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Pediatric Dentistry Handbook > Chapter 2: Dental Development, Morphology, Eruption > Flashcards

Chapter 2: Dental Development, Morphology, Eruption Flashcards

Dental Development, Morphology, Eruption, and Related Pathologies

1
Q

Neural Crest Cells

A
  • develop from ectoderm along lateral margins of neural plate
  • undergo extensive migration
  • responsible for many skeletal and connective tissues (bone, cartilage, dentin, dermis, not enamel)
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2
Q

Dental Lamina

A
  • Begins development at 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

3 Components of tooth bud

A
  1. Enamel Organ
  2. Dental Papilla
  3. Dental sac
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4
Q

Morphologic Developmental Stages

A 
Dental Lamina
Bud Stage
Cap Stage 
Bell Stage (early and late)
Hertwig's epithelial root sheath
Formation of enamel and dentin matrices
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5
Q

Dental Lamina Stage

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 caplike appearance
Characterized by proliferation, histodifferentiation, and morphodifferentiation
-inner and outer enamel epithelium
-stellate reticulum (center of epithelial enamel organ)
-dental papilla (neural crest origin; gives rise to dentin/pulp)
-dental sac (gives rise to cementum/PDL)

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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 and 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 is laid down
Remnants persist 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 2 stages
Both processes occur simultaneously
-immediate partial mineralization as matrix segments are formed
-maturation

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12
Q

Anomalies associated with Initiation Stage

A

Stage affected: dental lamina
Nature of anomaly: number
Deficient development: anodontia, hypodontia, oligodontia
Excessive development: hyperdontia

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13
Q

Anomalies associated with Proliferation Stage

A

Stages affected: bud, cap, bell stages
Nature of anomaly: number and structure
Deficient development: hypodontia, oligodontia
Excessive development: hyperdontia, odontoma, epithelial rests

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14
Q

Anomalies associated with Histodifferentiation

A

Stages affected: cap, bell
Nature of anomaly: enamel and dentin structure
Deficient development: amelogenesis imperfecta type I and IV, dentinogenesis imperfecta

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15
Q

Anomalies associated with Morphodifferentiation

A

Stages affected: bud, cap, bell
Nature of anomaly: size and shape
Deficient development: 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 evaginatus, dilaceration, fusion, concrescence

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16
Q

Anomalies associated with Apposition

A

Stages affected: deposition of enamel/dentin matrices
Nature of anomaly: enamel, dentin, cementum apposition
Deficient development: amelogenesis imperfecta type II and IV, enamel hypoplasia, dentin dysplasia, regional odontodysplasia
Excessive development: enamel pearls, hypercementosis, odontoma

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17
Q

Anomalies associated with Mineralization

A

Stages affected: mineralization of enamel/dentin
Nature of anomaly: enamel/dentin mineralization
Deficient development: amelogenesis imperfecta type III, enamel hypomineralization, fluorosis, interglobular dentin
Excessive development: sclerotic dentin

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18
Q

Anomalies associated with Maturation

A

Stages affected: maturation of enamel/dentin
Nature of anomaly: enamel/dentin maturation
Deficient development: amelogenesis imperfecta type II and IV

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19
Q

Anomalies associated with Eruption

A

Stage affected: eruption
Nature of anomaly: eruption
Deficient development: 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

A

Primary dentition: 0.3-0.8%
Permanent dentition: 0.1-3.8% in whites; higher in blacks and Asians
2:1 Male:Female
Most common in maxilla (95%) - mesiodens most common
Supplemental supernumerary = normal morphology
Rudimentary supernumerary = conical, tubuerculate, molariform

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21
Q

Conditions/Syndromes Associated with Hyperdontia

A 
Apert Syndrome (acrocephalosyndactyly)
Cleidocranial dysplasia
Gardner syndrome
Crouzon syndrome 
Down syndrome
Sturge-Weber syndrome
Orofaciodigital syndrome I
Cleft lip and palate
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22
Q

