Abnormalities of Teeth PDF

Abnormalities of teeth Dr Yohannes 1  Abnormalities teeth  Environmental & developmental alterations  Environmental - Environmental effects on tooth development - Post developmental structure loss - environmental discolorations of teeth - Localized...

Abnormalities of teeth Dr Yohannes 1  Abnormalities teeth  Environmental & developmental alterations  Environmental - Environmental effects on tooth development - Post developmental structure loss - environmental discolorations of teeth - Localized disturbances in eruption 2  Cont.  Developmental alterations – - in number - size - shape - structure 3  Environmental effects on tooth development Clinical features  3 patterns – hypoplasia, diffuse opacities & demarcated opacities  The tooth has to be viewed after cleaning & drying & in the dental operatory light  Hypoplasia – as pits, grooves or large areas of enamel defects 4 5  Cont.  Diffuse opacities – normal thickness of enamel with but it is more opaque than normal & there is no clear boundary with the normal enamel  Demarcated opacities – areas of increased opacity with sharp boundary with the adjacent enamel & the opacity may have white, yellow, brown or cream color 6  Types  Turner's hypoplasia  Hypoplasia caused by antineoplastic therapy (radiation)  Dental fluorosis  Syphilitic Hypoplasia 7  Turner's hypoplasia  Enamel defect seen in permanent tooth due to the periapical inflammation of overlying deciduous tooth due to caries or trauma & the affected tooth is called Turner's tooth  There can be local areas of brown, yellow or white color or may affect the whole crown 8  Cont.  Commonly affects the premolars (caries) & Maxillary central incisors (trauma)  Turner’s hypoplasia depends on the stage of tooth development, length of time infection remains untreated, virulence of organism, resistance of host  The trauma or infection of the deciduous tooth may cause dilaceration of crown or root 9 10  Hypoplasia caused by antineoplastic therapy  Hypodontia  Microdontia  Radicular hypoplasia  Enamel hypoplasia  Mandibular hypoplasia 11  Dental fluorosis  White chalky areas of enamel with yellow or dark brown discoloration  Sometimes deep, irregular, brown pits  Usually bilaterally symmetrical 12 13  Syphilitic Hypoplasia  Hutchinson's incisors - shaped like straight- edge screwdrivers with the greatest circumference present in middle one third of crown and a constricted incisal edge.  The middle portion of incisal edge often demonstrates a central hypoplastic notch.  Altered posterior teeth are termed mulberry molars. 14 15  Treatment:  Acid- etched composite resin restorations.  Labial veneers  Full crowns 16  Post developmental loss of tooth structure  Tooth wear  Internal & external resorption 17  Tooth wear  It is a normal physiologic process that occurs with aging but must be considered pathologic when the degree of destruction creates functional, aesthetic or dental sensitivity problems.  Causes: Attrition, Abrasion, Erosion & abfraction 18  Attrition  It is the loss of tooth structure caused by tooth-to tooth contact during occlusion & mastication.  Tooth destruction can be accelerated by: Poor quality or absent enamel (Fluorosis), Premature contacts (Edge to edge occlusion) & grinding habits. 19  Cont.  Clinical Features: occur in both dentitions - Most frequently incisal & occlusal surfaces are involved - sometimes labial of lower anteriors & lingual of upper anteriors - Large, flat, smooth and shiny wear facets are found in a relationship that corresponds to the pattern of occlusion. 20  Cont. - Inter proximal contact points also are affected from vertical movement of teeth during function which may cause decreased arch length - pulp exposure & dentin sensitivity are rare because of the slow process 21 22  Abrasion:  It is pathologic loss of tooth structure or restoration secondary to action of an external agent.  Cause: Tooth paste with heavy pressure and a horizontal brushing stroke, Pencils, Tooth picks, Pipe stems, Chewing tobacco & hair pins  Clinical features - Usually have sharply defined margins & a hard, smooth surface 23  Cont.  Tooth brush abrasion typically appears as horizontal cervical notches on buccal surface of exposed radicular cementum & dentin.  