ABNORMALITIES OF TEETH V. Žampachová Dental anomalies ndefects in tooth development nenvironmental alterations of teeth n ncauses - hereditary, systemic, traumatic or local factors (eg. drug) Developmental alterations nIdiopathic or hereditary conditions n nAlterations in the number of teeth nAlterations in the size of teeth nAlterations in the shape of teeth nAlterations in the structure of teeth > Environmental alterations nInfluenced by environmental forces n nDevelopmental tooth defects nPostdevelopmental structure loss nDiscoloration of teeth nLocalized disturbances in eruption > Environmental effects on tooth structure nTurner‘s hypoplasia nHypoplasia due to antineoplastic therapy nDental fluorosis nSyphilitic hypoplasia > Postdevelopmental loss of structure nTooth wear – attrition n abrasion n erosion n abfraction nInternal and external resorption > Environmental discoloration nExtrinsic stains nIntrinsic stains > Localized disturbances in eruption nPremature eruption nRetarded eruption nPremature loss nDeciduous teeth persistence nPrimary impaction nAnkylosis +/- reimpaction > Histology of enamel nFormed by ameloblasts •95% mineralized anorganic material •5% organic •98% calcified •Consists of enamel rods or prisms •Yellow to grayish white nStrong, but prone to splits and chips nHardest structure in body nNon-reparative nSubject to caries nSubject to wear > Environmental effects on tooth structure nAmeloblasts in the developing tooth germ highly sensitive to external forces → multiple posibilities of enamel abnormalities. nNo remodeling → permanent defects n3 stages: matrix formation n mineralization n maturation > Factors associated with enamel defects nSystemic nBirth-related trauma (hypoxia, premature b., prolonged labor) nChemicals (chemotherapy, fluoride, Pb, TTC, thalidomide) nChromosomal abnormalities (trisomy 21) nInfections (CMV, varicella, rubella, syphilis, ..) nInherited diseases (phenylketonuria, osseous dysplasia, ..) nMalnutrition (generalized, vit. A, D def.) nMetabolic diseases (celiac d., hypoparathyroidism, renal d.) nNeurologic disorders (mental retardation,..) 1. > Factors associated with enamel defects nLocal nLocal acute mechanic trauma (falls, traffic accidents, gunshot, mechanical ventilation, ritual mutilation,..) nElectric burn nIrradiation nLocal infection (periapical etc.) > Cause period nPrenatal nNeonatal nPostnatal n n > Prenatal nVertical transmission of infection, i.e. rubella, syphilis nMaternal systemic disease n > Neonatal nhaemolytic disease of the newborn nhypocalcaemia npremature birth/prolonged labour (ischaemia) n > Postnatal nsevere childhood infections, esp. viral exanthematic diseases nchronic diseases in childhood, e.g. congenital heart disease, gastrointestinal and endocrine diseases nnutritional deficiency, e.g. vitamin D ncancer chemotherapy nexcess fluoride ions ntrauma n > Enamel defects ndifferent causes may result in similar defects npossible timing of cause in deciduous enamel nrough estimate in permanent teeth nvery common (≥ 50%) > Enamel defects patterns nLocalized x multifocal (number of teeth affected) nPartial x global (amount of surface) n nHypoplasia (pits, grooves, parts missing) nDiffuse opacities (variations of translucence, white) nDemarcated opacities (decreased translucence, sharp demarcation, white → brown) > mild type n smooth-surface enamel n white, opaque spots, n brown after eruption Dsc00928 拷贝-1 Dsc01067 拷贝 copy 重症 severe type nhorizontal grooves in the enamel surface npits in the enamel surface ngeneral reduction in the thickness of the whole enamel Dsc00635 拷贝 Dsc00931 拷贝-1 symmetrical copy symmetrical Dsc00866 拷贝 Dsc00865 拷贝 Dsc00867 拷贝 copy Turner’s hypoplasia (Turner’s tooth) n - a local hypoplastic or hypomineralized defect in crown of a permanent tooth nextension of a periapical inflammatory disease (infection) or mechanical trauma from overlying deciduous tooth, disturbing the ameloblasts of the permanent tooth bud nmost common in lower premolars > Localized enamel hypoplasia (Turner's teeth) nlocal or extensive copy > Turner teeth nyellowish or brownish pigmentation of the enamel npits and irregularity of the surface nsmaller crown than normal Dsc00954 拷贝-1 Dsc00885 拷贝-1 copy DSC00197 DSC00198 DSC00199 DSC00198 Turner tooth copy Hypoplasia due to antineoplastic therapy nchildhood cancer nchemo and/or radiotherapy nenamel and dentin defects nhypodontia, microdontia, enamel hypoplasia, … > Dental fluorosis nFluorosis (mottled enamel) n fluoride in drinking water, toothpaste, supplements ® hypomineralization, event. enamel hypoplasia nmostly discoloration, true hypoplasia uncommon npaper-white patches ® brown npermanent teeth (Placenta barrier normally resists fluoride, fluorosis seldom in deciduous dentition.) nhydroxyapatite ® calcium fluorapatite nmatrix normal nfluorosis x caries resistance n > Dental