paeds Flashcards
Can a father give a consent for a child
only if married to mother at or after birth, or on birth certificate after 1st December 2003
if not, then have to get in mother at next visit to consent for treatment
4 types of abuse. which is most common in children. How to approach it if suspect in clinic
physical, emotional, neglect, sexual
neglect most common
-be empathetic, ask questions, tell them it is not their fault, cannot promise you won’t tell anyone, you want to put their best interests first, don’t assume it is whoever has brought them
what is smith and knight index used for
tooth wear
What treatment is for brown fluorosis staining
-tray based whitening
-then controlled acid-pumice micro abrasion as it is more destructive and deep (good for localised brown mottling, fluorosis and idiopathic stains)
-veneers is last resort as cannot do treatment after that
What does balancing of teeth do. which primary teeth to avoid with balancing
prevent centreline shift
can do Cs, sometimes Ds, never Es
Early loss of E causes medial drifting of 6 and 5 can become impacted
For compensating of opposing arch, do you avoid lowers or uppers
avoid taking out lowers for compensating. Because lowers don’t over erupt
Which tooth is likely to be the cause of child complaining of sinking into gums
primary molar- infraocclusion if it is retained when adult dentition coming through
-fail to maintain occlusion with opposing teeth
Fluoride values in fluoride varnish, normal tooth paste, high risk patients (for different ages), prescribed mouthwash
-Varnish = 22600ppm, 2.26% NaF. Applied every 3 months for high risk
<6 years = smear or pea size of 1000ppm
7+ years= 1450 ppm
-Mouthwashes =prescription is 230ppm 0.05%, only for 8+ who comply
-High risk:
-0-10= varnish, 1350-1500ppm paste (no prescription), fissure sealants, recall every 3 months, diet
-10+ =2800ppm “
-16+= 5000ppm
Safe dose, potential lethal dose, and lethal dose of fluoride
*1mgF/kg safety tolerated dose (STD- dose below which symptoms are unlikely to occur)
*5mgF/kg potentially lethal dose (PLD-lowed dose associated with fatality)
*32-64mgF/kg certainly lethal dose (CLD- survival after containing this amount is unlikely) – so a tube of fluoride varnish has 3750mg in. 10kg child = dead
how much fluoride is in fluoridated water
0.5-1.5 mg/l
Optimum= 1ppm
(introduced in 1955)
Daily sugar limits
-4-6 years: 5 sugar cubes (19g)
-7-10 years: 6 cubes (24g)
-11+ years: 7 cubes (30g)
Contraindications for duraphat fluoride varnish. What other varnishes can be used instead
-unstable asthma (colophony sensitivity)
-gingival stomatitis
-ulcerative gingivitis
-latex, avocado, kiwi or banana allergy
-Profluoride not licensed for caries. (For hypersnsitivty) But indicated if latex allergy or issue with taste of duraphat
-Fluor Protector S (7700ppm) does not contain colophony so inidcated in unstable asthma, ulcerative gingivits, stomatitis. Need to dicuss with consultant as off license for caries, for hypersensitivty
For 0-3 year olds, when to start brushing, how much toothpaste, diets
-start brushing when teeth start coming through at 6 months, twice daily with smear of 1000ppm
-<6 months= breast milk/ formula
-6 months=complementary feeding of soft food
-9 months= soft lumps, liquids in beaker or cup
-12 months =bottle discouraged, use free-flow cup. Can use cows milk as main source of milk
-breastfeeding up until 2 years
What makes someone high risk for caries
-exisiting caries
-previous caries
-caries in 6s at age 6
-hypoplastic/hypomineralised teeth
-crowding
-ortho appliances, dentures
-family history of caries
-deep pits and fissures
-manual dexterity issues
-unfluoridated area (<0.3ppmF)
-vulnerable groups= homeless, in care, prisoner, asylum seeker
-poor dental access/ attendance
-poor oral hygiene
-poor motivation
-diet (could be medical related)- number of sugar and acid exposures
-dry mouth (due to meds)
-poor manual dexterity due to disability
3 reasons why moisture control is needed. Options
-Protect operators from aerosol spread, Protect soft tissues from materials, Isolate the tooth to keep it dry
-dry tip over parotid, cotton wool rolls in sulcus, saliva ejector curly wurly lingually, high volume aspirator
Criteria for fissure sealants. Materials used and their technique
-fully set, well bonded, extended to include all pits and fissures, not over filled or under filled, 1/3 cusp height, no air blows.
