abnormalities of teeth environmental alterations of teeth developmental alterations of teeth...

ABNORMALITIES OF TEETH

Environmental Alterations of Teeth

Developmental Alterations of Teeth

牙齒的異常 - 環境與發育的影響

王文岑 高雄醫學大學 牙醫學系wcwang@kmu.edu.tw

Wen-Chen Wang

ENVIRONMENTAL ALTERATIONS OF TEETH

Developmental tooth defectsTurner’s toothHypoplasia caused by antineoplastic therapyFluorosisSyphilitic hypoplasia

Postdevelopmental structure lossTooth wearInternal and external resorption

Discolorations of teethIntrinsic stainsExtrinsic stains

Localized disturbances in eruption Primary impactionAnkylosis

Wen-Chen Wang

Enamel development Three stages:

1. Matrix formation: protein laid down

2. Mineralization: minerals deposition, majority of original prot. removed-- diffuse, opaque white, soft enamel

3. Maturation: final mineralization-- translucent, hard enamel

Amelogenesis imperfecta Enamel hypoplasia

Wen-Chen Wang

Enamel development

No remodeling after initial formation Timing of ameloblastic damage has a

great impact on location & appearance of the defect

Development of crown : from 14th week of gestation to 12 months of age in deciduous dentition; 6 months to 15 y/o in permanent dentition

Neonatal ring on deciduous enamel and deposition with a rate of 0.023mm/day

Wen-Chen Wang

Factors associated with enamel defects

Systemic-1. Birth-related trauma: premature birth 2. Chemicals: antineoplastic C/T, fluoride,

tetracycline 3. Chromosomal abnormalities: trisomy 214. Infections: chicken pox, CMV, syphilis5. Inherited diseases: Vit.D-dependent rickets 6. Malnutrition: Vit. A deficiency 7. Metabolic disorders: hypoparathyroidism,

maternal diabetes8. Neurologic disorders: cerebral palsy

See Box 2-2

Factors associated with enamel defects

Local-1.Local acute mechanical trauma 2. Electric burn3. Irradiation4. Local infection: periapical inflammatory

disease

See Box 2-2

Wen-Chen Wang

Clinical and Radiographic Features

Environmental enamel defects:1.Hypoplasia: pits, grooves or

large area of missing enamel

2. Diffuse opacities: variation in translucency, normal thickness, white opacity without clear boundary

3. Demarcated opacities: increased opacity, a sharp boundary with adjacent normal enamel, normal thickness

Wen-Chen Wang

Turner’s hypoplasia, Turner’s tooth

Permanent teeth

Periapical inflammatory disease of the overlying deciduous tooth, less frequently in anterior teeth

Traumatic injury- not rare -45% children sustain injury to

their deciduous teeth, 23% permanent teeth development disturbed

Turner’s hypoplasia secondary to previous trauma

Wen-Chen Wang

Turner’s teeth

Wen-Chen Wang

Hypoplasia caused by antineoplastic therapy

Under 12 y/o, esp. under 5y/o Age at treatment, forms of therapy

Chemotherapy-Chemotherapy- Less alteration than radiation Increased number of enamel hypoplasia

and discolorations, slight smaller tooth size, radicular hypoplasia

Wen-Chen Wang

Radiotherapy-Radiotherapy- 0.72 Gy related to mild defects in enamel,

dentin ( 一般成人頭頸癌照射一次約為 2Gy)

Dose, radiation field

Wen-Chen Wang

Developmental radicular hypoplasia and microdontia caused by radiotherapy

Wen-Chen Wang

Hypodontia, microdontia, radicular hypoplasia, enamel hypoplasia, mandibular hypoplpasia, reduced in vertical development of lower 1/3 of face

Mandibular hypoplpasia may caused by Radiation →impaired root development →reduced alveolar bone growth

Cranial radiation→ altered pituitary gland function→ growth failed

Wen-Chen Wang

*Dental fluorosis 1901, Dr. Frederick S. McKay: Colorado brown stain 1909, Dr. F.L. Robertson in Bauxite, Arkansas 1930, H.V. Churchill: high concentration of fluoride of

