversible pulpitis in a child

A
  • spontaneous pain, pain on biting, TTP
  • excessive mobility not associated with trauma or exfoliation
  • “gum boil”
  • bad taste
  • sinus tract
  • discolouration
  • facial swelling
  • furcation or apical RL
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125
Q

what is Vitapex? (components, use)

A
  • calcium hydroxide and iodoform
  • used in obturation in primary teeth as it resorbs with tooth
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126
Q

how far are the canals prepared in pulpectomy in deciduous teeth?

A

to 2mm short of the apex

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127
Q

what is the theory behind using the Hall technique?

A
  • manipulates plaque environment by sealing and separating from substrate
  • bacterial profile changes and lesion does not progress
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128
Q

indications for Hall technique (5)

A
  • any proximal/occlusal lesions that pt cannot tolerate conventional restoration/FS (asymptomatic or reversible only)
  • developmental defects (eg hypoplastic)
  • restoration of fractured primary molar
  • band of sound dentine between lesion and pulp
  • high caries risk (eg special needs)
129
Q

contraindications for Hall technique (7)

A
  • irreversible pulpal involvement
  • insufficient sound tooth tissue to retain crown
  • > 1/2 root has been resorbed
  • MH where infection poses a risk
  • nickel allergy
  • pt cooperation endangering airway
  • parent/child unhappy with aesthetics
130
Q

describe Hall technique procedure

A

1 space formation with orthodontic separators 3-5 days beforehand
2 crown selection with airway protection - trial and error
3 cementation with GIC luting cement and pressure
4 remove excess cement and inform that it will feel high for a week

131
Q

pros and cons of Hall technique

A

+ = good wear resistance, low failure rate, low incidence of CARS, simple
- = poor aesthetics, unsuitable if nickel allergy, may inhibit eruption of 6

132
Q

indications for conventional technique with PMC (5)

A
  • extensive caries (multiple surfaces)
  • developmental defects (AI, dI)
  • following pulpectomy/pulpotomy
  • restoring a primary tooth to be used as abutment for space maintainer
  • definitive restoration for high caries risk child
133
Q

different methods of crown selection for conventional technique (3)

A
  • measure M-D width with divider
  • trial and error after prep
  • impression and crown prep on a model
134
Q

which Act determines who can consent for a child? who can consent for a child? (7)

A

The Children Act 1989
- mother
- legally appointed guardian
- person with residency order for the child from a count
- local authority designated in a care order
- father if married at time of birth
- unmarried father who has acquired parental responsibility (married mother, court order)
- unmarried father after 2003 = registered at time of birth, or re-registered and natural father

135
Q

when can a young person consent?

A
  • ≥16yo can consent without parental/guardian consent (Family Reform Act 1969)
  • minors <16yo if deemed Gillick competent or Fraser competent
136
Q

when should the first dental assessment be conducted for a child?

A

before 6 months old

137
Q

general principles of treatment for primary tooth trauma (4)

A
  • do not replant avulsed primary teeth
  • leave and monitor if no occlusal interference and not excessively mobile/airway risk
  • reposition if occlusal interference but no splint
  • extract if airway risk
138
Q

what should be included in the notes of the first paediatric assessment visit? (10)

A
  • accompanying person
  • CO/HPC
  • MH
  • DH
  • SH
  • diet
  • OH, habits
  • EO and IO examinations and special tests
  • behaviour (Frankl)
  • diagnoses and caries risk
139
Q

general treatment plan format for paediatric patients

A

1 emergency/acute (pain relief, prevent further infection, maintain vitality)
2 stabilisation of active disease, including prevention and temporisation, behaviour management
3 corrective (restorative, prosthetic)
4 maintenance (reinforce prevention)
5 regular reassessment (6/12, 3/12 if high risk)

140
Q

indications for bitewings in children (4)

A
  • detect caries
  • dental injuries or trauma
  • disturbances of tooth development
  • examination of other pathological conditions (other than caries)
141
Q

describe the Frankl behavioural scale

A

1 = definitely negative = refuses treatment, forceful crying, fearfulness, other evidence of extreme negativism
2 = negative = reluctant to accept treatment, uncooperative, some evidence of negative attitude but not pronounced
3 = positive = accepts treatment, cautious at times, willingness to comply, at times with reservation but follows directions cooperatively
4 = definitely positive = good rapport with dentist, interest in dental procedures, laughter, enjoyment

142
Q

what might you ask about when taking a social history for paeds? (3)

A
  • caries experience and dental-related anxiety in parents or siblings (risk assessment)
  • school, social workers (safeguarding)
  • parental occupation and who takes care of child
143
Q

what might you ask when taking the past dental history for paeds? (5)

A
  • regular attendance?
  • past experiences and treatments
  • coping abilities
  • any specific difficulties or dislikes
  • child and parents’ attitudes towards dental treatment
144
Q

what might you ask when taking a diet history for paeds? (6)

A
  • bottle feeding (duration, when)
  • snacks, treats (frequency, sugar)
  • drinks (when, sugar)
  • medications (sugar-free)
  • lunches (school dinners or packed)
  • fruit and veg, 5/day
145
Q

what can affect a child’s cooperative potential? (4)

A
  • current pain
  • dental history, PMH, SH
  • level of understanding and potential cooperation
  • level of anxiety
146
Q

what is behaviour management?

