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Enamel and Dentin Defects (Continued); Abnormalities of the tongue

McDonald & Avery, Dentistry for the Child and Adolescent, 7th ed., Chapter 7 pp123-147. Italicized notes have been questioned on the Dental Decks

Inherited Defect--Dentinogenesis Imperfecta Prevalence : 1/8000 Bell Histodifferentiation thru apposition phases defect primary odontoblasts degenerate changing predentin matrix Presentation: Weak dentin--Red brown to gray opalescent color Undermineralized Slender roots/small pulp chambers-fracture easily Sound enamelbulbous crowns no support from dentin Enamel fractures easily without the support Exposed dentinabrades rapidly
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Inherited Defect--Dentinogenesis Imperfecta Shields classificationType I DI- always with Osteogenesis Imperfecta Type II DI- isolated trait, older terminology: Hereditary opalescent dentin DSPP gene mutation. DSPP codes for: Dentin Sialo-protein (DSP) matrix protein and Dentin Phospho-protein (DPP)

Type III DItype seen in an isolated Brandywine triracial group in Maryland


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Shields Type I DI
Autosomal dominant Osteogenesis Imperfecta Collagen defect brittle bones (osteoporotic) bowing limbs bitemporal bossing blue sclera Primary dentition-more severely affected
McDonald 124 7-27

Shields Type II DI
Older term: Hereditary opalescent dentin Autosomal dominant Isolated trait Reddish brown to gray opalescent color Primary & permanent dentitions equally affected

McDonald 125 7-29

Shields Type III DI


Isolated population in Brandywine, Maryland (near DC) population Shell-like appearance (radiograph) Multiple pulp exposures Premature exfoliation Thin layer of normal dentin next to enamel and cementum, then layer of disorganized dentin with few tubules.

McDonald 124 7-28

Dentinogenesis Imperfecta From Pediatric Dentistry, Linda Shaw, 1994.

Dentinogenesis Imperfecta
Radiographs:
Opacified pulps Short roots Bell-shaped crowns Constricted CEJ Type II & III Shell-like teeth Multiple pulp exposures McDonald 124 7-28
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Dentinogenesis Imperfecta
TX:
Protect tooth from wear Consider SSC on primary molars Restore/protect with crowns and veneers Do not use as abutments Consider overdenture Extract if root fractures (fractures commonly occur)
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Dentin Dysplasia
Rare disturbance of dentin formation related to DI 2,3 Type I- Radicular (root) dentin dysplasia Normal crown; short, pointed roots; rippled dentin Normal color (sometimes blue/brown/opalescent) Absent/Chevron-shaped coronal pulp Periapical radiolucencies Primary and Permanent teeth affected Autosomal dominant
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Dentin Dysplasia
Type II- Coronal dentin dysplasia Primary teeth-Opalescent Obliterated pulp chambers Permanent teeth--Normal color Normal length roots Pulp chamber--pulp stones Mutation of DSPP (related to Type II,III DI)

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Dentin Dysplasia
Type I- Radicular

Type II- Coronal Thistle tube pulp shape with pulp stones

From Contemporary oral and maxillofacial pathology 1997

Enamel Developmental Defects


Amelogenesis Imperfecta
Genetic Clinical presentation: Primary and permanent teeth 1/14,000 Skeletal anterior open bite association Pulp and root normal 3 major categories 14 subcategories

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Amelogenesis Imperfecta (AI) p127

Contemporary Oral and Maxillofacial Pathology 1997

Researchers disagree over classifications. We will use McDonalds Hypoplasticimperfect enamel matrix (bell stage) calcification is deficientless, but hard, enamel enamel rough/stains or smooth
Smooth hypoplastic-defective enamelin gene Local hypoplastic-defective enamelin gene

Hypomatured-imperfect calcification (apposition stage) Hypocalcifiedenamel matrix thickness is normal; imperfect calcification (calcification stage) enamel rough/stains soft enamel

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Contemporary Oral and Maxillofacial Pathology 1997 Hypoplastic Histodifferentiation Type 1 Timing: Bell stage Thickness: thin enamel thickness Surface: rough, pitted or smooth Hardness: normal enamel hardness (calcifies normally) McDonald 127 7-32 Radiographically: enamel contrasts normally with dentin

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Contemporary Oral and Maxillofacial Pathology 1997

Hypomaturation: Type II Timing: Apposition Phase Thickness: normal enamel thickness Surface: Chipped, porous, stained/mottled--enamel soft Hardness: less enamel hardness Radiographically: enamel has density of dentin
Differential diagnosis: often confused with fluorosisask about diet, family history

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Contemporary Oral and Maxillofacial Pathology 1997

Type III- Hypocalcified


Timing: calcification phase Thickness: normal enamel thickness Surface: smooth Radiographically: Enamel is less radiopaque than dentin poor quality of enamel Fractures easily leaving dentin cores

