Dental anoamlies Flashcards
4 classes of dental anonamlies
number
size and shape
structure - hard tissue defects
eruption and exfoliation
hypodontia
missing teeth from normal sequence
teeth commonly affected by hypodontia
3rd molars: 9-37% of population have more than 1 missing
1.0.1-0.9% in the primary dentition
4.3.5-6.5% in the permanent dentition
mandibular premolars: 1.2-2.5% (5s)
maxillary lateral incisors: 1.0-2.0% (2s)
The teeth least likely to be missing are the first permanent molars and upper central incisors
*tends to be end of series *
conditions associated with hypodontia
Ectodermal Dysplasia (sparse hair, small nose, sweating)
Down Syndrome
Cleft Palate
Hurler’s syndrome
Incontinentia pigmentii
hypodontia dental management
in chronological order
Diagnosis
Removable prosthesis (waiting to grow, full permanent dentition)
Orthodontics
Composite build ups – inc size and shape
Porcelain veneers
Crowns, bridges and implants – need to wait for gingival margin settle, early/mid 20s
class of preventative tx need for hypodontia pts
high risk as less teeth
enhanced prevention needed throughout life
possible dental issues associated with hypodontia pts
submergence/infraocclusion of permanent teeth
deep overbite
spacing
issues with occlusion - reduced LFH
abnormal shape/form
* cone shaped teeth or straight sided can happen
hypodontia tx aims
3
prevention
aesthetics
function
commmon solutions/tx for hypodontia pts
overdentures
partial dentures
composite additions
porcelain veneers
fixed prosthodontics
example tx plan for hypodontia pt
Local fixed orthodontics to oppose central incisors, and composite build up
Overdenture – restore face height
Implants
Bone augmantation, sinus lift, distraction osteogenesis
hyperdontia/supernumerary
extra teeth to normal sequence
most common hyperdontia/supernumerary
1.5-3.5% prevalence
males:females 2:1
higher frequency in Japanese
more common in maxilla
higher frequency in cleidocranial dysplasia
types of supernumerary
4
Conical (cone shaped)
Tuberculate (barrel shaped, has tubercles)
Supplemental (looks like tooth of normal series)
Odontome (irregular mass of dental hard tissue, compound or complex)
most common cause of delayed eruption of permanent incisor teeth
supernumerary teeth
*Conical supernumerary
Central incisors are at immature stage so wouldn’t go in at this stage
Wait till child is 7/8 then remove extra teeth as root formation of 1s complete *
microdontia
smaller teeth than normal
2.5%
F>M
e.g. peg shaped lateral incisors
macrodontia
bigger teeth than normal
rare
less than 1% for single teeth and 0.1% in generalised form in Caucasians
double teeth
2 types
Gemination (one tooth splits into 2)
Fusion (two teeth join to form 1)
odontomes
anomalies in size and shape
odd dentine/enamel masses
taurodontism
flame shaped pulp, teeth look normal but risk pulp exposure in restorations
6.3% in UK
dilaceration
can be to crown or root
due to trauma or anomaly
accessory cusp
e.g. talon cusp
Selective grinding over time, Fluoride on
Encourage pulp to regress
dens in dente
tooth in tooth
invagination on tooth, seal areas to prevent bacteria ingress as not able to RCT and plaque trap
anomalies in root structure
short root anomaly
* permanent maxillary incisors
* 2.5% incidence
* 15% of these children also have short roots on the canines and premolars
* Danger for orthodontic tx
Causes
* radiotherapy
* dentine dysplasias
* accessory roots
3 enamel anomalies
amelogenesis imperfecta
environmental enamel hypoplasia
localised enamel hypoplasia
types of amelogenesis imperfecta
100s but 4 main
hypoplastic
hypocalcified
hypomaturational
mixed forms
causes of environmental enamel hypoplasia
4
systemic (kidney/liver failure)
nutritional
metabolic e.g. Rhesus incompatability, liver disease
infection e.g. measles
causes of localised enamel hypoplasia
2
trauma
infection to primary tooth
hypomineralised enamel
all tooth tissue there
normal shape but have marks on them
correct thickness
hypoplasitc enamel
chunks of enamel missing
mineralisation fine
how to categorise hard tissue defects
localised/generalised
if generalised environental or hereditary
if localised - trauma or abscess/infection primary tooth
tell tale sign generalised environmental enamel defect
can see lines on teeth from onset of the generalised environmental defect to stop, different on each tooth as form at different times
example generalised enviornmental enamel defects
2
fluorosis
MIH associated with childhood illness or chronological hypomineralisation e.g. liver/kidney failure
possible tx for fluorosis
generalised environmental enamel defect
Treat using microabrasion therapy/veneers/vital bleaching
Microabrasion remove surface layer so teeth will look more dull as dark and light parts removed – ensure pt aware
generalised environmental enamel defects
3 times cause can happen
prenatal
neonatal
postnatal
prenatal factors for generalised environmental enamel defects
rubella, congenital syphilis, thalidomide, Fluoride, maternal A&D deficiency, cardiac & kidney disease
neonatal factors for generalised environmental enamel defects
prematurity
meningitis
postnatal factors for generalised environmental enamel defects
otitis media, measles, chickenpox, TB, pneumonia, diphtheria, deficiency of Vits A,C&D. heart disease. Long term health problem e.g. organ failure
example generlised hereditary enamel defect
amelogenesis imperfecta
prevalance of amelogenesis imperfecta
1: 14,000
4 main types:
* Hypoplastic
* Hypomineralised
* Hypomaturation
* mixed with taurodontism
familial inheritance
* autosomal dominant, recessive, and x-linked
no associated systemic disorder (studies ongoing)
5 parts of dx for amelogenesis imperfecta
family history
generally affects both dentitions (primary and permanent, worse in permanent)
affects all teeth
tooth size, structure, colour
radiographs
* fail to see change in radiolunceny between enamel and dentine
enamel formation and genes
Enamel formation needs multiple genes to transcribe the process of crystal growth and mineralisation.
