CHAPTER 3: ANOMALIES OF THE DEVELOPING DENTITION

sas

stage of tooth development

initiation → 8weeks → bud stage

proliferation → 9weeks → cap stage

differentiation (histology, morphology) → 11weeks → bell stage

calcification

attrition

initiation & proliferation

the stage of tooth development where anomalies on number of tooth usually occurs

conditions under histology defects

amelogenesis imprfecta

dentinogensis imperfecta

dentin dysplasia

anomalies on number of tooth

hyperdontia

hypodontia

under hyperdontia

mesiodens

distomolar

paramolars

hypodontia

occur more than hyperdontia

congenital absence of one or more teeth

occur more frequently in permanent

missing primary teeth are much less common than missing permanent teeth!

most common congenitally missing permanent teeth

lower 3rd molar

lower 2nd pm

upper lateral incisor

upper 2nd pm

hyperdontia

any number of extra (supernumerary) teeth

• it may occur:

  • as part of a genetic syndrome

  • as an isolated developmental trait

mesiodens

an isolated developmental anomaly

not associated with syndromes & not hereditary, despite occasional increased familial occurrence

• location:

  • located palatal to the permanent incisors

• can be positioned to:

  • erupt normally & be inverted

• clinical findings:

  • one or two extra teeth may be present

  • frequently conical or have an abnormal morphology

ectodermal dysplasia

a diverse group of genetic disorders that involves defects of the teeth, hair,sweat glands, mammary glands, salivary glands, fingernails.

• commonly affected:

  • teeth, hair, sweat glands

  • mammary glands, salivary glands

  • fingernails

oligodontia

missing more than six teeth, excluding third molars

anodontia

the complete absence of teeth

causes of hyper/hypodontia

genetic & molecular abnormalities affecting tooth development.

environmental stressors which may interrupt tooth bud development during later stages of development

2 chemotherapeutic agents commonly associated with dental anomalies are:

vincristine

cyclophosphamide (an alkylating agent)

—when these drugs are administered during tooth formation, pediatric patients are at risk of developing dental anomalies, including hypodontia

anomalies of tooth morphology

microdontia → more common

macrodontia

microdontia

refers to a reduction in tooth size.

• it may result from:

  • decrease in the overall tooth size.

  • reduction in enamel thickness.

  • combination of both.

under microdontia

peg lateral

hutchinson’s incisors

mulberry molars

triad to confirm syphilis

hutchinson’s incisors

interstitial keratitis

deafness

under macrodontia

fusion

gemination

taurodontism

gemination

2 crowns, 1 root

most common cause of localized macrodontia

incomplete splitting (twinning) of a developing primary or permanent tooth

• characteristics:

  • total number of teeth remains normal.

  • produces a tooth that may be almost twice the width of a normal tooth

• etiology:

  • no known genetic predisposition

  • no known hereditary cause.

fusion

1 crown, 2 roots

occurs when two developing teeth join together

• characteristics:

  • produces an enlarged tooth

  • more common in the primary dentition

  • results in one fewer tooth in the affected area.

taurodontism

enlarged pulp chamber, short roots

hutchinson’s incisor

tapered and notched incisal edges with screwdriver shapes

caused by congenital syphilis → treponema pallidum

tx: penicillin

mulberrymolars

associated with congenital syphilis

irregular, accentuated occlusal patterns

anomalies in shape

dens evaginatus

dens invaginatus (dens in dente)

dens evaginatus

approaching outward

an outfolding of the enamel organ that produces an extra cusp

pulp exposure can occur if excessive occlusal adjustment (equilibration) is performed bc pulp tissue extends into the cusp

• location:

  • central groove or ridge of posterior teeth

  • cingulum area of anterior teeth → talon cusp

  • mx premolar → leon’s premolar

• development:

  • results from evagination of the inner enamel epithelium, the cells that later become ameloblasts.

• extra cusp contains:

  • enamel, dentin, pulp tissue

• management:

  • careful enameloplasty.