Prevalence of anodontia, hypodontia, oligodontia

A

Primary dentition: less than 1%
Permanent dentition: 1.5-10% (excluding 3rds)
1.5:1 Female:Male
Most common is 3rd molars (20%), then MnPm2 (3.4%), then MxLt (2.2%) then MxPm2 (0.85%)

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23
Q

Facts about Anodontia/Hypodontia/Oligodontia

A

Significant correlation between missing primary and missing permanent successor
May be associated with microdontia: peg lateral incisors part of hypodontia spectrum
Agenesis of third molars is associated with agenesis of one or both permanent maxillary lateral incisors
Some patients have other ectodermal organs affected (salivary glands, skin, sweat)

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24
Q

Conditions/Syndromes Associated with Anodontia/Hypodontia/Oligodontia

A 
Ectodermal Dysplasia 
Crouzon Syndrome (note also hyperdontia)
Chondroectodermal dysplasia (Ellis-van Creveld) 
Williams Syndrome
Non-syndromic CL/CP
Achondroplasia
Incontinentia pigmenti 
Orofaciodigital syndrome I
Rieger Syndrome
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25
Prevalence of Microdontia
0.8-8.4% Most commonly affects maxillary laterals, 2nd premolars, third molars Usually follows autosomal dominant pattern
26
Prevalence of Macrodontia
Single tooth macrodontia is rare - rule out fusion, gemination Usually affects incisors and canines, often bilateral
27
Conditions/Syndromes Associated with Microdontia
``` Ectodermal Dysplasia Chondroectodermal dysplasia (Ellis-van Creveld) Hemifacial microsomia Down Syndrome Crouzon Syndrome Pituitary Dwarfism ```
28
Conditions/Syndromes Associated with Macrodontia
``` Hemifacial hyperplasia/hypertrophy Crouzon Syndrome Otodental Syndrome XYY Syndrome Pituitary gigantism Pineal hyperplasia with hyperinsulinism ```
29
Gemination
Definition: enlarged or joined tooth in which tooth count is normal Prevalence: primary dentition 0.5-2.5%; permanent 0.5% Characteristics: abortive attempt by single tooth to divide - bifid crown with single root and pulp chamber Crowding may retard eruption of permanent successor Site of fusion may be at increased risk for caries
30
Fusion
Definition: enlarged or joined tooth in which the tooth count is not normal (unless fused with supernumerary) Prevalence: 0.5% - more common in primary Characteristics: dentinal union of two embryologically developing teeth with 2 separate pulp chambers May retartd eruption of permanent successor Site of fusion may be at increased risk for caries
31
Concrescence
Prevalence: most common in maxillary posterior Characteristics: fusion that occurs after root formation is completed Etiology: trauma, crowding may occur pre- or post-eruption
32
Dens in dente
"tooth within a tooth" Prevalence: 0.3-10%; rare in African-Americans Maxillary lateral most affected; uncommon in primary teeth Characteristics: invagination of inner enamel epithelium Carious involvement via communication between oral environment and invaginated portion Treatment: sealant/composite; endo
33
Dens evaginatus
Type 1 = talon cusp Type 2 = semi-talon Type 3 = trace talon Prevalence: 1-8%; higher in Asian, Native American, Hispanic 77% permanent teeth; 88% maxillary incisors, 55% lateral incisors; may be unilateral or bilateral Characteristics: evagination of enamel epithelium; focal hyperplasia of pulp mesenchyme Pulp tissue within extra cusp may develop necrosis Conditions: Lobodontia, Rubinstein-Taybi syndrome
34
Taurodontism
"Bull's teeth" Prevalence: 2.5-3.2% in US Permanent molar most common Large pulp at expense of root
35
Conditions associated with Taurodontism
``` Klinefelter Tricho-dento-osseous syndrome (TDO) Mohr syndrome (orofaciodigital syndrome II) Hypohydrotic ectodermal dysplasia Amelogenesis Imperfecta Type IV Down Syndrome Williams Syndrome Smith-Magen's Syndrome ```
36
Dilaceration
