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REVISION BDS > paeds 430 > Flashcards

paeds 430 Flashcards

1
Q

caries pattern in children

A

caries rate in lower 6s higher than in uppers

pit and fissure caries - palatal of upper 6s and 2s and buccal of lower 6s

second molars erupting

host factors i.e. reduced salivary flow and high mutans counts

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2
Q

caries definition

A

‘‘disease of mineralised tissues; enamel, dentine and cementum, caused by action of micro-organisms on fermentable carbohydrates … In it’s very early stages the disease can bearrested since it is possible for remineralisation to take place”

(Kidd et al, 1987)

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3
Q

caries classification

A
  • Decalcification
    • White/Brown spot lesions
  • Pit and fissure caries
  • Smooth surface caries
    • Buccal
    • Lingual
    • Cervical
  • Interproximal
  • Early Childhood or nursing bottle caries
    • Max incisors, 1st molars, mandibular canines
    • lower incisors are protected by the tongue
  • Recurrent/Secondary caries
  • Arrested Caries
  • Rampant Caries
    • 10 or more new lesions per year
    • Lower anteriors affected
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4
Q

eval of dentition of child

A

restorability

pt and parent compliance

stage of development

space management (drifting, ortho considerations)

anticipated difficulties

overall prognosis

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5
Q

loss of upper first permanant molars

before complete eruption of 7s

A

7 rotates

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6
Q

loss of lower first permanent molars

after optimum age

A

7 tilts mesially

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7
Q

loss of lower first permanent molars

before optimum age

A

5s drift distally and rotate

rotates to form arbitrary occlusal contact

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8
Q

3 safety reason for rubber dam

A

damage to soft tissues

risk of inhalation

cross infection

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9
Q

benefits to operator and pt of rubber dam

A

increase

  • isolation and moisture control
  • retraction of gingivae and cheeks
  • effective inhalation sedation
  • pt confidence
  • operator confidence
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10
Q

SDCEP caries prevention guidance

A

Give toothbrushing advice at least once a year:

  • Brush at least twice daily, in the morning and last thing at night,
  • Use the correct amount of a toothpaste with age-appropriate fluoride concentration:
    • Under 3 years old: use a small smear of paste containing not less than 1000 ppm fluoride
    • 3–6 years inclusive: use a pea-sized amount of paste containing not less than 1000 ppm fluoride
    • 7 years old or over: use paste containing 1350–1500 ppm fluoride
  • Spit, don’t rinse.
  • Help children under 7 years old and continue to supervise older children until confident in their brushing habits.

In the early stages of providing care give hands-on brushing instruction.

Give dietary advice at least once a year:

  • Restrict foods and drinks containing sugar to meal times.
  • Drink only water or milk between meals.
  • Snack on sugar free snacks (e.g. fresh fruit, carrots, peppers, breadsticks, occasionally a little cheese).
  • Do not eat or drink after brushing at night.

Be aware of hidden sugars in some foods and the acid content of drinks. Apply sodium fluoride varnish (5%) twice a year to children over 2 years of age

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11
Q

caries risk factors

A

General

  • Social
    • Mother’s Secondary education
    • Dental attendance
    • Family unit - single parent/social class/employment status
  • Systemic Health
    • Generally unwell
    • Chronic illnesses
    • Sugar based medications - often contain sucrose

Local

  • Oral Hygiene
    • Poor, Irregular brushing, unassisted
  • Diet
    • 3 or more instances of sugar intake per day
  • Fluoride experience
    • Infrequent use of F- toothpaste
  • Past Caries experience
    • dmft - more than or equal to 5
    • DMFT - more than or equal to 5
    • 10 or more initial lesions
    • Caries in 6’s at eruption (6-7 years)
    • 3 years caries increments
  • Ortho treatment
    • fixed appliance therapy
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12
Q

acronym to remember caries risk factors

A

S ome

S tudents

O ver

D o

F luoride

C ocaine and

O rthodontics

Social Systemic OH Diet Fluoride experience Caries experience Ortho fixed applicances

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13
Q

Caries risk assessment

A
  1. clincial evidence
  2. dietary habits
  3. social history
  4. fluoride use
  5. plaque control
  6. saliva medical history
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14
Q