-Resin= moisture control, etch (10-30s), wash and dry, apply with thymosin probe, cure
-GIC= no etch or bond, apply with thymsion probe, no cure
What radiographs are required for primary/ mixed and permanent dentition for new patients. How often are they needed for high risks patients. How often for low risk.
-BWs and more views if indicated
-Primary low risk = 1-2 years
-Primary High risk = 6-12 months
Permanent/mixed low risk= 2-3 years
Permanent/mixed high risk= 1 year
(combo of FGDP and EAPD guidelines)
What are the 5 pillars of prevention
- Oral hygiene
- Diet
- Fluoride (water, milk, paste, varnish)
- Fissure sealants
- Review an recall
The 4 requirements for caries
-tooth, substrate (sugar), bacteria, time
What is the dosage for a single application of fluoride varnish for primary, mixed and permanent dentition (in ml)
-primary=0.25ml
-Mixed= 0.40ml
-Permanent=0.75ml
What is SDF. Fluoride concentration. How it is applied. Contraindications. Follow-up time and recall time
-silver diamine fluoride (44,800ppm, 38%)
-applied to carious lesions to arrest or slow the progress. Off license for caries but effective
-child needs to be able to sit still for at least 1 minute with isolation throughout
-Vaseline to lips, buccal mucosa and adjacent gingiva.
-Clean tooth and remove soft caries with excavator
-Dry tooth with cotton wool. Cotton wool in sulcus
-applied with micro brush, scrub for 10s, cure for 20s, blot dry and remove excess (1 drop per quadrant)
-simple application but stains caries black
-contraindications= infection, irreversible pulpits, caries into pulp, inflamed gingiva, allergy to metals, poor cooperation
-follow up in 2 weeks and reapply if necessary. 3-6 month recall according to caries risk
-Silver- bactericidal, protects the collagen
When should children start brushing on their own
-aged 6-7 usually have sufficient coordination to brush their teeth reasonably well, and be able to spit out toothpaste. Below that age many areas of the mouth will be missed and a tendency to swallow toothpaste , hence parental supervision is essential
-By 7, they can determine which messages merit attention and have better attention and concentration
what is classical conditioning and operant conditioning
-classical= when 2 things are associated with each other in someones mind (eg.feeling scared lying in a chair when treatment was done) so make environment different to situations in which the child felt scared or threatened
-operant= behaviour being rewarded, extinguished or punished. Positive or negative reinforcement (rewarding good behaviour or reward avoidance for bad behaviour)
Methods of calming an anxious patient
-acclimatisation- into them to environment
-tell, show, do
-distraction
-gradually introduce the fearful stimuli to desensitise them
-modelling: watching a parent having treatment
-sedation: oral diazepam/midazolam, nitrous oxide
Systemic and inherited diseases that can cause periodontitis
papillon-LeFevre syndrome (autosomal recessive)
ehlers-danlos syndrome
hypophosphatasia
chediak-higashi
neutropenia
leuokycte adhesion deficiency syndrome
diabetes
How the periodontium differs in children compared to adults
-marginal gingival tissues more vascular (red), fewer connective tissue fibres, thinner epithelia, less keratinization
-therefore look redder and often mistaken for inflammation.
-Thinner cementum and cortical plates.
-PDL less fibrous and more vascular. Bone more vascular and fewer trabeculae. [So perio disease progresses rapidly]
What altered BPE technique is used on children and why
-modified BPE technique used in <18 years
-BSP or BSPD
-6 index teeth (all 6s, UR1, LL1)
-start doing when 6s and incisors have erupted - 7 years
-Use codes 0, 1 and 2 for 7 yrs-11yrs
-Use full range of codes for 12yrs – 18 yrs. If codes 3 or 4 found = radiographs
-Eruption of primary dentition is accompanied by localized bleeding, leading to persistent swollen and rounded papillae and >3mm sulcus depths. due to tooth eruption, can seem more inflamed than it is
-Eruption of permanent teeth accompanied by migration of JE, leading to large sulcus depth. After full eruption, JE and gingival margin continue to shift. Will get different sulcus depths in BPE. Mistaken for gingival recession
Mouthrinse recommendations for children
<5 years = ¼ adult dose
>5 years= ½ adult dose
>10 years = adult dose
225ppm prescription for high risk 8+ who will comply
symptoms of Reye’s syndrome
causes by aspirin and viral illness (esp 5-10 years. Not used in <16 year olds)
-Sudden illness and vomiting. Increase in NH3 and H+ in blood, brain swells, liver inflames and fails, all organs affected.
