CHAPTER 1 TOOTH ANOMALIES 1. Anomalis of tooth number 1 Supernumerary tooth |A.- 3°60 population, more common in maxi. 8. Most common: mesiodens~ a supernumerary tooth located between tho maxilary cena incisors. ©. Sometimes these supernumerary teeth may block the normal eruption of permanent teth D. Associated syndrome: clidocranil dysplasia (autosomal dominant or mutations), Gardner’s syndrome. (Gominant and vad of soft tise tumer, osteoma, familial adenomatous poyposis and supemumerary teeth) Commonly n maxilla than manelble and more common in permanent F. Tx extraction of supernumerary teeth it a mesiodens is inhibiting development of eruption of other teeth, interering with orthodontic movement, developing pathology around it, or erupting into the nasal caviy (it can happen!) then | would lean towards ‘extraction. If a mesiodens is net interfering with eruption, orthodontic movement, has no pathology, and is asymptomatic, | woud lean towards observation 2 Congentaly missing teeth |A. Complete anodontia: congenital absenes of teeth, generally due to dev abnormalities suchas ectodermal aplasia. (atfectng the development o function of tho tooth, hair, nails and sweat glands 8. Pala: congenital absonce of 1 or more teeth. 4. Hypodonta: congental absence ofa few teth ©. Cigodonta: congenital absence of large numberof toth Most common congenitally missin teth: * molars> mand. 2°! pm > max latrais> max 2°! pm. {3 When 2% pm is missing on one side: wih extraction close the space to make it symmetrical For lateral incisor its much easier than the 2" pm, canine substitution and enamelopasty to ‘make it appoar more like latras or prosthetic replacoment (Maryland fridge) “take note that for primary dentition, the mest common congenital missing primary tooth is Most common ankyosed primary tooth is SiniAnBiAiGU SSSORATRB, which may bo related to common missing teeth of mandibular 2" pm. (succedaneous counterpart) 13 Ectodermal dysplasia: complao or partial anodontia hypodontia, ty, scaly skin, sparse, lanugo> lke ha, dystrophic nals. (loot, exoerine glands, har and nals ar affected). Tx dental implants x prosthotis 2. Anomalies of size: 1 Microdontia ‘A. Generalized: down syndrome , pituitary dwarfism, ectodermal dysplasia. B. Localized. isolated instances are common and include peg-shaped maxillary lateral “pog-shaped are often transmitted as autosomal dominant tat, 2 Macrodontia ‘A. Generalize: ptutary gigantism or pineal hyperplasia with B. Localized: hemifacial hypertrophy, teeth on the affected side are abnormally large compared with the unaffected sid. 3. Anomalies of shapeson and gems: DERE NES, A. Fusion a, 2 tooth buds merge into one tooth b. More common ©. Have confluent dentin but separate canals (ori can be shared) d, As the fused tooth is counted as one, thus the tooth count is one lass than normal B. Conecrescence Fusion of 2 completely formed teeth at their roots . Must have confluent cementum ©. May take place before or after eruption of teeth and is related to trauma or overcrowding. d » Most commonly seen in max 2nd and 3rd molars. Linked to hypercomentosis Germination (twinning) a. Development of 2 crowns from one tooth bud, Share a single root and root canal ©. Tooth count is normal when the tooth is counted as one. ny Dons invaginatus / Dens in dente. ‘A. Caused by invagination of IEE. (later becomes ameloblas!) B. Represents as exaggeration or accentuation of the ingual pit C. The iavagination is lined with enamel, creates a hole in the enamel and forms a tunnel through the tooth, this allow caries to progress very quickly through the tunnel Most common in permanent max. Lateral and central incisors. Bilateral involvement is commonly seen, ‘Should be diagnosed with x a ‘Tx: prophylactic filing ofthe pit, Large invaginations that disrupt normal coronal formation may need to be extracted, endodontic tx for pulptis. ens ivaginatis ons Evaginatus Ungualt exnsion — Sear ni : Dens evaginatus A. Relatively common developmental condition, in which a focal portion of the crown projects outward ‘reating an exa cusp. (The exta cusp contains enamel, dentin