Paediatrics Flashcards
behavioural management techniques (6)
positive reinforcement
tell show do
acclimatisation
desensitisation
distraction
role modelling
egs of acclimatisation
- introduce topical visit before using LA for 1st time
- give rubber dam sheet to ptx before planning to use it
- introduce 3:1, suction & cotton wool rolls on visit before fissure sealant
- use slow speed first with cup then bur then high speed later
communication with children
verbal = 5%
paralinguistic = 30% this refers to tone of voice
non verbal = 65%
5 sections of psychological development in children
- motor
- cognitive
- perceptual
- language
- social development
4 stages to cognitive development
- sensorimotor - until 2yrs
- preoperational thought - 2-7yrs
- concrete operations - 7-11yrs
- formal operations 11+yrs
calcification of teeth at birth
1/2 crown of a, d
1/3 crown of b, e
tip of c
tip of cusp 6
eruption sequence & dates of deciduous teeth
ABDCE
A - 6mths
B - 9mths
D - 12mths
C - 18mths
E - 24mths
teeth in same series erupt within 3mths of each other & primary dentition should be completed by 2.5-3yrs of age
ugly duckling phase
when there is transient spacing of 1st due to roots of centrals being in close proximity to 2s and 3s developing below
4 common anomalies in erupting dentition
- ED1 gene (x-linked) = peg shaped laterals in ectodermal dysplasia -> encodes ecdysplasmin A
- mutation of MSX1 gene on chromosome 4 (autosomal dominant) = missing 3rd molars & 2nd premolars
- PAX9 (autosomal dominant) gene on chromosome 14 = usually missing molars
- mutation of sonic hedgehog gene (SHH) chromosome 7 = solitary median central incisor & other developmental problems
hypodontia
missing tooth
if primary tooth missing, permanent successor most likely missing too
most often maxillary laterals & mandibular 2nd premolars
commonly associated with down syndrome & cleft lip and/or palate
management of hypodontia
retain primary tooth for as long as possible
bridge / rpd / overdenture
eventually implants but ptx must have excellent OH
hyperdontia / supernumeraries
more than the normal amount of teeth
supernumerary teeth are the most common cause for delayed eruption of a permanent incisor tooth
if contralateral tooth erupted 6mths ago & it hasn’t started yet then take radiograph to view positioning
types of supernumeraries
conical - cone shaped
tuberculate - barrel shaped, has tubercles
supplemental - looks like tooth of normal series, maybe smaller
odontome - irregular mass of dental hard tissue; compound / complex
anomalies of size & shape (8)
microdontia (F>M) e.g. peg shaped laterals
macrodontia
double teeth
odontomes
dilaceration - deviation or bend in the linear relationship of a tooth crown to its root
accessory cusps e.g. talon cusp
dens in dente - teeth growing within teeth
anomalies of root structure
short root anomaly - perm max incisors and 15% also have short roots on premolars; DO NOT PUT FIXED APPLIANCES ON THESE
accessory roots
dentine dysplasia
radiotherapy
anomalies of enamel structure (3)
congenital - amelogenesis imperfecta
environmental enamel hypoplasia
localised enamel hypoplasia
difference in hypoplasia & hypomineralisation
hypomineralisation - correct amount of enamel present but mineral content is not correct; often caused by trauma / MIH
hypoplasia - thin / absent enamel
amelogenesis imperfecta
hypomineralised - crystallites fail to grow in thickness & width in enamel
hypoplastic - enamel crystals do not grow to correct length
hypomature - enamel crystals grow incompletely in thickness / width with normal length; will also be incomplete mineralisation
problems associated with amelogenesis imperfecta (6)
sensitivity
caries/acid susceptibility
poor aesthetics
poor OH - hurts to brush, don’t like teeth so not bothered, calculus can act as barrier to protect from pain
delayed eruption
anterior open bite
solutions to amelogenesis imperfecta (6)
preventative therapy
comp veneers / wash
fissure sealants
metal onlays
ss crowns
orthodontics
problems with dentinogenesis imperfecta
aesthetics
caries/acid erosion susceptibility
spontaneous abscesses
solutions to dentinogenesis imperfecta
prevention - OHI
composite veneers
overdentures
removeable prosthesis
ss crowns
prognosis for teeth with this is very poor
radiograph of dentinogenesis imperfecta shows (3)
bulbous crowns
pulp canal obliteration
occult abscess formation
7 elements of caries risk
clinical evidence
dietary habits
social history
fluoride use
plaque control
saliva
medical history
8 elements of caries prevention
radiographs
toothbrushing instruction
strength of F in toothpaste
