05 - Early Development of Dentition

etiology of irregularities

1. systemic: affect all teeth at time of disturbance, creating systemic distribution of defects that share same chronological development period

   • enamel defect produced prior to eruption will persist after tooth erupts and will serve as a biological record of early systemic change

2. hereditary: affect tooth in either dentition or all teeth in primary and permanent dentitions in which both dentitions may not be affected equally

3. local: generally affects only one or a few adjacent developing teeth

teeth mineralization

• mineralization of all primary teeth begins prior to birth in utero

• mineralization of all permanent teeth begins after birth

  • only premolars and molars begin to mineralize after first birthday

enamel defects

1. enamel dysplasia: clinically observable defect as result of adverse effects during apposition and/or calcification

2. hypoplasia: occurs during appositional stage of development as a result of arrest from ameloblasts

   • deficient enamel structure at affected site

   • presents as series of pits or linear depressions in enamel crown

3. hypocalcification: occurs during calcification as a result from interference of precipitation of calcium salts into developing organic matrix

   • affected site less mineralized than surrounding normal enamel

   • refractive differences from surrounding enamel gives a chalky-white color

exanthematous fever

nonspecific high fever that causes systemic disturbance of apposition and/or mineralization phase of odontogenesis

• large number of hypoplastic and hypocalcific defects of enamel with no specific etiology

• high temperature of fever adversely affects ameloblastic activity that leaves permanent record

congenital syphilis

results from transplacental transmission of bacteria Treponema pallidum that affects teeth during morphodifferentiation

• not all children with syphilis will have condition

• infection in 50-80% of exposed neonates

• morphological changes that give rise to Hutchinson’s incisors (maxillary central and lateral incisors) and mulberry molars

• can affect both dentitions but most precipitous effect on active enamel organ when infant separated from placental circulation

• manifests at neonatal period (birth to 28 days), at time of morphogenesis of central incisors and permanent first molars

enamel fluorosis

ingestion of high fluoride content causes “mottled” enamel

• water containing 1.0-1.2ppm fluoride during tooth formation results in caries reduction by 58%

• ingesting water with fluoride content >1.5ppm increases probability of developing “mottled” enamel

• sources of fluoride: tap water, some bottled waters, food, toothpaste, supplementation (mouthwashes)

tetracycline staining

tetracycline antibiotic causes intrinsic staining of grayish-yellow to dark brown

• drug chelates calcium salts and gets incorporated into bone and teeth during mineralization

• can affect primary and/or permanent dentitions, depending on which teeth are developing at time of administration

• can pass through placenta barrier

• children do not invariably develop stain

  • one study showed discoloration was absent in 28% of children who received tetracycline

Rh incompatability/erythroblastosis fetalis

when Rh-positive child is born to previously sensitized Rh-negative mother and Rh-positive father that causes hemolysis of infant’s blood and breakdown into pigments producing jaundice

• pigments intrinsically stain developing teeth into a green color

• if father is Rh-positive or unknown, the Rh-negative mother receives immune globulin injection “RhoGAM” during second trimester and another injection within days after delivery if newborn is Rh-positive

amelogenesis imperfecta

inherited developmental disturbance of histodifferentiation or mineralization causing hypoplastic or hypocalcified food

• difference of quality and appearance of enamel due to stage of enamel development at time of defect

• defective structure limited to enamel only

  • radiographs show normal pulp and root morphology

• affects all or nearly all of teeth in both primary and permanent dentitions

• preventative care: early identification and early prevention for infants and children to avoid negative social and functional consequences

  • regular oral exams, meticulous oral hygiene, calculus removal, oral rinses

  • fluoride application and desensitizing agents may diminish tooth sensitivity

• restorative care: appearance, quality, and amount of affected enamel or dentin will dictate type of restorations necessary to achieve esthetic and functional health

  • enamel intact but discolored → bleach and/or microabrasion

  • enamel is hypocalcified → composite resin or porcelain veneers

  • enamel/dentin can’t be bonded → full coverage restorations

dentinogenesis imperfecta

inherited developmental disturbance of dentin from hisotdifferentiation stage that causes a defect of predentin

• results in amorphic disorganized atubular circumpulpal dentin

• ename wears down and breaks away from incisal or occlusal surfaces after eruption

• exposed soft dentin abrades rapidly (from acid erosion or attrition) so that smooth polished dentin surface is flush with gingiva

• severity of discoloration and enamel fracturing is highly variable

• preventative care: early identification and early prevention for infants and children to avoid negative social and functional consequences

  • regular oral exams, meticulous oral hygiene, calculus removal, oral rinses

  • fluoride application and desensitizing agents may diminish tooth sensitivity

• restorative care: treatments applied to permanent because permanent dentition is less severely affected

  • severe case of enamel fracturing → full coverage restoration in both primary and permanent dentition

  • restoration should be completed before excessive wear adn loss of vertical dimension

  • significant loss of tooth structure and vertical dimension → overdenture therapy

• Type I: occurs in conjunction with osteogenesis imperfecta

• Type II: same characteristics as Type I but does not involve osteogenesis imperfecta

• Type III: represents features of Type I and Type II with prominence of bell-shaped crowns in permanent dentition