A

the way in which a dentist effectively and efficiently performs treatment for a child

147
Q

list behaviour management techniques (12)

A
  • positive reinforcement
  • appropriate language
  • tell, show, do
  • acclimatisation
  • systematic desensitisation
  • voice control
  • role modelling
  • hand stop signal
  • distraction
  • appropriate touch
  • reward
  • hypnosis
    (- restraint but not in UK)
148
Q

describe positive reinforcement (what, how)

A
  • presentation of a stimulus that will increase the likelihood of behaviour being repeated
  • important to be clear and immediate
  • positive voice modulation, facial expression, descriptive verbal praise
149
Q

give examples of some appropriate and inappropriate language to use with children

A

good = buzzy brush, hoover, tooth pillow, raincoat, magic jelly, spoon

bad = sharp, needle, jaw, drill

150
Q

describe the tell, show, do technique (what, how)

A
  • method of introducing equipment and procedures
    1 tell child about instrument
    2 show the instrument and describe any sensation that might be felt (+/neutral)
    3 do what has been demonstrated without deviation with minimal delay
151
Q

define acclimatisation

A

planned sequential introduction of environment, people and instruments and procedures

152
Q

describe systematic desensitisation (what, how)

A
  • repeated non-distressing exposure to an anxiety-provoking stimulus to eventually decrease the anxiety
  • reassure pt, +/- hypnosis
    1 construct personalised hierarchy of anxiety-provoking stimuli
    2 expose to least anxiety provoking stimulus (imaginary or reality) until no anxiety produced)
    3 repeat for next least anxiety-provoking
153
Q

define voice control

A

controlled alteration of voice, volume, tone or pace to influence and direct a patient’s behaviour

154
Q

describe role modelling (what, why)

A
  • using a model to demonstrate similar treatment
  • children learn how to act by observing and imitating their peers
155
Q

what is the hand stop signal?

A

pt able to raise their hand as a stop signal to give them a degree of control over the dentist’s behaviour

156
Q

describe distraction (behaviour management) (what, how)

A
  • shifting the pt’s attention from the dental setting to some other situation, or from a potentially unpleasant procedure to some other action
  • verbal, short-term distracters, short breaks
157
Q

from when do the teeth start developing?

A

5 weeks in utero

158
Q

in what order do the primary teeth erupt?

A

A B D C E

159
Q

what is the first tooth to erupt in the mouth and when?

A

lower A (7-8 months)

160
Q

what is the last deciduous tooth to erupt?

A

upper E (25-33 months)

161
Q

what is the first permanent tooth erupt?

A

lower 6

162
Q

what are the anthropoid spaces?

A

spaces immediately mesial to UC and distal to LC

163
Q

what is leeway space?

A

amount by which the combined M-D width of the CDE exceeds that of the 345
(1.5mm U, 2.5mm L)

164
Q

give the order and ages in which the permanent teeth erupt

A

6yo = L1 and L6 (closely followed by U6)
7yo = U1 and L2
8yo = U2
9yo = laterals tilted distally by canine
10yo = L3 and all 4s, U3s palpable in buccal sulcus
11yo = U3, all 5s
12yo = all 7s

165
Q

what are the 3 main risk factors for developing caries within the next 3 years?

A
  • previous caries experience
  • resident in an area of deprivation
  • healthcare worker’s opinion (referral)
166
Q

what clinical findings would indicate low and high caries risk? (5/4)

A

LOW
- no new lesions, restorations years ago
- no carious extractions
- sound anterior teeth
- fissure sealants
- no appliances
HIGH
- new lesions, premature extractions, multiple recent restorations
- anterior caries/restorations
- no fissure sealants
- appliances

167
Q

what dietary habits would indicate low and high caries risk?

A

low = infrequent sugar intake
high = frequent sugar intake (non-milk extrinsic sugars)

168
Q

what social history factors would indicate low and high caries risk? (5/5)

A

LOW:
- social advantage
- siblings/parents with low caries
- dentally aware, regular attender
- limited availability of snacks
- high dental aspirations
HIGH:
- social deprivation
- high caries in family
- low dental disease knowledge, irregular attender
- readily available snacks
- low dental aspirations

169
Q

what OH habits would indicate low and high caries risk? (4/3)

A

LOW:
- fluoride in drinking water and TP
- fluoride supplements
- frequent effective cleaning
- good manual control
HIGH:
- no fluoride
- infrequent, ineffective cleaning
- poor manual control

170
Q

what medical history factors would indicate low and high caries risk? (3/3)

A

LOW:
- no medical or physical problems
- normal salivary flow
- no long term medications
HIGH:
- medically compromised, physical disability
- xerostomia
- long-term cariogenic medicine

171
Q

what salivary factors would indicate low and high caries risk?

A

LOW:
- normal flow rate
- high buffering capacity
- low S mutans and lactobacillus counts
HIGH:
- low flow rate (rare)
- low buffering capacity
- high S mutans and lactobacillus counts

172
Q

what does the caries risk assessment determine? (3)

A
  • preventive interventions
  • frequency of review radiographs
  • frequency of recall
173
Q

what are the four pillars of prevention?

A
  • plaque control
  • dietary advice
  • fluoride
  • fissure sealants
174
Q

give the standard prevention for 0-7+yo as per DBOH

A

0-3yo:
- breast feeding = best nutrition for babies
- from 6 months should introduce drinking from a free-flowing cup
- from 1yo, feeding from bottle should be discouraged
- sugar should not be added to food/drink
- parents/carers should supervise/do toothbrushing
- brush 2x daily with smear of at least 1000ppm F- toothpaste (last thing at night and one other occasion)
- frequency and amount of sugar
- sugar-free medications

3-6yo:
- supervised brushing at least 2x/day with pea sized fluoride toothpaste >1000ppm
- spit don’t rinse to maintain F- concentrations
- sugary food and drink frequency and amount should be reduced
- fluoride varnish 2.2% NaF 2x/year

7+yo:
- 1350-1500ppm F- TP
- decrease frequency and amount of sugary food/drink
- fluoride varnish 2.2% NaF 2x/year

175
Q

give the standard prevention for 0-3yo as per DBOH (8)

A

0-3yo:
- breast feeding = best nutrition for babies
- from 6 months should introduce drinking from a free-flowing cup
- from 1yo, feeding from bottle should be discouraged
- sugar should not be added to food/drink
- parents/carers should supervise/do toothbrushing
- brush 2x daily with smear of at least 1000ppm F- toothpaste (last thing at night and one other occasion)
- decrease frequency and amount of sugar
- sugar-free medications

176
Q

give the standard prevention for 3-6yo as per DBOH (4)

A

3-6yo:
- supervised brushing at least 2x/day with pea sized fluoride toothpaste >1000ppm
- spit don’t rinse to maintain F- concentrations
- sugary food and drink frequency and amount should be reduced
- fluoride varnish 2.2% NaF 2x/year

177
Q

give the standard prevention for 7+yo as per DBOH (3)

