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Dental Development, Morphology, Eruption and Related Pathologies Flashcards

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1
Q

Embryology: Neural crest cells

A
  • Develop from ectoderm along lateral margins of neural plate
  • Undergo extensive migration
  • Responsible for many skeletal and connect tissues:
    • Bone
    • Cartilage
    • Dentin
    • Dermis
    • NOT enamel
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2
Q

Embryology: Dental lamina

A
  • Begins development @ 6 weeks of embryonic age.
  • Dental lamina differentiates from expansion of basal layer of oral cavity epithelium.
  • Tooth buds arise from dental lamina.
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3
Q

Name the components of tooth buds

A
  • Enamel organ
  • Dental papilla
  • Dental sac
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4
Q

Name the morphologic stages of dental development

A
  • Dental lamina
  • Bud stage
  • Cap stage
  • Early bell stage
  • Advanced bell stage
  • Hertwig’s epithelial root sheath
  • Formation of enamel and dentin matrices
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5
Q

Dental lamina

A
  • Inductive phenomenon
  • Initial formation of dental development
  • Characterized by initiation
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6
Q

Bud stage

A
  • Initial swellings from dental lamina.
  • Formation of tooth buds.
  • Characterized by proliferation and morphodifferentiation.
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7
Q

Cap Stage

A
  • Expansion of tooth buds
  • Formation of tooth germ
  • Proliferation of tooth germ with cap-like appearance
    • Inner (concavity) and outer (convexity) enamel epithelium
    • Stellate reticulum (center of epithelial enamel organ): supports and protects ameloblasts
    • Dental papilla (neural crest origin): Formative organ of dentin and primordium of pulp
    • Dental sac: Gives rise to cementum and PDL
    • Characterized by proliferation, histodifferentiation, and morphodifferentiation.
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8
Q

Early Bell Stage

A
  • Invagination of epithelium deepens, margins continue to grow
    • Stratum intermedium: Essential for enamel production
    • Primordia of permanent teeth bud off primary dental lamina
  • Basic form an relative size established by differential growth
  • Characterized by proliferation, histodifferentiation, and morphodifferentiation
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9
Q

Advanced Bell Stage

A
  • Differentiation of odontoblasts precedes that of ameloblasts
  • Future DEJ outlined
  • Basal margin of enamel organ gives rise to Hertwig’s epithelial root sheath
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10
Q

Hertwig’s Epithelial Root Sheath

A
  • Composed of inner and outer enamel epithelia without stratum intermedium and stellate reticulum
  • Root sheath loses continuity once first layer of dentin laid down
  • Remnant persists as rests of Malassez
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11
Q

Formation of enamel and dentin matrices

A
  • Characterized by apposition
  • Regular and rhythmic deposition of matrix of hard dental structures
  • Takes place in waves from DEJ outward, from incisal to cervical
  • Takes place in two stages
  • Both processes occur simultaneously
    • Immediate partial mineralization as matrix segments are formed
    • Maturation
      • Gradual completion
      • The term “maturation” is also used to describe post-eruption mineralization
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12
Q

Initiation: Morphologic stage counterparts, nature of anomaly, deficient developments, excessive development

A
  • Morphologic stage counterparts: Dental lamina
  • Nature of anomaly: Number
  • Deficient developments: Anodontia, hypodontia, oligodontia
  • Excessive development: Hyperdontia
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13
Q

Proliferation: Morphologic stage counterparts, nature of anomaly, deficient developments, excessive development

A
  • Morphologic stage counterparts: Bud, cap, early and advanced bell
  • Nature of anomaly: Number and structure
  • Deficient developments: Hypodontia, oligodontia
  • Excessive development: Hyperdontia, odontoma, epithelial rests
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14
Q

Histodifferentiation: Morphologic stage counterparts, nature of anomaly, deficient developments, excessive development

A
  • Morphologic stage counterparts: Cap, early and advanced bell
  • Nature of anomaly: Enamel and dentin structures
  • Deficient developments:
    • Amelogenesis imperfecta type I (hypoplastic) & IV (hypoplastic/hypomaturation)
    • Dentinogenesis imperfecta
  • Excessive development: Hyperdontia, odontoma, epithelial rests
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15
Q

Morphodifferentiation: Morphologic stage counterparts, nature of anomaly, deficient developments, excessive development

A
  • Morphologic stage counterparts: Bud, cap, early and advanced bell
  • Nature of anomaly: Size and shape
  • Deficient developments:
    • Microdontia
    • Peg lateral
    • Mulberry molars
    • Hutchinson incisors
    • Absence of cusp or root
  • Excessive development:
    • Macrodontia
    • Tuberculated cusps
    • Carabelli’s cusp
    • Taurodontism
    • Dens in dente
    • Dens evaginarus
    • Dilaceration
    • Gemination
    • Fusion
    • Concresence
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16
Q

Apposition: Morphologic stage counterparts, nature of anomaly, deficient developments, excessive development

A
  • Morphologic stage counterparts: Deposition of enamel and dentin matrices
  • Nature of anomaly: Enamel, dentin and cementum apposition
  • Deficient developments:
    • Amelogenesis imperfecta type II (hypomaturation) and IV
    • Enamel hypoplasia
    • Dentin hypoplasia
    • Regional odontodysplasia
  • Excessive development:
    • Enamel pearls
    • Hypercementosis
    • Odontoma
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17
Q

Mineralization: Morphologic stage counterparts, nature of anomaly, deficient developments, excessive development

A
  • Morphologic stage counterparts: Mineralization of enamel and dentin matrices
  • Nature of anomaly: Enamel and dentin mineralization
  • Deficient developments:
    • Amelogenesis imperfecta type III (hypocalcified)
    • Enamel hypomineralization
    • Fluorosis
    • Interglobular dentin
  • Excessive development: Sclerotic dentin
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18
Q

Maturation: Morphologic stage counterparts, nature of anomaly, deficient developments, excessive development

A
  • Morphologic stage counterparts: Maturation of enamel and dentin matrices
  • Nature of anomaly: Enamel and dentin maturation
  • Deficient developments: Amelogenesis imperfecta type II & IV
  • Excessive development: N/A
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19
Q