-Death if undiagnosed. So instead use paracetamol or ibuprofen for viruses in children
Symptoms of sepsis in children
immune overreaction due to infection, causing inflammation, low BP, high RR, organ failure, fever, feels cold to touch, extreme pain, pale/ blue/ blotchy/ mottled skin/ lips/ tongue, confusion, lethargic, high HR, not urinating, low oxygen saturation, convulsion
-A purpuric rash, a weak high pitched cry, not responding normally (not interested in feeding or normal activities)
Symptoms of teething. Treatment
-ulcerated gingiva, won’t want to eat, sore to touch, dehydrated, drooling, rash around mouth, crying, disrupted sleeping.
-Treatment includes massage, dry the drool, teething toys/ foods, topical or systemic analgesia (bonjela, paracetamol elixir)
What are natal and neonatal teeth. Do they need removing
-natal teeth=born with teeth
-neonatal= come in within 30 days of birth
-underdeveloped, raged edges, hypoplastic, ulcer on tongue which affects feeding, wobbly, could be inhaled.
-Only remove if excessively mobile and airway risk, interferes with feeding, ulceration of ventral tongue. As part of normal denititon
What are eruption cysts. management
-blue area where bleeding in follicle. Will regress when tooth erupts so want it to erupt naturally
-Teething toys. May need ellipse of tissue, LA or GA If problematic. Be carful of bleeding as haemostasis can be difficult to achieve.
-do not touch as will bleed excessively. Heal on their own. Incise and drain only if symptomatic or interfering with occlusion.
what is gingivitis artefacta. Treatment
-picking or playing with gingiva causes recession and loss of attachment. Bitten nails can get impacted into gingiva and cause infection.
-Can be associated with dermatitis artefacta so consider referring to psychologist.
-Treated by removing cause, OHI, manage ulceration with chlorhexidine, soft diet/ fluids, review
Symptoms and treatment of acute necrotising ulcerative gingivitis
-bacterial inflection involving spirochetes.
-Interdental papilla destroyed (grey slough), erythema, painful, smell, commonly due to malnourished.
-Treatment involves OHI, debridement, smoking cessation, if infection then metronidazole (200mg) 3Xdaily for 3 days
What is cancrum oris/ noma. what its caused by. Treatment
-spirochete and fusobacterium infection due to malnourishment or previous bacterial or viral infection.
-Destroys soft and hard tissue, aggressive and gangrenous, due to poor sanitation. Subsaharan Africa.
-Treatment includes debridement, nutrition, antibiotics, hydration
Oral manifestations of HSV1 and 2, hand foot and mouth disease, herpangina, HHV3
-HSV1&2=vesicles in and around mouth, generalized gingiva erythema, herpetic gingiva stomatitis, heretic whitlow. Reactivation causes herpes labialis (cold sores)
-hand foot and mouth=coxsackie virus, very infectious, vesicles and ulcers (not on gingiva, more likely on palate)
-herpangina=coxsackie, Posterior aspect of oropharynx, progress to painful ulceration, sore throat, vomiting, general malaise. not on gingiva Can be misdiagnosed as tonsilitis
-HHV3= Runny nose, cold-like symptoms, precedes into skin rash, vesicle, ulcers, scabs – most infectious then. Itchy. Oral lesions can occur but never alone.
Reactivation causes shingles which is tingly
management of herpangina
Soft diet. Fluids. Analgesics and antipyretics. Benzydamine chloride 0.15% oral spray or rise every 2 hours (Difflam).
Management of chicken pox
Managed with bed rest, fluids, topical/ systemic analgesia (but not ibuprofen is it allows the virus to get deeper. Use paracetamol instead or lidocaine lollypop), ulcer coverage (orabase alone).