A

7+yo:
- 1350-1500ppm F- TP
- decrease frequency and amount of sugary food/drink
- fluoride varnish 2.2% NaF 2x/year

178
Q

give the enhanced prevention for 0-6yo as per DBOH (3)

A
  • fluoride toothpaste 1350-1500ppm
  • frequent long-term med should be sugar free (liaise with GP)
  • professional = decreased recall interval, F- varnish ≥2x/year, diet analysis and good dietary practice in line with Eat Well guide
179
Q

give the enhanced professional prevention for 7+yo as per DBOH (6)

A
  • resin FS on permanent molars
  • F- varnish ≥2x/year
  • 8+yo with active caries = daily 0.05% (225-230ppm) F- rinse prescribed
  • 10+yo with active caries = 2800ppm TP
  • 16+yo with active caries = 2800 or 5000ppm TP
  • investigate diet and assist to adopt good dietary practice in line with Eat Well guide
180
Q

periodontal disease prevention as per DBOH (5)

A
  • OHI to prevent gingivitis, achieve the lowest risk of periodontitis and tooth loss
  • correct factors impeding effective plaque control – calculus, open margins, overhangs, contours

12+yo:
- ID plaque control daily before brushing
- small spaces = floss or tape
- larger spaces = ID brushes or single tufted brushes

181
Q

DBOH recommendations for diet (5)

A
  • restrict sugary food and drink to no more than 4 occasions/day
  • grazing on sugary food, sipping soft drinks containing sugar/acid over prolonged periods should be discouraged
  • avoid sugar-containing food and drink at bedtime when saliva flow is decreased and buffering capacity is lost
  • only water/cow’s milk between meals
  • breast feeding best for babies
182
Q

topical fluoride modes of action (2)

A
  • NaF contacts enamel –> CaF2 and stays on the surface - reservoir of F-, protection against further acid attack
  • dentine hypersensitivity relief – CaF2 globules occlude the tubules
183
Q

which group should not have fluoride varnish?

A

<3yo with low caries risk

184
Q

describe how fluoride varnish is applied and post-operative instructions

A

1 remove XS plaque
2 isolate and dry one quadrant
3 thin layer applied to most susceptible areas of teeth – gingival margins, proximal areas, susceptible occlusal areas
4 repeat with other quadrants

post-op:
- no liquids/eating for 30mins, only soft foods after
- do not brush and avoid chewing for 4 hours

185
Q

what are the fluoride varnish recommended doses and how is this measured?

A

visual dispensing pad
- 0.25ml for primary dentition
- 0.4ml for mixed dentition
- 0.75ml for permanent dentition

186
Q

what concentration is Duraphat fluoride varnish and how much NaF is in 1ml?

A
  • 22.6% or 22600ppm
  • 1ml = 50mg of NaF (22.6mg F-)
187
Q

what is the toxic dose of fluoride varnish?

A

5mg/kg of F-

188
Q

contraindications for fluoride varnish (5)

A
  • hypersensitivity to colophony or other constituents
  • ulcerative gingivitis
  • stomatitis
  • bronchial asthma
  • pts who are allergic or unable to take alcohol for cultural/religious reasons
189
Q

what is the colophony for in fluoride varnish?

A

natural resin for stickiness

190
Q

radiographic intervals for high risk and low risk

A
  • high risk = 6-12 months
  • low risk = 12-18 months (primary), ~24 months (permanent)
191
Q

define early childhood caries (ECC)

A

at least 1 carious lesion in any primary tooth (dmfs) in <6yo

192
Q

define severe early childhood caries (S-ECC) (3)

A
  • smooth surface caries in a child <3yo
  • any dmfs affecting primary maxillary anterior teeth <6yo
  • dmfs > age for those <6yo
193
Q

how is a child’s body weight estimated (1-10yo)?

A

(age + 4) x 2

194
Q

what are the recommended doses and timings for paracetamol?

A
  • 3-12mo = 60-125mg (0.5-1 tsp)
  • 1-5yo = 125-250mg (1-2 tsp)
  • 5-12yo = 250-500mg (2-4 tsp)
  • 12-18yo = 500mg-1g (4-8 tsp)
    (Calpol = 125mg or 250mg/5ml)
  • every 4-6 hours, max 4 in 24 hours
195
Q

what is the toxic dose of paracetamol?

A

150mg/kg for adults (higher for children) = nausea and vomiting

196
Q

what are the recommended doses, max doses and timings for ibuprofen? (4)

A
  • 3-12mo = 50mg (max 30mg/kg)
  • 1-4yo = 100mg (max 30mg/kg)
  • 4-7yo = 150mg (max 30mg/kg)
  • 7-10yo = 200mg (max 2.4g/kg)
  • 10-12yo = 300mg (max 2.4g/kg)
  • 12-18yo = 300-400mg
  • every 8 hours
197
Q

contraindications for ibuprofen (4)

A
  • asthma
  • liver disease
  • renal failure
  • bleeding disorders
198
Q

s/s of ibuprofen overdose (3)

A
  • nausea, vomiting
  • epigastric pain (stomach ulcer with prolonged use)
  • tinnitus
199
Q

describe ID block technique in children

A
  • mandibular foramen = below occlusal plane, most posterior and lower than in most adults

1 mouth fully open
2 approach direct from contralateral primary molars, lateral to the pterygomandibular raphe and medial to the ascending ramus at SAME LEVEL of occlusal plane
3 insert 5mm above the occlusal plane (may be lower if younger)
4 advance until bone is hit (~15mm in young, 25mm in older), withdraw slightly, aspirate and deposit 1.5ml
5 withdraw halfway and deposit 0.5ml

200
Q

describe the Wand (LA) and its advantages and disadvantages

A
  • computer-controlled LA injection with dynamic pressure-sensing technology
    + = looks less threatening, induces less anxiety, precise control of flow rate ensures comfort
  • = more expensive, longer, more hazardous waste, needs space for machine
201
Q

what factors will affect whether you will extract or retain a child’s tooth? (6)

A
  • restorability
  • caries risk
  • relevant MH (oncology, haematology, immunology)
  • pt/parent compliance and attitude
  • stage of dental development - exfoliation, long term prognosis or permanent tooth
  • space management/maintenance
202
Q

what may be done during the stabilisation phase of paediatric treatment plan? (4)