8 aspects of prevention plan from CPCS

A
  1. radiographs (and frequency)
  2. toothbrushing instruction
  3. strength of F- toothpaste (ppm)
  4. F- varnish (frequency)
  5. F- supplements
  6. diet advice
  7. fissure sealants
  8. sugar free medications
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15
Q

most common trauma in primary dentition

A

luxation

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16
Q

most common trauma in permanent dentition

A

ED#

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17
Q

9mm+ overjet increases chance of trauma

A

200%

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18
Q

medical hx for trauma red flags

A

rheumatic fever

congenital heart defects

immunosuppression

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19
Q

EO for trauma look for

A
  • Laceration
  • Haematoma (bruise)
  • Haemorrhage/CSF - Emergency if straw coloured fluid from nose eyes or ears
  • Subconjunctival haemorrhage
  • Bony step deformity in mandible
  • Mouth opening difficulty
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20
Q

IE for trauma check

A

soft tissue

alveolar bone

occlusion changes

teeth

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21
Q

tooth mobility can be due to

A

displacement

root #

bone #

look for fracture lines (horizontal or vertical) and pulpal involvement

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22
Q

dull note on percussion indicates

A

root #

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23
Q

what requires urgent tx

A

traumatic occlusion post trauma

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24
Q

emergency management of avulsion

A
  1. hold crown only
  2. wash under running water
  3. replace in socket
  4. child bite on tissue or store in milk/saliva/saline
  5. seek dental advice ASAP
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25
Q

tx if EADT is <1hr

A
  • replant under LA
  • flex splint 2 weeks
  • antibiotics
  • tetanus status
  • extirpate pulp unless open apex in <10days

monitor

  • non vital - endo tx and 2 month intermediate steroid medicament
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26
Q

tx if EADT >1hr

A
  • replant under LA
  • heal by ankylosis
  • endo at 7 days
  • 4 week splint

if open apex

  • might revascularise
  • replant under LA
  • antibiotic prescription
  • watch for necrosis
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27
Q

external surface resorption

A

damage to PL which subsequently heals

non-progressive

e.g. maxillary canines/laterals through excessive orthodontic forces

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28
Q

external inflammatory resorption

A

damage to PL intially maintained and propagated with dentinal tubules

root surfaces are indistinct

tramlines of root canal intact

pulp extripation - mechanical and chemical irrigation NSCaOH

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29
Q

internal inflammatory resorption

A

intiated by non-vital pulp

progressive

dx: tramlines of root canal indistinct, root surfaces intact
tx: extirpation, mechanical and chemical irrigation, NSCaOH

change NSCaOH for 4-6 weeks to try and halt resorption

6 weeks obturate with GP

if resorption continues, plan pros tx

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30
Q

resorption - replacement ankylosis

A

initiated by severe damage to PL and cementum

normal repair does not occur

bone fused directly to dentine

progressive - tooth gradually resorbed as it is now part of bone remodelling

dx: loss of PL and lamina dura

Tx: nil

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31
Q

immedicate management for all trauma injuries

A
  • soft diet for 10-14 days
  • brush teeth with soft toothbrush after every meal
  • topical CHX by parent twice daily for one week (CWR for swabbing)
  • after intial tx review 1, 3, 6 monthly taking radiographs if possible 6 monthly
    • intrusion requires montly review for 6 months, then 6 monthly
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32
Q

enamel #

A

smooth sharp edges

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33
Q

enamel/dentine #

A

restore/bandage with composite (not GI)

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34
Q

EDP #

A

endo therapy or extract

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35
Q

crown and root #

A

extract coronal fragment, don’t remove any root fragments that aren’t obvious they will be resorbed physiologically

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36
Q

alveolar #

A

reposition segment

splint to adj teeth (only time for primary trauma where its used)

teeth may need extracted later

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37
Q

concussion/subluxation

A

observe

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38
Q

lateral luxation

A

increased PDL space apically

if no occlusal interference - allow it to reposition, if interfering then extract

39
Q

intrusion

A

if root displaced labially to tooth germ leave to re-erupt

if palatally toward tooth germ - extract

40
Q

extrusion

A

extract

41
Q

long term effects of trauma on primary teeth

A

immediate discolouration - vitality maybe maintained

discolouration over weeks - non-vital

  • sinus or PAP on radiograph
    • no sinus or PAP then leave and review
  • opaque - no tx

delayed exfoliation of primary tooth

  • XLA needed or permanent successor maybe extopic or not erupt
42
Q

child abuse definition

A
  • Significant harm to child
    • Carer has some responsibility for that harm
    • Significant connection between carer’s responsibility to the child and harm to said child
43
Q

signs of neglect

A
  • Failure to thrive/short stature
  • Inappropriate clothing, cold injury, sunburn
  • Ingrained dirt finger nails, head lice, dental caries, developmental delay
  • withdrawal or attention seeking behaviour

Dental Neglect
➡ Toothache
➡ Disturbed sleep
➡ Difficulty eating/change in food preference (only soft food etc)
➡ Absence from school

44
Q

management of child abuse/neglect

A

Preventive dental team management
‣ raise concerns with parents, offer support, set targets, keep records and monitor progress.

