Presentation on theme: "ABNORMALITIES OF TEETH"— Presentation transcript:
1 ABNORMALITIES OF TEETH Environmental Alterations of TeethDevelopmental 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
2 ENVIRONMENTAL ALTERATIONS OF TEETH Developmental tooth defectsTurner’s toothHypoplasia caused by antineoplastic therapyFluorosisSyphilitic hypoplasiaPostdevelopmental structure lossTooth wearInternal and external resorptionDiscolorations of teethIntrinsic stainsExtrinsic stainsLocalized disturbances in eruptionPrimary impactionAnkylosis
3 Enamel developmentThree stages: 1. Matrix formation: protein laid down2. Mineralization: minerals deposition, majority of original prot. removed-- diffuse, opaque white, soft enamel3. Maturation: final mineralization-- translucent, hard enamelAmelogenesis imperfectaEnamel hypoplasia
4 Enamel development No remodeling after initial formation Timing of ameloblastic damage has a great impact on location & appearance of the defectDevelopment of crown : from 14th week of gestation to 12 months of age in deciduous dentition; 6 months to 15 y/o in permanent dentitionNeonatal ring on deciduous enamel and deposition with a rate of 0.023mm/day初成形後沒有remodeling, 故受損的timing 是關鍵
6 Factors associated with enamel defects See Box 2-2Factors associated with enamel defectsLocal-1.Local acute mechanical trauma2. Electric burn3. Irradiation4. Local infection: periapical inflammatory disease
7 Clinical and Radiographic Features Environmental enamel defects:1.Hypoplasia: pits, grooves or large area of missing enamel2. Diffuse opacities: variation in translucency, normal thickness, white opacity without clear boundary3. Demarcated opacities: increased opacity, a sharp boundary with adjacent normal enamel, normal thickness
8 Turner’s hypoplasia, Turner’s tooth Permanent teethPeriapical inflammatory disease of the overlying deciduous tooth, less frequently in anterior teethTraumatic injury- not rare-45% children sustain injury to their deciduous teeth, 23% permanent teeth development disturbedTurner’s hypoplasia secondary to previous trauma
10 Hypoplasia caused by antineoplastic therapy Under 12 y/o, esp. under 5y/oAge at treatment, forms of therapyChemotherapy-Less alteration than radiationIncreased number of enamel hypoplasia and discolorations, slight smaller tooth size, radicular hypoplasia
11 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
12 Developmental radicular hypoplasia and microdontia caused by radiotherapy
13 Hypodontia, microdontia, radicular hypoplasia, enamel hypoplasia, mandibular hypoplpasia, reduced in vertical development of lower 1/3 of faceMandibular hypoplpasia may caused by Radiation →impaired root development →reduced alveolar bone growthCranial radiation→ altered pituitary gland function→ growth failed
14 *Dental fluorosis 1901, Dr. Frederick S. McKay: Colorado brown stain 1909, Dr. F.L. Robertson in Bauxite, Arkansas1930, H.V. Churchill: high concentration of fluoride of Bauxite(13.7ppm) and Colorado1931, Dr. H. Trendley Dean: association between fluoride, dental fluorosis and prevalence of caries among children1.0 ppm reduced caries by 50~70% and associated with low and mild mottled enamel0.7~1.2 ppm water fluoridation was recommended after 1962, currently 0.7ppm is recommended due to increased dental fluorosis
15 Dental fluorosisRetention of the amelogenin protein in enamel structure → hypomineralized enamel → permanent hypomaturation → increased surface and subsurface porosity → alters light reflection and create white, chalky area
16 Dental fluorosisCritical period for clinical dental fluorosis is the 2nd and 3rd year of life, dose dependentCaries resistant
18 POSTDEVELOPMENTAL LOSS OF TOOTH STRUCTURE Begin from enamel surface (tooth wear):Attrition, abrasion, erosion, abfractionBegin from dentin, cemental surface: internal or external resorption
19 AttritionTooth to tooth contact during occlusion and mastication, some are physiologicAccelerated by: poor quality or absent enamel, premature contact, intraoral abrasives, erosion, grinding habitsIncisal, occlusal and interproximal surfaces
20 AbrasionPathologic 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 handDemastication- when tooth wear is accelerated by chewing an abrasive substance between opposing teeth (both attrition and abrasion)
26 AbfractionRepeated 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 abrasionWedge-shaped cervical defects, deep, narrow V-shaped, not allow toothbrush to contact base; if the defect, often affect a single toothAlmost exclusively on facial surface and more often in bruxism, higher in mandibular dentition
28 Treatment and prognosis of tooth wear Resolve pain and sensitivityIdentify the cause of tooth structure lossProtection