Eruption: Morphologic stage counterparts, nature of anomaly, deficient developments, excessive development

A
  • Morphologic stage counterparts: Eruption of teeth
  • Nature of anomaly: Eruption
  • Deficient developments:
    • Primary failure of eruption
    • Ectopic eruption
    • Ankylosis
    • Impaction
    • Transposition
    • Delayed eruption
  • Excessive development:
    • Natal/neonatal teeth
    • Accelerated eruption
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20
Q

Hyperdontia: Prevalence, Frequency, Location, Genetics, Classification of supernumerary teeth

A

initiation and Proliferation

  • Prevalence:
    • Primary dentition: 0.3-0.8%
    • Permanent dentition: 0.1-3.8% in whites; higher in blacks and Asians
  • Frequency:
    • Males 2:1 females
    • Permanent dentition 5x as common as primary dentition
  • Location
    • 95% in maxilla, especially in anterior region
    • Mesiodens most common
  • Genetics: Variable with familial tendency
  • Classification of supernumerary teeth
    • Supplemental: Normal morphology
    • Rudimentary: Conical, tuberculate (barrel-shaped), molariform (differentiate from odontoma)
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21
Q

Conditions/Syndromes Associated with Hyperdontia

A
  • Apert (acrocephalosyndactyly)
    • Delayed or ectopic eruption
    • Shovel-shaped incisors
  • Cleidocranial dysplasia
    • Delayed development and eruption of permanent teeth
    • Supernumerary teeth
    • Delayed primary exfoliation
    • Enamel hypoplasia
  • Gardner syndrome
    • Delayed eruption
    • Supernumerary teeth
    • Osteomas of the jaw
  • Crouzon syndrome (craniofacial dysostosis)
  • Down syndrome
  • Sturge-Weber syndrome
  • Orofaciodigital syndrome I
  • Cleft lip and palate
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22
Q

Anodontia, Hypodontia, and Oligodontia: Prevalence, Frequency, Location, Genetics, Etiology, Associations

A

Initiation and Proliferation

  • Prevalence
    • Primary dentition: Less than 1% (0.5-0.9%)
    • Permanent dentition: 1.5-10% excluding 3rd molars
  • Frequency
    • Females 1.5:1 males
    • Third molars (20%), mandibular 2nd premolar (3.4%), maxillary lateral (2.2%), maxillary 2nd premolar (~0.85%)
  • Genetics
    • Inheritance pattern may be autosomal dominant or polygenic multifactorial
    • Familial patterns may play a role
    • Mutations of PAX9, MSX1, AXIN2 genes may be identified
  • Problems may arise from:
    • Failure of induction
    • Abnormality of lamina
    • Insufficient space
    • Physical obstruction of lamina
  • Significant correlation between missing primary and missing permanent successor
  • May be associated with microdontia: peg lateral incisors are part of spectrum of hypodontia
  • Agenesis of third molars is associated with agenesis of one or both permanent maxillary lateral incisors
  • In some patients with hypodontia, other ectodermal organs are also affected: salivary glands (hyposalivation), skin, sweat glands, but not always in association with ectodermal dysplasia
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23
Q

Conditions/Syndromes Associated with Anodontia, Hypodontia, and Oligodontia

A
  • Ectodermal dysplasia
    • Conical crowns
    • Hypodontia to anodontia
    • Deficient alveolar ridge
  • Crouzon syndrome (craniofacial dysostosis); also hyperdontia
  • Chondroectodermal dysplasia (Ellis-van Creveld)
    • Premature teeth - 25%
    • Absent maxillary sulcus
    • Conical crowns
    • Partial anodontia
    • Enamel hypoplasia
  • Williams syndrome (elfin appearance)
    • Partial anodontia
    • Prominent lips
    • Microdontia
    • Enamel hypoplasia
  • Non-syndromic cleft lip/palate
  • Achondroplasia
    • Midface hypoplasia
    • Frontal bossing
  • Incontinentia pigmenti
    • Conical crowns
    • Delayed eruption
    • Premature teeth
    • Cleft lip/palate
  • Orofaciodigital syndrome I
  • Rieger syndrome
    • Midface hypoplasia
    • Delayed eruption
    • Hypodontia, usually upper incisors
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24
Q

Size Anomalies

A
  • Types
    • True generalized: Small/large teeth in normal jaws
    • Relative generalized: Normal or slightly smaller/larger teeth in larger/smaller jaws

Proliferation and Morphodifferentiation

  • Microdontia
    • Prevalence: 0.8-8.4%
    • Frequency: Maxillary lateral incisors, 2nd premolars, 3rd molars
    • Genetics: Inheritance pattern autosomal dominant with incomplete penetrance
  • Macrodontia
    • Prevalence: Single tooth macrodontia is rare. Rule out fusion, germination.
    • Frequency: Usually incisors and canines, often bilateral
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25
Q

Conditions/Syndromes Associated with Microdontia

A
  • Ectodermal dysplasia
  • Chondroectodermal dysplasia (Ellis-van Creveld)
  • Hemifacial microsomia
  • Down syndrome
  • Crouzon syndrome
  • Pituitary dwarfism
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26
Q

Conditions/Syndromes Associated with Macrodontia

A
  • Hemifacial hyperplasia/hypertrophy
    • Accelerated eruption on affected side
  • Crouzon syndrome
  • Otodental syndrome
    • Macrodontia affects posterior teeth globodontia (primary second molars) molar fusion
  • XYY syndrome
  • Pituitary gigantism
  • Pineal hyperplasia with hyperinsulinism
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27
Q

Conjoined Teeth Anomalies

A

Proliferation and Morphodifferentiation

  • Gemination
  • Fusion
  • Concrescence
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28
Q

Gemination – Prevalence, characteristics, significance

A

Proliferation and Morphodifferentiation

  • Enlarged or joined teeth in which tooth count normal when enlarged tooth is counted as one.
    • Prevalence:
      • Primary dentition: 0.5-2.5%
      • Permanent dentition: 0.5%
    • Characteristics: Abortive attempt by single tooth to divide; bifid crown with single root and pulp chamber
    • Familial inheritance
    • Significance
      • Crowding may retard eruption of permanent successor
      • Site of fusion may be at increased risk for caries
        • Clinical diagnosis: Extra crown (assuming normal complement of other teeth)
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29
Q