Preventive multi-agency management
‣ liaise with other professionals (e.g. health visitor, school nurse, general medical practitioner, social worker) to see if concerns
are shared
‣ A child may be the subject of a CAF (Common Assessment Framework) at this level.
‣ Check if child is subject to a child protection plan (which replaced the child protection register)
‣ Agree joint plan of action, review at agreed intervals
‣ Letter to Health Visitor of children < 5 who fail appointments and have failed to respond to letter from dental practice
๏ “If this family is known to you, we would welcome working together to promote their oralhealth.”

Child protection referral
‣ In complex or deteriorating situations
‣ Follow local guidelines
‣ Referral is to social services
๏Usually by telephone followed up in writing

45
Q

signs of physical abuse

A
  • Bruising of face - punch, slap, pinch
  • Bruising of ears - pinch, pull
  • Abrasions and lacerations
  • Burns and bites
  • Neck - choke or cord marks
  • Eye injuries
  • Hair pulling
  • Fractures (nose>mandible>zygoma)

Misnomers to be aware of

  • Impetigo- similar to cigarette burns
  • Birthmarks- mistaken for bruises
  • Facial infection- mistaken for trauma
  • Coagulation problems- bruise easily
46
Q

expectation of dental team re abuse/neglect

A
  • Observe
  • Record
  • Communicate
  • Refer for assessment

NOT expected to diagnose

47
Q

plaque induced gingivitis in children

A

most apical extension of juctional epitheliym is still the CEJ with no periodontal loss of attachment

severe inflammation -> gingival swelling inc -> even deeper false gingival pocket

48
Q

necrotising ulcerative gingivitis

A

blunted papillae

malodour

painful gingivae

aetiology

‣ Fusiform and Spirochete bacilli
‣ Patient risk factors
๏Smoking
๏Stress
๏Immunosuppression
๏Poor Diet
๏HIV status
๏Other underlying conditions
๏Common in developing countries

49
Q

puberty gingivitis

A

increased inflammatory response to plaque

mediated by hormonal changes

can progress to early perio

local and systemic factors can influence progression

50
Q

systemic causes of gingivitis

A

haematological

  • *Agranulocytosis** - Acute condition with low white cell count
  • *Cyclic Neutropenia** - Low Neutrophil Count, in 3 week cycles lasting 4-6 days
  • *Granulomatosis** - autoimmune vasculitis, multi system disorder affecting mouth, URT and kidneys
51
Q

hyperplastic gingivitis

A

Genetic factors, local factors

Medication side effects

  • Cyclosporin
  • Nifedipine
  • Phenytoin

Greater incidence in puberty

Tx - rigorous home care, frequent scaling, often surgery required (esp. drug induced)

52
Q

key features of periodontitis

A

apical migration of JE below ACJ

loss of attachment fibres of cementum

change from JE to pocket epithelium (often thin and ulcerated)

alveolar bone loss

53
Q

chronic periodontitis

A

similar pathogens to adults with chronic perio can be found in subgingival microflora of teenagers with chronic perio

  • Porphyromonas Gingivalis
  • Prevotella intermedia
  • Aggregatibacter Actinomycetemcomitans
54
Q

aggressive periodontitis

A

Caused by Aggregatibacter Actinomycetemcomitans

Rapid attachment loss and bone destruction
Otherwise patient healthy

family history
should be referred

Localised
‣ Incisors
‣ First molars
‣ onset at puberty

Generalised
>3 permanent teeth other than incisors and first molar
onset usually older but sometimes <30 y/o