F varnish
F supplementation
diet advice
fissure sealants
sugar free medicine
health education
process where individuals / group of people have increased knowledge related to health. dental / dietary health education alone have been proven not to work so must form part of an overall prevention plan with health promotion
health promotion
supporting knowledge people have gained from health education and translating this into positive behaviours. it should impact a wide variety of areas i.e. social, economic, structural environments as well as improving policies of public & local institutions
what determines previous caries experience
dmft >5 or DMFT >5
>10 initial lesions
caries in 6s at 6yrs
3yrs caries increment >3
Bohn’s nodules
white benign keratinised marks from epithelial remnants of salivary glands found on buccal / lingual mucosa or on hard palate away from mucosa
epstein pearls
white benign keratinised marks found on palate filled with fluid
radiographs for mixed dentition
high risk - every 6 months
low risk - every 12-18 months
pattern of caries attack in primary dentition
- lower molars
- upper molars
2nd molars then 1st - upper anteriors
if upper and lower incisors affected there is uncontrolled caries
space maintenance
if primary toot extracted the permanent tooth will drift mesially causing crowding - earlier a tooth is lost the more space will be lost
primary tooth XLA affected by
tooth size
jaw relation
muscle behaviour
age at loss
which tooth is extracted
band & loop maintainers can be used to maintain space when 6s have erupted
when is optimum time to remove 6s
when the permanent 7 crown can be seen formed on a radiograph as well as calcification of the birfurcation
if maxillary 6s lost before complete 7 eruption
rotation & mesial movement of 7
distal drift of 5s
mandibular 6s lost before optimum age
tilting of 7s
mandibular 6s lost after optimum age
distal drift & rotation of 5s
benefits of using rubber dam (7)
decrease soft tissue damage
decrease risk of inhalation
decrease risk of cross infection
produces isolation & moisture control
retracts gingivae & cheeks
produces more effective inhalation sedation
increases ptx & operator confidence
ideal sequence of restoration
fissure sealants
preventative restorations
simple fillings e.g. shallow cervical caries
fillings requiring LA but not into pulp
pulpotomies / pulpectomies
XLA
what indicates pulpal involvement visually
marginal ridge breakdown
if caries is 2/3s into dentine
when to restore pit & fissure caries
- microcavitation
- shadowing under enamel after cleaning & drying tooth
- dental caries on radiograph
why should you not use duraphat
if patient is allergic to sticky plasters as they will be allergic to colophomy
or if they have been hospitalised for asthma in the last year
indications for pulp treatment in kids
good cooperation
want to avoid GA
space preservation
no permanent successor
medical history precludes XLA e.g. bleeding disorder
contraindications for pulp treatment in kids
poor cooperation
poor motivation
multiple grossly carious teeth
poor dental attendance
medical history precludes endo i.e. cardiac defect, immunosuppression or poor healing
XLA indications
severe pain
pus in pulp chamber
gross bone loss
advanced root resorption
cellulitis
non inflamed v inflamed pulp
non inflamed - normal bleeding, blood will be bright red & haemostasis will be achieved
inflamed - deep crimson blood with continued bleeding after pressure
when to do a vital pulpotomy
pulp minimally inflamed, marginal ridge destroyed, caries extends 2/3s into dentine or if any doubt pulp is involved
aim of vital pulpotomy
to stop bleeding, disinfect coronal part of radicular pulp yet preserve vitality of apical portion of pulp
technique of vital pulpotomy
LA rubber dam access
remove caries & roof of pulp chamber with diamond bur
remove coronal pulp with excavator
haemorrhage control with pressure & ferric sulfate for 4-5 mins
restore placing ZOE paste over pulp stumps with GIC core & preformed ss crown
success = 85-100% over 3yrs
when to do non vital pulpectomy
for non vital primary molar
indicated when hyperaemic pulp, pulpal necrosis & furcation involvement
symptoms inc - irreversible pulpitis, periapical periodontitis, chronic sinus
aim of non vital pulpectomy
to prevent / control infection by extirpation of radicular pulp followed by cleaning and obturation of canals
technique for non vital pulpectomy
LA rubber dam & access
coronal pulp extirpated with root canal prep to 2mm short of apex
canals obturated with vitapex then GIC core placed with ss crown
success = 90% over 3yrs