Bauxite(13.7ppm) and Colorado 1931, Dr. H. Trendley Dean: association between

fluoride, dental fluorosis and prevalence of caries among children

1.0 ppm reduced caries by 50~70% and associated with low and mild mottled enamel

0.7~1.2 ppm water fluoridation was recommended after 1962, currently 0.7ppm is recommended due to increased dental fluorosis

Wen-Chen Wang

Dental fluorosis Retention of the amelogenin protein in enamel

structure→ hypomineralized enamel→ permanent hypomaturation→ increased surface and subsurface porosity→ alters light reflection and create white, chalky area

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Dental fluorosis Critical period for clinical dental fluorosis is

the 2nd and 3rd year of life, dose dependent Caries resistant

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Syphilitic hypoplasia •Congenital syphilis •Hutchinson’s incisors & mulberry molars

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POSTDEVELOPMENTAL LOSS OF TOOTH STRUCTURE

Begin from enamel surface (tooth wear):

Attrition, abrasion, erosion, abfraction

Begin from dentin, cemental surface: internal or external resorption

Wen-Chen Wang

Attrition Tooth to tooth contact during occlusion and

mastication, some are physiologic Accelerated by: poor quality or absent enamel,

premature contact, intraoral abrasives, erosion, grinding habits

Incisal, occlusal and interproximal surfaces

Wen-Chen Wang

Abrasion Pathologic loss of tooth structure or restoration

secondary to the action of an external agent (ex. Toothbrush, hair grips, toothpicks, chewing tobacco, biting thread, dental flossing…)

Toothbrush abrasion: horizontal buccal cervical notches of exposed radicular cementum and dentin with smooth surface.

Greater on prominent teeth ( canines, premolars , and teeth adjacent to edentulous area) and side of the arch opposite to the dominant hand

Demastication- when tooth wear is accelerated by chewing an abrasive substance between opposing teeth (both attrition and abrasion)

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Abrasion

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Abrasion

Long-term use of tobacco pipe

Improper use of hair grips

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Erosion Chemical process, exposure to acidic foods or

drinks, medications (chewable Vit. C, aspirin), involuntary regurgitation (ex. esophagitis, pregnancy), voluntary regurgitation (ex. psychologic problems, bulimia)

Perimolysis- dental erosion from gastric secretion Facial surface of maxillary anteriors affected-

dietary source Posterior teeth extensive loss of occlusal surface,

and palatal surface concave dentin surrounded by an elevated enamel rim- regurgitation of gastric secretion

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Erosion

concave dentin surrounded by an elevated enamel rim

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A bulimia patient

Erosion

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Abfraction Repeated tooth flexure caused by occlusal stresses

(tensile stress)

→ concentrate at the cervical fulcrum

→ may produce disruption in the chemical bonds of enamel crystal

→cracked enamel can be lost or removed by erosion or abrasion

Wedge-shaped cervical defects, deep, narrow V-shaped, not allow toothbrush to contact base; if the defect, often affect a single tooth

Almost exclusively on facial surface and more often in bruxism, higher in mandibular dentition

Wen-Chen Wang

Abfraction

Wen-Chen Wang

Treatment and prognosis of tooth wear

Resolve pain and sensitivity Identify the cause of tooth

structure loss Protection

Wen-Chen Wang

INTERNAL & EXTERNAL RESORPTION Internal resorption- by cells located in pulp, rare Follows injury to pulp tissues, physical trauma

or caries, continue as long as vital pulp remains, may result in communication of the pulp and PDL

External resorption- by cells in PDL, common

Wen-Chen Wang

Factors associated with external resorption

Wen-Chen Wang

Clinical and Radiographic Features

Internal resorption- Inflammatory resorption-

dentin replaced by inflamed granulation tissue Pink tooth of Mummery:

internal resorption involved coronal pulp Balloonlike enlargement of the canal

Replacement, or metaplastic absorption- pulpal dentinal walls are replaced by bone or cementum-like bone

