5. Aquired Developmental Disturbances Flashcards
Is amelogenesis imperfecta inherited
yes
inheritance patterns of amelogenesis imperfect
- dominant
- recessive
- X-linked
- sporadic
Amelogenesis imperfecta affects the three major stages of enamel formation which are
- Elaboration of enamel matrix (hypoplastic)
- Mineralization of the matrix (hypocalcified)
- Maturation of the matrix (hypomaturation)
AI affects the (primary/permenant) teeth
both (uniformly throughout the dentition)
How many major types and subgroups of AI
4 major types and 14 subgroups
Dx of AI based on
- Family history
- Clinical exam (teeth may be discolored, sensitive and prone to disintegration)
What malocclusion is AI commonly associated with
anterior open bite
what are the 4 major types of AI
- Hypoplastic
- Hypocalcified
- Hypomaturation
- Hypomaturation with taurodontism
Describe hypoplastic AI
-Insufficient quanity of enamel
Describe hypomaturation AI
- Normal thickness
- Low mineral content
Describe Hypocalcified AI
- Normal quantity
- Poorly calcified
- Soft and fragile
Describe hypomaturation with taurodontism for AI
- Mottled and pitted
- Enlarged pulp chambers
- Associated with tricho-dento-osseous syndrome
Treatment for AI in primary dentition
- SSC molars
- Strip crow anteriors (resin or preformed)
- Usually done under general anesthesia
Treatment of AI in mixed dentition
- SSC molars
- Composite restorations on anterior teeth
When can you do a full coverage restoration on a child patient and why
when they are done growing… position of finishline will always change
Treatment for AI in permenant dentition
Full coverage crowns
Dentures/overdentures
Is dentinogenesis imperfecta inheritable
yes
inheritance pattern of DI
autosomal dominant
What is DI
- Defect in predentin matrix
- Histodifferentiation stage in tooth development
- Amorphic disorganized atubular circumpulpal dentin
Describe the color of teeth with DI
- Blue-brown (amber)
- Translucence
- Normal enamel (but tends to chip due to poor support)
DI radiographic findings
- Bulbous crowns
- Short roots
- Early obliteration of pulp chamber/root canals
- *Variation= shell teeth (large pulp chambers)
What are the three different types of DI
Sheilds types I, II, and III
Describe Sheilds Type I DI
- Osteogenesis imperfecta
- Brittle bones
- Bowing limbs
- Temporal bossing
- **Blue sclera
- Teet= periapical RLs and amber translucence
Which are more severely affected in Sheilds type I (primary/permanent) teeth
primary
Describe Sheilds Class II DI
- Both dentitions affected
- Same clinical findings as Shield’s type I but without osteogenesis imperfecta
Shell teeth is most commonly seen in what type of DI
Sheild’s class III
Describe Sheild’s type III
- Rare
- Brandywine population
- Bell shaped crowns
- Shell teeth (short roots and large pulp chambers)
- Multiple pulp exposures
Is dentin dysplasia an inherited disorder
yes
inheritance pattern of dentin dysplasia
autosomal dominant
What are the subtypes of dentin dysplasia
Sheilds Type I and II
Describe Sheild type I dentin dysplasia
- Radicular
- Normal color of crowns
- Both dentitions affected
- Short blunted roots
- Obliterated pulp chambers
- mobility
Describe Sheild Type II dentin dysplasia
- Coronal
- Amber colored primary teeth
- Normal root length
- Permanent tooth look normal but on X-ray –> Thistle tube shaped pulp and multiple pulp stones
Contraindications for patients with Osteogenesis imperfecta and why
physical restraint (can break their bones)
DI and DD treatment in permanent dentition
- Full coverage restorations
- Denture/overdenture (short roots –> early failure)
- Bonded restorations prone to failure
Another name for vitamin D resistant rickets
familial hypophosphatemic rickets
Inheitance pattern of VItDRR and what is the gene involves
X-linked PHEX gene
Describe VitDRR
- Decreased tubular reabsorption of phosphate in the kidney leads to hypophosphatemia
- Low levels of phosphate –> defective calcification of teeth and bones (bowing legs and frontal bossing)
Treatment for VitDRR
-Phosphate and calcitriol
Oral manifestations of VitDRR
- Abnormal dentin and enamel
- Large pulp chambers (can extend into DEJ)
- Spontaneous abscesses (25% have multiple abscesses in normal primary teeth)
- Variable penetration (depends on when treatment was intiated)
Treatment for VitDRR
Selants
- Prophylatic full coverage restorations (large pulps)
- Endo therapy for pulpally involved permanent teeth
Sources of intrinsic stains of teeth
- Congenital porphyrie- Purple brown *heme build up)
- Hyperbilirubinemia Absent bile duct –> bile accumulation
- Anemia - gray
- Cystic Fibrosis - (disease/therapy)= (yellow/brown)
- Tetracycline
Colors of hyperbilirubinemia
- Biliary atresia= green
- Rh incompatibility (erythroblastosis fetalis)= blue-green/brown
What is the name of the disease where there is enamel hypoplasia on one or more permanent molars and incisors
molar incisor hypomineralization (MIH)
Causes of Molar incisor hypomineralization