55
Q

early periodontitis

A

Typically

  • 1-2mm LOA interproximally
  • 4-5mm pocket
  • 0.5mm horizontal bone loss
56
Q

perio screening consists of

A

gingival condition

assess OH status

assess if any calculus present

assess local risk factors

57
Q

gingival condition in perio screening

A

colour

contour

swelling/recession

suppuration

inflammation - presence and location

marginal bleeding free chart

58
Q

OH status assessment in perio screening

A

description of plaque status

  • surfaces covered by plaque
  • easily visible?
  • dectectable only by probing
  • use of plaque free scores
    • motivational aid
59
Q

local risk factors assessment in perio screening

A

plaque retention factors

low frenal attachments

malocclusion

incompetent lips

reduced upper lip coverage (labial and palatla gingivitis)

increased lip separation

mouth breathing

palatal gingivitis

60
Q

BPE in primary dentition

A

Carried out on UR6 UR1 UL6 LR6 LL1 LL6

Start at 7 years when all the index teeth have erupted

Identifies patients who would benefit from further investigation

Primary teeth - perio disease rare
If mobility or suppuration - refer to specialist

codes restricted 0-2 to avoid false pocketing

from ages 11-17 full range of BPE used

BW’s posteriors, PA’s for anteriors

Always take BPE prior to ortho treatment

61
Q

primary herpetic gingivostomatitis

A

Variable incubation period

Widely varying severity of symptoms

  • Fever, Malaise, Loss of appetite
  • Can cause severe systemic upset

Features

  • Vesciles on mucosa
  • Gingivae are fiery red
  • Rupture of vesicles = Ulcers 1-3mm in diameter
  • Mouth is very painful
  • Refuse to eat
  • Refuse toothbrushing
  • Halitosis

Treatment

  • Fluids
  • Rest/Reassure = recover
  • NSAIDs
  • Aciclovir only in early stages/immunocompromised patient
62
Q

herpangina

A

Highest incidence in young children

2-9 day incubation

fever, malaise, muscle pain

pinhead vesicles on tonsils, uvula, soft palate

  • lesions all at the back of the mouth

vesicles rupture to form larger ulcers

heal within 5-7 days

No gingivitis

Less unwell

63
Q

hand foot and mouth

A

1 week incubation

Cozsackie A16

vesicular rash on limbs, fingers and toes

oral lesions on tongue and buccal mucosa

ulcers are shallow

painful

self limiting

64
Q

HPV (papilloma)

A

Cause
‣ Verruca Vulgaris
‣ Papillomas
‣ Focal Epithelial Hyperplasia (Heck’s Disease)

Warts on lips and tongue

Papillomas on gingivae and palate

Appearance
‣ Cauliflower like
‣ Localised
‣ Increased Incidence in Immunocompromised

65
Q

minor apthae

A

recurrent apthae on Non-Keratinised mucosa
- Labial, Buccal mucosa and floor of mouth

prevalance >2%

  • Stress/Family history/HLA type
  • Altered T cell ratio?
  • Some develop Crohn’s disease later
  • iron def. common in girls from menstrual blood demand - can cause apthae
  • Fe Replacement treatment of symptoms - diflam mouthwash

variable size
well demarcated
red halo round lesion
1-10 in number
heal 1-3 weeks
no scarring
more common in 20’s

66
Q

eruption cysts

A

dilation of follicular space around crown

compressible

can be infected

resolved when tooth erupts

blueish hue

67
Q

ranula

A

present as a swelling of connective tissue consisting of collected mucin (thick and jelly like) from a ruptured salivary gland caused by local trauma

68
Q

traumatic ulcer characteristics

A

history

non recurrent

less well defined

irregular outline

69
Q

radiation mucositis

A

Mucositis is a common complication of cancer therapy which
significantly affects the mucosa.

Oral mucositis refers to the oral erythematous and ulcerative
lesions commonly observed in patients undergoing cancer
therapy.

They are painful and affect nutrition and quality of life of the patient, and contribute to local and systemic infections

Radiation induced mucositis is initiated by direct injury to basa epithelial cells and cells in the underlying tissue. DNA-strand breaks can result in cell death or injury

70
Q

orofacial granulomatsis

A

associated with Crohns disease

High incidence in west of scotland

presents in 2nd or 3rd decade

  • Lip swelling
  • Biopsy shows non-caeseating granulomas
  • Langhans type giant cells
  • Lymphocytic infiltrate
  • Swelling due to oedema
  • Cobblestone mucosa
  • mucosal tags
  • deep penetrating ulcers
  • gingivitis
  • pyostomatitis
71
Q

fibro epithelial polyp

A

common

exagerrated response to trauma

should usually be excised

squamous epithelium overlying firbous CT, minimal inflammaiton

72
Q

pyogenic granuloma

A

‣ Fibro-endothelial growth
‣ Gingival margin
‣ Common in children
‣ Red/purple, very vascular
‣ Mimic haemangioma
‣ Ulcerate and can bleed
‣ profusely
‣ Complete excision ? Cryo

73
Q

giant cell granuloma (peripheral)

A

appears in the mouth as an overgrowth of tissue due to irritation or trauma

appears histologically as large number of multinucleated giant cells which can have dozens of nuclei

74
Q

malignant proliferative conditions in children

A

Malignacy is most common cause of death in childhood (14% in <15years)

Leukaemia

  • Peak age 2-5 years
  • Male>Female
  • 80% are ALL
  • Good rate of cure
  • Gingival bleeding, fatigue etc like primary herpes

Lymphoma

  • 1% childhood malignancies, older children

Rhabdomyosarcoma- majority are <4 years

75
Q

geographic tongue

A

2-10% prevalence

Children <4yrs mostcommon

Red zones of depapillation, move around!