Wen-Chen Wang

Clinical and Radiographic Features

External resorption- Moth-eaten loss of tooth

structure, less well-defined and variation in density in radiography

Most involved apical or midportions of root, occasionally, begin from cervical (invasive cervical resorption)

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Histopathologic Feature

• Increased cellularity, vascularity and collagenization • Numerous multinucleated dentinoclasts• Inflammatory cells infiltration

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Treatment and prognosis Internal resorption-

Removal of all soft tissue from site of resorption Endodontic treatment before perforation in internal

resorption Placement of calcium hydroxide paste for

remineralization Surgical exposure and restoration Extraction

External resorption- Identification and elimination the accelerating factor

Wen-Chen Wang

ENVIRONMENTAL DISCOLORATION OF TEETH

Extrinsic- surface accumulation of exogenous pigment

Intrinsic-secondary to endogenous factors that result in discoloration of underlying dentin

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Extrinsic stains Bacterial- Chromogenic bacteria, green, black-brown,

orange coloration Frequently in children, labial surface of maxillary ant. in gingival third

Iron- formation of ferric sulfide Tobacco Food and beverage- chlorophyll Gingival hemorrhage- Hb. breakdown to biliverdin Restorative material – ex. Amalgam Medications- iron, iodine, silver nitrate, chlorhexidine,

stannous fluoride

Wen-Chen Wang

Intrinsic stains Amelogenesis imperfecta Dentinogenesis imperfecta Dental fluorosis Erythropoietic porphyria –

autosomatic recessive disorder of porphyrin metabolism, increased synthesis and excretion of porphyrins and their related precursors

Porphyrin deposition in teeth, reddish-brown coloration, red fluorescence when exposed to a Wood’s UV light

Present both in dentin and enamel in deciduous teeth, but only dentin affected in permanent teeth

Wen-Chen Wang

Erythropoietic porphyria

Hyperbilirubinemia

Wen-Chen Wang

Intrinsic stains Hyperbilirubinemia- bilirubin, breakdown product

of RBC, jaundance (yellow-green discoloration), erythroblastosis fetalis, biliary atresia Biliverdin deposition, green discoloration of teeth

(chlorodontia)

Ochronosis-alkaptonuria, blue-black discoloration

Trauma- coronal discoloration, pulp necrosis

Localized RBC breakdown

Wen-Chen Wang

Intrinsic stains Medications-

Tetracycline (bright yellow to dark brown), chlortetracycline (gray-brown), oxytetracycline (yellow) , minocycline hydrochloride

Time of administration dose, duration Avoid from pregnancy up to 8 yrs of age

Wen-Chen Wang

Minocycline hydrochloride Tx for Acne

Blue-gray from incisal 3/4,

to dark green or black in

roots, also affect developed

teeth

Skin, nail, sclera,

conjunctiva, thyroid, bone

discoloration in susceptible

individuals Stained alveolar bone

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Treatment and prognosis

Extrinsic stains- polishing

Intrinsic stains- bleaching, bonded restoration, crowns

Wen-Chen Wang

LOCALIZED DISTURBANCES IN ERUPTION

PRIMARY IMPACTION- Teeth cease to eruption before emergence

ANKYLOSIS -Cease of eruption after emergence and anatomic fusion of tooth cementum or dentin with alveolar bone

Wen-Chen Wang

Impaction 3rd molars, maxillary canines, mandibular premolars,

mandibular canines, maxillary premolars, maxillary central incisors, maxillary lateral incisors, and mandibular second molars; usually angulated or diverted

Factors associated with impaction: Crowding and deficient maxillofacial development Overlying cysts or tumors Trauma Reconstructive surgery Thickened overlying bone or soft tissue A host of systemic disorders, diseases or syndromes