-If severe or immunosuppressed use acyclovir tablets, suspension or cream
Causes of recurrent aphthae stomatitis. Difference between minor and major
-ulcers on non-keratanised epithelium. Non-traumatic
-crohn’s, diet, stress, hormones, allergies, familial, trauma, deficiency (Fe/ folate/ B12) , Behcet’s, drugs
-Treat underlying cause, chlorehexidine, difflam spray (benztdamine hydrochloride 0.15%, antibacterial and reduces inflammation)
-Cover ulcer and reduce inflammation (adcortyl in orabase, gengigel)
minor=2-10mm
major ulcers=> 10mm diameter. Last >2 weeks. Heal with scarring
why good detection of caries is essential. What factors help us detect caries
-improve quality of life and wellbeing, aids prognosis, targeted prevention, decision making for treatment planning, allows us to inform the patient which can motivate them to change their behaviours, informs health service planning
-Detection requires: well lit, magnification (not essential for children though as want to see what they are doing), clean tooth (use dry brush or cotton wool), dry tooth (allows detection of early WSL by changing refractive index of enamel allowing greater light scattering), wet tooth (to allow detection of dentine shadowing), separators to allow vision of approximal regions (needs leaving on for a couple of days)
Explain these adjunctive detection methods for detecting caries (although rarely used as expensive and time consuming), Fiber-optic transillumination, Quantitative light-induced fluorescence, DIAGNOdent (Quantitative laser fluoresce),Electrical conductance measurement, Ultrasonic caries detector, Bioluminescence
- Fiber-optic transillumination: Lesion has lower index of light transmission and interrupts light beam so aids visual inspection, but not very specific and no numerical score given. More useful for anterior teeth and interproximal
- Quantitative light-induced fluorescence: blue light makes teeth green. Demineralisation of enamel reduces natural autofluorescence.
- DIAGNOdent (Quantitative laser fluoresce): Aids detection of non-cavitated caries. Healthy = little fluorescence. Carious = high value
- Electrical conductance measurement: intact enamel is a good insulator. Porosities in lesions fill with water and ions from saliva to increase conductance. More useful for pits and fissures and interproximal
- Ultrasonic caries detector: emits ultrasonic waves and measures echo. Cavities produce different echo than healthy tooth
- Bioluminescence: protein binds with calcium and camera picks up flash of light to indicate lesion.
Explain meanings of validity, reliability, sensitivity, specificity
Validity= measuring what you intend to measure
Reliability= consistently measuring the same thing
Sensitivity= getting True positives - detecting caries
Specificity= True negatives. Avoiding false alarms
Specificity is often higher than sensitivity in visual and radiographic detection - more likely to get false alarms
Explain the ICDAS codes 0-7
0= sound, no caries
1=first visual signs when dry, opacity or discolouration. Prisms still shiny and in tact
2=distinct visual change in enamel, early white spot lesion visible when dry. Frosty
3=localised enamel breakdown. Classic white or brown spot lesion, no cavitation, no dentine exposure
4=underlying dentine shadowing, with or without enamel breakdown
5=distinct cavity with visible dentine. Caries past ADJ
6=extensive cavity (>half the surface) with visible dentine
7=unrestorable
Radiographic scoring system of how deep the caries is (0-6) What scores are the initial, moderate and extensive stages of caries. How deep must the caries be before considering restoring
0=no radiolucency
1=radiolucency in outer 1/2 of enamel
2=inner 1/2 of enamel
3=outer 1/3 of dentine
4=middle 1/3 dentine
5=inner 1/3 dentine
6=into pulp
Initial: in enamel or outer 1/3 dentine
Moderate: middle 1/3 dentine
Extensive: inner 1/3 dentine or into pulp
Only restore when moderate or extensive
Aims and indications of pulp therapy (not extracting) in children. What are the contraindications
-to maintain primary tooth until exfoliation, if caries close proximity to pulp, maintain an intact arch, avoids physiological and psychological trauma of extraction, xtn may be medically contraindicated, no permanent successor, space maintenance (mixed dentition), co-operative child and carers
-Contraindications: uncooperative, risk of infection, neglected dentition (>3 pulpotomies required), severe acute infection, unrestorable crown, root caries, >2/3 root resorbed so near to exfoliation, pathology
Name types of vital and non-vital pulp therapies
-Non vital pulp = pulpectomy. When pulp is necrotic (no blood) Or if bleeding difficult to stop