A
  • stabilisation of restorable lesions (IRM, GIC, RMGIC)
  • acclimatisation to dentistry
  • removal of unrestorable teeth
  • prevention - OHI, diet advice, FS, FV
203
Q

options for managing caries in anterior primary teeth (4)

A
  • prevention (fluoride)
  • proximal stripping
  • strip crowns
  • extraction
204
Q

describe proximal stripping (what, 3 indications, +/-, technique)

A
  • opening the ID spaces of primary anterior teeth to allow fluoride to access
  • indications = exfoliation close, pre-cooperative but able to use soflex disks, superficial interproximal lesions
    + = simple, quick, self-cleansing allowed
  • = pulp vitality, food packing, space loss, poor aesthetics

1 create tapered smooth crown form with slow speed soflex discs (or bur)
2 polish + FV

205
Q

indications for proximal stripping for anterior primary teeth caries (3)

A
  • exfoliation close
  • pre-cooperative but able to use soflex disks
  • superficial interproximal lesions
206
Q

describe strip crowns for anterior primary teeth caries management (indications, technique)

A
  • enamel hypoplasia, dental anomalies in a compliant pt

1 LA, rubber dam
2 tapered preparation with high speed diamond (2mm incisal, labial groove)
3 cellulose acetate crown form and composite to restore

207
Q

when might you take an intraoral radiograph regarding the maxillary central incisors’ development in a child? (3)

A
  • erupted but grossly rotated
  • large diastema
  • unerupted beyond normal timing (asymmetry >6 months or disturbed order)
208
Q

what are the differences between the conventional and Hall technique with preformed metal crowns? (3)

A
  • conventional requires LA and tooth preparation and caries removal but Hall does not
  • conventional requires excellent pt cooperation, Hall can be done in less compliant pts
  • Hall technique can only be used for asymptomatic teeth or reversible pulpitis
209
Q

describe indirect pulp therapy (why, indication, steps)

A
  • arrest caries process and encourage reactionary dentine formation and remineralisation of remaining carious dentine
  • maintain pulp vitality
  • indication = teeth with deep carious lesion but no s/s of pulpal pathology
    1 LA, rubber dam
    2 remove all caries at EDJ
    3 remove soft deep carious dentine over pulp with care to avoid exposure
    4 appropriate lining (eg RMGIC, CaOH)
    5 definitive restoration for coronal seal, ideally PMC
210
Q

define molar-incisor hypomineralisation

A
  • developmentally-derived dental defect
  • involving hypomineralisation of 1-4 first permanent molars
  • frequently associated with similarly affected permanent incisors
211
Q

give the features of mild MIH (3)

A
  • demarcated opacities located in non-stress bearing areas, mild incisor involvement if present
  • no caries associated with affected enamel
  • no hypersensitivity
212
Q

give the features of moderate MIH (4)

A
  • demarcated opacities on molars and incisors
  • post-eruptive enamel breakdown limited to 1-2 surfaces without cuspal involvement
  • atypical restorations may be needed
  • normal dental sensitivity
213
Q

give the features of severe MIH (4)

A
  • post-eruptive enamel breakdown and crown destruction
  • caries associated with affected enamel
  • history of dental sensitivity
  • aesthetic concerns
214
Q

what age is the critical period for causing enamel defects of FPMs and incisors?

A

first 2.5 years of life (early maturation)

215
Q

factors causing MIH (up to 15)

A

1 prenatal:
- maternal pyrexia
- medication
- prolonged vomiting

2 perinatal (difficult birth):
- c-section
- prolonged or complicated delivery
- hypoxia
- premature, low birth weight
- hypocalcaemia

3 post-natal:
- ENT infections (recurrent and needing antibiotics)
- chicken pox, measles, mumps
- respiratory problems
- pyrexia
- prolonged medication
- antibiotics
- breast feeding

216
Q

what does the colour of the demarcated opacities indicate in MIH? (Jalevik & Noren 2000)

A
  • yellowish-brownish = full thickness and more porous = more likely to have PEB
  • creamy, yellow, whitish = less porous, variable depth
217
Q

what is the 6 step management of MIH? (William et al 2006)

A

1 risk identification
2 early diagnosis
3 remineralisation and desensitisation
4 prevention of caries and PEB
5 restorations or extractions
6 maintenance

218
Q

what does CPP-ACP stand for and which patients might not be suitable?

A
  • casein phosphopeptide-amorphous calcium phosphate
  • milk protein - consider those who are lactose intolerant
219
Q

which restorative materials may be used to restore FPMs for those with MIH? (4)

A
  • RMGIC or GIC = temporary, non-stress bearing areas
  • composite = ≥1 surface needs restoration (but may be sensitive and decreased bond strength)
  • PMC = must be replaced by cast onlay/crown at some point (teens)
  • cast onlays/crowns
220
Q

what are the 2 approaches that may be taken when restoring MIH-affected teeth and why are they good/bad?

A

1 remove all defective enamel = loss of more tooth tissue but better bond
2 remove only porous enamel until resistance to bur/probe is felt = less invasive but defective enamel may continue to chip away

221
Q

factors to consider when extracting molars affected by MIH (4)

A
  • other molars (should definitely be unaffected)
  • severity (mild may be acceptable)
  • occlusion (other teeth present, minimal crowding, inclination of 5s, stage of 7s, presence of 8s)
  • timing
222
Q

what factors guide the timing for extraction of FPMs in children? (2)

A
  • calcification of bifurcation of the lower 7s (usually ~9yo)
  • angulation of 7s (15-30º)
223
Q

give the factors for consideration of loss of FPMs (6)

A
  • underlying malocclusion
  • no missing teeth (including the 8s)
  • timing (early means loss of space, late means space not closed)
  • extent and location of crowding
  • long term prognosis
  • which FPM (lowers may need compensation)
224
Q

what options are there for treating incisors affected in MIH? (6)

A
  • bleaching (>18yo only)
  • resin infiltration (ICON)
  • microabrasion only
  • direct composite restoration
  • microabrasion and composite
  • porcelain/composite veneers in adulthood
225
Q

treatment for mildly affected FPMs in MIH (3)

A
  • FV on PE molars
  • FS on fully erupted molars
  • composite restoration if breakdown or caries
226
Q

treatment for moderately/severely affected FPMs in MIH (4)

A
  • consider extraction
  • FV or GIC on PE molars
  • composite restoration for ≤3 surfaces
  • PMC/copings for >3 surfaces
227
Q

indications for inhalation sedation (5)

A
  • mild-moderate anxiety
  • special healthcare needs
  • pronounced gag reflex
  • LA not possible
  • cooperative child but challenging/traumatic dental procedure
228
Q

define conscious sedation

A
  • technique that produces a state of CNS depression to enable treatment to be delivered
  • during which verbal contact with the patient is maintained throughout
229
Q

what are the 3 modes of action of inhalation sedation/nitrous oxide gas?