Wen-Chen Wang

Classification : Partially erupted or full bony impaction according to angulation: Mesioangular,

distoangular, vertical, horizontal or inverted

Eruption sequestrum

Wen-Chen Wang

Treatment and PrognosisChoice of treatment: Long-term observation Orthodontically assisted eruption Transplantation Surgical removal

The risks associated with nonintervention: Crowding dentition Resorption and worsening of the periodontal

status of adjacent teeth Development of pathologic conditions, ex

infections, cysts or tumors

Wen-Chen Wang

The risks associated with intervention:

Transient or permanent sensory loss Alveolitis Trismus Infection Fracture TMJ injury Periodontal injury Injury to adjacent teeth

Wen-Chen Wang

ANKYLOSIS

Infraocclusion, secondary retention, submergence, reimpaction, reinclusion

Wen-Chen Wang

ANKYLOSISClinical And Radiographic Features Pathogenesis is unknown, may be secondary to

many factors and result in PDL barrier deficiency. May occur at any age, any tooth Most affect 8~9yr-old children and D , E , D , E PDL absent Occlusal, periodontal problems, impaction of the

underlying teeth

Treatment and Prognosis Variable : extraction, orthodontics, segmental

osteotomy

Wen-Chen Wang

DEVELOPMENTAL ALTERATIONS OF TEETH

SHAPE Gemination, Fusion, Concrescence

Accessary cusps Dense in dente Ectopic Enamel Taurodontism Dilaceration Hypercementosis Supernumerary roots

NUMBER Hypodontia Hyperdontia

SIZE Microdontia Macrodontia

STRUCTURE Amelogenesis imperfecta Dentinogenesis imperfecta Dentin dysplasia I & II Regional odontodysplasia

Wen-Chen Wang

Missing teeth 1.6-9.6% , excluding 3rd molars, female predominance Hypodontia: missing one or more teeth Oligodontia: missing 6 or more teeth Anodontia: total missing 8 > 5 > 2 > 1 Deciduous mandibular incisors Gene mutation, ex: PAX9, MSX1, AXIN2 gene, He-Zhao

deficiency, maps to chromosome 10q11.2 AXIN2 mutation: associated with the development of

adenomatous polyps of colon, and colorectal carcinoma

Ectodermal dysplasiaorofaciodigital syndrome

Wen-Chen Wang

Hypodontia

Wen-Chen Wang

Ectodermal dysplasia

Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

Wen-Chen Wang

Supernumerary teeth, hyperdontia

Mesiodens 4th molar Paramolar Distomolar, distodens deciduous - lat. incisors 86% single supernumerary multiple & impaction

cleidocranial dysostosis Gardner’s syndrome

Wen-Chen Wang

Mesiodens

The most common in supernumerary.Premaxillary area , usually between upper central incisorsCone-shaped crown & short rootOne or two in number

Wen-Chen WangKaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

Wen-Chen Wang

Cleidocranial dysostosis

1.Skull: flat appearance, sutures remain open

2.Jaws: underdeveloped, high narrow palate

3.Teeth: prolonged retained deciduous teeth,

delayed eruption of permanent teeth

4.Clavicles: complete or partial absent

Wen-Chen WangKaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

Wen-Chen WangKaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

Wen-Chen WangKaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

Wen-Chen WangKaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

Wen-Chen Wang

Wen-Chen Wang

Gardner’s syndrome

1.multiple polyposis of the large intestine2.osteoma of the bone3.multiple epidermoid cysts or sebaceous cysts

of the skin4.desmoid tumors5.impacted supernumerary & permanent teeth

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Predeciduous dentition

Neonatal teeth: within 30 days Natal teeth: newborns Most are prematurely erupted deciduous teeth Removal only if mobile and at risk of aspiration

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Wen-Chen Wang

Microdontia True: 1.General -pituitary dwarfism 2. Single -peg lat., 3rd molar Relative microdontia

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Macrodontia

True macrodontia :