and pulp ) B. Affecting predominantly premolar teeth (Leong's premolars), common in Chinese. C. A prominent dens evaginatus often seen on anterior teeth is called a (alo GUS. D. Common in Asians, Inulls and native Americans ° Inim 9. Often bilateral. An anomalous tubercle, or cusp located at the center of the occlusal surface. Due to ‘occlusal abrasion, the tubercle wears relatively fast, and cause early exposure of an accessory pulp horn that extends into the tubercle. F, Typical nial: caries-free teeth often before completion of root dev and apical closure , making root fling ‘more difficult ‘Tx: sealant, pulp capping and partial pulpotomy rae ‘Taurodontism (bull shaped tooth) ‘A.A molar with an elongated root trunk, elongated pulp chamber and short root. 8. Generally occurs in patient with type 4 amelogneesis imperfecta, Kinefelter syndrome (xxv) of Down's syndrome, ‘Supernumerary roots: Accessory roots are most commonly seen in mandibular canines, premolars and molars i A Aovomal bend ot Conia enal prepcans: conmon tor antral tt sctancmebtne ears inih dov. of eons Mos common fond on he Buss a6 oe ans Gran ence a peerer © Grae! decree oaerion ecomencenanal zion war ta talon ©. Gree eam ete wthout ise) Grade oerang the talon rea cate oe ous SV oa rare pat A. A.small focal mass of enamel formed apical to the CE B. Blocking the attachment of Sharpey's fibers.2. Patient wil automatically have a periodontal pocket, as the periodontal ligament attachment will not ‘happen and hygiene would be more dificult. ‘Commonly in bifurcation or trifurcation but can also appear in premolar ai molars AFS ow Commonly affected than mandibular. 4. Defects in the structure Enamel 1 A. Enamel hypoplasia Flue in the apposition stage . Quanttatvely defective enamel but wih Rimalnaranads) . Tumers hypoplasia: periapical infection or vauma to primary tooth causes inflammatory response ‘at messes up ameloblasts of de. permanent tooth > alfa single Tooth, Only involves the permanent teeth Usually on the labial of max incisor or facial of cusp tip of pm Can aso cause hypocaleieation 4. Congenital syphilis Acquired by infected mothe. Hutchinson triad: intesttial Keratis, malformed teeth (Hutchinson incisors and muberr molars), and eighth nerve deainess. 1) Hutchinson’ incisors: rypoplaste notch 1) Mulberry molars: lobular name = Hutchinson’s incisors= hypoplastic notch — Mulberry molars= globular enamel Enamel hypocaletication ‘a, Abnormal mineralization resulting in white spot. 'b. Qualitative defective enamel, with normal amounts of enamel produced but are hypomineralized ©. The enamels softer than normal a. Failure in the maturation stage_(after the apposition)luorosis can cause hypoplasia or hypocaletication. “For systemic factors (suchas infection) to have an eifecton developing permanent teth, the ener mist oeeuratan C. Amelogenesis imperfecta ‘Can be autosomal dominant (mostly), recessive or x inked Intrinsic alteration of enamel, disturbance in bell tae, Trin to no enamel but dentin and pulp are normal 4 types: 1B Type 1: Hypoplast (majority {@_Insufficient amounts of enamel but normal enamel matrix. Banging from pits and groove in one patient to complete absence in another. B Cinically Goneraized: small pits scattered across surfaces of teeth, Localized: large areas of hypoplastic enamel, typically onthe buccal middle 3 ofthe tooth In rough hypoplastic type the enamel is denser than that of the smooth pattern, Xray: Enamel appears normal ‘A relatively thin radiopaque layer of enamel, low or absent cusps, and mutiple open Contacts between the teeth. The anterior teeth on images are said to have a “picket fonco"—type appearance. ee ee ‘Type2/ Hypomaturation (last stage) Adequate deposition and mineralization of enamel matrix but inadequate maturation of crystal structure, Soft enamel and appears less radiopaque compared to dentine on radiographs. Fadiodensiy the same as dentin Creamy opaque to yellow or brown with sensitivity, appear mottled and wear away and break. 