Etiology: trauma | Conditions associated: Axenfeld-Rieger, Ehlers-Danlos, Lamellar congenital ichthyosis, Smith-Magenis syndrome
37
Amelogenesis Imperfecta (overview)
Incidence 1:14,000 | Multiple inheritance patterns
38
AI Type I (Hypoplastic)
Insufficient quality of enamel Both dentitions affected Most commonly autosomal dominant Anterior openbite common
39
AI Type II (hypomaturation)
Normal enamel thickness Poor mineralization Mottled brown-yellow-white color X-linked recessive, autosomal recessive
40
AI Type III (hypocalcification)
``` Soft enamel with normal thickness Enamel lost soon after eruption anterior openbite >60% High calculus formation due to rough enamel Delays in eruption Autosomal dominant and rescessive ```
41
AI Type IV (hypomaturation-hypoplastic with taurodontism)
Distinct from trichodento-osseous syndrome (AI+taurodontism+hair/nail defects) Mottle yellow-brown enamel with pitting Molars are taurodont
42
Dentinogenesis Imperfecta
Incidence 1:8000 Heritable defect of predentin matrix Normal mantle dentin
43
DI Type I
``` Least severe Occurs with osteogenesis imperfecta Autosomal dominant Type 1 collagen defect Primary teeth more severely affected Amber translucence and bulbous crowns with short roots Many periapical radiolucencies/alveolar abscesses Rapid attrition Pulpal obliteration ```
44
DI Type II
``` "Hereditary opalescent dentin" Occurs alone: no OI Autosomal dominant Both dentitions equally affected Same characteristics as DI ```
45
DI Type III
``` Most severe Brandywine tri-racial isolate population Bell-shaped crowns Opalescent hue Shell teeth in primary dentition Multiple pulp exposures Rapid wear ```
46
Conditions/Syndromes associated with DI
Osteogenesis Imperfecta Ehlers Danlos Goldblatt Syndrome Schimke immune-osseous dysplasia
47
Osteogenesis Imperfecta
``` 4 major types Type I most common; Type II lethal in perinatal Dentinogenesis imperfecta Types III and IV Bowing of legs Fragile bones (many fractures) Blue sclera Bitemporal bossing Impaired hearing Macrocephaly Autosomal dominant ```
48
Enamel Hypoplasia
Environmental etiologies: physiologic (developmental or ingestional), infectious, traumatic, iatrogenic Genetic etiology: amelogenesis imperfecta Potential marker for celiac disease Associated also with epidermolysis bullosa
49
Enamel pearls
Cells of epithelial root sheath may remain attached to dentin May differentiate into ameloblasts and produce enamel May contain dentin and pulp
50
Dentin Dysplasia Type I
``` "Rootless teeth" Shot, blunt roots with normal crowns Obliterated pulp chambers Multiple PA radiolucencies Root sheath problem Autosomal dominant ```
51
Dentin Dysplasia Type II
``` "Thistle-tube pulps" in permanent teeth Coronal dentin dysplasia Primary teeth more affected Amber color (looks like DI-II) Autosomal dominant ```
52
Regional odontodysplasia
"ghost teeth" Localized arrest in tooth development Affects both dentitions, usually in maxilla Single or several teeth moderate/severe hypoplasia Thin enamel with diffuse shell appearance Large pulps with little dentin No inheritance pattern or etiology known Failure of eruption Gingival hyperplasia
53
Vitamin-D-resistant rickets
``` X-linked dominant; autosomal recessive Failure of distal tubular reabsorption of phosphate in kidneys Hypophosphatemic rickets Hypomineralized dentin Enlarged pulp and pulp horns ```
54
Hypoparathyroidism
Rare endocrinopathy with unknown origin Deficiency of PTH causes low serum calcium and increased serum phosphorus Enamel hypoplasia, delayed eruption, hypodontia, shortened roots
55
Psuedohypoparathyroidism
Rare X-linked dominant disorder of hypocalcemia | Enamel hypoplasia, delayed eruption, short roots
56
Albright Hereditary Osteodystrophy
Mutation in GNAS1 gene chromosome 20 Autosomal dominant Elevated parathyroid hormonoe Mild mental deficiencies, round facies, short stature Enamel hypoplasia, enlarged pulp chambers, delayed eruption, short roots
57
Ehlers-Danlos