White margins due to heavy infiltration

No successful tx

76
Q

heriditary gingival fibromatosis

A

non specific progressive enlargement

maybe localised e.g. palatal aspect of tuberositiess, or generalised

maybe isolated or part of a syndrome

drug induced - nifidipine, cyclosporin, phenytoin

77
Q

haemangioma

A

Present at birth or soon after

Grow rapidly

Benign tumour, endothelial proliferation

Capillary/Cavernous

Can occur within bone

Most will involute spontaneously

78
Q

occlusal cavity restoration

A
  1. Occlusal portion no greater than 1.5mm depth with fissure bur or round bur
  2. Include all pits and fissures but preserve transverse ridges unless undermined

Upper E

  1. Banana Distal
  2. Kidney Mesial

Lower E
3. Follow fissure pattern but dont breach marginal ridges (squiggly S)

79
Q

approximal cavity

A
  1. Isthmus should be 1/2 to 1/3
  2. Axial wall follows contour of tooth
  3. Don’t encroach onto the occlusal surface
  4. Remove marginal ridge then sink box
80
Q

minimal box preparations

A
  1. Basically a proximal box with no occlusal portion
  2. Rounded line angles
  3. No occlusal extension
  4. Dam and wedge for good contact pt
  5. Use narrow fissure bur
81
Q

cervical caries management

A
  1. Hand excavate caries using slow speed with round bur
  2. Wash and isolate with rubber dam
  3. Either GIC covered with vaseline or compomer (composite has tendency to #)
82
Q

anterior caries management

A
  1. Hand excavate or use a slow speed round bur
  2. Wash and isolate preferably with rubber dam
  3. Acetate into contact pts
83
Q

Stainless steel crown placement

A

Instruments Needed

  • Tapered diamond separating bur
  • Straight fissure bur
  • Crown Crimping pliers
  • Curved crown scissors
  • GI luting cement

Crown Selection - measure M/D length of crown or simple trial and error

Procedure

  1. Marginal ridge reduction w/ round bur
  2. Break contact area and produce knife edge finish with tapered separating bur
  3. Remove any ledges at GM
  4. Occlusal reduction of 1-2mm
  5. Reduce crown bucco-lingually
  6. Test fit crown and should snap fit
  7. Mix GI and fill up crown
  8. Seat crown L to B

Problems with Crowns

  1. Rocking - When cervical margin is >1mm beyond
  2. Canting - due to uneven reduction of occlusal surface
84
Q

hall crown technique

A

Requirements

  1. No LA, Caries removal or tooth prep
  2. Child v cooperative
  3. Right size crown
  4. No pulpal involvement
  5. Sufficient coronal tissue left

Instruments
- Essential

  • MPT
  • Excavator (to remove crown if necessary)
  • Flat plastic to load crown with cement
  • Cotton wool rolls - to wipe away cement
  • Useful
  • Ortho biting stick - good for seating the crowns
  • Bond forming pliers (especially good if loss of M/D length)
  • Gauze for between tooth and tongue
  • Elastoplast or sticky microbrush

Separation

  • Ortho donut with floss looped through either end
  • Held taught and wiggled into contact
  • may need to disc the tooth
  • Remove at crown fitting appt

Procedure - same as SS crown

85
Q

follow up for stainless steel crowns

A

Minor Failure

  1. Sec. caries
  2. Crown worn or lost
  3. Restoration lost but tooth restorable4. Reversible pulpitis treated without pulpotomy or extraction

Major Failure

  1. Irreversible pulpitis
  2. Abscess requiring pulpotomy or XLA
  3. Interadicular radiolucency
  4. Filling lost and tooth unrestorable
86
Q

vital tooth pulpotomy

A

Indications

  • Carious or traumatic exposure of a bleeding pulp
  • Radicular pulp preserved and bleeding controlled
  • Pt able to take LA and rubber dam

