Dental Development, Morphology, Eruption and Related Pathologies Flashcards
Handbook (143 cards)
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
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.
3
Q
Name the components of tooth buds
A
- Enamel organ
- Dental papilla
- Dental sac
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
5
Q
Dental lamina
A
- Inductive phenomenon
- Initial formation of dental development
- Characterized by initiation
6
Q
Bud stage
A
- Initial swellings from dental lamina.
- Formation of tooth buds.
- Characterized by proliferation and morphodifferentiation.
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.
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
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
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
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
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
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
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
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
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
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
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
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
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)
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
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
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
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
25
Conditions/Syndromes Associated with **Microdontia**
* **Ectodermal dysplasia**
* **Chondroectodermal dysplasia (Ellis-van Creveld)**
* **Hemifacial microsomia**
* **Down syndrome**
* **Crouzon syndrome**
* **Pituitary dwarfism**
26
Conditions/Syndromes Associated with **Macrodontia**
* **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**
27
**Conjoined Teeth Anomalies**
**Proliferation and Morphodifferentiation**
* Gemination
* Fusion
* Concrescence
28
Gemination – Prevalence, characteristics, significance
**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)
29
Fusion – Prevalence, characteristics, significance
**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)
30
Concrescence – Prevalence, characteristics, significance
**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
31
Anomalies of **Morphodifferentiation -- Size and Shape**
* Dens in dente
* Dens evaginatus
* Taurodontism
* Dilaceration
32
Dens in dente – Prevalence, characteristics, significance, treatment
**Morphodifferentiation -- Size and Shape**
* Dens **_in_**vaginatus; "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
33
**Dens evaginatus** - Types, prevalence, frequency, characteristics, significance
**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
34
Conditions/syndromes associated with **dens evaginatus**
* Lobodontia - "wolf-like teeth", "fang-like cusps"
* Rubenstein-Taybi syndrome
35
**Taurodontism** - Types, prevalence, frequency, characteristics, significance
**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
36
Conditions/Syndromes Associated with **Taurodontism**
* **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**
37
**Dilaceration** - Etiology
Anomalies of **Morphodifferentiation -- Size and Shape**
## Footnote
Etiology: Trauma to primary dentition, especially intrusion or idiopathic developmental disturbance.
38
Conditions/Syndromes Associated with **Dilaceration**
* **Axenfeld-Rieger syndrome**
* **Ehlers-Danlos syndrome**
* **Lamellar congenital ichthyosis**
* **Smith-Magenis syndrome**
39
Anomalies of **Histodifferentiation -- Structure**
* Amelogenesis imperfecta
* Dentinogenesis imperfecta
40
Amelogenesis imperfecta
* 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**
41
**AI Type I -- Hypoplastic –** Characteristics, subgroups
* 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
42
Dentinogenesis imperfecta
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)
43
Dentinogenesis imperfecta – **Shields Type I:** Severity, clinical characteristics
**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
44
Dentinogenesis imperfecta – **Shields Type II**: Characteristics
**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
45
Dentinogenesis imperfecta – **Shields Type III:** Severity, clinical characteristics
* **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
46
**Conditions/Syndromes Associated with DI**
* **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**
47
Anomalies of **Apposition -- Enamel Structure**
* Enamel hypoplasia
* Enamel pearls
48
Enamel hypoplasia: Etiology, marker for what disease, predominant locations
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**
49
Enamel pearls
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
50
Anomalies of **Apposition -- Dentin Structure**
* Dentin dysplasia
* Regional odontodysplasia
51
Shields Type I Dentin Dysplasia: Clinical features, inheritance, primary defect
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**
52
Shields Type II Dentin Dysplasia: Clinical features, inheritance
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
53
Regional Odontodysplasia
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
54
Anomalies of **Apposition -- Cementum Structure**
* Hypophosphatasia
* Epidermolysis bullosa
* Cleidocranial dysplasia
55
**Hypophosphatasia:** Etiology, clinical presentation, inheritance
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
56
Epidermolysis bullosa
Anomalies of **Apposition -- Cementum Structure**