A
  • anxiolytic (similar to benzodiazepines via GABA A receptors)
  • analgesic (stimulates opioid release)
  • anaesthetic (non-competitive inhibitor for NMDA-type glutamate recepts)
230
Q

s/s of ideal sedation in children (up to 10)

A
  • normal relaxed respiration
  • peripheral vasodilation
  • decreased muscle tone
  • pupil dilation, eyelids relax
  • delayed response to questions
  • tingling/numbness in hands/feet
  • warmth
  • light-headed, dizziness
  • euphoric feeling
  • numbness of IO soft tissues
231
Q

contraindications for IHS (up to 10)

A
  • ASA III+ cannot be done in PDC
  • pre-cooperative
  • phobic
  • nasal obstructions, severe respiratory diseases
  • recent medical procedures involving intracranial gases (expansion)
  • middle ear infection, recent ENT operation (2wks)
  • neuromuscular disorders
  • porphyria
  • antifolate medication (methotrexate)
  • bleomycin chemotherapy
232
Q

advantages of IHS (up to 9)

A
  • non-invasive, well-tolerated
  • titrated
  • wide margin of safety
  • rapidly absorbed (2-3mins)
  • rapidly eliminated (5mins)
  • minimal impairment of reflexes
  • some analgesic properties esp with semihypnotic suggestion
  • reduces anxiety at following visits
  • cost-effective alternative to GA
233
Q

disadvantages of IHS (up to 9)

A
  • lacks potency
  • heavily reliant on psychological support
  • needs nasal breathing and compliance
  • variable post-op amnesia
  • nasal hood may impede access
  • may still need LA
  • nitrous oxide pollution
  • can have unfavourable psychological reactions and LOC in some
  • headache, vomiting, nausea with higher levels of sedation
234
Q

give some of the effects of prolonged nitrous oxide exposure on staff (2)

A
  • haematological = impaired RBC production, pernicious anaemia
  • reproductive (avoid in first trimester)
235
Q

what is diffusion hypoxia? (3)

A
  • potential complication during recovery period after IHS
  • rapid release of nitrous oxide from blood into alveoli = decreased oxygen concentration leading to hypoxia
  • disorientation, headache, nausea, vomiting
236
Q

how is diffusion hypoxia prevented?

A

administering 100% oxygen for 3-5 mins after nitrous oxide gas is stopped

237
Q

pre-operative instructions for IHS (3)

A
  • light meal before treatment
  • do not bring other children
  • reschedule if child is unwell or nasal obstruction
238
Q

pre-operative checks for IHS (5)

A
  • suitable escort
  • MH, no nasal obstruction
  • light meal
  • toilet
  • second stage consent
239
Q

what is involved in clinical monitoring of a child during IHS? (5)

A
  • responsiveness
  • colour
  • respiratory rate and rhythm
  • muscle tone
  • eyes
240
Q

risks of GA (up to 10)

A
  • 1/10 headache, nausea, vomiting, dizziness, agitation on waking (1/5), sore nose or sore throat, tummy ache
  • allergy 1/10,000
  • death <1/100,000
241
Q

GA indications (4)

A
  • very young child, too anxious or uncooperative for other means
  • medically compromised
  • difficult or complex dental treatment
  • extractions in multiple quadrants
242
Q

define general anaesthesia

A

state of controlled unconsciousness during which you feel nothing and can be described as “anaesthetised”

243
Q

when is GA not appropriate for dental treatment? (3)

A
  • carious asymptomatic teeth with no signs of sepsis
  • orthodontic extractions of sound permanent premolars in a healthy child
  • pt/carer preference only
244
Q

describe different types of GA airway management (4)

A
  • McKesson nasal mask - mouth free for access, only for single tooth extractions
  • laryngeal mask - sits over vocal cords, for more extensive dental treatment but limited access and easily dislodged
  • oral intubation - for longer treatments (more robust) but difficult access
  • nasal intubation - more associated complications but less access issues
245
Q

what does the UN Convention on Rights of the Child 1989 say regarding children’s rights? (2)

A
  • children should be protected from all forms of physical or mental violence, injury or abuse, neglect or negligent treatment, maltreatment or exploitation
  • children have a right to enjoy the highest attainable standard of health and to facilities for the treatment of illness and rehabilitation
246
Q

what does the Children’s Act 2004 say about safeguarding (in short)?

A

safeguarding children is the responsibility of everyone

247
Q

what is “safeguarding” and what does it involve? (4)

A
  • wider range of measures are taken to minimise risks and harm to children
  • protecting from maltreatment
  • preventing impairment of children’s health or development
  • ensuring children grow up in a safe and caring environment
248
Q

what is “child protection”?