Most common in cuspids, bicuspids and teeth adjacent to edentulous and on side of arch opposite dominant hand.  Use of pipes or bobby pins usually produces rounded or V-shaped notches in the incisal edges of anterior teeth. 24 25  Erosion:  It is loss of tooth structure caused by a chemical process beyond that associated with bacterial interaction with tooth  Causes: Acids, Chelating agents, Medications (e.g. chewable vitamin, Aspirin tab.), Swimming pools with poorly monitored pH, c/c regurgitation (bulimia, pregnancy, alcoholism) & Industrial environmental exposure. 26  Cont.  Clinical features - Commonly affects facial surfaces of maxillary anteriors & appears as shallow spoon-shaped depressions in the cervical portion of crown.  When palatal surfaces are affected, exposed dentin has a concave surface and shows a peripheral white line of enamel. 27  Cont.  Active areas are clean unstained areas  Erosion limited to the facial surfaces of maxillary anterior dentition often is associated with dietary sources of acid.  When the tooth loss is confined to incisal portions of anterior dentition of both arches, an external environmental sources is suggested. 28  Cont.  When erosion is located on palatal surfaces of maxillary anterior teeth and occlusal surfaces of posterior teeth of both dentitions, regurgitation of gastric secretions is a probable cause. 29 30  Abfraction:  The loss of tooth structure that results from respected tooth flexure caused by occlusal stresses (enamel is having less tensile strength)  Abfraction appears as wedge-shaped defects limited to cervical area of teeth.  Defects that are deep, narrow & V-shaped & often affect a single tooth with adjacent unaffected teeth. 31  Cont.  Lesion are seen in facial surface,  Common in mandibular teeth  More in patients with bruxism (more lingual inclination of teeth) 32 33  Treatment  Removal of cause  Mouth guards  Mouth washes, varnishes, tooth pastes containing stannous fluoride, and mono- fluorophosphates.  Glass ionomer restoration.  Composite resins, and full crown. 34  Internal & External Resorption  Resorption by the cells located in the dental pulp is called internal resorption.  Resorption by the cells located in periodontal ligament is called external resorption.  Internal resorption is caused by physical injury to pulp tissue, trauma, caries-related pulpitis. 35  Cont.  Factors associated with external resorption  - Cysts & tumors  - Dental trauma  - Periradicular inflammation  - Hormonal imbalances  - Excessive mechanical forces (e.g. orthodontic therapy) 36  Cont.  2 types of resorption – inflammatory & replacement resorption  Inflammatory – resorbed area is replaced by granulation tissue  Replacement - resorbed area is replaced by bone or cementum 37  Cont.  Clinical features - Internal resorption: Pain if there is pulpal inflammation & if coronal pulp is involved crown will have pink discoloration. (pink tooth of Mummery)  Radiographic features - well- circumscribed symmetric radiolucent enlargement of pulp chamber or canal.  External resorption - appears as a "moth-eaten" in radiolucency in radiograph. 38 39 40 41  Cont.  Usually seen in apical area of root.  Histopathologic Features: In internal resorption, pulp tissue in area of destruction is vascular & exhibits increased cellularity.  Adjacent to dentinal wall are numerous multinucleated dentinoclasts.  External resorption similar to internal resorption with numerous multinucleated dentinoclasts 42  Cont.  Treatment: Internal resorption- endodontic treatment or extraction if radicular perforation occurred  External resorption- removal cause & restoration of the lost tooth part after removing the soft tissues 43  Environmental discoloration of teeth  Two types - Extrinsic & intrinsic stains  Extrinsic stains: Causes:- Bacterial stains - Iron - Tobacco - Foods & Beverages - Gingival hemorrhage - Restorative materials. 44  Cont.  Clinical features: Chromogenic bacteria produce green or black- brown orange stains, - Most frequently in children. - Usually seen in maxillary anterior teeth in gingival 1/3 {ferrous sulfide = H2S (bacteria) + Fe (saliva or crevicular fluid). 45  Cont.  Iron – black discoloration  Tobacco stain – brown discoloration commonly involve lingual surface of mandibular incisors.  