McDonald 127 7-33

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Treatment for Amelogenesis Imperfecta


(remember, dentin is normal) Depends on severity Esthetic improvement Full coverage restorations (dentin is normal) Bonded veneer restorations Porcelain laminate veneer restorations
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Aplasia--Enamel & Dentin Aplasia

Similar to DI and AI Controversy over terminology (Also called Odontogenesis Imperfecta) Both enamel & dentin are affected Normal bone Little or no enamel Large pulp chambers Acellular cementum No secondary dentin TX:SSC on erupting permanent molars McDonald p 129 7-36
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Collaboration Activity Handout Consult with student sitting next to you about the cases on the handout

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Intrinsic Discoloration of Teeth Timing: embryonic and beyond (Pigmentation of Teeth) as the result of: Hyper-Bilirubinemia (yellow-green) caused by: Biliary atresia Premature birth ABO incompatibility Neonatal complications Erythroblastosis fetalis (Rh factor) PorphyriaHeme pathway compromised Cystic Fibrosis Tetracycline Therapy Treatment: Primary teethgenerally not treated may consider composite veneers McDonald has report of bleaching a 4 yo Permanent teeth-microabrasion and/or bleaching with carbamide peroxide

Bleaching protocol at WVUcase by case basis child must be caries-free


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Erythroblastosis Fetalis
Mother RhTransplacental passage of maternal antibody active against RBC antigens of infant Increased rate of fetal RBC destruction Infant is anemic and jaundiced Discoloration of primary teeth resultblue green/brown

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Porphyria
Enzymes of heme pathway compromised Excess porphyrin Red urine Child is hypersensitive to lightsubepidermal bullous lesions when exposed to light Porphyrin accumulates in the primary and permanent teethPink/purple/brown; but scarlet in UV
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Cystic Fibrosis
Inherited chronic multisystem disorder Many die young-20s Many airway infections Many digestive problems Unknown if teeth are discolored by the disease or therapeutics for it Yellow-gray to brown Mice studies indicate abnormal enamel gene handling saltmost reliable diagnostic tool is the sweat test/ salty skin

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Tetracycline Stains
Rare nowphysicians avoid it during tooth-forming and calcifying years and during pregnancy (it crosses placenta) Tetracycline chelates calcium salts Adult onset has been reported with minocycline (3-6%) blue-gray crowns; black-green roots Sanchez, 2003 IJDermatology Incorporates into bones and teeth (mostly dentin, some enamel) Yellow to brown Severity--dose related TX: Vital bleaching with carbamide peroxide Bleaching may take several months or restore

McDonald 134 7-40

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Tetracycline-anterior teeth induced discoloration


Primary dentition will be affected by tetracycline from: Mx central14 w iu to 1.5 months Md central14 w iu to 2.5 months Mx lateral16 w iu to 2.5 months Md lateral16 w iu to 3 months Mx/Md canine17 w iu to 9 months Permanent dentition will be affected from Mx/Md central; Md laterals--3-4 mo to 4-5 y Mx/Md canines4-5 mo to 6-7 y MX lateral10-12 mo to 4-5 y (Premolars 12 yearsso avoid tetracyline prenatally thru 12 years) Adult onset has been reported with minocycline (3-6%) blue-gray crowns; black-green roots Sanchez, 2003 IJDermatology McDonald-135
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Anomalies of the tongue, etc.


Macroglossia (large tongue) Ankyloglossia (Tongue-tie) Geographic tongue (Benign migratory glossitis) Coated tongue Median rhomboid glossitis Injuries to the tongue
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Macroglossia Jaw development concerns: Cl III Occlusion conerns: flared lower ant. Associated with: Hypothyroidism Fissured Extend from mouth Down Syndrome Tx: surgical reduction

Geographic tongue (Benign migratory glossitis)

Fissures on dorsum of tongue Generally clinically insignificant Associated with Vitamin B deficiency Down syndrome Hypothyroidism No treatment is required Self-limiting.

McDonald 139 7-45

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Coated Tongue local factors, debris, TX: clean tongue

McDonald 140 7-46

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Median Rhomboid Glossitis asymptomatic chronic candida infection TX--anti-fungals


Example prescription for teens and older who are not allergic or hypersensitive to Nystantin or any component of the formulation. Rx: Nystantin Oral Suspension 100,000 units/ ml Dispense: 250 ml Sig: Swish and swallow 1 teaspoon 4 times a day for 10 days. Label, no refills

Wynn, RL. Drug Information Handbook for Dentistry, 12th edition


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Injuries to the Tongue


Causes:Traumas/Falls/Piercings Management: Airway May need sutures for Hemorrhage control Piercing complications: Airway compromise Infections-brain abscess endocarditis tetanus Fractured teeth/abrasion/recession
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Ankyloglossia short lingual frenum limits movement possible speech problems possible gingival stripping TX: surgery laser surgery

McDonald p138 7-43 7-44

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