Fusion – Prevalence, characteristics, significance

A

Proliferation and Morphodifferentiation

  • Enlarged or joined tooth in which the tooth count is normal when enlarged tooth is counted as one.
    • Prevalence: 0.5% and more common in primary dentition
    • Characteristics:
      • Dentinal union of two embryologically developing teeth with two separate pulp chambers
      • Separate or fused canals may appear as large bifid crown with one chamber
      • Dentin always confluent
    • Clinical diagnosis: Missing a tooth (unless fusion occurs with supernumerary tooth)
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30
Q

Concrescence – Prevalence, characteristics, significance

A

Proliferation and Morphodifferentiation

  • Technically not a developmental defect because it can occur after tooth formation is complete
    • Prevalence: Most common in the maxillary posterior region
    • Characteristics: Fusion that occurs after root formation is complete (why it is technically not a developmental defect)
    • Etiology: Trauma, crowding that may occur pre- or post-eruption
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31
Q

Anomalies of Morphodifferentiation – Size and Shape

A
  • Dens in dente
  • Dens evaginatus
  • Taurodontism
  • Dilaceration
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32
Q

Dens in dente – Prevalence, characteristics, significance, treatment

A

Morphodifferentiation – Size and Shape

  • Dens invaginatus; “tooth within a tooth”
    • Prevalence: 0.3-10%; rare in African Americans
    • Frequency: Maxillary lateral most affected; uncommon in primary teeth
    • Characteristics
      • Invagination of inner enamel epithelium
      • In severe types – Hertwig’s epithelial root sheath folds into developing root
    • Significance: Carious involvement via communication between oral environment and invaginated portion
    • Treatment:
      • Simple type: Sealant or composite restoration
      • Deeper lesions require direct or indirect pulp capping, conventional RCT, MTA/RCT, combined RCT/surgical treatment
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33
Q

Dens evaginatus - Types, prevalence, frequency, characteristics, significance

A

Morphodifferentiation – Size and Shape

  • Types
    • Type I: Talon cusp
    • Type II: Semi-talon
    • Type III: Trace talon
  • Prevalence: 1-8%
    • Higher in some racial groups – Asian, Native American, Hispanic, Inuit
  • Frequency
    • Both sexes affected
    • 77% are permanent teeth
    • 88% are maxillary incisors
    • 55% are lateral incisors
    • May be unilateral or bilateral
  • Characteristics: Evagination of enamel epithelium; focal hyperplasia of pulp mesenchyme
  • Significance: Pulp tissue within extra cusp may develop pulp necrosis
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34
Q

Conditions/syndromes associated with dens evaginatus

A
  • Lobodontia - “wolf-like teeth”, “fang-like cusps”
  • Rubenstein-Taybi syndrome
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35
Q

Taurodontism - Types, prevalence, frequency, characteristics, significance

A

Morphodifferentiation – Size and Shape

  • Types
    • Hypotaurodontism
    • Mesotaurodontism
    • Hypertaurodontism
  • Prevalence: 2.5-3.2% in US
    • Higher in some racial groups and hypophosphatasia
  • Frequency: Permanent molar is most affected
  • Characteristics:
    • Failure of normal invagination of Hertwig’s epithelial root sheath
    • Elongation of crown at the expense of the roots
  • Significance: Large pulps
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36
Q

Conditions/Syndromes Associated with Taurodontism

A
  • Klinefelter syndrome
    • Small cranial dimension
    • Bimaxillary prognathism
    • Taurodontism in 30%
  • Tricho-dento-osseous syndrome (TDO)
    • Dolichocephalic with frontal bossing
    • Taurodont teeth have periapical radiopacities and high pulp horns with likely microexposures
    • Delayed eruption
  • Mohr syndrome (orofaciodigital syndrome II)
    • Lobed tongue
    • Upper lip midline cleft
    • Oligodontia
  • Hypohydrotic ectodermal dysplasia
  • Amelogenesis imperfecta type IV
  • Down syndrome
  • Williams syndrome
  • Smith-Magenis syndrome
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37
Q

Dilaceration - Etiology

A

Anomalies of Morphodifferentiation – Size and Shape

Etiology: Trauma to primary dentition, especially intrusion or idiopathic developmental disturbance.

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38
Q

Conditions/Syndromes Associated with Dilaceration

A
  • Axenfeld-Rieger syndrome
  • Ehlers-Danlos syndrome
  • Lamellar congenital ichthyosis
  • Smith-Magenis syndrome
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39
Q

Anomalies of Histodifferentiation – Structure

A
  • Amelogenesis imperfecta
  • Dentinogenesis imperfecta
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40
Q

Amelogenesis imperfecta

A
  • Heritable enamel defect with multiple inheritance patterns
  • Incidence variably reported as 1:14,000, 1:8,000, 1:4,000 – first figure is generally accepted
  • Clinically diverse with potential for overlaps of types
    • 14 subgroups under 4 major types – based on clinical/histologic features and mode of inheritance
  • Distinguished from other enamel defects: Confinement to distinct patterns of inheritance; occurrence apart from syndromic, metabolic, or systemic condition.
    • AI Type I – Hypoplastic
    • AI Type II – Hypomaturation
    • AI Type III – Hypocalcified
    • AI Type IV – Hypoplastic/Hypomaturation +/- Taurodontism
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41
Q

AI Type I – Hypoplastic – Characteristics, subgroups

A
  • Insufficient quantity of enamel
    • Lack of complete inner enamel epithelium
    • Enamel matrix defect
  • Both dentitions affected
  • Most common subgroup (AD)
  • Anterior open bite in 44%
  • Long lower face
  • Subgroups (Witkop)
    • Pitted: AD
    • Localized: AD
    • Localized: AR
    • Smooth: AD
    • Smooth: X-linked recessive
    • Rough: AD
    • Enamel agenesis: AR
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42
Q

Dentinogenesis imperfecta

A

Anomalies of Histodifferentiation – Structure

  • Heritable defect of predentin matrix
  • Normal mantle dentin
  • Amorphic and atubular circumpulpal dentin
  • Incidence: 1:8,000
  • 3 subtypes - (Shields I, II, and III)
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43
Q