Beverages stain are also involve lingual surface of anterior teeth.  Foods with chlorophyll may cause green discoloration 46 47  Cont.  Gingival hemorrhage – green discoloration in patients with poor oral hygiene& erythematous enlarged gingiva  Dental restorative materials, especially amalgam in black-gray discolorations of teeth  Treatment: Polishing with fine pumice powder or 3% hydrogen peroxide with pumice powder - removal of the cause. 48 49  Cont.  Intrinsic stains: Causes:- Amelogenesis imperpecta - Dentinogenesis imperpecta - Dental fluorosis - Erythropoietic porphyria - Hyperbilirubinemia - Trauma - Medications 50  Cont.  Clinical Features: Congenital Erythropoietic porphyria - diffuse reddish- brown discoloration. - Deciduous teeth have more discoloration (both enamel & dentin are affected but in permanent only enamel is affected)  Hyperbilirubinemia - deciduous teeth have more discoloration 51 52  Cont. - yellow to green discoloration (biliverdin) - usually a sharp dividing line separating the discoloration  Trauma - dark-gray discoloration due to pulpal damage - temporary pink discoloration after 2-3 weeks of trauma due to vascular damage which turns back to normal in 3 weeks 53  Cont. - yellow discoloration – due to calcific metamorphosis of pulp in later stages  Medications – Tetracycline - bright yellow to dark brown - minocycline – blue gray discoloration 54 55  Cont.  Treatment: External bleaching of vital teeth. - Internal bleaching for non vital teeth. - Composite buildups - Veneer crowns - full crowns. 56  Localized Disturbances in Eruption:  Ankylosis: Cessation of eruption after emergence is termed ankylosis  There is fusion of cementum or dentin to alveolar bone  Causes: Trauma - Injury - Chemical or thermal irritation - Local failure of bone growth. - Abnormal pressure from tongue 57  Cont.  Clinical Features: Most commonly involved tooth is primary first molar - Majority of cases occur in mandible. - The occlusal plane of involved tooth is below that of the adjacent dentition. - A sharp, solid sound may be noted on percussion of the involved tooth. Radiographic features; Absence of periodontal ligament space 58  Cont.  Complications – adjacent teeth incline towards the affected tooth, over eruption of opposing tooth causing periodontal problems & impaction of underlying permanent tooth  Treatment: Extraction & space maintenance  If underlying permanent tooth is absent fabrication of crown 59 60 Developmental alteration in number of teeth  Hypodontia  Hyperdontia 61  Hypodontia  Less number of teeth which are congenitally missing  More common in females  Associated with hereditary ectodermal dysplasia  Causes – trauma, infection, medications, endocrine disturbances causing damage to dental lamina 62  Cont.  Not common in deciduous dentition. if present common on mandibular incisors  Oligodontia – lack of development of more than 6 teeth  In permanent dentition, 3rd molars, 2nd premolars & lateral incisors are commonly affected  Treatment – replacement of missing teeth 63 64  Hyperdontia  More number of teeth  Caused by development of excess dental lamina  Additional tooth - supernumerary teeth  Occurs more frequently in permanent dentition  More in maxillary anterior region  Male predominance 65  Cont.  Supernumerary tooth in maxillary anterior incisor region –mesiodens  Accessory 4th molar – distomolar or distodens  Posterior supernumerary tooth situated lingually or buccally to a molar tooth – paramolar  Teeth in newborn – natal teeth 66 67  Cont.  Teeth erupting in 30 days of life is neonatal teeth  Treatment – extraction -natal teeth – extraction if mobile 68 69 Developmental alterations in size of teeth  Microdontia  Macrodontia 70  Microdontia  Small teeth  Relative microdontia – normal sized teeth appears small if widely spaced in arch which is larger than normal  True diffuse microdontia in Down’s syndrome & pituitary dwarfism  Associated with hypodontia  More in females 71 72  Cont.  Isolated microdontia is common in maxillary lateral incisor (peg shaped – proximal surfaces converge to the incisal edge) also in 3rd molars  Treatment – restoration to the original size 73 74  Macrodontia  Larger teeth  Relative macrodontia – normal sized teeth in small jaws with crowded teeth  True macrodontia I in pituitary gigantism, pineal hyperplasia with hyperinsulinism & unilateral hemi hyperplasia  Seen in association with hyperdontia  More common ion males 75 Developmental alterations in shape of teeth  Gemination  Fusion  Concrescence  Accessory cusps  Dens invaginatus  Ectopic enamel  Taurodontism  Hypercementosis 76  Cont.  