* Fibrous acellular cementum
* Excess cellular cementum
57
Cleidocranial dysplasia
Anomalies of **Apposition -- Cementum Structure**
* Deficient cellular cementum
* May be related to lack of eruption
58
Anomalies of **Mineralization -- Enamel**
* Enamel hypomineralization
* Molar-incisor hypomineralization (MIH)
* Amelogenesis imperfecta Type III (hypocalcified)
* Enamel fluorosis
* Sclerotic dentin
59
**Molar-Incisor Hypomineralization (MIH):** Etiology, associated conditions
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
**Amelogenesis imperfecta Type III (Hypocalcified):** Etiology, inheritance, clinical presentation
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
**Enamel fluorosis:** Amount of fluoride in water, indices
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
Sclerotic dentin
Anomalies of **Mineralization -- Enamel**
* Deposition of calcium in tubules as result of trauma or normal aging
63
Anomalies of **_Maturation_ -- Enamel Structure**
* Amelogenesis Imperfecta Type III (hypomaturation)
* Amelogenesis Imperfecta Type IV (hypomaturation-hypoplastic with taurodontism)
64
**Amelogenesis Imperfecta Type II - Hypomaturation:** Clinical presentation, genetic etiology, subgroups
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
**Amelogenesis Imperfecta Type IV - Hypomaturation-Hypoplastic with Taurodontism** (also involves histodifferentiation): Clinical presentation, subgroups
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
Intrinsic (endogenous in nature) abnormalities of color
* Blood-borne pigments
* Drug administration - tetracyclines
* Cystic fibrosis
* Trauma
* Hypoplasia/hypomineralization disorders
* Excessive systemic fluoride
67
Intrinsic abnormalities of color - Blood-borne pigments
* 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
Intrinsic abnormalities of color: Anemias-hemosiderin
Grey
69
Intrinsic abnormalities of color: Bile duct defects
Green
70
Intrinsic abnormalities of color: Dental trauma
Red, gray, black
71
Intrinsic abnormalities of color: Neonatal hepatitis - bilirubin
Black, gray
72
Intrinsic abnormalities of color: Porphyria-porphyrin
Purplish-brown
73
Intrinsic abnormalities of color: Rh incompatibility (erythroblastosis fetalis) - bilirubin, biliverdin
Blue-green, brown
74
Intrinsic abnormalities of color - Drug administration (tetracyclines): Affected dentitions, threshold, when not to prescribe,
* 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
Intrinsic abnormalities of color: Cystic fibrosis
* May be related to disease, tetracycline, or combination
* Color yellowish gray to dark brown
76
Intrinsic abnormalities of color: Hypoplasia/hypomineralization disorders
* Amelogenesis imperfecta
* Dentinogenesis imperfecta
* Dental caries
* Enamel and dentin dysplasias
77
Intrinsic abnormalities of color: Excessive systemic fluoride
* Must know community water concentration before describing
* Non-esthetic appearance of teeth; more resistant to caries
78
Extrinsic abnormalities of color
* Bacteria (chromogenic)
* Discoloring agents
79
Extrinsic abnormalities of color: Bacteria (chromogenic)
* 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
Extrinsic abnormalities of color: Bacteria (chromogenic)
## Footnote
**Brown/black**
Much less common, difficult to remove
81
Extrinsic abnormalities of color: Bacteria (chromogenic)
## Footnote
**Green**
***Bacillus pyocaneus, Aspergillis***: Most common
82
Extrinsic abnormalities of color: Bacteria (chromogenic)
## Footnote
**Orange**
***Serratia marcescens, Flavobacterium lutescens***: poor OH, more easily removed than green
83
Extrinsic abnormalities of color: Discoloring Agents
* 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
Extrinsic abnormalities of color: Discoloring Agents
## Footnote
**Chlorhexidine**
Brown
85
Extrinsic abnormalities of color: Discoloring Agents
## Footnote
**Cola**
Coloring agents
86
Extrinsic abnormalities of color: Discoloring Agents
## Footnote
**Foods**
Coffee and tea (tannins)
87
Extrinsic abnormalities of color: Discoloring Agents
## Footnote
**Iron sulfide**
Black
88
Extrinsic abnormalities of color: Discoloring Agents
## Footnote
**Marijuana**
Gray-green (oils, resins and pigments)
89
Extrinsic abnormalities of color: Discoloring Agents
**Silver nitrate**
Black
90
Extrinsic abnormalities of color: Discoloring Agents
## Footnote
**Stannous fluoride**
Black
91
Extrinsic abnormalities of color: Discoloring Agents
## Footnote
**Tobacco**
Dark brown to black
92
**Variables influencing Permanent Tooth Eruption**
* **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 eruptio_**n
93
**Theories of Eruption**
* 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
**Sequences of Eruption -- Primary**
**A B D C E**
95
**Sequences of Eruption -- Permanent**
* **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
**Stages of Eruption -- Permanent Teeth**
* Follicular growth
* Pre-emergent eruptive spurt
* Post-emergent eruptive spurt
* Juvenile occlusal eruption
* Circumpubertal eruptive spurt
* Adult occlusal equilibrium
97
Premature teeth
Erupt prior to 3mo
98
Natal teeth
Present at birth
99
Neonatal teeth
Present within the first 30 days of life
100
Incidence of natal : neonatal
Natal : Neonatal
3 : 1
101
Incidence of premature teeth
1 : 2000-3500
102
Premature teeth: Incidence, etiology, associated findings, syndromes
* 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
Structures present in newborns often confused with premature teeth
* **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
What are Bohns nodules?