3 main conditions to ask about in trauma medical history
rheumatic fever
congenital heart defects
immunosuppression
when undertaking sensibility tests & radiographs
compare with contralateral uninjured tooth & adjacent teeth
sensibility tests continued for 2yrs after injury
if tooth - to sensibility tests do not RCT straight away as it can revascularise in time (~30days), only RCT if signs & symptoms of necrotic pulp
splinting times
flexible 2wks = subluxation, extrusion, avulsion
flexible 4wks = luxation, apical / middle 1/3 root #
flexible 4mths = coronal 1/3 root #
rigid 4wks = dento-alveolar root #
4 forms of root resorption in traumatic injury
- external surface
- external inflammatory
- internal inflammatory
- replacement resorption
external surface root resorption
often produced from excessive orthodontic forces
non progressive problem
external inflammatory resorption
produced by trauma
initially damage to PDL which is maintained & propagated by necrotic pulp tissue due to acid from pulp travelling along dentinal tubules
tx - extirpate pulp, mechanically & chemically irrigate, place non setting CaOH for 4-6wks then RCT and fill with GP
internal inflammatory resorption
very rare
initiated by non vital pulp which progressively resorbs internal surfaces of roots
tx - same as external inflammatory resorption
prognosis worse if open apex
replacement resorption
ankylosis - bone fuses directly to dentine
EDP# - if exposure of pulp
small exposure <24hrs = direct pulp cap or CaOH with a hemetic seal of either composite or compomer
large exposure >24hrs = partial / full coronal pulpotomy then CaOH with hemetic seal placed on top
partial pulpotomy -> full coronal pulpotomy -> pulpectomy i.e. complete removal
intrusion open apex <6mm impaction
disimpacted with forceps & allowed to spontaneously erupt for 3wks
if no movement ortho used to reposition
flexible 4wk splint
intrusion open apex >6mm impaction
disimpacted then surgically repositioned as it will not spontaneously erupt
4wk flexible splint
intrusion closed apex <6mm impaction
disimpacted & moved orthodontically
4wk flexible splint
intrusion closed apex >6mm impaction
disimpact & surgically reposition
4wk flexible splint
acquired intrinsic discolouration of teeth caused by (6)
molar / incisor hypomineralisation
trauma
infection
systemic upset / illness
fluorosis
tetracycline
what is the main cause of MIH
a febrile illness in the 1st 2yrs of life
how to differentiate fluorosis & MIH
MIH is asymmetrical unlike fluorosis
2 main problems in ptx with MIH
- difficult to anaesthetise
- very sensitive so even fissure sealant can be difficult so dry with cotton wool roll
treatment of hypomineralised molars
molars should get lots of fluoride to try keep them as strong as possible & they should be sealed
may need compomer / preformed crowns
usually XLA at ideal time i.e. bifurcation of 7s, GA usually needed due to poor anaesthesia
treatment of hypomineralised incisors
main issue is aesthetics but have to wait until fully erupted. treat via leaving, microabrasion, localised composites, composite veneers, porcelain veneers
microabrasion helpful for brown spots
veneers needed for white patches
4 issues that can happen following trauma
- localised hypoplasia (incomplete / underdevelopment of organ / tissue)
- loss of vitality - dark grey discolouration wks - months later; or sclerosis of root canal in 2dary dentine formation which causes yellowish discolouration
- internal resorption - pink discolouration / pink spot as pulp closer to surface
- haemorrhage - dark purple or brown colour
infection in a primary tooth
if periapical infection in primary tooth this can cause permanent successor to be hypomineralised
most commonly 1st/2nd premolars - known as Turner’s tooth
to diagnose fluorosis
must affect 2 or more PAIRS of teeth and there will be a history of fluoride ingestion
microabrasion treatment
etching with HCl and pumice to remove 100 microns of surface enamel
3 elements of definition of child abuse
- has there been significant harm to the child
- is the child’s carer responsible for the harm
- is there significant connection between the carer’s responsibility for the child and the harm caused
2 forms of physical abuse
- acute - anyone; anyone is capable of causing acute physical abuse in a spontaneous uncalculated reaction & they will feel remorse and child’s need will be a priority
- chronic - calculated; it is more the way of life where no remorse is felt where child’s needs are not a priority & help is not actively sought
legalisation in child protection
UN Convention on the Rights of the Child 1989
