Pediatric tooth development and disturbances

McDonald Avery & Dean, Dentistry for the Child and Adolescent, 8th ed., Chapter 4 pp50-54, Chapter 7 103-123Bring the textbook to classItalicized notes have been questioned on the Dental Decks

Overview

Life cycle of TeethInitiationBudProliferationDifferentiationAppositionCalcificationEruptionAttrition

Calcification timingDevelopmental Disturbances

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6th week in utero:Initiation/Induction. The

mesenchyme induces ectodermal changes:

Primordium of ectodermal portion of the teeth: Base layer of oral epithelial cells thicken, forming:

Dental lamina (also called the Common dental germ) which:

Becomes part of the embryonic jawsGives rise to: primary teeth and all permanent

molars

Life cycle of Teeth

Bud Cap

Bell AppositionMcDonald p 52 4-1

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Life Cycle

6-9th weeks iuBud stage

Special Dental Germs— 10 swellings bud in each dental lamina enamel organ starts to form

Researchers disagree about the overlap of each of these stages.

We will use McDonald’s dates as our reference. Evidence of human teeth is as early as 6 weeks iu

McDonald p 52 4-1

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Life Cycle

10th week iuCap/Proliferation StageRapid growth:Cap of epithelial cellsPapilla—epithelial cells under

the cap—will form dentin and pulp

Tooth germ is complete by end of cap and has enamel organ, dental papilla and dental sac with morpho-and histo-differentiation

McDonald p 52 4-1

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Life Cycle Collaboration Activity

Handouts—Embryos

Consult with the student sitting next to you about the approximate ages of the embryos.

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Life Cycle 11th week iu--Bell Stage—final shapingContinued Histo- and Morpho-differentiationElongation of inner enamel epithelial cells of

enamel organ causes mesenchymal cells next to dental papilla to become odontoblasts; Inner enamel epithelium will become ameloblasts.

Enamel is from ectoderm; all other tooth structure is from mesenchyme.

Hertwig’s epithelial root sheath (HERS)-inner and outer epithelium at the cervical of the enamel organ which directs root shape (number) as well as dentin formation in the root Therefore, ectodermal cells determine the crown and root shapes.

Follicle or dental sac will form PDL and

cementum

A. Bud

B. Cap

C. Bell McDonald p 52 4-1

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Life Cycle

Morphodifferentiation:11wk iu-primary centrals13wk iu-primary laterals14 wk iu-primary canines

McDonald p. 52 4-1

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Life CycleAppositionAmeloblasts and odontoblasts 1. Line up at DEJ and DCJ2. Secrete matrix at “growth

centers” deposits of the first layer of dentin preceeds deposition of the first layer of enamel

3. Start at the apex of cusps

McDonald p. 52 4-1

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Life Cycle CalcificationPrecipitation of calcium saltsEnamel droplets-small nidus

beginning at the 4 lobes (cusp/mamelon/cingula)

Concentric laminationsFusion of calcospheritesResearchers disagree over chronology.

We will use McDonald’s as our reference. Primary teeth begin to calcify at about 4 mo iu and permanent teeth begin to develop at about 4 mo iu

The buds of the primary teeth begin to develop permanent incisors, canines, and premolars buccal to the primary tooth, but the permanent teeth will erupt lingual to the primary

McDonald p. 52 4-1; p 178

Calcification

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Primary Calcification

Primary hard tissue formation begins (weeks in utero):

Centrals— 14 13 to 16 w iu

1st molars— 15 ½ 14 ½-17 w iu

Laterals—16 14 2/3 to 16 ½ w iu

Mx canines– 17 15-18 w iu

Md canines—17 16-17 w iu

Md 2nd molars—18 16-23 ½ w iu

Mx 2nd molars—19 16-23 ½ w iuAll 20 primary teeth begin to calcify

by 4-6 mo iu and take 10 months for completion.

McDonald 52 4-1

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Primary Calcification is complete after birth:

Mx central 1.5 moMx lateral Md central 2.5 moMd lateral 3 moMx 1st molars 5.5

moMx 1st molars 6

moCanines 9 moMd 2nd molars 10 moMx 2nd molars 11 moResearchers disagree over

chronology. We will use McDonald’s as our reference.

