Anomalies pt 2 Flashcards
MIH - what teeth must it affect for diagnosis? what appear on teeth? where to lesion start/progress? how does colour of lesion change from deeper to more superficial?
must affect at least 1 first permanent molar
well demarcated lesions - white, cream to brown
lesion start in inner aspect of enamel and work outwards
more superficial lesions are whiter, browner lesions further into enamel
what does hypomineralised enamel mean? what is it prone to? how do bond strengths differ?
right quantity of enamel but defect in quality - softer enamel prone to post eruptive breakdown
poorer bond strengths
when should first permanent molars be XLA’d in MIH? what will this allow?
8-10yrs
space will spontaneously close w/ 7s erupting in (7s erupt around 11-13yrs)
what will happen if 6s XLA’d too early or too late?
too early = 7s will drift distally
too late = 7s will not close space as already erupted/partially erupted
explain balancing and compensating XLA approach - what does each approach ensure?
balancing = take out contralateral tooth at same time - maintains midline
compensating = take out opposing tooth at same time as XLA - prevents overeruption
how is LA affected in MIH teeth? what LA techniques are often required? possible resolution?
LA harder to achieve as inflamed pulp
buccal/palatal infiltration w/ articaine, IDB and intraligamentary often required
could do comp dressing of pulp to help settle down inflammation so easier to achieve LA at next appt
what could be done to FPMs prior to XLA time to stabilise?
hall crown
how do margins and caries resistance of white patches on fluorosis differ to MIH?
fluorosis show diffused patches - whereas MIH patches are well demarcated
fluorosis teeth caries resistant whereas MIH caries prone
list 6 ways to manage MIH & fluorosis?
microabraison - removes white patches to match rest of teeth
bleaching - matches normal tooth to whiter patches
resin infiltration
localised comps on lesions
veneers
is amelogeneis imperfecta caused by genetic or environmental factors? how does this differ from MIH/fluorisis?
completely genetic - no environemntal factors (unlike MIH & fluorosis)
name 3 types of AI - explain appearance
hypomaturation - enamel thinner and less dense/hypomineralised/pitted
hypoplastic - normal strength but not right shape (thin or absent enamel)
hypocalcified - enamel contains less calcium so thinner and weaker
what type of AI is associated w/ taurodontism?
hypomature enamel
give differing physical differences in the types of AI
hypomature - snow capped (white/brown striations), mottled/spotted/pitted
hypoplastic - not right size/shape but normal hardness, may be sensitive due to thin/absent enamel
hypocalcified - discoloured, opaque, chalky, extremely sensitive
chronological enamel hypoplasia - cause? presentation of enamel?
caused by environmental factor
thin or absent enamel - teeth look yellow
what is a turner tooth? what are they prone to? clinically present as?
permanent tooth that has been affected by infection or insult to primary tooth
prone to post eruptive breakdown and caries
may be sensitive
hypolasia/hypoplastic definition - how does this affect bond strength?
underdevelopment or absence of tissue - normal bond strength
list 4 dentine defects
dentinogenesis imperfecta - pulp absent, bulbous crowns
dentine dysplasia - short roots, extreme mobility
hypophosphatemia rickets - spontaneous abcesses
intrinsic staining
Dentinogenesis Imperfecta - how do teeth present?
funny shape
short thin roots
normal enamel - but shearing off of enamel due to poor bond between enamel and dentine
looks worse in primary teeth as enamel usually thinner
teeth are brown/orange
what occurs in teeth with dentogenesis imperfecta? how does pulp respond after sclerosis? what can present if pulp stays massive? how do teeth look on radiograph?
enormous pulp, rapid secondary dentine laid down to shrink and sclerose pulp
teeth therefore have low pulpal inflamm. response and hardly get painful
lots of spontaneous abcesses if pulp stays enormous
bulbous crowns, no pulp, cevrical constriction so crowns eventually ping off
management for DI
aesthetic management
cuspal coverage
MCC if attrtion to prevent pulp exposure
dentine dysplasia - how do teeth appear clinically? consequence to teeth? how do teeth appear radiographically?
normal enamel
atypical dentine formation w/ abnormal pulp morphology
teeth appear normal in appearance and colour
bur extreme mobility and often exfoliated prematurely
how do teeth W/ dentine dysplasia present on radiograph?
pulp chamber does not extend down roots
hypophosphatemia rickets (XLH) - clinical presentation? what causes this?
spontaneous abcesses
caused by larger pulps and pulp horns extending to the ADJ
intrinsic staining - what may this be caused by?
tetracycline
how should intrinsic staining be managed? how may caries diagnosis in these teeth be aided?
may not respond to bleaching - so direct comp veneers in kids/traditional veneers in adults
consider BW interval - harder to diagnose caries clinically
name a disorder of cementum - how does this condition affect the body?
hypophosphatasia - endocrine disorder affecting the skeleton
skeletal deformaties, restricted growth, fractures, bone pain
how does hypophosphatasia affect teeth? in what order do the teeth fall out? which teeth first?
fully rooted teeth fall out
cementum does not form properly and is patchy - not covering whole root
teeth will fall out in eruption pattern - lower 1s first
what is odontohypophosphatasia?
hypophosphatasia with only dental features
what is regional odontodysplasia?
mixed tooth structure disorder
segment of the arch does not form properly
disorder does not cross midline
more common in maxilla
how does regional odontodysplasia present?
unerupted teeth
may be alveolar expansion
teeth that do erupt have abnormal shape, size and mineralisation