Dentinogenesis imperfecta – Shields Type I: Severity, clinical characteristics

A

Histodifferentiation – Structure

  • Least severe
  • Occurs with osteogenesis imperfecta Types IB an IVB
  • Autosomal dominant
  • Defect of matrix common to teeth and bones
  • Dentinal manifestation of underlying type 1 collagen defect
  • Primary teeth more severely affected; permanent teeth most often affected are central incisors and 1st molars
  • Occurs prior or soon after eruption
  • Degree of expressivity is variable, even with same individual
  • Clinical characteristics:
    • Amber translucence
    • Bulbous crowns
    • Short roots
    • Periapical radiolucencies
    • Alveolar abscesses
    • Rapid attrition
    • Pulpal obliteration
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44
Q

Dentinogenesis imperfecta – Shields Type II: Characteristics

A

Histodifferentiation – Structure

  • “Hereditary opalescent dentin”
  • Occurs alone: no OI
  • Autosomal dominant
  • Both dentitions equally affected
  • Same characteristics as DI-I
    • Amber translucence
    • Bulbous crowns
    • Short roots
    • Periapical radiolucencies
    • Alveolar abscesses
    • Rapid attrition
    • Pulpal obliteration
  • Irregular or tubular pattern
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45
Q

Dentinogenesis imperfecta – Shields Type III: Severity, clinical characteristics

A
  • Most severe
  • Rare: Brandywine tri-racial isolate population (Caucasian/African American/American Indian)
  • Clinical characteristics:
    • Bell-shaped crowns
    • Opalescent hue
    • Shell teeth (esp. primary dentition) with short roots and enlarged pulp chambers
    • Only mantle dentin formed
    • Rapid wear of primary and permanent crowns
    • Permanent tooth pulps small or completely obliterated
    • Multiple pulp exposures (esp. primary dentition)
    • Regular tubules
    • Enamel pitting
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46
Q

Conditions/Syndromes Associated with DI

A
  • Osteogenesis Imperfecta
    • Autosomal dominant
    • 4 major types
      • OI Type I: Most common
      • OI Type II: Lethal in perinatal period
      • Dentinogenesis imperfecta more common in Types III and IV
    • Bowing of legs
    • Fragile bones – fractures
    • Blue sclera
    • Bitemporal bossing
    • Defective collagen > loose ligaments
    • Impaired hearing
    • Macrocephaly
  • Some variants of Ehlers-Danlos syndrome
  • Goldblatt syndrome
  • Schimke immune-osseous dysplasia
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47
Q

Anomalies of Apposition – Enamel Structure

A
  • Enamel hypoplasia
  • Enamel pearls
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48
Q

Enamel hypoplasia: Etiology, marker for what disease, predominant locations

A

Anomalies of Apposition – Enamel Structure

  • Environmentally induced
    • Physiologic: Developmental, ingestional (vitamin deficiency, A, C, D, calcium, phosphate, fluoride), erosion
    • Infectious: Debilitating disease, apical infection of predecessor, chronic fungal infection, prenatal (syphilis, rubella, Rh incompatibility)
    • Traumatic: Injury to predecessor, attrition, abrasion
    • Iatrogenic: Tetracycline, fluoride, surgery, irradiation
  • Genetic etiologies: Amelogenesis imperfecta
  • Enamel hypoplasia is a potential marker for celiac disease
    • Predominant locations: Maxillary/mandibular, primary/permanent central and lateral incisors
    • Enamel hypoplasia is associated with epidermolysis bullosa, junctional form
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49
Q

Enamel pearls

A

Anomalies of Apposition – Enamel Structure

  • Cells of epithelial root sheath may remain attached to dentin
  • May differentiate into ameloblasts and produce enamel
  • May contain dentin and pulp
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50
Q

Anomalies of Apposition – Dentin Structure

A
  • Dentin dysplasia
  • Regional odontodysplasia
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51
Q

Shields Type I Dentin Dysplasia: Clinical features, inheritance, primary defect

A

Anomalies of Apposition – Dentin Structure

  • Radicular dentin dysplasia
  • “Rootless teeth”
  • Clinical features:
    • Short, blunted roots or rootless in both dentitions
    • Normal crown morphology
    • Slightly translucent
    • Obliterated pulp chambers
    • Multiple periapical radiolucencies
    • Root sheath problems
    • Severe mobility and malalignment
  • Autosomal dominant
  • Primary defect is epithelial root sheath that invaginates too early/often
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52
Q

Shields Type II Dentin Dysplasia: Clinical features, inheritance

A

Anomalies of Apposition – Dentin Structure

  • Coronal (and radicular) dentin dysplasia
  • Very rare
  • Primary teeth affected
  • Amber color
  • Looks like DI-II
  • Coronal dentin is involved as well as root dentin
  • Permanent teeth look normal, but radiographically demonstrate thistle-tube shaped pulps, multiple pulp stones
  • Some cases, features characteristic of DI-II are seen (bulbous crowns, cervical constriction, mild discoloration, pulp obliteration
  • Autosomal dominant
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53
Q

Regional Odontodysplasia

A

Anomalies of Apposition – Dentin Structure

  • “Ghost teeth”
  • Localized arrest in tooth development
  • Variable presentation
  • Affects primary and permanent teeth
    • Usually maxilla
    • 80% involve central incisors
  • Single or several teeth may be involved with moderate to severe hypoplasia
  • Atubular tracts, irregular tubules, interglobular mineralization, no odontoblastic layer
  • Cementum can be normal or aberrant
  • Thin enamel with diffuse shell appearance
  • Large pulps
  • Little dentin
  • No established etiology or inheritance pattern
  • Gingival hyperplasia
  • Failure of teeth to erupt
  • No established etiology or inheritance pattern but alteration in vascular supply is most popular theory
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54
Q

Anomalies of Apposition – Cementum Structure

A
  • Hypophosphatasia
  • Epidermolysis bullosa
  • Cleidocranial dysplasia
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55
Q

Hypophosphatasia: Etiology, clinical presentation, inheritance

A

Anomalies of Apposition – Cementum Structure

  • Lack of serum alkaline phosphatase
  • Increased urinary phosphoethanolamine
  • Autosomal dominant or recessive
  • Lack of cementum on root surfaces
  • Premature loss of primary teeth with little/no resorption
  • Bone abnormalities that resemble rickets
  • Large pulp chambers
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56
Q