McDonald p.52 4-1

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Bud represents the beginning of formation of the dental lamina and special dental germs

Overview of Disturbances in Bud stage:

Congenital absence of tooth/teeth lack of initiation

Supernumerary teeth—continued budding

McDonald-p.667 shows a

Mesiodens-midline supernumerary

Odontoma (enamel/dentin tumor) p107 (often with odontoma-dysphagia syndrome)

McDonald 667 27-54McDonald 107 7-5

Developmental Disturbances

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Odontoma or Odontogenic tumorAbnormal proliferationAsymptomaticOften with unerupted tooth/cystOften with odontoma-dysphasia syn.Compound-miniature teeth

anterior maxilla occurrence-14.8 yo

(mean)Complex-amorphous/opaque

posterior mandible occurrence-20.3 yo (mean) affects both genders

equallyTX: enucleate rarely recursResearchers disagree over the

distinctions compound/complexMcDonald p 107 7-5

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Cap Stage--cell multiplication

Overview of Problems:Congenially missing teeth and

Supernumerary teeth may also occur in cap stage

Odontoma which replaces the normal tooth p107

Extra cusps and roots

Suppression of cusps and roots

Fusion (2 teeth unite into 1 tooth)

Gemination (bifid crown)

Epithelial rests cyst

McDonald 108 7-7 Fusion

McDonald 109 7-8 Gemination

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Cap disturbancesFusion—2 teeth unite into 1 tooth so

there are separate pulp canals & chambers

anterior location (generally) missing succedaneous teeth (often) family tendency primary or permanent teeth

Differential diagnosis—count teeth TX: may need restoration along line of fusion

McDonald p108 7-7

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Cap DistrubancesGemination—bifud crown Single tooth tries to divide Wide crown Familial tendency Primary or Permanent teeth Differential from fusion-count teeth TX: Recontour mesiodistal width

If dentin is exposed-restore If pulp is exposed-RCT

Mcdonald 109 7-8

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Bell—shape and cell finalization Overview of Disturbances:Abnormal forms and sizes:

Dens invaginatisDens evaginatus

Microdontia (such as peg lateral) Macrodontia Taurodontism Dilaceration Hutchinson’s incisors and Mulberry

molarsAmelogenesis Imperfecta

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Bell DisturbancesDens Invaginatus Dens in Dente—

Lingual invagination of enamelDeep lingual pits;

foramen cecum--some to pulpMaxillary perm. Laterals (7.7%)Frequent (1/77 Caucasians)Familial tendency (autosomal dominant)

Early diagnosis—early TXTX: apply sealant/restoration

Dens in MX lateral McDonald 110 7-10

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Bell DisturbancesDens Evaginatus

Lingual evagination of toothCone can interfere with eruption

occlusionCones contain pulp hornsTalon cusp—resembles an eagle claw—the term is reserved for anterior teethTX: may need to reduce

interference may require RCT

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Bell Disturbances Taurodontism Resemble cattle (taurus) teethElongated pulp chamberShort roots 2.5% occurrence in CaucasiansMay occur with syndromes: Otodental dysplasia X-chromosome aneuploidies

(change in number of X’s)Tricho-dento-osseous syndrome

(curly hair, dense bone)Late invagination-Hertwig’s

epithelial root sheath (HERS)

Clinically significant in a RCT

McDonald 123 7-26

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Bell DisturbancesDilacerationA sharp bend or

angulation of the root

• Result from trauma during tooth development

Clinical significance:• Can complicate tooth

extraction

McDonald 482 21-34

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Infections during BellCongenital Syphilis—child is

infected iu or while passing through birth canal.

Rare in US due to early detection and treatment

Hutchinson Incisors – result of congenital syphilis

– “screwdriver-shaped” permanent incisors

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Infections during the Bell stag

Mulberry molars Congenital Syphilis

From - Marquette University School of Dentistry

- Oral & Maxiollofacial Pathology website

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Apposition--matrix formation of ameloblasts and odontoblasts

Overview of Disturbances:– Enamel hypoplasia

defect in enamel matrix formation

Enamel Hypoplasia from trauma

Enamel Hypoplasia from infection

in apposition stage:

Hutchinson Incisor

Mulberry molar

Turner tooth

Amelogenesis Imperfecta Type 2– Hypoplasia of dentin

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Enamel hypoplasia (defect in matrix formation) is