Accessory roots  Dilaceration 77  Gemination  An attempt of a single tooth bud to divide with resultant formation of a tooth with bifid crown & a common root & root canal  Appears both in primary & permanent dentition  More in anterior maxillary region  Treatment – in deciduous dentition – extraction to prevent malocclusion - permanent dentition – endodontic treatment & full crown 78 79  Fusion  Union of 2 normally separated tooth buds with the resultant formation of a joined tooth with confluence of dentin  Appears both in primary & permanent dentition  More in anterior maxillary region  Separate root canals are present  Treatment – endodontic treatment & full crown 80 81  Concrescence  Union of 2 teeth by cementum without confluence of dentin  More common in maxillary posterior region  Caused by inflammation  Treatment – if interferes with eruption extraction 82 83  Accessory cusps  Cusp of carabelli  Talon cusp  Dens evaginatus 84  Cusp of carabelli  Accessory cusp located on palatal surface of mesiolingual cusp of maxillary molar  Seen in deciduous & permanent dentition  When present it is more obvious on 1st molar  Tooth will be larger than normal mesiodistally  Treatment – deep groove b/w cusp of carabelli & mesiolingual cusp is sealed 85 86  Talon cusp  Additional cusp located on the surface of anterior tooth & extends half the distance from cementoenamel junction to incisal edge  Seen in permanent dentition (maxillary lateral & central incisors)  Resembles an eagle’s talon  Associated with Rubin stein taybi & Sturge Weber syndrome 87 88  Cont.  Radiographic features - cusp is seen overlying the central portion of crown including enamel & dentin  Treatment – periodic grinding if interferes with occlusion - at the end of each session of grinding fluoride varnish is placed to prevent sensitivity - after finishing grinding either ca hydroxide or composite is placed  If deep fissure is present b/w talon’s cusp & tooth it should be restored 89  Dens evaginatus  Cusp like elevation of enamel located in central groove or lingual ridge of buccal cusp of permanent premolar or molar teeth  Usually bilateral in mandible  Consists of enamel, dentin & pulp  Radiographically there is pulpal extension into the tubercle  Treatment – occlusal interference is removed 90 91  Dens invaginatus (dens in dente)  Deep surface invagination of crown or root which is lined by enamel  2 forms – coronal & radicular  Coronal - commonly affects permanent maxillary lateral incisors, central incisors, premolars, canines & molars - invagination varies from slight enlargement of cingulum pit to a deep infolding that extends to apex 92  Cont.  Before eruption it is filled with soft tissue  3 types  Type 1 – invagination confined to the crown  Type 2 – extends below CEJ with or without communication with the pulp  Type 3 – extends through the root & perforates in apical or lateral radicular area without communication with pulp, 93 94  Cont. - close to the radicular perforation usually enamel is replaced by cementum  Radiographically there is invagination lined by radiopaque enamel  Radicular – arises secondary to proliferation of Hertwig`s root sheath with a strip of enamel extending along the root surface 95 96  Cont.  Radiogarphically – invagination in root lined by enamel with opening along the lateral aspect of root  Treatment – if there is no pulpal involvement it can be restored with calcium hydroxide base - if pulp is involved endodontic therapy 97  Ectopic enamel  Presence of enamel in unusual locations mainly the tooth root  Widely known as enamel pearls  Produced from the bulging of odontoblastic layer which causes prolonged contact with Hertwig`s epithelial root sheath which causes developing dentin, triggering enamel formation 98 99  Cont.  