-Vital pulp = Indirect pulp therapy (hall technique)
=Single visit Pulpotomy
=Desensitizing pulpotomy (lerdamix)
=Pulpectomy
=(Direct pulp cap – never used for caries exposure, only if child happens to bite on bur causing clean pulp exposure)
What is indirect pulp capping. When it is done. The process
-protects a tooth that has no pulp exposure, pulp is vital, caries is deep into dentine
-a thin layer of dentine is left in place to reduce pulp exposure risk . selective caries removal where only infected is removed and affected is left to remineralise
-protective dressing is placed on top on remaining dentine - calcium silicate cement (eg. biodentine or GIC) Then restored and a preformed metal crown placed. Reactionary dentine will be produced
What is involved in a pulpotomy, for vital pulps
-Excising affected pulp tissue. Cut back to healthy pulp
-Disinfect pulp with formaldehyde
-Ferrous sulphate (15.5%) applied for 15s to arrest bleeding, dry with cotton wool
-Place Calcium silicate cement over pulp stumps to create dentine bridge
-Then ZOE lining
-Then restore, doing preformed metal crown
-Partial – 1-2mm of superficial pulp
-Full – clear full pulp chamber
Calcium hydroxide and MTA uses and properties
-Direct pulp cap materials after exposures
-calcium hydroxide= -stimulates calcific barriers. Irritates pulp to create dentine bridge. Doesn’t work well with inflamed pulp so needs removing. Alkaline
-Mineral trioxide aggregate(MTA)= (Silicates, aluminates, calcium sulphate, bismuth oxide) Stimulates cytokine release from pulpal fibroblasts stimulating hard tissue formation
What to do if copious bleeding after coronal amputation
2 applications of ferric sulphate or pulpectomy if doesn’t stop bleeding
What to do if sensitive exposure
temporary dressing with Ledermix
Then in next visit ferric sulphate pulpotomy
Explain the process of 1 stage pulpectomy and when it is done and what primary teeth it is done on. When is a 2 stage pulpectomy done
-if necrotic pulp (bloodless carious exposure)
- 1 stage pulpectomy =remove coronal and radicular pulp staying 2mm from apices, clean, don’t shape, irrigate with chlorhexidine or saline as hypochlorite risks damaging the successor, dress and seal with PMFC
-if necrotic with PAP= 2 stage pulpectomy (use calcium hydroxide dressing in between to get rid of infection)
Only do this for 2nd primary molars only
Material options for restorations in children
-use composites mainly
-compomers (poly acid modified composite resin)
-Pre-formed metal crowns popular (extra-coronal) for multi surface tooth
-composite strip crowns-preload crown with composite and fit onto tooth, fiddly, useful for amelogenesis imperfecta
-GIC- not as common, temporary. For single surface occlusal restoration
Properties of GIC. Why not as common for intra-coronal restorations
adhesive, aestheitcly pleasing, fluoride leaching, useful in caries control, no need for moisture control
BUT long setting time, more brittle than composite so more likely to fail so not routinely used for multi-surface restoration, susceptible to erosion and wear, radiolucent, command set
Pros and cons of composite
Adhesive, very good aesthetic, command set
BUT technique sensitive, needs rubber dam and therefore LA, expensive, need good co-operation and low caries risk
Pros and cons of performed metal crowns
gold standard. Quick to use, results in more durable restorations, no ditching (unlike with amalgam)
Risk of them pinging off if cement gets weak or if picked one too big
Use the OAP technique or Hall technique.
What is the OAP and Hall technique. And the modified Hall technique
-techniques for applying PFMC
-OAP= occlusal approximal peripheral bevel. Involves removing tooth tissue all the way around the tooth
-Hall technqiue= biologically sealing decay in so don’t need to remove caries. No tooth prep or LA needed
-Modified Hall technique= clear interproximal area but no occlusal reduction or peripheral bevel. This is used if the crown does not fit perfectly
What is hypomineralisation and its appearance
-normal amount of enamel but poorly mineralised (qualitative defect)
-Abnormal enamel rods mean that when occlusal forces are applied they cause enamel to chip off and breakdown
-tips of enamel different shade to base
-yellowing of molars
-affects all cusps of a tooth
-opacities on incisors which can extend from tip to gingival margin
What is hypoplasia and its appearance
insufficient amount of enamel and occasionally poorly mineralised (quantitative defect)
-tooth almost looks concave
-thin translucent enamel with dentine visible through
What is molar incisor hypomineralisation
-qualitative defect of 1-4 first permanent molars with or without the permanent incisors.