``` Hypermobility of joints Skin elasticity and easily hemorrhages Tissue heals by papyraceous scarring Autosomal dominant (some X-linked) Abnormal collagen production Irregular dentin tubules with inclusions Intrapulpal calcifications ```
58
Hypophosphatasia
``` Lack of serum alkaline phosphatase Autosomal dominant or recessive Lack of cementum on root surfaces Premature loss of primary teeth Bone abnormalities Large pulp chambers ```
59
Epidermolysis bullosa
Fibrous acellular cementum | Excess cellular cementum
60
Molar-incisal hypomineralization (MIH)
Hypomineralization of 1-4 permanent first molars frequently associated w/ affected incisors 4-25% prevalence (Europe) Possible problem with ameloblast function Associated with febrile illness, antibiotics, nutritional deficiencies, preterm birth, dioxin in breastmilk
61
Enamel Fluorosis
Amount of fluoride in water: >2 ppm = 10% chance; >6ppm = 90% chance 84.5% unaffected in optimally fluoridated areas
62
Blood-borne pigmentation
``` Anemia: gray Bile duct defects: green Dental trauma: red/gray/black Neonatal hepatitis: black/gray Porphyria: purple/brown Rh incompatibility: blue-green/brown ```
63
Tetracycline and Color Abnormalities
Both dentitions affected Related to dose and duration Threshold: 21-26 mg/kg/day Should not prescribe from 5th month in utero to 8 years Teeth darken with increased exposure to UV light
64
Cystic Fibrosis Tooth Color
Yellow/gray to dark brown | May be related to disease, tetracycline or combination
65
Chromogenic Bacteria
Brown/black: less common, difficult to remove Green: Bacillus pyocaneus, Aspergillis Orange: Serratia marcescens, Flavobacterium lutescens
66
Theories of tooth eruption
Root growth - strong association Vascular pressure Bone growth PDL traction - need dental follicle to erupt Connective tissue proliferation and pulp apex
67
Sequences of Primary Tooth Eruption
ABDCE is most favorable eruption | central -> lateral -> first molar -> canine -> second molar
68
Sequences of Permanent Tooth eruption
Maxilla: 61245378 Mandible: 61234578 *mandible is only one that goes in order (12345) Sequence is more important than timing
69
Stages of Eruption - Permanent Teeth
``` Follicular growth Pre-emergent eruptive spurt Post-emergent eruptive spurt Juvenile occlusal eruption Circumpubertal eruptive spurt Adult occlusal equilibrium ```
70
Variables Influencing Tooth Eruption
Genetic (78%) -Race: Black and Hispanic earlier than white -Sex: females ahead of males Environmental -low birth weight = delayed eruption -nutrition has little/no effect -Prematurity: delayed eruption w/ ventilator dependency Systemic -endocrine system contributory -high correlation with hypopituitarism/hypothyroidism
71
Timing of primary tooth loss considerations
Before age 5: delays premolar After age 8: accelerates premolar Prior to crown completion of successor: delays eruption After crown completion of successor: accelerates eruption
72
Natal vs Neonatal Teeth
``` Premature teeth erupt before 3 months Natal - present at birth Neonatal - present within first 30 days Natal:neonatal 3:1 Incidence 1:2000-3500 90% true primary teeth; 10% supernumerary Slightly more common in females ```
73
Structures in newborns confused with premature teeth
Bohn nodules Dental lamina cysts Epstein pearls
74
Bohn nodules
Buccal, lingual aspects of maxillary alveolar ridge | Mucous gland tissue
75
Dental lamina cysts
Found on crest of alveolar ridge | Derived from remnant of dental lamina
76
Epstein pearls
Midpalatal raphe Trapped epithelial remnants Visible cysts in 80% of newborns
77
Teething problems (systemic symptoms)
Diarrhea GERD Otitis media Paroxysmal atrial tachycardia Rule out bronchitis, dehydration, eczema, febrile convusions, fever *Fevere > 101F not attributed to teething No available evidence suggests signs/symptoms sufficiently specific to teething
78
Eruption hematoma
