Chapter 2: Dental Development, Morphology, Eruption Flashcards
Dental Development, Morphology, Eruption, and Related Pathologies
Neural Crest Cells
- 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)
Dental Lamina
- 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
3 Components of tooth bud
- Enamel Organ
- Dental Papilla
- Dental sac
Morphologic Developmental Stages
Dental Lamina Bud Stage Cap Stage Bell Stage (early and late) Hertwig's epithelial root sheath Formation of enamel and dentin matrices
Dental Lamina Stage
Inductive phenomenon
Initial formation of dental development
Characterized by Initiation
Bud Stage
Initial swellings from dental lamina
Formation of tooth buds
Characterized by proliferation and morphodifferentiation
Cap Stage
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)
Early Bell Stage
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
Advanced Bell Stage
Differentiation of odontoblasts precedes that of ameloblasts
Future DEJ outlined
Basal margin of enamel organ gives rise to Hertwig’s epithelial root sheath
Hertwig’s Epithelial Root Sheath
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
Formation of Enamel and Dentin Matrices
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
Anomalies associated with Initiation Stage
Stage affected: dental lamina
Nature of anomaly: number
Deficient development: anodontia, hypodontia, oligodontia
Excessive development: hyperdontia
Anomalies associated with Proliferation Stage
Stages affected: bud, cap, bell stages
Nature of anomaly: number and structure
Deficient development: hypodontia, oligodontia
Excessive development: hyperdontia, odontoma, epithelial rests
Anomalies associated with Histodifferentiation
Stages affected: cap, bell
Nature of anomaly: enamel and dentin structure
Deficient development: amelogenesis imperfecta type I and IV, dentinogenesis imperfecta
Anomalies associated with Morphodifferentiation
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
Anomalies associated with Apposition
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
Anomalies associated with Mineralization
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
Anomalies associated with Maturation
Stages affected: maturation of enamel/dentin
Nature of anomaly: enamel/dentin maturation
Deficient development: amelogenesis imperfecta type II and IV
Anomalies associated with Eruption
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
Hyperdontia Prevalence
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
Conditions/Syndromes Associated with Hyperdontia
Apert Syndrome (acrocephalosyndactyly) Cleidocranial dysplasia Gardner syndrome Crouzon syndrome Down syndrome Sturge-Weber syndrome Orofaciodigital syndrome I Cleft lip and palate
Prevalence of anodontia, hypodontia, oligodontia
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%)
Facts about Anodontia/Hypodontia/Oligodontia
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)
Conditions/Syndromes Associated with Anodontia/Hypodontia/Oligodontia
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
Prevalence of Microdontia
0.8-8.4%
Most commonly affects maxillary laterals, 2nd premolars, third molars
Usually follows autosomal dominant pattern
Prevalence of Macrodontia
Single tooth macrodontia is rare - rule out fusion, gemination
Usually affects incisors and canines, often bilateral
Conditions/Syndromes Associated with Microdontia
Ectodermal Dysplasia Chondroectodermal dysplasia (Ellis-van Creveld) Hemifacial microsomia Down Syndrome Crouzon Syndrome Pituitary Dwarfism
Conditions/Syndromes Associated with Macrodontia
Hemifacial hyperplasia/hypertrophy Crouzon Syndrome Otodental Syndrome XYY Syndrome Pituitary gigantism Pineal hyperplasia with hyperinsulinism
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
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
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
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
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
Taurodontism
“Bull’s teeth”
Prevalence: 2.5-3.2% in US
Permanent molar most common
Large pulp at expense of root
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
Dilaceration
Etiology: trauma
Conditions associated: Axenfeld-Rieger, Ehlers-Danlos, Lamellar congenital ichthyosis, Smith-Magenis syndrome
Amelogenesis Imperfecta (overview)
Incidence 1:14,000
Multiple inheritance patterns
AI Type I (Hypoplastic)
Insufficient quality of enamel
Both dentitions affected
Most commonly autosomal dominant
Anterior openbite common
AI Type II (hypomaturation)
Normal enamel thickness
Poor mineralization
Mottled brown-yellow-white color
X-linked recessive, autosomal recessive
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
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
Dentinogenesis Imperfecta
Incidence 1:8000