8 8 81 Typeavttypocatitied (intial stage) [Normal quantity’ thickness but soft and friable, so it fractures easily and wears readly. “The color varies from tooth to tooth include white opaque to yellow to brown. RX: the is th less than the dentin, Tend to darken with age as a resull of exogenous staining but are not caries prone Tx; focus on esthotic and protection of tooth tissue. (such as full coverage rows) 1 Hypomaturation/hypoplasiatauradontism (type IV) taurodontism, sensitivity of teeth 8 @ Enamel appears mottled and yellowish-brown @ Pits on buccal suraces. Enamel show lower radlolucency a ‘common feature might include- B_Hypoplastic -dominant pattern: thin enamel “Tx: depend on type and degree of Al can be veneers, full crown coverage, overdentures and full dentures. (main objectives ~ pain relief, occlusal vertical height) 1 ane ae estan inte deed pie ponent ‘oth ech comm ora it te t——— rae ed pmlc argectmponinses Harvie! porate ain " ttionacm meshTresor AL Irene Pareen ‘Caen. Fearne Hypoplastic ‘Autosomal dominant ited ‘Autosomal dominant autosomal recessive Locale ‘Autosomal dominant orxnked dominant Smooth ‘Autosomal dominant ough ypomatwraion Autosomal recessive or Xnked recessive Pigmented inked or autosomal dominant Snow capped ypocaicfed Autosomal dominant or autosomal ecessive Coronal enamel et ypamature and Autoromal dominant “uradontem hypoplastic 2 Dentin ‘A. Dentinagenesis imperfecta ‘Autosomal dominant Intrinsic atteration of dentin, bell stage. b. 4. Systemic manifestation: Types Type 1 syndrome-associate: dentin abnormality occurs in patient with concurrent osteogenesis Imperfecta, primary teeth are more severely affected than permanent teeth; mutation in the {gone that encode collagen type t Type 2:patients have only dentin abnormalities and no bone disease. With pronounced cervical constriction, Type 2/ brandywine type: only dentin abnormalties. multiple pulp exposures. periapical tadiolueencies and a variable radiographic appearance, 1 Xray Short roots, belshaped crowns and obliterated pulps (opacification observed In type 1 and 2 due to excessive deposition of abnormal dentin) Type 3: the dentin appears thin and the pulp chambers and root canals are extremely large {iving the appearance of thin dentin shells- shal teeth. (esp. primary tooth) ‘The bullous crowns in radiographs due to consticied DEW, Cinical appearance 1B Tooth color appears yellow. brown to blue-gray discoloration and opalescent Extreme occlusal wear. fractures easily. Excessive CEJ consticion, iL Histologic: smooth DEJ (instead of scalloped in normal), fewer but larger and lrregular dentinal tubules. j. Te full-coverage crowns for esthetics and protection from the wear, but it should not be used as ze abutment.b. a Dentin dysplasia ~ shell teeth, ‘Autosomal dominant All teeth from both dentitions are affected X ray finding: obiterated (X17) pulps, periapical cysts/ granulomas. 1 rootless teeth: more common. (lft Both denttions are of normal color. a {Clinical the crown appears normal in color and shape. Ae obliterated pulps and short root. Pulp chambers are usualy absent except for a chevro shaped remnant in the crown, ‘Type 2: bulbous tooth may also show chevron pul. (right and bottom) {Mutation in dentin silophosphoprotein gene just like dentinogenesis imperfecta 2 and 3. The color of the primary dentition is opalescent, (lue-brown tanslucence), bulbous and the eemanent dentiion ig normal, ‘Tho pulps are filed with globules of abnormal dentin or pulp stones Xray Deciduous tooth ar similar in radiographic appearance to those in DGI type 4. Permanent teeth exhibit enlarged pulp chambers that have thistle tube in appearance ‘roatmentis directed toward retention of test or as ong as possible. However, because ofthe short roots and periapical lesions, the prognosis for prolonged retention is poor. This dental condition has not been associated with any systemic connective tissue problem3 Detects of enamel and dentin- iol BOnIGAyspI, A, GHOST teeth, 'B. volves the hard tissues derived from both epithelial (enamel) and mesenchymal dentin and comentum) ‘components ofthe tooth-forming apparatus C._The teeth in a region oF quadrant ofthe maxilla or mandible are affected to the extent