1. Generalized-pituitary gigantism

2. Localized- single, hemifacial hypertrophy Relative macrodontia: small jaw, child

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Wen-Chen Wang

Gemination, Fusion, Concrescence

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Gemination

single tooth germ division

single root & root canal + 2 complete or incomplete separated crowns

tooth no.: normal twinning

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Fusion

Union of 2 separate tooth germsContact of tooth germ before calcifiedConfluent of the dentinComplete- form a single tooth Incomplete- after calcified beginsTooth no. : less one

Wen-Chen Wang

Concrescence

Fusion after root formationCementun unitedTraumatic injury or crowdingPre-extraction x-ray check

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Talon cusp

Eagle’s talonLingual projection from the cingulum area of ant. teethMost contain a pulp hornBoth in deciduous & permanent dentition

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Dens evaginatus

( central tubercle, occlusal tuberculated premolar; Leong’s premolar; evaginated odontome; occlusal enamel pearl )

An accessory cusp or a globule of enamel on central groove or buccal cusp of premolars or molars; unilateral or bilateral.

15% in Asians, rare in whites

Wen-Chen Wang

Dens evaginatus

Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

Wen-Chen Wang

Shovel-shaped incisors

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Dens in dente(Dens invaginatus; Dilated composite odontome)

Tooth within a tooth, incidence 5% Invagination of the enamel organ into

dental papilla before calcification

Coronal type: 3 types maxillary lateral incisors are common

Wen-Chen Wang

Dens invaginatus, coronal type II

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Dens invaginatus Radicular type

Hertwig’s sheath invagination

Food deposition→ caries → pulp infection Restorated as soon as possible

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Taurodontism

“Bull-like “ teethBi- or trifurcation near the apexPulp chamber : greater apico-occlusal height and no constriction at the cervical of the tooth

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Syndromes associated with taurodontism

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Hypercementosis

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Supernumerary roots Any tooth may develop accessary roots No tx required, but critical important in

endodontic procedure

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Dilaceration

Angulation, sharp bend of root or crownTrauma during tooth is formingPre-extraction x-ray check

Wen-Chen Wang

Amelogenesis imperfecta (Hereditary enamel dysplasia; Hereditary brown

enamel; Hereditary brown opalescent teeth)

Defects in-- Formative stage→hypoplastic type → defective

formation of matrix Calcification stage →hypocalified → defective

mineralization of formed matrix Maturation stage → hypomaturation → enamel

crystallites remain immature Genes mutation : AMELX, ENAM, MMP-20, KLK4,

DLX3

Wen-Chen Wang

Amelogenesis imperfecta

Wen-Chen Wang

Thin enamel with pitted, rough or smooth & glossy surface; yellowish to brown

undersized, squared crown, lack of contact

flat occlusal surface & low cusps, attrition

1.Hypoplastic type

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Hypoplastic type

Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

Wen-Chen Wang

Hypoplastic type

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2.Hypomaturation

normal thickness of enamel, but mottled surface; cloudy white, yellow or brown, opaque in color

softer than normal same density as dentin

Wen-Chen Wang

Hypomaturation type

Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

Wen-Chen Wang

normal thickness of enamel, density less than dentin

normal size & shape when erupt, abrade or fracture away rapidly

permeability increase, darkened & stained

3.Hypocalcified type

4.Hypomaturation-hypocalcified with taurodontism

Wen-Chen Wang

Hypocalcified type

Wen-Chen Wang

Tricho-dento-osseous syndrome

Hypoplastic-Hypomaturation type

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Dentinogenesis imperfecta

(Hereditary opalescent dentin)

Classification of DI : (Shields)

Type I : DI + OI (osteogenesis imperfecta) COL1A1,

COL1A2 Type II : Isolated DI. (1/8000) DSPP Type III: DI of the Brandywine type * DSPP

A racial isolate in Maryland, DI + multiple pulp exposures in deciduous teeth

Wen-Chen Wang

Osteosclerosis imperfecta

Blue sclera

M Greenwood, J G Meechan,:General medicine and surgery for dental practitioners Part 8: Musculoskeletal system. British Dental Journal 2003 (195) 243 - 248 ,

Wen-Chen Wang

Clinical features type I : deciduous severe than permanent teeth; type II: equally affected; type III: both dentitions affected. Gray to brownish violet or yellowish brown

color, with translucent or opalescent hue. Enamel lost early through fracture, esp. on the

incisal & occlusal surface, and dentin attrition rapidly.