A

action taken to protect children who are suffering or at risk of harm

249
Q

define “child abuse” and give the 4 different types

A
  • term to describe a number of ways in which a child can be harmed
  • any child, isolated or recurrent
  • physical
  • emotional
  • sexual
  • neglect
250
Q

what environmental factors may increase the risk of child abuse? (5)

A
  • poverty
  • social isolation
  • poor housing
  • domestic violence at home
  • poor access to facilities
251
Q

give some characteristics which may increase the risk of someone being a child abuser (up to 6)

A
  • younger parent
  • mental health problem
  • drug/alcohol abuse
  • victim of abuse themselves
  • personality traits - impulsiveness, low tolerance, aggressive tendencies
  • unrealistic expectations from a child
252
Q

give some characteristics which may increase the risk of a child being abused (up to 6)

A
  • younger children
  • disabilities
  • unwanted pregnancy
  • premature/low BW babies
  • prolonged separation from mother
  • characteristics which evoke negative response (persistent crying, behavioural difficulties)
253
Q

define physical abuse and give examples (up to 4)

A
  • “deliberate physical injury to a child or failure to prevent physical injury or suffering”
  • hitting, shaking, squeezing, burning, biting
  • injury from restraining
  • harm as a result of giving alcohol, inappropriate drugs or poison
  • fabricated or induced illness (FII)
254
Q

what features of the history taking would raise suspicions of child abuse? (2)

A
  • delayed presentation
  • story inconsistent with injury or variation between child vs carer account
255
Q

describe the differences in features of accidental and non-accidental injuries (3)

A
  • accidental = usually bony prominences, match developmental age/stage of child
  • non-accidental = bilateral, soft tissue sites, triangle of safety
  • non accidental may also have imprints of fingers, teeth, cigarette-shaped burns
256
Q

what is the triangle of safety?

A
  • area including ears, side of face, neck and top of shoulders
  • unlikely to be traumatised accidentally
257
Q

define neglect and give examples (up to 4)

A
  • “persistent failure to meet a child’s needs (physical, emotional +/or psychological), likely to result in the serious impairment of the child’s health/development”
  • failure to provide adequate diet, make arrangements for health care
  • inadequate clothing
  • lack of appropriate supervision, stimulation
  • leaving child alone at an inappropriate age
258
Q

give some signs of child neglect (up to 7)

A
  • frequent minor injuries or recurrent infections, lice infestations
  • poor hygiene
  • abnormalities of hair/skin
  • developmental delay
  • inappropriate/inadequate clothing for season/weather
  • non-attendance at school
  • constant hunger/stealing
259
Q

define emotional abuse and give examples (up to 5)

A
  • “persistent emotional ill treatment of a child such as to cause severe and persistent adverse effects on the child’s emotional development”
  • persistently withholding love and affection
  • constantly shouting at, threatening or demeaning
  • being overprotective (child unable to mix with others)
  • racial or other forms of harassment undermining a child’s self-esteem
  • telling them they wish they were dead
260
Q

how may the parent and child present if emotional abuse is occurring?

A
  • parent = negative view of child, ignores child, constantly undermining and criticising, ridiculing
  • child = low self-esteem, delayed development, no sense of fun, self-harm, constantly seeking approval
261
Q

define sexual abuse and give examples (up to 3)

A
  • “forcing or enticing a child to take part in sexual activities”
  • making a child engage in/observe sexual activities
  • showing a child pornographic material
  • engaging a child in inappropriate discussion about sexual matters
262
Q

what are some possible signs of child sexual abuse? (7)

A
  • sudden unexplained changes in behaviour
  • running away from home
  • self-harm or attempted suicide
  • eating disorders
  • oral signs (eg STIs)
  • alluding to secrets which they cannot reveal
  • disclosure
263
Q

describe how we deal with suspected child abuse (flowchart)

A

1 assess the child (hx, ex, talk)
2 discuss concerns with appropriately experienced colleague
- local safeguarding board, safeguarding children advisory service telephone helpline
- consultant paediatrician
- child protection nurse
- social services
- HV, GP

STILL HAVE CONCERNS:
3 provide urgent dental care
4 talk to child and parents and explain concerns, inform of intentions to refer and seek consent to share info
5 refer for medical examination if needed, keep full clinical record
6 refer to children’s services, following up in writing within 48 hours
7 confirm referral has been received, arrange dental follow up

NO LONGER CONCERNED:
3 provide necessary dental care
4 keep full clinical records, consider liaison with HV/school nurse
5 arrange dental follow up

264
Q

when might it not be appropriate to inform the parents about a child protection referral? (4)

A
  • contrary to child’s welfare
  • putting yourself or your team at risk
  • suspicions of sexual abuse
  • suspicions of fabricated or induced illness (FII)
265
Q

define dental neglect

A

“the persistent failure to meet a child’s basic oral health needs, likely to result in the serious impairment of a child’s oral or general health or development”

266
Q

what are the possible effects of dental neglect? (up to 8)

A
  • toothache
  • disturbed sleep
  • difficulty eating
  • absence from school, interference in performance
  • repeated antibiotic use
  • exposure to GA-associated morbidity
  • Turner’s tooth
  • life-threatening systemic illness
267
Q

what features may raise concerns with regards to dental neglect? (up to 8)

A
  • severe untreated dental disease (obvious to a layperson)
  • dental disease with significant impact on the child
  • parent/carer has access to but persistently fails to obtain treatment for the child
    – irregular attendance
    – repeated failed appointments
    – failure to complete treatment
    – returning in pain at repeated intervals
    – requiring repeated GA
268
Q

what is the tiered response to dental neglect?

A

1 preventive dental team management
2 preventive multi-agency management
3 child protection referral
- implemented according to level of concern

269
Q

describe the “was not brought” pathway

A

1 - reception calls parent within 24 hours for reason for WNB and offer new appointment, also offer discussion about any worries
2a - phone contact success = send WNB1 letter home and document
2b - phone contact failure = send WNB2 letter home, document and wait
- parent contacts = step 1 and documentation
- parent fails to contact within 3 weeks = clinician informed and risk assessment (sharing of information, contact GP) and decide if further action is required, document

270
Q

give some barriers to the management of dental disease in medically compromised children (3)

A
  • reluctance of GDPs to treat as they may feel inadequately trained
  • children may become sensitised to treatment and have increased anxiety
  • dental health seen as low priority in the face of other chronic illness demands
271
Q

list the main types of medically compromising conditions we need to look out for in children (6)

A
  • CV disorders
  • haematological disorders
  • respiratory system disease
  • metabolic and endocrine disorders
  • oncology
  • organ transplants
272
Q

what kinds of CV disorders should we be aware of when treating children? (3)