  • preventive resin restorations (PRR)

dens invaginatus / dens in dente

approaching inward

this creates the appearance of a tooth within a tooth

results from invagination of the inner enamel epithelium

• most commonly affected tooth:

  • maxillary lateral incisors

• clinical significance:

  • high risk of dental caries and pulpal involvement bc the invaginated portion on the lingual surface may communicate with the oral environment

• management:

  • early diagnosis

  • prompt preventive treatment, including:

    • pit and fissure sealants

    • restorations if necessary

dilaceration vs flexium

dilaceration → >90 degrees

flexium → < 90 degrees

causes of root abnormalities

environmental

trauma

• root dilacerations (abnormal bending or curvature of the roots

severe infections:

• stevens-Johnson syndrome

• meningococcemia

chemotherapy and radiation:

• V-shaped roots

• stunted (shortened) roots

genetic

• tumoral calcinosis

• singleton-merten syndrome

syndromes associated with short roots

sponastrime dysplasia

bardet-biedl syndrome 1

rothmund-rhomson syndrome

associated with short root anomaly specific gene mutations in this syndrome

short root anomaly

frequently misdiagnosed as pathologic root resorption

• these conditions are different because:

  • this anomaly is a developmental variation

  • root resorption is a pathologic process

oculo-facio-cardio-dental syndrome

an elongated root

• cause:

  • mutations in the BCOR gene

• mechanism:

  • uncontrolled root growth

  • increased proliferation of PDL cells

• most commonly affected teeth:

  • permanent canines

hypercementosis

an excessive deposition of cementum on the root surface

• produces:

  • an abnormal root shape.

  • a bulbous enlargement at the root apex.

• may result from:

  • trauma to the PDL

  • abnormal developmental processes

  • reactive response to periapical inflammation

associated systemic conditions of hypercementosis

acromegaly

paget disease

atherosclerosis

taurodontism

enlargement of the body and pulp chamber of a multirooted tooth

• characterized by:

  • an elongated pulp chamber.

  • apical displacement of the pulpal floor.

• effects on root anatomy:

  • root furcation is displaced apically

  • individual roots become greatly shortened

  • overall root length may remain normal.

• development:

  • root furcation forms through invagination of Hertwig's epithelial root sheath

  • bc of this developmental process, many ectodermal dysplasias exhibit this condition

2 major types of enamel defects

enamel hypoplasia

enamel hypomineralization

hyperbilirubinemia

caused by biliary atresia

frequently produces green discoloration of teeth

tetracycline staining

exposure to ultraviolet light oxidizes this complex, producing pigments that stain dental hard tissues

• may cause severe intrinsic discoloration of:

  • primary teeth & permanent teeth

• tooth discoloration may occur after treatment lasting as little as 3 days

• among tetracycline antibiotics:

  • tetracycline hydrochloride → has the greatest staining potential

• forms an orthocalcium phosphate complex with:

  • dentin & enamel

• greatest risk occurs from:

  • intrauterine development

  • through 8 years of age

international association of dental traumatology (IADT)

recommends systemic doxycycline 2x daily for 7 days for avulsion injuries

dental fluorosis

hypomineralization of enamel due to excessive exposure to fluoride during enamel mineralization

• severity ranges from:

  • mild, moderate, severe

• degree of hypomineralization depends on the fluoride concentration in the serum during amelogenesis

• individual susceptibility varies due to:

  • genetic makeup

  • overall health status

  • multiple genes contribute to differences in fluorosis susceptibility

• mechanism:

  • fluoride contributes to fluorosis by affecting:

    • ameloblasts

    • developing enamel matrix

    • processing (maturation) of the enamel matrix

enamel hypoplasia (reduced enamel formation)

most common hereditary enamel phenotype

defect involving the amount (quantity) of enamel formed

amelogenesis imperfecta (AI)

yellowish

characterized by defective or missing tooth enamel

refers to hereditary conditions that primarily affect enamel formation

• classified according to:

  • mode of inheritance

  • mechanism causing the enamel defect

  • clinical phenotype (appearance of enamel)

• secondary effects:

  • cracked tooth, early tooth decay

  • sensitivity to hot or cold exposures

  • susceptibility to multiple diseases of the tissues surrounding the teeth (periodontal tissues)

3 major types of amelogenesis imperfecta (AI)

hypoplastic amelogenesis imperfecta

hypocalcified amelogenesis imperfecta

hypomaturation amelogenesis imperfecta

hypoplastic amelogenesis imperfecta

quantity defect

results in reduced enamel thickness

caused by deficient enamel matrix formation

clinical appearance:

• generalized thin enamel with pits/grooves

hypomaturation amelogenesis imperfecta

low value amount of ameloblast

produces hypomineralized enamel

caused by defective crystal growth and mineralization during the maturation stage of enamel development

clinical appearance:

• mottled white-yellow-brown enamel that chips

• soft

hypocalcified amelogenesis imperfecta

quality defect

also produces hypomineralized enamel

caused by abnormal initiation of enamel crystallites followed by defective mineralization

clinical appearance:

• chalky yellow-brown enamel that wears rapidly

• very soft

enamel hypomineralization

reduced mineral content

altered enamel translucency

higher protein content than normal enamel

weaker enamel, depending on the degree of mineral loss

defect involving the mineral content (quality) of enamel.

dentin

most abundant tissue in the tooth

poorly organized & less mineralized than normal

primarily responsible for determining crown-root morphology

• as a result:

  • enamel frequently fractures away

  • it provides inadequate support for enamel

  • teeth become susceptible to rapid attrition bc hypomineralized dentin has poor wear resistance

vit. D deficiency during tooth development may result in:

large pulp chambers

reduced dentin production

reduced dentin mineral content

hereditary dentin defects

dentin dysplasia (DD)

dentinogenesis imperfecta (DGI)

• are characterized by:

  • altered tooth morphology

  • abnormal dentin mineralization

dentinogenesis imperfecta (DGI)

discoloration results from abnormal dentin showing through translucent enamel

• clinical features:

  • discolored teeth → blue-gray or yellow-brown

  • prone to rapid wear, breakage, loss

• radiographic findings:

  • pronounced cervical constriction at the CEJ

  • small root structures that may appear:

    • sharp & tent peg-like

• management:

  • once significant enamel loss and rapid attrition begin:

    • full-coverage crowns → treatment of choice

3 types of dentinogenesis imperfecta (DGI)

DGI type I

DGI type II

DGI type III

both type II and type II are:

• autosomal dominant

• highly penetrant

dentinogenesis imperfecta type I

bone involvement

blue-sclera on eyes, osteogensis imperfecta

occurs in people who have osteogenesis imperfecta

a genetic condition in which bones are brittle, causing them to break easily

dentinogenesis imperfecta type II

no bone involvement

not associated with a syndrome

most common type of dentinogenesis imperfecta

occurs in people without another inherited disorder

caused by mutations in the DSPP (dentin sialophosphoprotein) gene

dentinogenesis imperfecta type III

shell tooth

generally the same as dentinogenesis imperfecta type II except initially have large pulp chambers that obliterate with age results to multiple pulp exposure

osteogenesis imperfecta

aka: brittle bone disease

• caused by mutations affecting:

  • type I collagen

  • proteins involved in fibrillogenesis

dentin dysplasia (DD)

normal-looking crowns but abnormal roots and pulp

• clinical features

  • short or no roots

  • pulp chamber obliteration

  • normal clinical crown morphology

• radiographic features:

  • bowtie-shaped pulp chambers → molars

  • thistle tube-shaped pulp chambers → anterior

  • crescent-shaped root

  • sometimes absent root

2 types of dentin dysplasia (DD)

DD type I / radicular dentin dysplasia

DD type II / coronal dentin dysplasia

dentin dysplasia type I / radicular dentin dysplasia

affects the roots → rootless on xray

the exact cause remains unknown

tooth crowns appear clinically normal

• dentin formation is markedly abnormal, characterized by:

  • pulp chamber obliteration

  • abnormal or nearly absent root development

  • a pathognomonic cascading waterfall histologic appearance

DD type II / coronal dentin dysplasia

affects the crown

pulp chamber has thistle tube appearance

2 stages of eruption of permanent dentition

preemergent eruption

postemergent eruption

eruption begins once root formation starts during the preemergent stage

normal eruption requires:

resorption of alveolar bone

resorption of primary tooth roots

propulsive movement of the tooth in an occlusal direction

mechanism of tooth eruption

one theory suggests that hard tissue proliferation at the root apex → the primary driving force for eruption

• however, this does not explain all cases because:

  • intruded or luxated teeth may re-erupt without apical proliferation

• tooth eruption is therefore considered a complex process involving multiple structures, including:

  • dental follicle

  • periodontal ligament (PDL)

ectopic eruption

one of the most common eruption anomalies

occurs when a tooth erupts along an abnormal eruption path

• most commonly affected teeth:

  • permanent first molars

  • permanent lateral incisors

  • permanent canines

• other eruption anomalies:

  • delayed exfoliation of primary teeth

  • delayed eruption of permanent teeth

environmental defects altering tooth color

excess fluoride exposure

fever, starvation, tetracycline

low birth weight, hyperbilirubinemia

trauma, hypoxia (e.g., severe cardiac defect)

infection (congenital syphilis, cytomegalovirus, congenital rubella)

practice question in sas