Systemic insult during child’s first 3 years of life
- Medical condition
- Antibiotic usage
- Preterm birth
- Environmental pollutants (PCDD in breast milk)
Prevalence of MIH
4-25%
Difficulties with treating MIH teeth are
Teeth are sensitive
- OH difficult
- Anesthesia difficult (pulps are chronically inflammed)
Poor bonding
Treatment for MIH teeth
- Remineralization therapy (MI paste and fluoride varnish)
- Fuji sealants (retention is poor- frequent replacing)
- Incisors= microabrasion, composite bonding and veneer
- *depends on the severity**
Treatment for molars affected with MIH
- Mild
- Moderate
- Severe
- Mild= composite restorations
- Moderate= SSC
- Severe= Exo
Fluorosis stains are (intrinsic/extrinsic)
intrinsic (white brown)
What causes fluorosis
excess fluoride disrupts enamel formation
Disruption of enamel formation by excess fluoride is commonly caused when
during the first few years of life
The enamel in fluorosis is (hypoplastic/hypomineralized/Hypomaturated)
hypomineralized
Current recommendation for water fluoridation is
0.7 ppm
Incidence of mild and moderate fluorosis in 12-15 year olds
8% mild and 5% moderate
Potential sources of fluoride causing fluorosis are
- Halo effect
- Infant formula
- Toothpaste consumption
- Inappropriate fluoride supplements
Fluorosis treatment
Esthetics only
- Microabrasion
- Bonding
- veneer
Eruption cyst is the soft tissue analog of
dentigerous cyst
What causes an eruption cyst
when the dental follicle forms around the crown of an erupting tooth
what is the name of an eruption cyst filled with blood
eruption hematoma
Treatment for eruption cyst
None-usually spontaneously erupts on its own
-Can excise the roof of the cyst to aid in eruption
Radiographic evidence of ankylosis
Loss of PDL (sometimes not evident)
Clinical sign of ankylosis
solid sound on percussion
-Marginal ridge discrepancy
Ankylosis in anterior teeth is common following
trauma
T?F the alveolar bone around the impacted tooth doesn’t continue to growth
f it does
Incidence of ankylosis in primary molars
2-4%
Ankylosis is more common in the (maxilla/mandible)
mandible
T/F Exfoliation of ankylosed teeth usually occurs normally
t
Under what circumstances should you extract an ankylosed tooth
-Marginal ridge discrepancy is severe (tipping of adjacent teeth into the space (prevent trapping erupting teeth)
What is ectopic eruption
when a permanent tooth causes either resorption of a primary tooth other than the one it is supposed to replace or resorption of an adjacent primary tooth
Ectopic eruption is most commonly seen in what teeth
- Lateral incisor
- First maxillary molar
- Maxillary canines
In what arch is the lateral incisor often involved in ectopic eruption
both arches
Describe what happens when a lateral incisor ectopically erupts
premature exfoliation of the primary canine
Ectopic eruption of the lateral incisors typically indicates
crowding
Treatment for ectopic eruption of the lateral incisor
- If unilateral, consider extraction of the other primary canine to prevent midline shift
- LLHA with a spur
- Refer to orthodontitis
Ectopic eruption of the maxillary first molar leads to early exfoliation of what tooth
primary 2nd molar
Prevalence of ectopically erupted maxillary first molar
3-4%
How many ectopically erupted maxillary first molars self-correct
66%
Treatment options for ectopically erupted maxillary first molars
- Ortho separator
- Brass wire
- Ortho appliances
- Severe case will result in loss of 2nd primary molar
Consequence of ectopic eruption of maxillary first molar
- Space loss
- 2nd primary molar may develop access (requiring exo)
Ectopically erupting maxillary canines (impacted) are positioned how
mesioangular (possible overlap with the root of the lateral incisor)
How many impacted maxillary canines are palatally and labially positioned
Palatal= 2/3 Labial= 1/3
Incidence of impacted maxillary canines
1.5-2%
Palatal impaction of the canine can be suspected when
the canine buldge can’t be palpated
Impacted maxillary canine is more commonly seen when
the lateral incisor is missing or small
Improvement of the eruption path of the impacted canine can be improved how
extraction of the primary canine
- Overlapping less than half the lateral incisor –> 91% success
- When overlap is more than 1/2 extraction is 64% successful
What will happen if eruption of the impacted canine is unsuccessful
remains impacted
The maxillary incisor is ectopic or impacted in _% of the population
2
Causes of impacted/ectopic maxillary incisor
- Supernumerary tooth
- Trauma
- Pulpal treatment of primary incisor
Treatment of impacted maxillary incisor
Impaction
-Exo supernumerary tooth or overretained primary tooth
Ectopic
- Depends on severity and etiology
- Exo overretained primary tooth
- Supernumerary tooth- consider root development of permanent incisors
Permanent mandibular incisors often erupt (buccally/lingually) relative to the primary
lingually
O and P can be extracted when
24 and 25 (lingually erupted are mostly erupted and O and P aren’t mobile