Type I dentinogenesis imperfecta

occurs in conjunction with osteogenesis imperfecta

• associated with brittle bones, bowling of limbs, bitemporal bossing (skull malformation), blue sclera in eyes

• characteristics: bulbous crowns, pulp chamber obliterated, multiple root fractures, unexplained periapical radiolucencies

• primary teeth more severely

Type II dentinogenesis imperfecta

same characteristics as Type I but does not involve osteogenesis imperfecta

• characteristics: bulbous crowns, pulp chamber obliterated, multiple root fractures, unexplained periapical radiolucencies

• both primary and permanent dentition are equally affected

Type III dentinogenesis imperfecta

represents features of Type I and Type II with prominence of bell-shaped crowns in permanent dentition

• involves teeth with shell-like appearance and multiple pulp exposures

• very rare and occurs in tri-racial isolate groups in southern Maryland (Brandywine population)

erythropoeitic porphyria

inherited disorder where enzyme activities in heme biosynthesis pathway are partially or completely deficient

• have abnormally elevated levels of porphyrins that accumulate in tissue and are excreted from tissue and deposited into teeth

• congenital erythropoeitic porphyria (Gunther disease) is rare autosomal recessive

• symptoms: red-colored urine, light hypersensitivity, subepidermal bulbous lesions when exposed to light

• primary teeth → purplish-brown from porphyrin deposition

• permanent teeth → intrinsic staining but a lesser degree (purple or red-brown)

gemination

disturbance in proliferation phase of cap stage in odontogenesis that causes single tooth germ to unsuccessfully completely divide itself into two

• bifid crown with a singular root and one enlarged pulp chamber

• “splitting” detected as a cleft with varying depths in incisal surface

  • can appear as two crowns

• familial pattern (genetic)

• 0.5% frequency, seen more in maxillary anteriors and primary dentition

fusion

disturbance in proliferation phase of cap stage that causes union of two adjacent tooth germs due to pressure in region that leads to broader tooth

• occurs usually in crown of tooth but can involve crown and root

dens invaginatus

disturbance in morphodifferentiation of cap stage that leads to enamel organ abnormally growing into dental papilla

• “dens in dente”

• produced enamel-lined pocket that extends from lingual surface and leaves tooth with a deep lingual pit where invagination occurred

• lingual pit may lead to pulpal exposure and pathology and endodontic therapy

• early detection is important

• mosts commonly affects maxillary incisors, especially lateral incisors

dens evanginatus

disturbance in morphodifferentiation phase of cap stage that results in talon cusps

• unusual lingual or labial projection with enamel and dentin containing varying degrees of pulp tissue

• incidence of 77% in permanent dentition, with 94% in maxilla and 55% in lateral incisors (unilateral or bilateral)

• common problems: occlusal interference, displacement or rotation of teeth, dental caries, periodontal problems, tongue irritation during speech and mastication, compromised esthetics

peg laterals

disturbance during morphodifferentiation that causes peg-shaped teeth associated with missing permanent tooth

• hereditary

taurodontism

improper degree of horizontal invagination of Hertwig’s epithelial root sheath during morphodifferentiation

• morpho-anatomic change in tooth shape, involving elongation of pulp chamber and short stunted roots

• reported in deciduous and permanent teeth

• occurs in molars and premolars, with higher prevalence in permanent molars

• incidence range of 0.5-5% more likely to show association with conditions

supernumary teeth

issue during initiation of bud stage that causes continual budding of enamel organs

• extra teeth can resemble normal (supplemental) dentition or be conical or tubercular (rudimentary) shape

• unerupted supernumaries often interfere with normal tooth eruption and require surgical extraction

• 90% exist in maxilla but can occur in either arch, anteriorly or posteriorly, in isolation or not

• associated with certain syndromes

hypodontia

disturbance in initiation or proliferation phase that results in failure of 1-5 teeth to develop

• frequently missing: 3rd molars → mandibular 2nd premolars → maxillary laterals → maxillary 2nd premolars

  • propensity for last tooth in each sequence to be missing

• frequently missing primary teeth: maxillary or mandibular incisors

• missing primary tooth usually means missing permanent associated tooth

  • analogues of permanent tooth bud derived from primary tooth bud

• can be unilateral or bilateral, more common in permanent dentition

• prevalence of missing permanent teeth is 2.3-9.6%

• prevalence of missing primary teeth is 0.1-0.7%

• genetic, usually isolated but can be part of a syndrome

ectodermal dysplasia

group of inherited disorders that involve defects of hair, nails, teeth, and sweat glands

• oral manifestations divided into categories

  • numerical

  • structural

  • morphological

  • compositional

  • positional

effects of traumatic events on teeth

traumatic events can happen during any time of odontogenesis and can have varying consequences

• appositional phase → injured ameloblastic activity causes enamel hypoplasia

• eruption or attrition phase → changes in tooth position

infection of primary tooth

infection spreads through bone and around buds of successors and can damage protective layer of young enamel epithelium

• enamel of permanent tooth exposed to inflammatory edema and granulation tissue that will erode enamel and deposit well-calcified, cementum-like substance on surface of tooth

• called “turner tooth”