Procedure

  • Access - High speed bur
  • Amputation - Haemorrhage control with Ferric Sulphate 15.5% for 20s (N.B If anterior or permanent then use saline!)
  • Restoration - cover with CaOH, GI Core, PFMC

Pulpal Evaluation

  • Normal bleeding - Uninflamed - bright red and good haemostasis
  • Abnormal bleeding - Inflamed - deep crimson and continued bleeding after pressure

Apexogenesis

  1. Radicular pulp left
  2. Calcific barrier formed over the radicular pulp with CaOH
  3. Permits normal physiological apexogenesis of the root

*Cvek Partial Pulpotomy is indicated where there is a exposed pulp <24 hours

87
Q

non vital tooth pulpectomy

A

Indications

  • Excellent pt cooperation
  • Hyperaemic pulp
  • Pulp necrosis
  • Caries into furaction
  • Irreversible pulpitiis
  • PA PDitis
  • Chronic Sinus
  • N.B if severe infection with facial swelling then AB’s and extraction

Procedure

  • Use slow speed bur or excavator
  • Remove contents of pulp chamber
  • Instrument to 2mm short of apex
  • Irrigate with CHX 0.2%
  • Dry with paper points
  • Obturate with Vitapex - CaOH and Iodoform paste OR MTA (leave for 30 mins to form apical barrier) and Gutta percha
    ➡ CaOH can dessicate dentinal proteins causing premature root fracture
  • Seal with mix of ZOE/GI
  • Take PA radiograph
  • Restore with PFMC

Apexification

  • Induces formation of osteocementum in a pulpless tooth via chemical means e.g CaoH or MTA
  • very rarely normal root development may take place
  • takes 9 months
88
Q

fissure sealants

A
  • Protective plastic coating used to seal fissures and pits to prevent food and bacterial accumulation that can cause caries
  • Isolate under single tooth dam
  • Tie ligatures into both holes of the clamp
  • Can alternartively use Cotton wool rolls and parotid guard

Indications

  1. High risk children
  2. Medically compromised
  3. Learning difficulties
  4. Permanent Molars, Cingulum pits upper incisors, buccal pits lower molars, palatal pits upper molars

Procedure

  1. Etch with 37% Orthophosphoric acid
  2. Wash off etch
  3. Bis-GMA resin painted onto fissure pattern
  4. No air blows
  5. Cure
  6. use probe to try and flick off - should be smooth and glassy
89
Q

XLA of FPMs

A
  • may help with spacing later on if prognosis poor
  • optimal occlusal relationship attained when
  • Bifurcation of lower 7 is formed on an OPT - 8.5-10 years
  • 5’s and 8’s are all pfesent and in good position
  • Mild buccal segment crowding
  • Class I incisor relationship

16/26

  • Loss before complete eruption of 7 - 7 rotates

36/46 >

  • Loss after optimum age - tilting 7’s - tilts mesially
  • Loss before optimum age - 5’s drift distally and rotate - rotates to form arbitrary occlusal contact
90
Q

microabrasion

A

Associated with
‣ Amelogenesis Imperfecta
‣ Trauma related staining
‣ MIH

Procedure

  1. Dental Dam with ligatures
  2. Polish the teeth pumice and water
  3. Apply Sodium bicarbonate to the cervical areas of the dam to create an alkaline barrier
  4. Apply 18% Hydrochloric acid or Opalustre 6%
  5. Use wooden popsicle stick to scrub on for 5 secs
  6. wash off with very good aspiration
  7. Dry teeth and reapply bicarb and start again
  8. Gold standard is 10 rounds of therapy

Works best on Brown staining
White stains can actually look worse and go yellowish
Best to do one tooth at a time so as not to over treat with acid, if doing >2 teeth as part of treatment, can remove the labial profile

91
Q

pulp canal obliteration

A
  • Narrowing of the pulp chamber and or root canal by dentine
  • mediated by odontoblasts, but not really known why this is
  • It will have a vital response but will be reduced
  • Tx - Do nothing but monitor vitality as only 1% form a PA area
  • Crown takes a yellow appearance - vital bleaching
92
Q

sequalae if trauma to primary tooth

A

Delayed eruption

  • Damage to perm tooth germ
  • Dilaceration of root
  • Odontome formation
  • Hypoplasia of enamel
  • Hypomineralisation
  • Root resorption
  • Ectopic eruption
  • Absent successor
  • Non-vitality
  • Sequestrum of successor
93
Q

amelogenesis imperfecta

A

REVISION BDS (43 decks)

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