The Children (Scotland) Act 1995
The Age of Legal Capacity (Scotland) Act 1991
The Human Rights Act 1998
Protection of Children (Scotland) Act 2003
PHG symptoms
incubation 3-7 days
symptoms - fever, malaise, vomiting, loss of appetite, 1-2 days later firey red oral vesicles on gingival mucosa which may rupture leading to 1-3mm diameter uclers
tongue white - often misdiagnosed for candidiasis
resolves in 10-14 days
herpangina causes & symptoms
incubation 2-9 days
caused by Coxsackie virus A
symptoms - fever, malaise, vomiting, muscle pain & pinhead vesicles surrounded by halo on tonsils, uvula, soft palate which progress to large ulcers covered by fibrin - last 3-5 days then heal quickly
avoid aspirin
difference in PHG & herpangina
no acute gingivitis in herpangina and is less painful with a shorter duration compared to PHG
hand foot & mouth disease
incubation 7 days
caused by coxsackie virus a16
vascular rash
oral lesions non specific affecting buccal mucosa - not back of mouth / gingiva
ulcers shallow and painful but resolves in a wk
pseudomembranous
layer of exudate resembling a membrane formed on surface of skin / mucous membrane
erythematous
abnormal redness of skin & mucous membranes due to accumulation of blood in dilated vessels
to remember about candida
must always test type of candida
acute candidiasis
may be pseudomembranous which will occur in neonates (<4wks old)
chronic candidiasis
can be erythematous due to partial dentures or orthodontic appliances trapping candida biofilm and causing trauma
median rhomboid glossitis
shiny oval diamond shaped elevation on the dorsum of the tongue in the midline in front of the circumvallate papillae
infectious causes of angular cheilitis
infection with either C albicans or S aureus
mucoceles
small bumps especially to lower lip due to chewing and damaging salivary glands blocking them resulting in a swelling
what is a ranula
a large bump / swelling on floor of mouth caused by blockage of salivary glands & tends to interfere with speech & swallowing
eruption cysts
blue/black elevated compressible dome shaped lesions on alveolar ridge superficial to crown of erupting tooth
lined with non keratinising stratified squamous epithelium & caused by dilation of follicular space around erupting crown
orofacial granulomatosis
can occur in isolation / in Crohn’s
lips become swollen, mucosa cobblestoned & may be mucosal tags, desquamative gingivitis, ulceration & inflammatory stomatitis
fibro epithelial polyp
common exaggerated response to trauma where a squamous epithelium overlying fibrous connective tissue is produced with minimal inflammation
can be left but usually excised
pyogenic granuloma
fibro-endothelial growth arising from marginal gingivae and present as round red/purple overgrowth
can ulcerate / bleed profusely so require complete excision with cryogenic or lasers to prevent recurrence
giant cell epulis
peripheral giant cell granuloma
arises at gingival margin and consists of highly vascular stroma with multinucleated giant cells
geographic tongue
multiple red zones of desquamation of filiform papillae surrounded by white elevated margins and this makes fungiform stand out
hereditary gingival fibromatosis
non specific progressive enlargement of gingivae which can be localised (palatal aspect of tuberosities) or generalised
idiopathic / autosomal dominant or part of a syndrome
haemangiomas
can be present at birth or appear son after growing rapidly
can be capillary or cavernous
capillary - small fine blood vessels
cavernous - large thin walled vessels with a single layer of endothelium & may blanch under pressure
dental aspect of congenital heart disease
must have good OH to prevent infective endocarditis
antibiotic prophylaxis - consult with cardiologist if necessary
make take anti coags & have trouble under sedation due to decreased O2 intake
oral manifestations of down’s syndrome
mouth small with open lip posture
tongue protrusive & fissured
circumvallate papillae enlarged with filiform not present
occlusion - anterior open bite, posterior crossbite, class III malocclusion
palate may be high with bifid uvula & commonly cleft lip and/or palate
hypodontia, microdontia, hypoplasia
asthma is a 3 disease process of
excess mucous production
inflammation of epithelial lining of airways
increased bronchial smooth muscle tone
if asthma attack in dental surgery
allow to breathe how they feel comfortable
give O2 through non re breathing mask
give salbutamol
likely to be allergic to penicillin so avoid it as well as aspirin & other NSAIDs
what kind of sedation should be given in asthmatics