that they exhibit ‘One or both dentin may be affected, and permanent teeth are more affected than the primary teeth, and the maxillary anterior teeth are more affected than others, Eruption o the affected tooth is delayed or does not occur. “Tx: support eruption (to bring healthy alveolar bone) extraction then prosthesis or implant ig 4 Pulp caletieation A. The difuse, o near, deposits are typically found inthe root canals and generally are parallel tothe blood vessels. Pulp stones usually are found in the pulp chamber. When they are composed predominantly of dentin, they are referred to as te demic, B, False denticies: represent foci of dystrophic caleicaion. C. Subdlvided into attached and free type. 5. Acquired anomalies 1 Atttion: physiologic wearing of teeth as a result of mastication ‘A. Factors such as det, dentition, jaw muscularture and chewing habits can influence the pattern and extent of atttion B, Tooth to tooth ©. Common cause: bruxism, poor occlusal contact after dental restoration. D. Clinically: affected site are occlusal surfaces. lingual surfaces of maxillary dentition , and labial surtaces of the mandibular teeth, ‘Tooth wear facets are characterized as flat, round or sharply angled and polished surfaces on the occlusal or incisal areas ‘of the teeth and may be the result of excessive attrition of one tooth against the other. Abrasion and erosion can also ‘contribute tothe excessive wear of the occlusal and incisal suraces. Wear facets usually develop at: Lingual-incisal edge of max. centrals and canines, Facial edge of mand. canines2 Abrasion ‘A. Loss of tooth structure due to abnormal habit or abnormal use of abrasive substances orally B. Pipe smoking, tobacco chewing, aggressive toothbrushing and use of abrasive dontifices, as fingernal iting. ©. Tooth to object. 1D. The damage caused by abrasion is flat unlike V-shaped abfraction, E. Clinical sign sy ‘a, Toothbrush abrasion presents as horizontal notches on the buccal and cervical aspect of the posterior tweth. Exposure of dentin and comentum and gingival recession is common. Biting of nails, pins or pencils can result in Wahaped notches on the incisal edge of the incisors. habits euch as Figure 1616 Aras fem casi wt gar chaning * FAME ET Eeshn atesio ni nso re, 3 Erosion A. Tooth to acid 3. Consumption ofa foods and inks (cilia), ulmi, GERD ing palatal suace cine doesnt corespond to funciona war pans. a Spoorshaped depression re sen in th ceria prion of malar arteritoth Poster tosh show conten losses on he ozclalsulecas. Typical th a SS SBBra@ ince denn reds fat han ene. Inputs, he palatal sues o te marily tet ptcalygresnt wih exposed dentin. (cure onthe tt) _ lr zB } i 4 aston A Noneaous ooh sue oss tht oc along he gingival margin. The damages wedge-shaped or Vshaped an is ulated caves, acter, or fection C. I's caused by friction and pressure on the tooth and gums, which causes the neck of the tooth to start breaking offD. Cause: bruxism, malocclusion, occlusal trauma, ‘5 Treatment ‘A. Prvention through education on proper tooth brushing technniques and nutritional education, B. Tooth structure can be replaced by veneers. crowns or composite resins. . Pathologie occlusions and premature contacts should be addressed, 6. Ankyosis 1 The fusion of a tooth to suroundling bone, Considered tobe ankyiosed when thee is no passive eruption Usually occurs associated with erupted primary molars, it may resul in impaction of a subsequent permanent tooth. [No known cause,May be related to periapical inflammation and subsequent bone repair due to trauma, abnormal pressure form the fongue, disturbances in oot resorption, smaler periodontal ligament gap. 5 Clinical sign and symptoms ‘A. Occlusal plane ofthe affected tooth is below the adjacent tot, B. x [oss of periodontal igament space and evidence of replacement resorption. Ankyioss usualy italy Cccurs on the labial and ngual rot surfaces making radiographic detection inthe early stages dificult Early diagnosis alows the practtioner to plan fo future complications. ©. General symploms include decreased tooth count, abnormal tooth enamel, curving