A
  • congenital structural defects = shunts, valve defects
  • acquired = rheumatic fever, Kawasaki’s disease, cardiomyopathy, prosthetic valves
  • previous IE
273
Q

how may a child with congenital structural heart defects present? (6)

A
  • breathlessness on exertion
  • tire easily
  • recurrent respiratory infections
  • cyanosis
  • finger clubbing
  • delayed growth or development
274
Q

list some congenital structural heart defects (3)

A
  • shunts = atrial septal defects, ventricular septal defects, patent ductus arteriosus
  • valve = aortic/pulmonary stenosis
  • complex = Fallot’s tetralogy, transposition of the great vessels, coarctation of aorta
275
Q

list some acquired heart diseases (5)

A
  • rheumatic fever
  • Kawasaki’s disease
  • cardiomyopathy
  • prosthetic valves
  • infective endocarditis
276
Q

describe infective endocarditis (what, fatality rate, risk)

A
  • life-threatening infection of endocardium, especially affecting heart valves
  • fatality rate of 30%
  • those with some cardiac defects have increased risk
277
Q

how does infective endocarditis develop?

A

1 turbulence of blood flow, endothelial damage
2 fibrin and platelet deposition
3 seeding with bacteria
4 colonisation and multiplication
5 increased fibrin and bacteria = vegetations, risk of embolism to lung/brain

278
Q

which cardiac conditions have increased risk of developing IE according to NICE? (5)

A
  • structural congenital heart disease, including surgically corrected or palliated conditions (excluding fully repaired defects or endothelialised closure devices)
  • acquired valvular disease with stenosis or regurgitation
  • valve replacements
  • hypertrophic cardiomyopathy
  • previous IE
279
Q

what information should be offered to patients at increased risk of IE regarding dental treatment? (4)

A
  • risks/benefits of antibiotic prophylaxis and why it is no longer routinely recommended
  • importance of maintaining good oral health
  • symptoms that may indicate IE and when to seek expert advice
  • risks of undergoing any invasive procedure (inc non-medical)
280
Q

why is antibiotic prophylaxis not recommended routinely for dental procedures? (3)

A
  • dental procedures not thought to be the main cause of IE (2-3%)
  • unclear if prophylaxis actually prevents IE
  • side effects (nausea, diarrhoea, allergy, anaphylaxis)
281
Q

how does dental treatment planning vary for children with CV disorders? (5)

A
  • aggressive prevention (diet, F-, FS,OHI) with regular clinical and radiographic monitoring
  • dental disease treated before any cardiac surgery
  • no antibiotic cover for routine procedures, consider cover if chronic infection
  • more radical treatment planning due to risk of chronic infections and IE
  • do not conduct routine dental tx until symptomatic cardiac disease is thoroughly investigated
282
Q

how may avulsed permanent tooth management differ for children with CV disorders? (2)

A
  • risk of bacteraemia and possible chronic infection = must discuss risk/benefit
  • replantation may proceed immediately but do not replant if high risk cardiac pt or poor prognosis (prolonged EADT)
    (antibiotics usually indicated anyway)
283
Q

list some types of inherited haematological disorders (3)

A

1 clotting:
- haemophilia A (FVIII deficiency)
- haemophilia B (FIX deficiency)
- von Willebrand’s disease
2 platelet = immune thrombocytic purpura (ITP)
3 blood dyscrasias
- thalassaemia (minor or major)
- sickle cell anaemia

284
Q

describe haemophilia A (what, demographic, effect)

A
  • x-linked recessive, factor VIII deficiency
  • males
  • varying levels with increased bleeding risk
285
Q

describe von Willebrand’s disease (what, effects)

A
  • most common inherited bleeding disorder
  • dominant, von Willebrand’s factor deficiency
  • vascular abnormalities, defective platelets, decreased FVIII
286
Q

give 2 acquired haematological disorders/conditions

A
  • vitamin deficiency
  • anticoagulant therapy (warfarin, heparin)
287
Q

how does dental treatment planning vary for children with haematological disorders? (6)

A
  • prevention and regular review
  • pulp therapy favoured to avoid extractions
  • restore early lesions
  • liaise with haematologist for any extractions and consider local measures
  • infiltrations&raquo_space;, avoid ID blocks (haematoma, airway compromise)
  • if blocks required then factor supplements are needed +/- tranexamic acid
    (best in hospital setting)
288
Q

describe sickle cell anaemia (what, effects, s/s, GA)

A
  • autosomal recessive mutation
  • RBCs clump together under certain conditions (blockages, necrosis, pain) - eg infection, hypoxia
  • pale, tired, weak, breathless, painful joints, growth retardation, increased susceptibility to infection
  • risk for GA (need to keep oxygen high)
289
Q

give 2 respiratory system diseases we should be aware of in children

A
  • asthma
  • cystic fibrosis
290
Q

describe asthma (what, dental triggers)

A
  • obstructive reversible lung disease causing breathlessness, coughing, wheezing - associated with hyperreactivity of airways to various stimuli
  • dental triggers = anxiety, dust, aerosols, NSAIDs
291
Q

how does dental treatment planning vary for children with asthma? (5)

A
  • increased prevention - higher risk for caries, erosion, candida
  • decrease anxiety as much as possible, may take a puff before treatment
  • medications must be brought to appointments
  • normal routine care
  • LA and IHS better, avoid GA if possible
292
Q

describe cystic fibrosis (what, s/s)

A
  • autosomal recessive, multisystem disorder mostly affecting exocrine glands
  • thick mucus, especially in the lungs causing obstruction and airway infections, malabsorption
  • delayed dental development, enamel opacities, more prone to calculus development
293
Q

how does cystic fibrosis affect a child’s dental health/treatment? (4)

A

1 high caries risk
- snack on highly refined carbohydrates (need high calorific intake)
- decreased buffering of saliva
2 clotting defects due to liver cirrhosis
3 antibiotic sensitivities, sometimes prescribed tetracycline (intrinsic staining)
4 avoid GA due to pulmonary involvement

294
Q

what is the most common endocrine disorder in children?