29 INTERNAL & EXTERNAL RESORPTION Internal resorption- by cells located in pulp, rareFollows injury to pulp tissues, physical trauma or caries, continue as long as vital pulp remains, may result in communication of the pulp and PDLExternal resorption- by cells in PDL, common
31 Clinical and Radiographic Features Internal resorption-Inflammatory resorption- dentin replaced by inflamed granulation tissuePink tooth of Mummery: internal resorption involved coronal pulp Balloonlike enlargement of the canalReplacement, or metaplastic absorption- pulpal dentinal walls are replaced by bone or cementum-like bone
32 Clinical and Radiographic Features External resorption-Moth-eaten loss of tooth structure, less well-defined and variation in density in radiographyMost involved apical or midportions of root, occasionally, begin from cervical (invasive cervical resorption)
34 Treatment and prognosis Internal resorption-Removal of all soft tissue from site of resorptionEndodontic treatment before perforation in internal resorptionPlacement of calcium hydroxide paste for remineralizationSurgical exposure and restorationExtractionExternal resorption-Identification and elimination the accelerating factor
35 ENVIRONMENTAL DISCOLORATION OF TEETH Extrinsic- surface accumulation of exogenous pigmentIntrinsic-secondary to endogenous factors that result in discoloration of underlying dentin
36 Extrinsic stainsBacterial- Chromogenic bacteria, green, black-brown, orange coloration Frequently in children, labial surface of maxillary ant. in gingival thirdIron- formation of ferric sulfideTobaccoFood and beverage- chlorophyllGingival hemorrhage- Hb. breakdown to biliverdinRestorative material – ex. AmalgamMedications- iron, iodine, silver nitrate, chlorhexidine, stannous fluoride
37 Intrinsic stains Amelogenesis imperfecta Dentinogenesis imperfecta Dental fluorosisErythropoietic porphyria –autosomatic recessive disorder of porphyrin metabolism, increased synthesis and excretion of porphyrins and their related precursorsPorphyrin deposition in teeth, reddish-brown coloration, red fluorescence when exposed to a Wood’s UV lightPresent both in dentin and enamel in deciduous teeth, but only dentin affected in permanent teeth
40 Intrinsic stains Medications- Tetracycline (bright yellow to dark brown), chlortetracycline (gray-brown), oxytetracycline (yellow) , minocycline hydrochlorideTime of administration dose, durationAvoid from pregnancy up to 8 yrs of age
41 Minocycline hydrochloride Tx for AcneBlue-gray from incisal 3/4, to dark green or black in roots, also affect developed teethSkin, nail, sclera, conjunctiva, thyroid, bone discoloration in susceptible individualsStained alveolar bone
43 LOCALIZED DISTURBANCES IN ERUPTION PRIMARY IMPACTION- Teeth cease to eruption before emergenceANKYLOSIS -Cease of eruption after emergence and anatomic fusion of tooth cementum or dentin with alveolar bone
44 Impaction3rd molars, maxillary canines, mandibular premolars, mandibular canines, maxillary premolars, maxillary central incisors, maxillary lateral incisors, and mandibular second molars; usually angulated or divertedFactors associated with impaction:Crowding and deficient maxillofacial developmentOverlying cysts or tumorsTraumaReconstructive surgeryThickened overlying bone or soft tissueA host of systemic disorders, diseases or syndromes
45 Eruption sequestrum Classification : Partially erupted or full bony impactionaccording to angulation: Mesioangular, distoangular, vertical, horizontal or invertedEruption sequestrum
46 Treatment and Prognosis Choice of treatment:Long-term observationOrthodontically assisted eruptionTransplantationSurgical removalThe risks associated with nonintervention:Crowding dentitionResorption and worsening of the periodontal status of adjacent teethDevelopment of pathologic conditions, ex infections, cysts or tumors
47 The risks associated with intervention: Transient or permanent sensory lossAlveolitisTrismusInfectionFractureTMJ injuryPeriodontal injuryInjury to adjacent teeth
49 ANKYLOSIS Clinical And Radiographic Features Pathogenesis is unknown, may be secondary to many factors and result in PDL barrier deficiency.May occur at any age, any toothMost affect 8~9yr-old children and D , E , D , EPDL absentOcclusal, periodontal problems, impaction of the underlying teethTreatment and PrognosisVariable : extraction, orthodontics, segmental osteotomy
50 DEVELOPMENTAL ALTERATIONS OF TEETH NUMBER HypodontiaHyperdontiaSIZE Microdontia MacrodontiaSTRUCTURE Amelogenesis imperfecta Dentinogenesis imperfectaDentin dysplasia I & II Regional odontodysplasiaSHAPE Gemination, Fusion, Concrescence Accessary cuspsDense in dente Ectopic EnamelTaurodontismDilaceration HypercementosisSupernumerary roots