Form of dentigerous cyst around crown Occurs in both dentitions Translucent to bluish color Usually ruptures spontaneously; may excise if symptomatic
79
Primordial cyst: stellate reticulum
Many believe all primordial cysts are odontogenic keratocysts WHO classification is odontogenic keratocyst
80
Dentigerous cyst
Most common type of odontogenic cyst Originates from separation of follicle from around crown of unerupted tooth Treated with enucleation
81
Ameloblastoma
Most common clinically significant odontogenic tumor Slow growing, locally invasive, benign Unilocular or multilocular Excision or en bloc resection Common in mandibular ramus or mandibular molars
82
Local causes of delayed primary exfoliation and permanent tooth eruption
Ankylosis Impaction Supernumerary Teeth Trauma
83
Systemic conditions associated with delayed primary exfoliation and permanent eruption
``` Achondroplasia Albright's hereditary osteodystrophy Apert Syndrome Ellis-van Creveld (chondroectodermal dysplasia) Cleidocranial dysplasia DeLange syndrome Down syndrome Gardner syndrome Hunter syndrome Hypopituitarism Hypothyroidism Ichthyosis Incontinentia pigmenti Low birth weight/prematurity Osteogenesis imperfecta ```
84
Primary failure to erupt
Malfunction of eruption mechanism with non-ankylosed teeth Failure of affected tooth to move through eruption path Teeth may partially erupt Abnormal or complete lack of response to ortho forces
85
Systemic conditions associated with accelerated eruption of teeth
``` Chondroectodermal dysplasia (Ellis-van Creveld) Hemifacial hypertrophy Hyperthyroidism Osteogenesis imperfecta Precocious puberty Sotos syndrome Sturge-Weber ```
86
Premature exfoliation of primary teeth - systemic conditions
``` Bone disease (fibrous dysplasia, Vitamin-D resistant rickets) Perio disease (Aggressive perio, Papillon-Lefevre) Metabolic disease (hypophosphatasia) Blood disease (Burkitt's lymphoma, Chediak-Higashi, Cyclic neutropenia, Langerhans cell histiocytosis, leukemia) Physical/chemical injuries (acrodynia, facial burns) Dental anomalies (dentin dysplasia I, regional odontodysplasia) ```
87
Ectopic eruption of permanent first molars
Incidence: 3-4% Self-corrects 66% - but only 22% in CLP Etiology: larger permanent teeth, small maxilla, small SNA, abnormal angulation of erupting tooth, delayed mineralization of some permanent teeth
88
Order of ectopic eruption of permanent teeth (most to least common)
Maxillary first molars Mandibular lateral incisors Maxillary canines
89
Ankylosis (infraocclusion)
Fusion of cementum with alveolar bone Can occur at any stage of eruption Clinically diagnosed as "submerged tooth" - radiographs not detected Unknown etiology Prevalence: 1.3-38.5% Primary mandibular first molar most common Associated with agenesis of permanent successor
90
Problems with ankylosed teeth
``` Deflected eruption paths Delayed eruption of permanent successor Impacted premolars Loss of arch length and alveolar bone Supraeruption of opposing teeth ```
91
Treatment of ankylosed teeth
Observe Extract Restore to occlusion Luxate (permanent teeth)
92
Maxillary central diastema prevalence
44-97% in 6 year olds (ugly duckling stage) 33-46% 9 year olds 7-20% in 14 year olds 2x more common in African-Americans
93
Etiology of maxillary central diastema
``` Normal development of mixed dentition Excessive skeletal growth Habits (digit sucking, pacifier use) Small teeth or spaced dentition Physical impediment to normal closure (enlarged labial frenum, macroglossia, mesiodens, midline pathology, retained primary teeth) Artificial (rapid palate expansion) ```
94
Treatment of maxillary central diastema
Usually occurs after eruption of permanent canines Based on cause -eliminate habits -mesial tipping of central incisors -reduction of overjet -surgical intervention (transseptal fibers, frenum) -enlargement of incisors

Pediatric Dentistry Handbook (9 decks)

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