-6s affected in severe cases
-contralateral (opposite tooth of arch will be affected)
-70% of children with MIH have incisor involvement
-Yellowing of molars. Opacities on incisors. Brown areas have higher protein content.
-Chalky, brown, motled
-occurs in 1 in 8 children
-can cause pain, hypersensitivity (dentine less protected), poor aesthetics
-can cause post-eruptive breakdown when tooth crumbles away
What is the cause of molar incisor hypomineralisation
-Aetiology unknown
-trauma. At the point of impact, this will cause hypomineralisation on the permanent tooth
-Acute or chronic childhood illness - hypoxic event, fever, long term use of antibiotics (normally amoxicillin), asthma, pneumonia, hypocalcaemia
-Amelogenesis/Dentinogenesis imperfecta
-Generalised hypomineralisation
-Prenatal -maternal obesity, stress, illness, vit D deficiency, smoking, medications
-Perinatal -breastfeeding, fever, birthweight, caesarean delivery
What is post-eruptive breakdown
enamel crumbling away, after tooth eruption, that has hypomineralisation and/or hypoplasia. Attrition, erosion, abrasion and caries can speed it up
Appearance of hypo plastic amelogensis imperfecta and fluorosis
- Hypoplastic amelogenesis imperfecta – affects all teeth, symmetrical pattern. Primary and permanent. Yellowing. pitting and grooving, thin enamel
- Fluorosis – chronological and symmetrical pattern. White or brown spots on teeth. Porous enamel. Lacework pattern. Premolars less affected. Don’t affect primary
Questions to ask when suspect fluorosis or AI
-What did/do the primary teeth look like?
-Does anyone else in the family have similar teeth?
-Any difficulties during birth?
-Any illnesses during late pregnancy?
-Any illnesses during baby’s first year of life?
-Any injuries or infection affecting primary teeth?
-Lived in another country during childhood?
-Fluoride supplements?
-Excessive consumption of fluoride up to age 3?
Ways of managing hypomineralised molars
-Preventative counselling
-Desensitising (fluoride varnish, toothpaste prescription, tooth mousse)
-SDF (minimal use in MIH as does not restore structure, just reduced carious activity)
-Fissure sealants (resin based. If mild. GIC only if uncooperative)
-Direct restorations (but poorer bonding due to hypo mineralised so may fail. Use composite, not GIC)
-PFMC (for severe cases. Best option for 2nd molar. Temporary choice until xtn or cast)
-Indirect/cast restorations (mild to moderate)
-Extraction (if severe) and ortho
When would you consider restoring or extracting hypo mineralised molars
-Restore if… mildly/ moderately affected, good cooperation, hypodontia, risk of drifting
-minimal tooth reduction, minimises pulp trauma, provides cusp coverage, controls sensitivity
-Extract if… symptomatic, severely affected, ortho considerations, poor cooperation. Extract at appropriate time
Management of hypo mineralised incisors
-Want something minimally invasive to reduce sensitivity, improve aesthetics and maintain tissue
1. Tooth mousse (replenishes Ca, P, F to remineralise)
2. Pumice acid microabrasion (18% HCl acid and gently removing outer layers, but removal of sound tooth tissue)
3. Resin infiltration ( into most porous parts of the teeth, but very expensive)
4. Bleaching (18% carbamide peroxide - 6% hydrogen peroxide – done in close-fitting trays) If <18 normally illegal, however since 2016 can be used by specialists for therapeutic reasons
5. Composite masking (localised composite over the opacity – can leave a shine through, but this avoided by putting fissure sealant after etch and before the composite
6. Composite restorations
7. Composite veneers - last resort as won’t be able to do the other less destructive treatments after this
What resin infiltration involves
-Microinvasive treatment, without necessity for tooth tissue removal
-Unfilled, low viscosity resin flows into porous enamel
-Can penetrate between 5 to 25 micrometres
-Rubber dam
-2 mins etching (15% HCl), thorough drying, infiltration of resin and then light curing