51 Missing teeth Ectodermal dysplasia orofaciodigital syndrome % , excluding 3rd molars, female predominanceHypodontia: missing one or more teethOligodontia: missing 6 or more teethAnodontia: total missing8 > 5 > 2 > 1Deciduous mandibular incisorsGene mutation, ex: PAX9, MSX1, AXIN2 gene, He-Zhao deficiency, maps to chromosome 10q11.2AXIN2 mutation: associated with the development of adenomatous polyps of colon, and colorectal carcinomaEctodermal dysplasiaorofaciodigital syndrome%4
63 3.multiple epidermoid cysts or sebaceous cysts of the skin Gardner’s syndrome1.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
64 Predeciduous dentition Neonatal teeth: within 30 daysNatal teeth: newbornsMost are prematurely erupted deciduous teethRemoval only if mobile and at risk of aspiration
70 Gemination single tooth germ division tooth no.: normal single root & root canal + 2 complete or incomplete separated crownstooth no.: normaltwinning
71 Fusion Union of 2 separate tooth germs Contact of tooth germ before calcifiedConfluent of the dentinComplete- form a single toothIncomplete- after calcified beginsTooth no. : less one
72 Fusion after root formation Cementun united ConcrescenceFusion after root formationCementun unitedTraumatic injury or crowdingPre-extraction x-ray check
73 Talon cusp Eagle’s talon Lingual projection from the cingulum area of ant. teethMost contain a pulp hornBoth in deciduous & permanent dentition
74 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
75 Dens evaginatusKaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
77 Tooth within a tooth, incidence 5% Dens in dente(Dens invaginatus; Dilated composite odontome)Tooth within a tooth, incidence 5%Invagination of the enamel organ into dental papilla before calcificationCoronal type: 3 typesmaxillary lateral incisors are common
90 2.Hypomaturationnormal thickness of enamel, but mottled surface; cloudy white, yellow or brown, opaque in colorsofter than normalsame density as dentin
91 Hypomaturation typeKaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
92 3.Hypocalcified typenormal thickness of enamel, density less than dentinnormal size & shape when erupt, abrade or fracture away rapidlypermeability increase, darkened & stained4.Hypomaturation-hypocalcifiedwith taurodontism
94 Tricho-dento-osseous syndrome Hypoplastic-Hypomaturation type
95 Dentinogenesis imperfecta (Hereditary opalescent dentin)Classification of DI : (Shields)Type I : DI + OI (osteogenesis imperfecta) COL1A1,COL1A2Type II : Isolated DI. (1/8000) DSPPType III: DI of the Brandywine type * DSPPA racial isolate in Maryland,DI + multiple pulp exposures in deciduous teeth
96 Osteosclerosis imperfecta Blue scleraM Greenwood, J G Meechan,:General medicine and surgery for dental practitioners Part 8: Musculoskeletal system. British Dental Journal 2003 (195) ,
97 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.
99 Dentinogenesis imperfecta Histology:1.pulp chamber obliterated with dentin2.flatten D-E junction3.atypical granular dentin, enlarged tubles, poor calcificationwater contents: 50% above normal
100 Radiographic features Partial or total obliteration of the pulp chamber & root canal by continued formation of dentin, in both dentitions.Short and blunted rootsNormal cementum, PDL & supporting bone
101 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.
102 Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
103 Dentin dysplasiaHereditary, autosomal dominant. Normal enamel but atypical dentin formation with abnormal pulp morphologyType I (radicular type): “Rootless teeth”Type II (coronal) DSPP (dentin sialophosphoprotein) gene mutation
104 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 featuresNormal coronal enamel& dentin.In root: tubular dentin and atypical osteodentin surrounded with normal dentin --- appearance of “ Lava flowing around boulders”.
106 Type II (coronal)Normal root length in both dentitions.Primary dentition similar to DI:bulbous crowns, cervical constrictionthin roots , early obliterated pulp.Permanent teeth : normal coloration, thistle tube-shaped or flame-shaped pulp chamber with pulp stones.
108 “Lava flowing around boulders”. Dentin dysplasiaLarge pulp stones
109 Regional odontodysplasia (odontodysplasia; odontogenic dysplasia; odontogenesis imperfecta; ghost teeth)One or several teeth in a localized areaMaxi. > Mand.; both dentitionsmost in ant. areaDelayed or total failure eruptionIrregular appearanceDefective mineralization
110 Radiographic features 1. Radiodensity ↓, “ghost appearance”2. Large pulp, thin enamel & dentinHistologic features1. Dentin↓2.Widening of the predentin layer,3. Interglobular dentin and an irregular tubular pattern of dentin ↑4.Calcification of the reduced enamel epi.