Pediatric tooth development and disturbances

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

Overview
Life cycle of Teeth Initiation Bud Proliferation Differentiation Apposition Calcification Eruption Attrition Calcification timing Developmental Disturbances

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 jaws Gives rise to: primary teeth and all permanent molars

Life cycle of Teeth

Bud Cap

Bell Apposition McDonald p 52 4-1

Life Cycle

6-9th weeks iu
Bud 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 McDonalds 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 iu Cap/Proliferation Stage Rapid growth: Cap of epithelial cells Papillaepithelial cells under the capwill 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

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

Life Cycle 11th week iu-Bell Stagefinal shaping Continued Histo- and Morpho-differentiation Elongation 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.

Hertwigs 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. B. C.

Bud Cap Bell McDonald p 52 4-1

Life Cycle Morphodifferentiation: 11wk iu-primary centrals 13wk iu-primary laterals 14 wk iu-primary canines

McDonald p. 52 4-1

Life Cycle Apposition Ameloblasts and odontoblasts 1. Line up at DEJ and DCJ 2. 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

Life Cycle Calcification Precipitation of calcium salts Enamel droplets-small nidus beginning at the 4 lobes (cusp/mamelon/cingula) Concentric laminations Fusion of calcospherites
Researchers disagree over chronology. We will use McDonalds 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 14 -17 w iu Laterals16 14 2/3 to 16 w iu Mx canines 17 15-18 w iu Md canines17 16-17 w iu Md 2nd molars18 16-23 w iu Mx 2nd molars19 16-23 w iu All 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 mo Mx lateral Md central 2.5 mo Md lateral 3 mo Mx 1st molars 5.5 mo Mx 1st molars 6 mo Canines 9 mo Md 2nd molars 10 mo Mx 2nd molars 11 mo Researchers disagree over chronology. We will use McDonalds as our reference. McDonald p.52 4-1
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Developmental Disturbances 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 teethcontinued budding McDonald-p.667 shows a Mesiodens-midline supernumerary Odontoma (enamel/dentin tumor) p107 (often with odontoma-dysphagia syndrome)

McDonald 667 27-54 McDonald 107 7-5

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Odontoma or Odontogenic tumor Abnormal proliferation Asymptomatic Often with unerupted tooth/cyst Often 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 equally TX: enucleate rarely recurs Researchers disagree over the distinctions compound/complex

McDonald 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 15

Cap disturbances Fusion2 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 diagnosiscount teeth TX: may need restoration along line of fusion
McDonald p108 7-7

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Cap Distrubances Geminationbifud 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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Bellshape and cell finalization Overview of Disturbances: Abnormal forms and sizes:
Dens invaginatis Dens evaginatus Microdontia (such as peg lateral) Macrodontia Taurodontism Dilaceration Hutchinsons incisors and Mulberry molars Amelogenesis Imperfecta

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Bell Disturbances Dens Invaginatus Dens in Dente Lingual invagination of enamel Deep lingual pits; foramen cecum--some to pulp Maxillary perm. Laterals (7.7%) Frequent (1/77 Caucasians) Familial tendency (autosomal dominant) Early diagnosisearly TX TX: apply sealant/restoration
Dens in MX lateral McDonald 110 7-10

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Bell Disturbances Dens Evaginatus Lingual evagination of tooth Cone can interfere with eruption occlusion Cones contain pulp horns Talon cuspresembles an eagle clawthe term is reserved for anterior teeth TX: may need to reduce interference may require RCT

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Bell Disturbances Taurodontism Resemble cattle (taurus) teeth Elongated pulp chamber Short roots 2.5% occurrence in Caucasians May occur with syndromes: Otodental dysplasia X-chromosome aneuploidies (change in number of Xs) Tricho-dento-osseous syndrome (curly hair, dense bone) Late invagination-Hertwigs epithelial root sheath (HERS) Clinically significant in a RCT

McDonald 123 7-26

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Bell Disturbances Dilaceration A 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 Bell Congenital Syphilischild 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: enamelhard/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 embryopathy Congenital syphilis Hypoparathyroidism Growth problems 0-6 mo X-ray radiation- can also effect dentin Fluoride; Chronic pediatric lead poisoning Nutritional deficiencies Vitamins A, C , Ca and P Cleft 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 disturbances Enamel hypoplasia from infections Hutchinson 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 TraumaTurners 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/kg Moderate 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 . 35 2006;39(3):163-172.

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

Supplementation schedule for .3-.6ppm:

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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 m 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
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Next weekcontinuation of enamel and dentin defects