Clinically: enamel—hard/thin

pitted/irregular surface

esthetic problems

sensitive teeth

yellow or brown

permanent and/or primary teeth

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Some causes of enamel hypoplasia:Local infection (localized problem)Local trauma (localized problem)Systemic diseases/conditions, such as

Rubella embryopathyCongenital syphilisHypoparathyroidismGrowth problems 0-6 mo

X-ray radiation- can also effect dentinFluoride; Chronic pediatric lead poisoningNutritional deficiencies – Vitamins A, C , Ca and PCleft lip and palate repair – permanent teeth more

likely to be damaged

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Enamel hypoplasia may be associated with

• Brain injury

• Neurologic defects

• Nephrotic syndrome

• Allergies

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Apposition disturbancesEnamel hypoplasia from

infectionsHutchinson Incisor –

result of congenital syphilis

– “screwdriver-shaped” permanent incisors

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Apposition Disturbances

Enamel hypoplasia from infection

Mulberry molars Congenital Syphilis

From - Marquette University School of Dentistry

- Oral & Maxiollofacial Pathology website

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Appostion Disturbances: Enamel Hypoplasia Due to local Infection or local Trauma—Turner’s tooth

Infections/caries in primary teeth may malform successors

McDonald 118 7-18

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Appostion Disturbances: The Location of the localized enamel defect is used to

calculate the timing of the infection/trauma/disease/insult.

At 4-5 years permanent centrals have completed calcification

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Apposition Disturbances: Enamel hypoplasia from radiation therapy which caused stunted of root

development McDonald p119 7-20

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Apposition Disturbances: Enamel Hypoplasia resulting from Rubella Embryopathy—

McDonald p 120 7-22

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Apposition Disturbances: Enamel Hypoplasia

caused by Fluoride- Fluorosis Mottled enamel-splotchy areas

of white and brown pigmentations

Irreversible Lethal dose: 20-50 mg/kg—

call 911; induce vomiting; force milk; (cardiac failure)

Acute toxic level: 1 mg/kgModerate to severe fluorosis:

0.1 mg/kg/d (Institute of Medicine) or 0.06 mg/kg/d (EPA Risk Information System Database)

Fluorisis on MX incisors McDonald 121 7-23

Carton RJ. Review of the 2006 United States National Research Council Report: Fluoride in Drinking Water. Fluoride. 2006;39(3):163-172.

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American Academy of Pediatric Dentistry Guideline, revised 2008

• Asses all sources of fluoride: water from home, day care, school; sodas, juices, formula, foods, toothpaste

• Assess caries risk• Recommend: smear of Fluoridated toothpaste

under 2yo; pea-size 2-5yo.• Supplementation schedule for <0.3ppm:

– 0-6m-0; 6m-3y-.25mg; 3-6y-.5 mg 6-16y-1mg

• Supplementation schedule for .3-.6ppm: – 0-6m-0; 6m-3y-0; 3-6y-.25mg 6-16y-.5mg

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Treatment of defective or carious hypoplastic teeth:

• Confine restoration to involved area • Use composite resin or glass

ionomer in minor defects or caries• Larger defects/carious areas may

require amalgams or Stainless Steel Crowns

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Treatment of hypoplastic teeth with esthetic problems

• Enamel microabrasion to remove superficial enamel discoloration (less than 250 μm depth)

• Vital tooth bleaching

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Calcification– precipitation of hydroxyapatite crystallites

[Ca10(PO4)6OH2] in matrix

Overview of Disturbances:Enamel Hypocalcification

A defect in enamel calcification and/or maturation

Pre-eruptive intracoronal resporption

Concrescence

Tetracycline stain

Interglobular dentin

Amelogenesis Imperfecta Type III

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Calcification disturbances: Pre-eruptive

intracoronal resorption or pre-eruptive caries • Defect in enamel formation• Results in connective tissue

growth into the defect• Not consdered classical

caries involving microorganisms and acids

• Infrequent (<10%)• Examine developing • teeth on radiographs for

such defects.

McDonald 121 7-24

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Calcification Disturbances: Concrescence

Fusion of two teeth by cementum only

Clinical significance: Important to recognize it and not

extract two teeth when intending to extract one

Considered to be caused by trauma

From “Contemporary oral and maxillofacial pathology” 1997

Next week—continuation of enamel and dentin defects