Epidermolysis bullosa

A

Anomalies of Apposition – Cementum Structure

  • Fibrous acellular cementum
  • Excess cellular cementum
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57
Q

Cleidocranial dysplasia

A

Anomalies of Apposition – Cementum Structure

  • Deficient cellular cementum
  • May be related to lack of eruption
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58
Q

Anomalies of Mineralization – Enamel

A
  • Enamel hypomineralization
  • Molar-incisor hypomineralization (MIH)
  • Amelogenesis imperfecta Type III (hypocalcified)
  • Enamel fluorosis
  • Sclerotic dentin
59
Q

Molar-Incisor Hypomineralization (MIH): Etiology, associated conditions

A

Anomalies of Mineralization – Enamel

  • Hypomineralization of 1-4 permanent first molars frequently associated with affected permanent incisors.
    • MIH prevalence 4-25% (Europe); varies with different aged birth cohorts, suggesting potential environmental factors.
    • Possible problem with ameloblast function after full matrix completion, and/or insufficient uptake of minerals.
    • Associated with:
      • Febrile illness
      • Antibiotics (confounding factor with febrile illness)
      • Nutritional deficiencies
      • Preterm birth
      • Dioxin compounds in breast milk
60
Q

Amelogenesis imperfecta Type III (Hypocalcified): Etiology, inheritance, clinical presentation

A

Anomalies of Mineralization – Enamel

  • Deficit in mineralization of matrix
  • Very soft enamel with normal thickness
  • Enamel lost soon after eruption
  • Anterior openbite >60%
  • Rough enamel results in high calculus formation
  • Delays in eruption
  • 2 subgroups
    • AD
    • AR
61
Q

Enamel fluorosis: Amount of fluoride in water, indices

A

Anomalies of Mineralization – Enamel

  • Critical issue is additive effects of fluoride (halo effect)
  • Amount of fluoride in water
    • Greater than 2ppm - 10% chance
    • Greater than 6ppm - 90% chance
  • Dean’s index: Normal, questionable, very mild, mild, moderate, severe
  • Tooth Surface Index of Fluorosis (TSIF) - Combines Dean’s and TF index
    • Defines the time which fluoride exposure occurs
    • Relates fluorosis risk with tooth development stage
  • 84.5% unaffected in optimally fluoridated areas
  • 78.1% had some degree of fluorosis when fluoride was 4x optimal
62
Q

Sclerotic dentin

A

Anomalies of Mineralization – Enamel

  • Deposition of calcium in tubules as result of trauma or normal aging
63
Q

Anomalies of Maturation – Enamel Structure

A
  • Amelogenesis Imperfecta Type III (hypomaturation)
  • Amelogenesis Imperfecta Type IV (hypomaturation-hypoplastic with taurodontism)
64
Q

Amelogenesis Imperfecta Type II - Hypomaturation: Clinical presentation, genetic etiology, subgroups

A

Anomalies of Maturation – Enamel Structure

  • Clinical presentation:
    • Normal enamel thickness
    • Low radiodensity, poorly mineralized
    • Less severely hypomineralized than hypocalcified type
    • Mottled brown-yellow-white color - porous surface; soft, chips away
    • Persistence of organic content
    • Defective or absent rod sheath, defective formation of apatite
    • Sheath may be filled with debris
  • X-linked recessive, AR (and AD)
  • Subgroups:
    • Pigmented – AR
    • X-linked recessive
    • Snowcapped – AD? *Fairly common*
65
Q

Amelogenesis Imperfecta Type IV - Hypomaturation-Hypoplastic with Taurodontism (also involves histodifferentiation): Clinical presentation, subgroups

A

Anomalies of Maturation – Enamel Structure

  • Distinct from trichodento-osseous syndrome (AI + taurodontism + nail/hair defects)
  • Clinical presentation:
    • Mottled yellow-brown, enamel with pits
    • Molars are taurodont
    • Subgroups:
      • Hypomaturation-hypoplastic: AD
      • Hypoplastic-hypomaturation: AD
66
Q

Intrinsic (endogenous in nature) abnormalities of color

A
  • Blood-borne pigments
  • Drug administration - tetracyclines
  • Cystic fibrosis
  • Trauma
  • Hypoplasia/hypomineralization disorders
  • Excessive systemic fluoride
67
Q

Intrinsic abnormalities of color - Blood-borne pigments

A
  • Anemias - hemosiderin: Grey
  • Bile duct defects: Green
  • Dental trauma: Red, gray, black
  • Neonatal hepatitis - bilirubin: Black, gray
  • Porphyria-porphyrin: Purplish-brown
  • Rh incompatibility (erythroblastosis fetalis) - bilirubin, biliverdin: Blue-green, brown
68
Q

Intrinsic abnormalities of color: Anemias-hemosiderin

A

Grey

69
Q

Intrinsic abnormalities of color: Bile duct defects

A

Green

70
Q

Intrinsic abnormalities of color: Dental trauma

A

Red, gray, black

71
Q

Intrinsic abnormalities of color: Neonatal hepatitis - bilirubin

A

Black, gray

72
Q

Intrinsic abnormalities of color: Porphyria-porphyrin

A

Purplish-brown

73
Q

Intrinsic abnormalities of color: Rh incompatibility (erythroblastosis fetalis) - bilirubin, biliverdin

A

Blue-green, brown

74
Q

Intrinsic abnormalities of color - Drug administration (tetracyclines): Affected dentitions, threshold, when not to prescribe,

A
  • Both dentitions may be affected
  • Related to dose and duration
  • Staining may result even after just 3 days administration
  • Threshold: 21-26 mg/kg/day
  • Should not prescribe from 5th month in utero to 8 years
  • Primary teeth are more intense
  • Tetracycline HCl stains more
  • Oxytetracycline stains less
  • Teeth darken with increased exposure to UV light
75
Q

Intrinsic abnormalities of color: Cystic fibrosis

A
  • May be related to disease, tetracycline, or combination
  • Color yellowish gray to dark brown
76
Q