give inhalation sedation not IV sedation as IV can cause respiratory failure
can’t give inhalation in severe asthma as nitrous oxide will act as airway irritant
asthma medication side effects (2)
inhaled corticosteroids - throat irritation, dryness of mouth, hoarseness, oropharyngeal candidiasis
beta-2 agonists - decrease saliva production, increased caries rate/dryness/calculus, LOS may be relaxed causing GORD
high levels of oral corticosteroids over time can cause
adrenal suppression leading to similar effects as Addison’s disease i.e. weight loss, lethargy, hair loss, low levels of aldosterone
dental management of cystic fibrosis
thickened saliva, increased calculus, likely to have enamel defects
increased risk from GA & sedation contraindicated due to respiratory failure so prevention is key
oral mucosal changes with childhood cancer
ulceration & mucositis after 12-15 days in radiotherapy or 3-10 days in chemotherapy
stomatitis will initially form & develop into ulcerations on all types of mucosa but mucositis usually localised only to pharynx
haemorrhage
when platelet count is below 20-30 there may be spontaneous gingival haemorrhage but this can be reduced with good OH
eliminate hard foods & smooth sharp cusps
before treatment ensure count is >80 for injections XLA and deep scaling
herpes simplex treated with
acyclovir 5x 400mg/10ml for 5 days
gram negative bacilli treated with
e.g. E coli treated with systemic antibiotics
candida treated with
nystatin / miconazole / fluconazole
aspergillus / phagomycosis treated with
systemic antifungal
when would antibiotic prophylaxis be needed for dental treatment
if granulocyte count is <2.0 and anaesthetic agent dosage may be modified if erythrocyte count is <5.0
aplastic anaemia
not enough red blood cells produced in bone marrow
they will be normochromic & normocytic but just not enough
dental considerations in chronic renal failure
bleeding tendencies & problems with haemostasis
dental treatment should be done day after dialysis
dental considerations in renal transplants
pre op assessment to remove all sources of infection and to maximise preventative efforts
elective tx may have to wait 6mths after surgery and may need antibiotic prophylaxis
oral manifestations of diabetes
reduced salivary flow -> xerostomia which can cause burning mouth, altered taste & candida infection
hypoglycaemia
most dangerous of the 2 so sugar should always be given just in case; presents as - irritability, disorientation with blurred vision, lethargy, slurred speech, strong bounding pulse, nausea, sweaty skin, shaking, tingling around mouth, hypothermia, loss of consciousness over time
hyperglycaemia
sugar levels are too high; presents as - weak pulse, rapid deep breathing, dry skin, acetone breath, thirst, severe hypotension, abdominal pain & vomiting or loss of consciousness
in epilepsy there is
decreased GABA transmitter levels causing abnormal cell to cell message propagation which can be:
- generalised; tonic/clonic, absence (petit mal), myoclonic
- partial; simple partial, complex partial, simple sensory
if seizure in surgery
remove anything causing damage from area & ptx should not be restrained
if recurrent fits give midazolam buccally
drug therapy in epilepsy
phenytonin used which can cause gingival hyperplasia
what is thrombocytopenia
low blood platelet count
deficiency state anaemias
deficiency of Fe, B12 or folate - there will be candida infections, angular cheilitis, aphthous ulceration or pale mucosa
iron deficiency in kids
microcytic blood cells with low serum iron and ferritin
can be due to prolonged bottle feeding & will have rampant caries
vit B12 deficiency in kids
causes macrocytic anaemia
may be seen in coeliac / crohns / strict vegans or autoimmune diseases
folate deficiency in kids
causes macrocytic anaemia
chrons / coeliac
coeliac disease
gluten sensitivity due to alpha-gliadin in gluten this reacts with the jejunum leading to inflammation and villous atrophy which can cause insufficient nutrient absorption and macrocytic anaemia
congenital haemostasis disorders
haemophilia A - factor VIII
haemophilia B - factor IX
von willebrands
single clotting factors - XI, XII
oral signs of cerebral palsy
higher caries incidence
if peg fed - increased calculus levels
poor OH
if birth trauma then enamel hypoplasia
dental trauma, malocclusion, drooling, NCTSL due to grinding & reflux
oral management of cerebral palsy
prevention
toothbrush with modified handle
inhalation sedation but GA usually required
drooling treated by changing posture, training appliances, drugs or surgery