Consists entirely of enamel or enamel, dentin & pulp  More common on the roots of maxillary molars  Usually seen near the furcation area  Radiographically – well defined radiopaque nodules along the root surface  Treatment – maintenance of oral hygiene to prevent attachment loss 100  Taurodontism  It is an enlargement of body & pulp chamber of multirooted tooth with apical displacement of pulpal floor & bifurcation of roots  Affect more commonly permanent tooth especially molars with increasing severity in last molars & decreasing towards the 1st molar  Tooth is commonly rectangular in shape 101  Cont.  Pulp chamber is having more apico - occlusal height  Depending on the severity it is classified as hypo, meso & hypertaurodontism  Treatment – no treatment 102 103  Hypercementosis  Non neoplastic deposition of excessive cementum that is continuous with the normal radicular cementum  Radiographically – thickening or blunting of root & normal periodontal ligament space & lamina dura around the root  Most common in premolars 104 105  Cont.  Factors associated with hypercementosis – local – occlusal trauma, inflammation, unopposed tooth) - systemic – Paget’s disease, pituitary gigantism, acromegaly  Histopathologic features – excessive amount of cementum on the periphery of root over the original layer of primary cementum 106  Cont. - the excessive cementum is cellular  Treatment – no treatment - extraction may be difficult 107  Dilaceration  Abnormal angulation or bend in the root  Usually arise after an injury that displaces calcified portion of tooth germ & remainder of tooth is formed at an abnormal angle  Common in maxillary permanent incisors  Treatment – dilacerated deciduous teeth usually retains, so extraction to help the permanent tooth to erupt - excessively deformed roots – extraction 108 109  Supernumerary roots  Development of an increased number of roots  Usually involve both the dentition  Commonly affect 3rd molars  Radiographically small additional root is superimposed over the normal root  Treatment – no treatment 110 111  Developmental alterations in structure of teeth  Amelogenesis imperfecta  Dentinogenesis imperfecta  Dentin dysplasia type І  Dentin dysplasia type ІІ  Regional odonto dysplasia 112  Amelogenesis imperfecta  Defective enamel formation  Both deciduous & permanent dentition are affected  3 types – 1.Hypoplasia- defective elaboration of enamel matrix 2. Hypocalcification – defective mineralization 3. Hypomaturation – defective maturation of enamel 113  Hypoplastic Amelogenesis imperfecta  Generalized – pinpoint to pinhead sized pits are scattered across the surfaces of teeth - pit may be stained - buccal surfaces of the teeth are affected more - enamel b/w pits are normal 114 115  Cont.  Localized – horizontal rows of pits, linear depression, one large area of hypoplastic enamel surrounded by a zone of hypocalcification - altered area is located on the middle 1/3 of the buccal surface 116  Cont.  Smooth pattern – enamel of all teeth exhibits smooth surface & thin, hard & glossy enamel - open contact points - color of teeth are opaque white to translucent brown - anterior open bite - Radiographically – thin radiopaque outline of enamel 117  Cont.  Rough pattern – thin, hard & rough surfaced enamel - Teeth tapering towards the incisal or occlusal surface - open contact points - color varies from white to yellow white - anterior openbite - radiographically – thin outline of enamel 118  Cont.  Enamel agenesis – total lack of enamel formation - teeth have color & shape of dentin with yellow to brown hue - Open contact points - crowns taper towards incisal or occlusal surface - surface dentin is rough 119  Cont. - anterior openbite - Radiographically – no peripheral enamel over dentin  Treatment – full crown or full denture 120 121 Hypomaturation amelogenesis imperfecta  Exhibit mottled, opaque white - brown - yellow discoloration  Enamel is softer than normal & tends to chip from underlying dentin  Radiographically affected enamel exhibits a radiodensity that is similar to dentin  Pigmented pattern - surface enamel is mottled & agar brown 122  Cont. - Enamel often fractures from underlying dentin & is soft enough to be punctured by a dental explorer - Anterior open bite  Snow capped pattern – zone of white opaque enamel on the incisal ¼ - 1/3 of crown 123 124 Cont. 125  Cont. - both dentitions are affected  Treatment – full crown or full dentures 126 127  Hypocalcified amelogenesis imperfecta  Enamel is very soft & easily lost  On eruption enamel is yellow - brown or orange, but it often becomes stained brown to black & exhibits rapid calculus apposition  Cervical portion is calcified better  Anterior open bite  Radiographically - density of enamel & dentin are similar 128  Cont.  