Intrinsic abnormalities of color: Hypoplasia/hypomineralization disorders

A
  • Amelogenesis imperfecta
  • Dentinogenesis imperfecta
  • Dental caries
  • Enamel and dentin dysplasias
77
Q

Intrinsic abnormalities of color: Excessive systemic fluoride

A
  • Must know community water concentration before describing
  • Non-esthetic appearance of teeth; more resistant to caries
78
Q

Extrinsic abnormalities of color

A
  • Bacteria (chromogenic)
  • Discoloring agents
79
Q

Extrinsic abnormalities of color: Bacteria (chromogenic)

A
  • Brown/black: Much less common, difficult to remove
  • Green: Bacillus pyocaneus, Aspergillis: Most common
  • Orange: Serratia marcescens, Flavobacterium lutescens: poor OH, more easily removed than green
80
Q

Extrinsic abnormalities of color: Bacteria (chromogenic)

Brown/black

A

Much less common, difficult to remove

81
Q

Extrinsic abnormalities of color: Bacteria (chromogenic)

Green

A

Bacillus pyocaneus, Aspergillis: Most common

82
Q

Extrinsic abnormalities of color: Bacteria (chromogenic)

Orange

A

Serratia marcescens, Flavobacterium lutescens: poor OH, more easily removed than green

83
Q

Extrinsic abnormalities of color: Discoloring Agents

A
  • Chlorhexidine: Brown
  • Cola drinks: Coloring agents
  • Foods: Coffee and tea (tannins)
  • Iron sulfide: Black
  • Marijuana: Gray-green (oils, resins and pigments)
  • Medicaments
  • Restorative materials
  • Silver nitrate: Black
  • Stannous fluoride: Black
  • Tobacco: Dark brown to black
84
Q

Extrinsic abnormalities of color: Discoloring Agents

Chlorhexidine

A

Brown

85
Q

Extrinsic abnormalities of color: Discoloring Agents

Cola

A

Coloring agents

86
Q

Extrinsic abnormalities of color: Discoloring Agents

Foods

A

Coffee and tea (tannins)

87
Q

Extrinsic abnormalities of color: Discoloring Agents

Iron sulfide

A

Black

88
Q

Extrinsic abnormalities of color: Discoloring Agents

Marijuana

A

Gray-green (oils, resins and pigments)

89
Q

Extrinsic abnormalities of color: Discoloring Agents

Silver nitrate

A

Black

90
Q

Extrinsic abnormalities of color: Discoloring Agents

Stannous fluoride

A

Black

91
Q

Extrinsic abnormalities of color: Discoloring Agents

Tobacco

A

Dark brown to black

92
Q

Variables influencing Permanent Tooth Eruption

A
  • Genetic: Estimated at 78%
    • Familial: High correlation based on twin studies
    • Race: African American and Hispanics slightly earlier than whites
    • Sex: Females ahead of males
  • Environmental
    • Low birth weight: Delayed eruption
    • Nutrition: Little or no effect
    • Prematurity: Delayed eruption with ventilator dependency
  • Systemic
    • Endocrine system contributory
    • High correlation with hypopituitarism and hypothyroidism
    • Low correlation with altered growth
  • Clinical guides for use in assessing eruption stage/rate of permanent dentition
    • Root development
    • Overlying bone
    • Infection
    • Timing of primary tooth loss considerations
      • Before 5yo: Delays premolar
      • After 8yo: Accelerates premolar
      • Prior to crown completion of successor: Delays eruption
      • After crown completion of successor: Accelerates eruption
93
Q

Theories of Eruption

A
  • Root growth – strong association
  • Vascular pressure
  • Bone growth
  • Periodontal ligament traction – need dental follicle to erupt
  • Connective tissue proliferation at the pulp apex
  • Latter two theories
94
Q

Sequences of Eruption – Primary

A

A B D C E

95
Q

Sequences of Eruption – Permanent

A
  • Maxilla: 6 1 2 4 5 3 7 8
  • Mandible: 6 1 2 3 4 5 7 8
  • Sequence is more important than the timing
96
Q

Stages of Eruption – Permanent Teeth

A
  • Follicular growth
  • Pre-emergent eruptive spurt
  • Post-emergent eruptive spurt
  • Juvenile occlusal eruption
  • Circumpubertal eruptive spurt
  • Adult occlusal equilibrium
97
Q

Premature teeth

A

Erupt prior to 3mo

98
Q

Natal teeth

A

Present at birth

99
Q

Neonatal teeth

A

Present within the first 30 days of life

100
Q

Incidence of natal : neonatal

A

Natal : Neonatal

3 : 1

101
Q

Incidence of premature teeth

A

1 : 2000-3500

102
Q

Premature teeth: Incidence, etiology, associated findings, syndromes

A
  • Natal, neonatal teeth - erupt prior to 3mo
  • Incidence - 1 : 2000-3500
  • 90% are true primary teeth; 10% supernumerary
  • Slightly more common in females
  • Etiology: Unknown - superficially positioned tooth bud?
  • Familial hx reported in 62% of cases
  • Most are poorly formed, risk of aspiration, and nursing obstacle
  • Associated findings: Riga-Fede disease
    • Sublingual traumatic ulceration due to natal or neonatal teeth
    • Syndromes: chondroectodermal dysplasia (Ellis-van Creveld)
      • 25% pachyonychia congenital (Jadassohn-Lewandosky)
103
Q

Structures present in newborns often confused with premature teeth

A
  • Bohn nodules
    • Buccal, lingual aspects of the maxillary alveolar ridge (away from the midline raphe)
    • Mucous gland tissue
  • Dental lamina cysts
    • Found on the crest of the alveolar ridge
    • Derived from the remnants of the dental lamina
  • Epstein pearls
    • Midpalatal raphe
    • Trapped epithelial remnants
    • Visible cysts in 80% of newborns
104
Q

What are Bohns nodules?

A
  • Buccal, lingual aspects of the maxillary alveolar ridge (away from the midline raphe)
  • Mucous gland tissue
105
Q

What are dental lamina cysts?

A
  • Found on the crest of the alveolar ridge
  • Derived from the remnants of the dental lamina
106
Q

What are Epstein pearls?