Commercialised under the brand name ICON
-microbrasion can be done first to open up the surface
When should you usually wait before extracting a 6
8.5-10 years olds - usually 9.5 years
-until 7 has bifurcated, which will then naturally drift into place of 6. [7 crown completion at 8 years, bifurcation at 8.5]
-Ideally need to have 8s
-Good angulation of 5s to prevent it tipping distally
-(6s first permanents to erupt so likely to be carious and hypominerlaised)
What is amelogenesis imperfecta. The 3 varieties and its appearance
-hypoplastic (rough or smooth) - pitted, thin enamel
-hypocalcified/hypomineralised= opaque, yellow, soft
- hypo mature= diffuse white opacities. snowcapped
-inherited enamel disorder. Genetic
-affects primary and permanent teeth
can cause rapid attrition, sensitive, increased calculus, elongated root, post-eruptive breakdown
What is dentinogenesis imperfecta
-Hereditary defect in dentine
-May be associated with osteogenesis imperfecta (associated with Type 1) – other bone fractures
-Rapid tooth loss – treat before vertical tooth loss
-Put preformed metal crowns on primary teeth
-appearance= even grey-brown colour with altered translucency. bulbous. Thin roots. Gradual pulp obliteration by dentine. Enamel fractures and severe wear follow shortly after eruption
-more severe in primary teeth
Extrinsic (direct & indirect) and intrinsic (enamel & dentine) causes of tooth staining
-Extrinsic (direct)= coffee, tomato sauce, wine smoking, poor OH, iron supplements, post orthodontic treatment
-Extrinsic (indirect)= CHX
-Intrinsic (enamel staining)= trauma or infection from primary predecessor, caries, internal resorption, amelogenesis imperfecta, fluorosis, illness.infection/radiation/deficiency during tooth formation, tetracycline, idiopathic
-Intrisnic (dentine staining)= necrotic pulp, metallic restorations, caries, dentinogenesis imperfecta, tetracycline, congenital porphyria, excess bilirubin, idiopathic, RCT
Treatment options for tooth staining
- Enamel microabrasion - brown patches
- Resin infiltration (ICON)
- Tooth whitening – vital or non-vital
- Veneers – composite or porcelain (porcelain less likely in child as they grow and cannot add to it)
- Crowns
What stains does acid-pumice micro abrasion remove
-uses acid to remove intrinsic brown opacities and diffuse white opacities in outer 1/3 of enamel.
-Not suitable for non-vital teeth or tetracycline stains
-for fluorosis, idiopathic speckling, turner teeth, post-ortho demineralisation, Removes surface enamel to improve discolouration
-Prior to veneers
Lesions on enamel
[-brown fluorosis stains easier to remove than white as less deep]
The process of acid-pumice micro abrasion
- Clean teeth with pumice and water, wash and dry
- Isolate teeth with rubber dam
- Don’t tuck the dam into margin, instead seal edge of dam with Copalite varnish
- Place sodium bicarbonate and water paste around the dam to neutralise any splashes of acid. Also cover patients neck
- Mix 18% HCl and pumice to a slurry and apply a small amount to tooth on a rubber cup (or a wooden stick). The cup should be rotating slowly and in contact with the tooth for 5 seconds
- Wash for 5 seconds directly into the aspirator tip
- Repeat up to a max of 10 applications, until achieved what you want to achieve
- Apply fluoride varnish for 3 minutes to reminieralise. NOT Duraphat as it is yellow!
- Polish with finest Soflex discs
- Warn not to eat highly coloured foods for 24 hours
- Review in 1 month.
How long after fluoride varnish application can you eat
Wait 30 mins
4 hours soft food
What is vital and non-vital bleaching
-oxidation process, whereby pigmented carbon ring structures are broken down into colourless structures.
-using H2O2
-Non-Vital - for root filled teeth
-In surgery ‘powerbleaching’ and ‘thermocatalytic’. Also Walking bleach. 37% phosphoric acid
Vital- for severe extrinsic stains, ageing, fluorosis, tetracyclic stains.