Treatment - Aesthetic crown - Full denture 129  Hypomaturation- hypoplastic amelogenesis imperfecta  Mottled yellowish white to yellowish brown enamel  Pits may be there on the buccal aspect  Radiographically – enamel is having the same density as dentin  There may have taurodontism  Treatment – full crown or denture 130  Dentinogenesis Imperfecta  Developmental defect of dentin  Also known as hereditary opalescent dentin  It may associated with osteogenesis imperfecta  Clinical & radiographic features - - Teeth in both dentitions are affected - Deciduous teeth are more affected 131  Cont. - The dentitions have a blue - to - brown discoloration with translucence - Enamel frequently separates easily from underlying defective dentin - Attrition  Radiographically - teeth have bulbous crowns , cervical constriction , thin roots & early obliteration of root canals & pulp chambers 132  Cont.  Dentinogenesis imperfecta 1 - osteogenesis imperfecta with opalescent teeth  Dentinogenesis imperfecta 2 - isolated opalescent teeth  Shell teeth - normal thickness enamel in association with thin dentin & enlarged pulps - Most frequently in deciduous teeth 133 134  Cont.  Histopathologic features - Short misshapen tubules course through an atypical granular dentin matrix with interglobular calcification  Treatment - overdentures - composite restoration in areas of occlusal wear 135 136  Dentin Dysplasia  Dentin dysplasia type 1 - Referred by rootless teeth or radicular dentin dysplasia - Enamel & coronal dentin are normal clinically & well formed - The radicular dentin organization is lost early in tooth development with markedly deficient roots 137  Cont. - Severity depends on the disorganization that occurs in which stage of tooth development - Extreme tooth mobility & premature exfoliation - tendency for root # during extraction - periapical lesions appears without deep caries 138 139  Cont.  Radiographically little or no detectable pulp & roots are markedly short or absent - later disorganization results in crescent shaped pulp chambers with short roots & without pulp canals - in milder forms there is normal pulp chamber with a large pulp stone 140  Cont.  Histopathologic features – apical to the disorganization, central portion of root forms whorls of tubular dentin & atypical osteodentin giving appearance of a “ stream flowing around boulders  Treatment - Oral hygiene to prevent caries - endodontic therapy 141 142  Cont.  Dentin dysplasia type 2  Also known as coronal dentin dysplasia  Normal root length  Clinical features – deciduous teeth have blue - to - amber- to brown translucence  Radiographically – Deciduous teeth - bulbous crowns, cervical constriction, early obliteration of pulp & thin roots 143 144  Cont. - permanent teeth - pulp chambers exhibit enlargement & apical extension (thistle tube shaped or flame shaped)  Histopathologic features – - deciduous teeth – same as dentinogenesis imperfecta - permanent teeth - radicular dentin is tubular, amorphous & hypertrophic 145  Cont.  Treatment - oral hygiene maintenance - endodontic therapy 146  Regional Odontodysplasia  It occurs both dentitions  Commonly affect maxillary anterior teeth  Small irregular crowns that are yellow to brown with a very rough surface  Pulpal necrosis is common because of dentinal clefts &long pulp horns  Many of the affected teeth do not erupt  Early exfoliation 147  Cont.  Erupted teeth have small irregular crowns with yellow to brown color & rough surface  Caries & periapical infection are common  Radiographically - Extremely thin enamel & dentin surrounding an enlarged radiolucent pulp (ghost teeth) - lack of contrast b/w enamel & dentin 148 149  Cont.  Histopathologic features – enamel is irregular & lack laminated appearance - dentin have clefts & tubular dentin & scattered cellular inclusions - pulp have free or attached stones  Treatment – endodontic therapy if sufficient hard tissue is available - if teeth are not restorable - denture 150