A
  • Midpalatal raphe
  • Trapped epithelial remnants
  • Visible cysts in 80% of newborns
107
Q

Symptoms children experience during teething

A
  • 50% or more children have one or more problems during teething, but no cause-effect relationship
    • Diarrhea
    • GERD
    • Otitis media
    • Paroxysmal atrial tachycardia
108
Q

Teething differential

A
  • Bronchitis
  • Dehydration
  • Eczema
  • Febrile convulsions
  • Fever >101*F not attributed to teeth - look for other causes
  • H. flu meningitis
  • URI
  • No available evidence suggests s/s sufficiently specific to teething to allow confident diagnosis w/o excluding other organic pathology
109
Q

Why should oral viscous lidocaine not be used for teething pain? (FDA alerts)

A

Excessive amounts can result in seizures, severe brain injury and heart problems. Misuse has lead to hospitalizations and death.

110
Q

Why should homeopathic teething tablets and gels not be given to children? (FDA alerts)

A

Due to reported adverse events. These substances have never been evaluated by the FDA for safety or efficacy.

111
Q

Cystic development associated with eruption

A
  • Eruption hematoma
    • Form of dentigerous cyst occurring around the crown
    • Occurs in either dentition
    • No gender predilection
    • Dilation of follicular space with blood or tissue
    • Translucent to bluish color
    • Infrequently delays tooth eruption
    • Usually ruptures spontaneously; may excise if symptomatic
  • Primordial cyst: stellate reticulum
    • Many believe all primordial cysts are odontogenic keratocysts
    • WHO classification is OKC
  • Dentigerous cyst
    • Most common type of odontogenic cyst
    • Originates from separation of follicle from around the crown of unerupted tooth
    • Usual tx is enucleation
  • Ameloblastoma
    • Most common clinically significant odontogenic tumor
    • Odontogenic epithelial origin
    • Arise from rests of dental lamina, developing enamel organ, basal cells of oral mucosa
    • Slow growing, locally invasive, generally run a benign course
    • Unilocular or multilocular
    • Excision or en bloc resection
    • Common sites: mandibular molars or ramus
112
Q

Eruption hematoma

A

Cystic development associated with eruption

  • Form of dentigerous cyst occurring around the crown
  • Occurs in either dentition
  • No gender predilection
  • Dilation of follicular space with blood or tissue
  • Translucent to bluish color
  • Infrequently delays tooth eruption
  • Usually ruptures spontaneously; may excise if symptomatic
113
Q

Primordial cyst: stellate reticulum

A

Cystic developments associated with eruption

  • Many believe all primordial cysts are odontogenic keratocysts
  • WHO classification is OKC
114
Q

Dentigerous cyst

A

Cystic development associated with eruption

  • Most common type of odontogenic cyst
  • Originates from separation of follicle from around the crown of unerupted tooth
  • Usual tx is enucleation
115
Q

What is the most common type of odontogenic cyst?

A

Dentigerous cyst

116
Q

Ameloblastoma

A

Cystic development associated with eruption

  • Most common clinically significant odontogenic tumor
  • Odontogenic epithelial origin
  • Arise from rests of dental lamina, developing enamel organ, basal cells of oral mucosa
  • Slow growing, locally invasive, generally run a benign course
  • Unilocular or multilocular
  • Excision or en bloc resection
  • Common sites: mandibular molars or ramus
117
Q

What is the most common clinically significant odontogenic tumor?

A

Ameloblastoma

118
Q

Local causes of delayed primary exfoliation and permanent eruption

A
  • Ankylosis
  • Impaction
  • Supernumerary teeth
  • Trauma
119
Q

Systemic conditions of delayed primary exfoliation and permanent eruption (not all-inclusive)

A
  • Achondroplasia
  • Albright’s hereditary osteodystrophy
  • Apert syndrome
  • Chondroectodermal dysplasia
  • DeLange syndrome
  • Down syndrome
  • Fibromatosis gingivae
  • Gardner syndrome
  • Hunter syndrome
  • Hypopituitarism
  • Hypothyroidism
  • Ichthyosis (also associated with ankyloses)
  • Incontinentia pigmenti
  • Low birth weight and/or prematurity
  • Osteogenesis imperfecta
120
Q

Primary failure to erupt may be due to:

A
  • Malfunction of eruption mechanism with non-ankylosed teeth
  • Failure of affected tooth to move through eruption path cleared for it
  • Teeth may partially erupt – submerged
  • Abnormal or complete lack of response to orthodontic forces
121
Q

Local causes of accelerated eruption of primary and permanent teeth

A

Early loss of primary tooth (closer to normal time of permanent tooth eruption)

122
Q

Systemic conditions that may cause accelerated eruption of primary and permanent teeth (not all-inclusive)

A
  • Chondroectodermal dysplasia (Ellis-van Creveld)
  • Hemifacial hypertrophy
  • Hyperthyroidism
  • Osteogenesis imperfecta
  • Pachyonychia congenita
  • Precocious puberty
  • Sotos syndrome (cerebral gigantism)
  • Sturge-Weber syndrome
123
Q

What may cause premature exfoliation of primary teeth? (diseases, conditions, injuries)

A
  • Bone diseases
    • Fibrous dysplasia
    • Vitamin D-resistant rickets
  • Periodontal diseases
    • Aggressive periodontitis
    • Papillon-LeFevre syndrome
  • Metabolic diseases
    • Hypophosphatasia
  • Deviations in growth and development
    • Hemihypertrophy
    • Premature teeth
  • Blood diseases
    • Burkitt’s lymphoma
    • Chediak-Higashi syndrome
    • Cyclic neutropenia
    • Langerhans cell histiocytosis
    • Leukemia
  • Physical and chemical injuries
    • Acrodynia
    • Facial burns
  • Dental anomalies
    • Dentin dysplasia type I (“rootless” teeth)
    • Regional odontodysplasia
124
Q

Treatment for premature exfoliation of primary teeth

A
  • Refer for a thorough physical assessment to rule out underlying systemic disorders
  • Treatment will be supportive in associated with rigorous OH and periodontal care, including regular scaling, antibiotics, preventive measures, and continued monitoring
125
Q

Ectopic eruption of permanent molars: Etiology, most often associated teeth, etiology, % of self-correction