Heritable defect of predentin matrix
Normal mantle dentin
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
DI Type II
"Hereditary opalescent dentin" Occurs alone: no OI Autosomal dominant Both dentitions equally affected Same characteristics as DI
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
Conditions/Syndromes associated with DI
Osteogenesis Imperfecta
Ehlers Danlos
Goldblatt Syndrome
Schimke immune-osseous dysplasia
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
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
Enamel pearls
Cells of epithelial root sheath may remain attached to dentin
May differentiate into ameloblasts and produce enamel
May contain dentin and pulp
Dentin Dysplasia Type I
"Rootless teeth" Shot, blunt roots with normal crowns Obliterated pulp chambers Multiple PA radiolucencies Root sheath problem Autosomal dominant
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
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
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
Hypoparathyroidism
Rare endocrinopathy with unknown origin
Deficiency of PTH causes low serum calcium and increased serum phosphorus
Enamel hypoplasia, delayed eruption, hypodontia, shortened roots
Psuedohypoparathyroidism
Rare X-linked dominant disorder of hypocalcemia
Enamel hypoplasia, delayed eruption, short roots
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
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
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
Epidermolysis bullosa
Fibrous acellular cementum
Excess cellular cementum
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
Enamel Fluorosis
Amount of fluoride in water: >2 ppm = 10% chance; >6ppm = 90% chance
84.5% unaffected in optimally fluoridated areas
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
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
Cystic Fibrosis Tooth Color
Yellow/gray to dark brown
May be related to disease, tetracycline or combination
Chromogenic Bacteria
Brown/black: less common, difficult to remove
Green: Bacillus pyocaneus, Aspergillis
Orange: Serratia marcescens, Flavobacterium lutescens
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
Sequences of Primary Tooth Eruption
ABDCE is most favorable eruption
central -> lateral -> first molar -> canine -> second molar
Sequences of Permanent Tooth eruption
Maxilla: 61245378
Mandible: 61234578
*mandible is only one that goes in order (12345)
Sequence is more important than timing
Stages of Eruption - Permanent Teeth
Follicular growth Pre-emergent eruptive spurt Post-emergent eruptive spurt Juvenile occlusal eruption Circumpubertal eruptive spurt Adult occlusal equilibrium
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
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
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
Structures in newborns confused with premature teeth
Bohn nodules
Dental lamina cysts
Epstein pearls
Bohn nodules
Buccal, lingual aspects of maxillary alveolar ridge
Mucous gland tissue
Dental lamina cysts
Found on crest of alveolar ridge
Derived from remnant of dental lamina
Epstein pearls
Midpalatal raphe
Trapped epithelial remnants
Visible cysts in 80% of newborns
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
Eruption hematoma
Form of dentigerous cyst around crown
Occurs in both dentitions
Translucent to bluish color
Usually ruptures spontaneously; may excise if symptomatic
Primordial cyst: stellate reticulum
Many believe all primordial cysts are odontogenic keratocysts
WHO classification is odontogenic keratocyst
Dentigerous cyst
Most common type of odontogenic cyst
Originates from separation of follicle from around crown of unerupted tooth
Treated with enucleation
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
Local causes of delayed primary exfoliation and permanent tooth eruption
Ankylosis
Impaction
Supernumerary Teeth
Trauma
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
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
Systemic conditions associated with accelerated eruption of teeth
Chondroectodermal dysplasia (Ellis-van Creveld) Hemifacial hypertrophy Hyperthyroidism Osteogenesis imperfecta Precocious puberty Sotos syndrome Sturge-Weber
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)
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
Order of ectopic eruption of permanent teeth (most to least common)
Maxillary first molars
Mandibular lateral incisors
Maxillary canines
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
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
Treatment of ankylosed teeth
Observe
Extract
Restore to occlusion
Luxate (permanent teeth)
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
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)
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