-15% carbamide peroxide gel which breaks down to produce H2O2 which causes the whitening. Can also just use max 6% hydrogen peroxide
-Over the counter preparations (e.g. toothpaste, boil and form kits) Also Matrix bleaching using trays (Nightguard vital bleaching)
Side effects and contraindications for vital bleaching
-Not used in under 18s (large pulp chambers), teeth with large/ defective restorations, teeth with apical pathology, fracture, worn, deep surface cracks, pregnancy, unrealistic expectations, sensitive teeth
-sensitivity, less likely to brush teeth, bleaching can fade and have to be re-done, soft-tissue burns, potential adverse effects on restorative materials
Guidlines for tooth whitening in children
Illegal to use vital tooth whitening in <18. This is because they have larger pulp chambers, less secondary dentine, possibly poorer plaque control, increased potential for pulpal hyperemia. Need to be qualified as can cause lots of damage.
In 2012 GDC allowed the use of H2O2 (<6%) in dentistry for 18+. Must be prescribed by dentists and delivered o supervised by dentist, and consent gained.
In 2014, allowed to use it in children for therapeutic reasons. Controversy around this.
Cannot whiten at NDH
Method involved in veneers (for correcting tooth discolouration) Inidcations and contraindications
-Composite veneers (direct technique)
-enamel reduction is needed to prevent bulky restorations and bond strength is increased if buccally removed. But over contouring increases plaque retention in gingival margin, and children have large pulp chambers and unstable soft tissue so not as much enamel reduction than in adults
-Indications: morphology, diastema, fractures, failed acid pumice, inherited disorder, growing child so porcelain cannot be used.
-Porcelain veneers
-rarely used in children as growing. Mainly 16+ girls who have stopped growing
Indications= discoloration, enamel defects, diastema, malpositioned teeth, malocclusion, poor restorations, ageing, wear patterns, deep pits and ridges
Contraindications= unavailable enamel, oral habits (nail biting etc.)
The 3 types of non carious TSL. Which is most common in children
-Abrasion= uncommon (foreign object)
-Attrition=common (grinding)
-Erosion=most common (intrinsic or extrinsic acid eg. vomitting, GORD, eating disorder, dietary, meds, xerostomia, alcohol)
1/3 of 5 year olds had evidence of TSL on 1+ of buccal surfaces of the primary upper incisors, although only 4% overall had TSL involving dentine or pulp
Clinical appearance of erosion
-silky or glassy appearance
-bucco-lingual/ palatal flattening
-dished out/ cupping occlusal appearance
-dentine exposure
-high enamel ridges
-pulp wear, loss of vitality
-sensitivity
-reduction in length of incisors
Management options for TSL
-early diagnosis to stop progression
-wait and see, if no complaints of pain/sensitivity, function, aesthetics
-patient info leaflets
-recording the process: study casts, photographs, silicone putty impression, radiographs
-diet analysis and counselling
-OHI, remineralisation (F toothpaste, varnish. Amorphous calcium phosphate), desensitisation
-if teeth sensitive, cover anteriors with composite, or PFMC for posteriors, or extraction
-If can see pulpal shine through then teeth should be extracted. Don’t want to risk damaging tooth germ so need action
-Avoid PFMC if about to erupt
-follow up
-nocuturnal splint for grinding not ideal due to children growing and poor compliance
Treatment objectives for TSL
Resolve sensitivity
Restore missing tooth surface
Prevent further tooth tissue loss
Maintain a balanced occlusion
What is the tripple headed brush handy for special needs patients
Dr Barman’s brush
How to manage primary herpetic ginigvostomatitis. appearance
common in ages 1-3 (as mothers antibodies give protection up to 1 year)
-Aggressive gingivitis, fluid filled vesicles on the palate, tongue, and buccal mucosa which burst to leave ulcers
-rest etc, Orabase (carboxymehtylcellulose) on ulcers to protect/sooth, topical analgesia (Bongela)
-Systemic analgesia + antipyretics, 5% topical Aciclovir every 4 hours, systemic aciclovir 200mg Aciclovir 5Xdaily 5 days (half dose if less than 2)
Treatment for 1) reversible pulpits of an E, and 2) irreversible pulpits of an E
1) Indirect pulp therapy- setting CaOH or GIC or biodentine
OR Pulpotomy- remove coronal pulp, 15.5% ferric sulphate, MTA, CaOH, then PFMC
2) Pulpectomy or XLA