fluorosis nfluoride opacities symmetrically around the arch nfaint white flecking of the enamel, white patches or striations nin severe cases may be associated with loss of the normal tooth form nthe deciduous teeth may be involved in severe cases and in areas of endemic fluorosis nhighly acid-resistant, rapid loss by abrasion and attrition n n > Fluorosis Dsc00704 拷贝-1 copy Therapy nbleaching ncomposite resin n > Congenital syphilis nCongenital syphilis - Hutchinson nlater fetal infection, now very rare ndental follicle infection by T. pallidum npermanent teeth nupper 1. I (Hutchinson´s incisors) – barrel-shaped n fissure on incisal edge n1. M (mulberry, Moon´s molar) – pitted + bumpy occlusal surface > Congenital syphilis n30 % of infected fetuses develop dental hypoplasia > Congenital syphilis nHutchinson´s incisors mulberry molar Dsc00825 拷贝-1 Dsc00870 拷贝-1 copy Postdevelopmental loss of structure nNon-bacterial (x caries) nNon-traumatic (x fracture) nTooth wear (enamel) – attrition n abrasion n erosion n abfraction nInternal and external resorption (dentin, cement) > Habitual disorders nAbrasion is the abnormal wearing away of tooth structure caused by a repetitive mechanical habit. nexternal cause (friction of a foreign body, abrasive material, pressure) nimproper toothbrushing – common, on exposed roots, maxillary > mandibular, anterior > molars, grooves + polished dentine ngripping objects with teeth – habitual (pipe, pencils), occupational > Toothbrushing injury nV-shaped groove in cervical area nSensitive nMaxillary premolars >canines > incisors nR-L (mostly) defect at cervical level, well-defined semilunar shapes abrasion copy > Toothbrushing abrasion n 17_039 > Habitual disorders nAttrition: wearing away of tooth structure during mastication (chewing) through tooth-to-tooth contact nIncisal, occlusal and interproximal surfaces (contact points) nCrown shortened, reduction of pulp chamber, canals nPhysiological (contact points and areas, abrasive foods, exposion of dentine → accelerated attrition) nDentin sensitivity rare due to slow loss + secondary dentin formation n > Attrition n 17_040a 17_040b > Habitual disorders nPathological attrition nabnormal occlusion (prolongated contact, developmental, acquired – extraction) nbruxism; long-term use of intraoral abrasives (tobacco or betel chewing) nabnormal tooth structure (poor quality or absent enamel – fluorosis, amelogenesis or dentinogenesis imperfecta) > 17-36attrition Attrition Toothbrushing injury copy Habitual disorders nBruxism: an oral habit consisting of involuntary grinding and clenching of the teeth in movements other than chewing. nUsually performed during sleep, commonly associated with stress or tension. > Bruxism n 17_041 > Habitual disorders nErosion – loss of tooth structure by a chemical process (acid) not asssociated with bacterial interaction. Possible combination (↑ attrition, abrasion). nDietary – carbonated soft drinks, fruit juices; shallow polished concavities nMedication – aspirin, vit. C chewing nStomach regurgitation – involuntary (gastric reflux, pregnancy), voluntary (repeated vomiting) n > Habitual disorders nCrown shortened, reduction of pulp chamber, canals ndentin reactive changes, incl. tertiary reactionary dentine formation npossible hypersensitive dentin if rapid course > Erosion caused by bulimia. 17_042a 17_042b Habitual disorders nAbfraction – due to the repeated tooth flexure (occlusion stress) → disruption of enamel crystals → cracked enamel → loss by erosion, abrasion nwedge-shaped defect on cervical area of the teeth, facial surface nsingle tooth often affected > Habitual disorders n ncommonly multifactorial etiology + result nfunctional, dental sensitivity, aesthetic problems > Histology of dentin nFormed by odontoblasts n70% anorganic matter n30% organic matter nMakes up bulk of tooth nDentinal tubules nNot as hard as enamel nSomewhat elastic nPale yellow nSomewhat transparent nMore radiolucent than enamel nCan repair itself > Histology of cementum nFormed by cementoblasts nCovering of root n50% to 55% anorganic material n45% organic nPrimary cementum nSecondary cementum nAnchors tooth to socket via periodontal ligaments n > Secondary dentin n Dentin deposited in pulp chamber after primary dentin formed completely nNormal aging process ntertiary dentin: pathologic condition after chronic trauma nReduction in size of pulp chamber and canals nBegins in the region adjacent to source of stimuli and alters normal shape of chamber 17-42secondary dentin > Internal and external resorption nresorption of dentin or cementum ninternal surface – cells in the pulp nexternal surface – cells in the periodontal ligament > Internal and external resorption nInternal resorption – macrophages (dentinoclasts) on pulpal surface, vital pulp necessary nloss of odontoblasts nasociated with pulpitis, physical trauma