Gene mutations found so far, involve enamel extracellular matrix molecules amelogenin and enamelin and kallikrein 4
Hypoplastic type
* Enamel crystals do not grow to the correct length
Hypomineralised
* Crystallites fail to grow in thickness and width
Hypomaturational
* Enamel crystals grow incompletely in thickness or width but to normal length with incomplete mineralisation
dental problems in amelogenesis imperfecta
sensitivity
caries/ acid susceptibility - erosion
poor aesthetics (brown colour, white teeth with flecks, alike fluorosis)
poor oral hygiene
delayed eruption
anterior open bite
solutions for dental problems in amelogensis imperfecta
preventive therapy
composite veneers/ composite wash (aid sensitivity)
fissure sealants
metal onlays
stainless steel crowns (replace at older age)
orthodontics (troublesome to bond to)
systemic disorders associated with enamel defects (not amelogensis imperfecta)
8
epidermolysis bullosa
incontinenta pigmenti
Down’s
Prader-Willi
porphyria
tuberous sclerosis
pseudohypoparathyroidism
Hurler’s
4 anomalies of dentine structure
dentinogenesis imperfecta
dentine dysplasia
odontodysplasia
systemic disturbance (nutritional, metabolic, drugs)
dentine dysplasia
normal crown morphology, amber radiolucency, pulpal obliteration, short constricted roots
odontodysplasia
localised arrest in tooth development, thin layers of enamel and dentine, large pulp chambers, “Ghost Teeth”
dentinogenesis imperfecta
uncommon
3 types
* Type I osteogenesis imperfecta (issue with bone)
* Type II autosomal dominant (no underlying medical conditions)
* Brandywine
type I dentinogenesis imperfecta
have osteogenesis imperfecta (issue with bone)
blue sclera of eye
teeth amber/translucent/grey
dx dentiogenesis imperfecta
appearance
family history
associated osteogenesis imperfecta
both dentitions affected
enamel loss
radiography:
* bulbous crowns
* obliterated pulps (I & II)
Crowns look like primary teeth but roots are like adult
Pulps quickly become obliterated
Get occult abscess, impossible to tx due obliteration
type III dentinogenesis imperfecta -Bradywine
Brandywine, Maryland, USA. – genetic defect in that area
dental problems in dentinogenesis imperfecta
3
aesthetics
caries/acid susceptibilty
spontaneous abscess
dental solutions to dentinogenesis imperfecta
5
prevention (enhanced)
composite veneers
overdentures –* cover vulnerable dentine *
removable prostheses
stainless steel crowns – varied success, but prevents wear
POOR PROGNOSIS
hereditary dentine defects
limited to dentine only
3
dentinogenesis imperfecta type II
dentine dysplasia Types I & II
fibrous dysplasia of dentine
hereditary dentine defects
associated with general disorder
5
osteogenesis imperfecta
Ehlers-Danlos syndrome
brachio-skeletal genital syndrome
rickets
hypophosphatasia
tooth structure defects tx overview
prevention and pain control
harness growth
restoration of lost tissue
overview of dental management
anomalies in paeds
continous dental care
management of growth and development
removable prosthesis
crowns and bridges
interceptive ortho
anomalies of cementum
2
cleidocranial dysplasia
* hypoplasia of cellular component of cementum
* no clavicle
hypophosphatasia
* hypoplasia or aplasia of cementum
* early loss of primary teeth (nothing holding them into bone)
premature eruption causes
3
high birth weight
precocious puberty
natal / neonatal teeth
* 1: 2000-3000 births
* Just early – try to get to stay as usually part of series
* But extract if issue with feeding or inhalation risk
delayed eruption causes
4
pre-term & low birth-weight children
malnutrition
associated general conditions:
* Downs, hypothyroidism, hypopituitarism, cleidocranial dysplasia
gingival hyperplasia/ overgrowth
premautre exfoliation causes
6
trauma
following pulpotomy
hypophosphatasia
immunological deficiency e.g. cyclic neutropaenia
Chediak-Higashi syndrome
Histiocytosis X
delayed exfoliation causes
5
‘double’ primary teeth
Hypodontia – retain primary tooth
ectopic permanent successors
following trauma
infra-occlusion
* 1-9%, m=f, lower 1st primary molar most common
* congenital absence of premolar
* the majority exfoliate normally by age 11-12 yrs