Caries rate is not increased.

Wen-Chen Wang

Dentinogenesis imperfecta

Wen-Chen Wang

Dentinogenesis imperfecta

Histology: 1.pulp chamber obliterated with dentin 2.flatten D-E junction 3.atypical granular dentin, enlarged tubles, poor calcification

water contents: 50% above normal

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Radiographic featuresPartial or total obliteration of the pulp chamber & root canal by continued formation of dentin, in both dentitions.

Short and blunted roots

Normal cementum, PDL & supporting bone

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Shell teeth Initial reported in the Brandywine population Normal thickness of enamel associated with extremely thin dentin and dramatically enlarged pulps (due to insufficent and deffective dentin formation) Short roots.

Wen-Chen WangKaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

Wen-Chen Wang

Dentin dysplasia

Hereditary, autosomal dominant. Normal enamel but atypical dentin formation with abnormal pulp morphology

Type I (radicular type): “Rootless teeth”

Type II (coronal) DSPP (dentin sialophosphoprotein) gene mutation

Wen-Chen Wang

Type I (radicular type)Radiographically: deciduous teeth affected more severely, little or no pulp,

short or absent roots. If disorganization late---normal pulp chambers, with a

large pulp stone. periapical lesions (R-L) no obvious cause.

Histologic features Normal coronal enamel& dentin. In root: tubular dentin and atypical osteodentin

surrounded with normal dentin --- appearance of “ Lava flowing around boulders”.

Wen-Chen Wang

Dentin dysplasia, type I

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Type II (coronal)

Normal root length in both dentitions.

Primary dentition similar to DI:

bulbous crowns, cervical constriction

thin roots , early obliterated pulp.

Permanent teeth : normal coloration, thistle tube-shaped or flame-shaped pulp chamber with pulp stones.

Wen-Chen Wang

Dentin dysplasia, type II (coronal)

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Dentin dysplasia

“Lava flowing around boulders”.

Large pulp stones

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Regional odontodysplasia

(odontodysplasia; odontogenic dysplasia; odontogenesis imperfecta; ghost teeth)

One or several teeth in a localized area Maxi. > Mand.; both dentitions most in ant. area Delayed or total failure eruption Irregular appearance Defective mineralization

Wen-Chen Wang

Radiographic features

1. Radiodensity ↓, “ghost appearance”

2. Large pulp, thin enamel & dentin

Histologic features

1. Dentin↓

2.Widening of the predentin layer,

3. Interglobular dentin and an irregular tubular pattern of dentin ↑

4.Calcification of the reduced enamel epi.

Wen-Chen Wang

Regional odontodysplasia

Enameloid conglomerates Odontogenic epithelium

Wen-Chen Wang

ENVIRONMENTAL ALTERATIONS OF TEETH

Developmental tooth defectsTurner’s toothHypoplasia caused by antineoplastic therapyFluorosisSyphilitic hypoplasia

Postdevelopmental structure lossTooth wearInternal and external resorption

Discolorations of teethIntrinsic stainsExtrinsic stains

Localized disturbances in eruption Primary impactionAnkylosis

Summary

Wen-Chen Wang

DEVELOPMENTAL ALTERATIONS OF TEETH

SHAPE Gemination, Fusion, Concrescence

Accessary cusps Dense in dente Ectopic Enamel Taurodontism Dilaceration Hypercementosis Supernumerary roots

NUMBER Hypodontia Hyperdontia

SIZE Microdontia Macrodontia

STRUCTURE Amelogenesis imperfecta Dentinogenesis imperfecta Dentin dysplasia I & II Regional odontodysplasia

Summary