A
  • Incidence of permanent first molars: 3-4% (25% in CLP)
  • Most often associated with U6s, then L2s and U3s
  • Etiology
    • Larger mean sizes of all maxillary permanent and primary teeth
    • Larger affected E’s and 6’s
    • Smaller maxilla
    • Posterior position of maxilla related to cranial base (smaller SNA)
    • Abnormal angulation of erupting 6 causing resorption of distal portion of E
    • Delayed mineralization of some affected 6s
  • Self-correction
    • 66% (only 22% in CLP)
126
Q

Ankylosis (infraocclusion): Diagnosis, etiology, association

A
  • Histological diagnosis: Fusion of cementum with alveolar bone
  • Clinical diagnosis: Submerged tooth; ankylosed area often not diagnosed in radiograph, so ankylosis may be incorrect clinical terminology
  • May occur prior to emergence or occlusal contact, or after tooth is in occlusion
  • Dull noise to percussion (controversial)
  • Etiology: Unknown; some follow familial pattern
  • May be association between ankylosed primary teeth and agenesis of missing successors
127
Q

Ankylosis (infraocclusion): Possible extrinsic factors

A
  • Disturbed local metabolism
  • Localized infection
  • Tooth replantation
  • Trauma
128
Q

Ankylosis (infraocclusion): Possible intrinsic factors

A
  • Break in continuity of periodontal membrane
  • Aberrant deposition of cementum or bone
129
Q

Ankylosis (infraocclusion): Prevalence, teeth most often affected

A
  • 1.3-38.5% (handbook; McDonald and Avery 7-14%) depending on diagnostic criteria, sample characteristics
  • Most affected are Ld’s, followed by Le’s, Ud’s, Ue’s (prevalence variably reported)
  • Associated with agenesis of permanent successor
  • Multiple teeth seen as frequently as single
    • 50% have more than 1 ankylosis
130
Q

Ankylosis (infraocclusion): Sequelae

A
  • Deflected eruption paths
  • Delayed eruption of permanent successors
  • Impacted premolars
  • Loss of arch length and alveolar bone
  • Supraeruption of opposing teeth (esp. maxilla)
131
Q

Ankylosis (infraocclusion): Treatment - empirical

A
  • Observe (esp. for Ld’s, esp. for mandibular teeth)
  • Extract
  • Restore to occlusion
  • Luxate (permanent teeth)
132
Q

Ankylosis (infraocclusion): Timing

A
  • Primary mandibular 1st molars
    • Demonstrate infraocclusion when permanent first molars erupt
    • Often exfoliate on schedule
    • Do not infraocclude dramatically
    • Can be restored to occlusion
  • Primary mandibular 2nd molars
    • Later onset than Ld’s
    • Likely bilateral
    • Usually more severe infraocclusion than Ld’s
    • Usually need extraction
  • Primary maxillary 1st and 2nd molars
    • Relatively rapid progression
    • Occurs close to or ahead of eruption of 6s
    • Usually must be extracted
133
Q

Maxillary central diastema: Prevalence at 6yo, 9yo, 14yo

A
  • 44-97% in 6yo (ugly duckling stage)
  • 33-46% in 9yo
  • 7-20% in 14yo
134
Q

Maxillary central diastema: Distribution

A
  • African Americans >2x more likely than whites or Hispanics
  • Higher in females at 6yo; higher in males at 14yo
135
Q

Maxillary central diastema: Etiology

A
  • Normal development of mixed dentition
    • Familial/racial - associated with bimaxillary protrusion
  • Excessive skeletal growth: Acromegaly
  • Pernicious habits: Lip biting, digit sucking, pacifier, infantile swallow with tongue thrust
  • Deficiency of teeth in arch due to: Spaced dentition, missing/peg laterals, extractions, excessive OJ, excessive OB, ectopic laterals/crowded to lingual
  • Physical impediment to normal closure
    • Enlarged labial frenum (may be effect, rather than cause)
    • Interruption of transseptal fibers caused by midline bony clefts
    • Macroglossia
    • Mesiodens
    • Midline pathology (cysts, fibromas)
    • Retained primary teeth
  • Artificial
    • RPE
136
Q

Maxillary central diastema: Treatment

A
  • Usually after eruption of U3s
  • Based on diagnosis of cause: Bolton analysis is helpful
    • Eliminate habits if present
    • Mesial tipping of central incisors
    • Bodily movement of central incisors
    • Reduction of excess OJ
    • Surgical intervention - transseptal fibers/frenum
    • Enlargement of incisors
137
Q

Classification of supernumerary teeth

A
  • Supplemental: Normal morphology
  • Rudimentary: Conical, tuberculate (barrel-shaped), molariform (differentiate from odontoma)
138
Q

Conditions w/ microdontia

A
  • Ectodermal dysplasia
  • Chondroectodermal dysplasia
  • Hemifacial microsomia
  • Down syndrome
  • Crouzon
  • Pituitary dwarfism
139
Q

Conditions w/ macrodontia

A
  • Hemifacial hyperplasia/hypertrophy
  • Crouzon
  • Otodental syndrome – microdeletion of FGF3
  • XYY syndrome
  • Pituitary gigantism
  • Pineal hyperplasia
140
Q

Syndromes w/ natal/neonatal teeth

A
  • Ellis van Creveld syndrome
  • Hallerman-Streiff syndrome
  • Pachyonychia congenita syndrome
141
Q

Down syndrome: dental manifestations

A
  • Delayed eruption
  • Missing and supernumerary teeth
  • Malformed Teeth (taurodontism)
  • Microdontia
  • Increased risk of perio (Down syndrome : neutrophil chemotaxis defect)
  • Low levels of caries
  • Open Bite
  • Class III tendency
  • Appearance of Macroglossia
  • Fissured tongue
142
Q

Down syndrome: dental tx considerations

A
  • Cardiac defects (40%)(SBE)- Atrioventricular septal defect
  • Leukemia (15x) (AML)
  • Atlantoaxial instability (contraindication in restraint)
  • 3 copies of chromosome 21 (47 total)
  • Risk of airway obstruction due to large tonsils/adenoids
  • Possible reduced risk to infection
143
Q

Cleido

A

* (22 decks)

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