A

diabetes (type 1)

295
Q

how does dental treatment planning vary for children with diabetes? (5)

A
  • intense prevention and regular review
  • normal dental tx if well controlled
  • early morning or early afternoon appointments
  • advise normal insulin and normal eating - glucose drink if hypo
  • minimal stress, may refer for GA
296
Q

oral manifestations of diabetes in children (4)

A
  • xerostomia (salivary gland dysfunction, increased salivary glucose, polyuria)
  • increased caries in low risk areas (salivary hypofunction, increased salivary glucose, poor OH)
  • candidiasis (salivary hypofunction, underlying deficiencies) - acute pseudomembraneous, angular cheilitis
  • periodontal disease (increased pro-inflammatory mediators, increased GCF glucose)
297
Q

what is the most common malignancy in childhood?

A
  • acute lymphoblastic leukaemia (peak at 4yo)
298
Q

list some oral complications that child oncology pts may have (8)

A
  • periodontal inflammation
  • oral mucositis
  • tooth morphology - agenesis, microdontia, short roots, enamel/dentine developmental defects, discolouration
  • reduced salivary flow (caries)
  • candida infections
  • loss of taste (improves over time) - may eat sweets
  • difficulty swallowing - Difflam, moist food
  • jaw stiffness
299
Q

how does dental treatment planning vary for children with cancer? (5)

A
  • intense prevention and regular review
  • dentally fit before cancer treatment = prioritise infections, extractions and sources of tissue irritation
  • pulp therapy not recommended due to immunosuppression - radical treatment planning
  • defer elective dental care during therapy, liaise with oncologist for any essential tx
300
Q

describe autism spectrum disorders (what, up to 5 characteristics)

A
  • group of developmental disorders defined by a significant impairment in social interaction, communication and the presence of unusual behaviours and interests
  • impaired communication and socialisation
  • difficulty recognising others’ emotions and expressing their own
  • lack of social imagination, inability to read social cues
  • hyper or hyposensitivity to normal stimuli
  • repetitive or restrictive patterns of behaviour
301
Q

what other comorbidities may a patient with ASD have? (7)

A
  • ADHD
  • OCD
  • depression
  • epilepsy
  • dyspraxia
  • dyslexia
  • insomnia
    (etc)
302
Q

oral features commonly associated with patients with ASD (4)

A
  • poor OH - poor tongue and cheek coordination, hyperreactive to stimuli
  • caries
  • xerostomia (s/e of medication)
  • orofacial pain - bruxism, self-abusive injuries (gingival defects, biting, self-extraction)
303
Q

how may diet be affected in a child with ASD? (3)

A
  • eating disturbances (“picky eater”)
  • preferences for soft, high sugar content food
  • pocketing and pouching of food
304
Q

how may a child with ASD be prepared for the dental visit? (4)

A
  • pre-appointment questionnaire (developmental age, ability to read, toilet training, social interactions, likes and dislikes)
  • visual supports eg calendar, pictures
  • pre-visit sessions
  • social story books
305
Q

how may your practice change for a child with ASD? (4)

A
  • first appointment of the day (minimise wait time, waiting room)
  • double appointment (more time)
  • not changing any plan of the appointment once it has been explained
  • removing overwhelming sensory stimuli
306
Q

what is the GDP’s role with oral pathology in children? (4)

A
  • careful examination and diagnosis and documentation
  • reassurance to parents
  • appropriate treatment or referral to specialist
  • provide routine dental care
307
Q

where is most oral pathology found in children?

A

soft tissues

308
Q

give some developmental soft tissue lesions which may present in children (6)

A
  • Bohn’s nodules
  • eruption cyst
  • tongue tie/ankyloglossia
  • geographic tongue/erythema migrans/benign migratory glossitis
  • white sponge naevus
  • Fordyce’s spot
309
Q

management of Bohn’s nodules

A

leave and monitor (should disappear spontaneously by 3 months)

310
Q

describe eruption cysts in children (what, presentation, management)

A
  • developmental odontogenic
  • purple/red swellings of alveolar mucosa which may delay eruption
  • radiographically may appear as enlarged follicle
  • monitor (burst with spontaneous eruption) or incision if causing significant problems
311
Q

describe ankyloglossia (what, management)

A
  • lingual frenulum attaching near the tip of the tongue
  • excised only if interfering with breastfeeding, speech development, oral hygiene or causing gingival recession
312
Q

describe geographic tongue (associations, presentation)

A
  • genetic, may be associated with psoriasis or atopy
  • defined, irregular smooth/shiny red areas surrounded by distinct yellowish, slightly raised margins on tongue dorsum
  • changes in shape, moves around on tongue
  • usually asymptomatic, may be sore to acidic foods, cheese, toothpaste
313
Q

describe white sponge naevus (what, presentation, management, histology)

A
  • inherited AD disorder of keratin, benign
  • white soft thickened folded mucosa with undefined margins, usually bilateral on buccal mucosae
  • monitored
    histology:
  • “basket-weave” appearance of cell membranes, no dysplasia or inflammation
  • hyperkeratosis, thickened epidermis with spongy appearance
314
Q

describe Fordyce’s spots (presentation, management)

A
  • small yellowish ectopic sebaceous glands
  • buccal mucosa, anterior pillar of fauces, lips
  • become more prominent in puberty
  • no intervention required
315
Q

list some reactive soft tissue lesions that may be seen in children

A
  • mucocele/mucous extravasation cyst
  • infections = primary herpetic gingivostomatitis, ulceration, VZV, candidiasis, squamous papilloma
  • gingival enlargements = inflammation, gingival fibromatosis, DIGO, OFG, etc
  • ulcerative = RAS (minor)
316
Q

what is an important differential for gingival enlargement in children?

A

leukaemia

317
Q

most common site for pyogenic granuloma in children

A

maxillary palatal gingiva of incisors/premolars

318
Q

describe hereditary gingival fibromatosis (cause, presentation, histology, tx)

A
  • genetic (associated with hypertrichosis and LD) or idiopathic
  • diffuse, multinodular overgrowth of fibrous tissue of gingiva
  • associated with delayed tooth eruption
  • histology = epithelial hyperplasia, increased collagen, little/no inflammation
  • tx = improve OH, gingivectomy after puberty (recurrence common)

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