* Buccal, lingual aspects of the maxillary alveolar ridge (away from the midline raphe)
* Mucous gland tissue
105
What are dental lamina cysts?
* Found on the crest of the alveolar ridge
* Derived from the remnants of the dental lamina
106
What are Epstein pearls?
* Midpalatal raphe
* Trapped epithelial remnants
* Visible cysts in 80% of newborns
107
Symptoms children experience during teething
* 50% or more children have one or more problems during teething, but no cause-effect relationship
* Diarrhea
* GERD
* Otitis media
* Paroxysmal atrial tachycardia
108
Teething differential
* 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
Why should oral viscous lidocaine not be used for teething pain? (FDA alerts)
Excessive amounts can result in seizures, severe brain injury and heart problems. Misuse has lead to hospitalizations and death.
110
Why should homeopathic teething tablets and gels not be given to children? (FDA alerts)
Due to reported adverse events. These substances have never been evaluated by the FDA for safety or efficacy.
111
Cystic development associated with eruption
* **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
**Eruption hematoma**
**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
**Primordial cyst: stellate reticulum**
**Cystic developments associated with eruption**
* Many believe all primordial cysts are odontogenic keratocysts
* WHO classification is OKC
114
**Dentigerous cyst**
**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
What is the most common type of odontogenic cyst?
Dentigerous cyst
116
**Ameloblastoma**
**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
What is the most common clinically significant odontogenic tumor?
Ameloblastoma
118
Local causes of delayed primary exfoliation and permanent eruption
* Ankylosis
* Impaction
* Supernumerary teeth
* Trauma
119
Systemic conditions of delayed primary exfoliation and permanent eruption (not all-inclusive)
* 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
Primary failure to erupt may be due to:
* 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
Local causes of accelerated eruption of primary and permanent teeth
Early loss of primary tooth (closer to normal time of permanent tooth eruption)
122
Systemic conditions that may cause accelerated eruption of primary and permanent teeth (not all-inclusive)
* Chondroectodermal dysplasia (Ellis-van Creveld)
* Hemifacial hypertrophy
* Hyperthyroidism
* Osteogenesis imperfecta
* Pachyonychia congenita
* Precocious puberty
* Sotos syndrome (cerebral gigantism)
* Sturge-Weber syndrome
123
What may cause premature exfoliation of primary teeth? (diseases, conditions, injuries)
* 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
Treatment for premature exfoliation of primary teeth
* 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
Ectopic eruption of permanent molars: Etiology, most often associated teeth, etiology, % of self-correction
* 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
Ankylosis (infraocclusion): Diagnosis, etiology, association
* 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
Ankylosis (infraocclusion): Possible extrinsic factors
* Disturbed local metabolism
* Localized infection
* Tooth replantation
* Trauma
128
Ankylosis (infraocclusion): Possible intrinsic factors
* Break in continuity of periodontal membrane
* Aberrant deposition of cementum or bone
129
Ankylosis (infraocclusion): Prevalence, teeth most often affected
* 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
Ankylosis (infraocclusion): Sequelae
* Deflected eruption paths
* Delayed eruption of permanent successors
* Impacted premolars
* Loss of arch length and alveolar bone
* Supraeruption of opposing teeth (esp. maxilla)
131
Ankylosis (infraocclusion): Treatment - empirical
* Observe (esp. for Ld's, esp. for mandibular teeth)
* Extract
* Restore to occlusion
* Luxate (permanent teeth)
132
Ankylosis (infraocclusion): Timing
* 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
Maxillary central diastema: Prevalence at 6yo, 9yo, 14yo
* **44-97%** in 6yo (ugly duckling stage)
* **33-46%** in 9yo
* **7-20%** in 14yo
134
Maxillary central diastema: Distribution
* **African Americans _\>2x_ more likely than whites or Hispanics**
* Higher in females at 6yo; higher in males at 14yo
135
Maxillary central diastema: Etiology
* **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
Maxillary central diastema: Treatment
* 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
Classification of supernumerary teeth
* **Supplemental:** Normal morphology
* **Rudimentary:** Conical, tuberculate (barrel-shaped), molariform (differentiate from odontoma)
138
Conditions w/ microdontia
* Ectodermal dysplasia
* Chondroectodermal dysplasia
* Hemifacial microsomia
* Down syndrome
* Crouzon
* Pituitary dwarfism
139
Conditions w/ macrodontia
* Hemifacial hyperplasia/hypertrophy
* Crouzon
* Otodental syndrome – microdeletion of FGF3
* XYY syndrome
* Pituitary gigantism
* Pineal hyperplasia
140
Syndromes w/ natal/neonatal teeth
* Ellis van Creveld syndrome
* Hallerman-Streiff syndrome
* Pachyonychia congenita syndrome
141
Down syndrome: dental manifestations
* 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
**Down syndrome:** dental tx considerations
* 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
Cleido