nrare idiopathic nless common than external resorption npulp tissue visible through enamel – pink spot n > Internal and external resorption nInternal resorption n2 main patterns: ninflammatory resorption: replacement of dentin by granulation tissue, in pulpitis nmetaplastic resorption: replacement by bone or cementum-like bone > Internal resorption nWithin the pulp chamber or canal, involves resorption of surrounding dentin, results in enlarged pulp space nM>F, commonly begins during 3rd-5th decade nRadiographs reveal symptomless early lesions of IR nRadiolucent, round, oval, or elongated within root or crown and continuous with pulp chamber or canal nSharply defined and smooth or slightly scalloped → irregular widening of the pulp chamber or canal nMetaplastic bone may lead to partial obliteration of the canal n n > 17-38internal root resorption-3 17-38internal root resorption 17-38internal root resorption-2 Internal resorption Internal and external resorption nExternal resorption nfrom root surface nvariable individual susceptibility to external resorption – most important factor nextremely common, in 10% serious nvariable radiolucency (moth-eaten) nresorption by multinucleated dentinoclasts, inflammatory reaction + woven bone, may lead to ankylosis n > Internal and external resorption nExternal resorption ninflammatory res. – periapical inflammation, root res., layer of granulation tissue (later fibrotic), layer of woven bone npressure/mechanical res. - ? aseptic necrosis → repair nidiopathic – burrowing from root surface into dentine → granulation tissue → bone (event. ankylosis); invasive cervical resorption > nApical ER: n-blunting with normal bone and lamina dura n-root shortening, except due to periapical inflammatory lesions n canal is visible and abnormal wide at apex n nLateral root surface ER: n-presence of an unerupted adjacent tooth Internal and external resorption > Internal and external resorption nExternal resorption risk factors ncysts ndental trauma nexcessive external forces (mechanical, occlusal) ntherapy (orthodontic, bleaching, teeth reimplantation, …) nlocal diseases (periradicular inflammation, herpes zoster, Paget‘s bone disease, tumors… ngeneralized disorders (hormonal imbalances) nidiopathic > 17-39external root resorption 17-40external root resorption Apical ER Lateral root surface ER copy Teeth discoloration nextrinsic – surface deposits nbacterial stain niron, other metals ntobacco, betel nfood + beverages ngingival haemorrhage nrestorative materials nmedication n > Teeth discoloration nIntrinsic: nchanges in the structure or thickness (amelo-, dentinogenesis imperfecta, developmental enamel hypoplasia, caries) ndiffusion of pigments after formation of tissues - ↑ in preexisting enamel or dentin changes (root filling material, pulp necrosis + haemorrhage) n > Teeth discoloration nIntrinsic: npigment incorporation during formation of enamel/dentin ncongenital hyperbilirubinemia (greenish) ncongenital porphyria (red-brown, UV red fluorescence) nTTC pigmentation (yellow dentin bands, UV yellow, later brown) > TTC pigmentation n Dsc00707 拷贝-1 Dsc00914 拷贝-1 Pigment disorders therapy ncomposite resin nbleaching n > Composite resin Dsc00914 拷贝-2 Dsc00916 拷贝-3 copy Tooth trauma nMaxillary central incisors - 70-80% of all fractured teeth nComplications: failure to complete eruption, color change of the tooth, abscess, loss of space in the dental arch, ankylosis, abnormal exfoliation, root resorption. > Tooth fracture nI.- enamel, usually no complication nII. – enamel+dentin: risk of pulp necrosis nIII. – into pulp, 10-30% necrosis bbmapAsset?appID=MDC&isbn=978-1-4160-3623-4&eid=4-u1 copy > Tooth luxation nA. extrusive luxation – partially out of socket nB. intrusive luxation – pulp compression, bone crush nC. lateral luxation – commonly + alveolar bone fracture nComplete luxation (complete avulsion) – entire tooth out of socket bbmapAsset?appID=MDC&isbn=978-1-4160-3623-4&eid=4-u1 copy > Tooth trauma - intrusion nThe missing tooth could be lost, fully intruded, aspirated or swallowed. nupper tooth into maxillary sinus → recurrent sinusitis ninto the nasal cavity → infection or bleeding naspiration into the airway bbmapAsset?appID=MDC&isbn=978-1-4160-3623-4&eid=4-u1 copy > Tooth trauma nDeciduous tooth trauma: typical direction of force in a forward fall (A), the apex of the deciduous tooth levered away from the developing tooth bud (B). n bbmapAsset?appID=MDC&isbn=978-0-323-03228-5&eid=4-u1 copy > Root fracture nMultiple factors affecting healing: location, degree, fragment position and mobility nSterile x infected nSterile: similar to bone fracture healing - organisation of haematoma by granulation tissue → maturation + calcification. nMalposition: fragments rounded, covered by cementum, more or less separated, gaps filled by fibrotic tissue nInfected: abscess, gangrene >