of the fth igi, enlarged lower jaw and abnormal dentition, with decreased tooth count asthe most frequent symptom 1D. Opposing teeth can migrate In vertical dimension, resulting in orverruption. ‘A. Primary dentition: Extraction of the ankylosed teeth and maintained with space maintenance, 'B. When infraocclusion is less than § mm, itis possible to carry out restorative treatment with the use of restorative materials or prosthetic erowms for oestablshing dental occlusion. (Orthodontics associated with luxation -may help to reestablish anew PDL although there aro risks of fracture recurrence of ankylosis and endodontic problems. Ie 7. Hypercementosis 1. Excessive deposition of comentum on the radicular cementum 2 Sis ‘A, Uncomfortable sensation in the tooth followed by an aching pain B. Re a. Apical 2 aro commonly afocted . Thickening ofthe root surrounded by radiolucent periodontal igament space and intact lamina dura 3 Cause: PIG ON TAP P: Ieidiopathic G:gigantsm occlusal trauma NN: nonfunctional tooth truama, A athrits4 Treatment ifficutios A. May interore with extractions, especially if adjacent toeth become fused (concrescence). B. may also result in pulpal necrosis by blocking blood supply via the apical foramen CC. _Dificuty in endodontic x as dificult in assessing the Cementum-Dentin Canal (CDC) junction. 8 Root resorption: progressive loss of dentin and cementum by the action of odontoclast Normal physiologic for exfoliation of the primary dentition. 1 Internal root resorption ‘A. Caused by injury to pulpal tissue related to trauma or caries, orthodontic treatment, cracked teeth, excessive heat generated during restoration, B.Usualy aysmptomatic and identified by chance. CC. Cirical signs and symptoms a. Xray: Woll-ctcumscribed oval or round radiolucency with smooth, well-defined margins in the pulp chamber of root canal. Ballooning out of the root canal b ©. If pulp is stil vital patient may experience symptoms of pulptis. If entire pulp is necrotic then the pationt may experience symptoms of apical periodontitis D. Treatment is aimed at severing the blood supply tothe resorbing tissues by means of conventional root canal treatment (use of ultrasonic irigation and inra-canal medicaments such as Calcium hydroxide will be necessary and flowable obturation materials or MTA in suspected cases of root perforation will bo necessary) E. Extensive resorption can eventually lead to root perforation resulting in the formation of a sinus tract Wich result in poorer prognosis 2 External root resorption (more common) ‘A. More difficult to treat. It tends to be more aggressive, is usually asymptomatic and is characterized by an Invasion of blood vessels and connective tissue into tooth’ root B. Cause:trauma periodontal tx, orthodontics. footh whitening, increase occlusal forces that lead to periradicular inflammation are the most common stimulants of inflammatory resorption (Other uncommon cause include pressure from ectopic teeth, cyst and tumors.©. Can be further classtied into a, laflammatory : following prolonged insult leading to continuing pathologeal resoption such as trauma of damage tothe POL. ». Surface asiont inflammatory resorption: sol.simiting process and soften and incidental Rx finding Undergoes healing after 2-8 weeks of osteodast activity. ©. Cemveal localized resorption lesion on the corvcal area ofthe tooth, below the epithelial attachment. 4. Replacement: occurs following ankylosis of the roots of the alveolar bone. The tooth tissue is resorbed and replaced wih bone. D._ Radiographicaly: moth-eaten loss of root structure, typically in the apex or midroot portion ofthe tooth E. Tic case-dependent, may be elimination of etiologic factors, remave sot tissue adjacent to resoption sito or replacoment of the lost root structures with restorative material last if extensive, extraction 8. Tooth staining 1. Exogenous: tobacco, colfee, red wine, amalgam. bacteria (colored byproducs of chromogenic bacteria in dental plaque). Can be removed with abrasives. Cause oF Sou Stanane Covor ‘CaracaPaesexanon crea Green Frequently seen in cléren. Blac-brown Labial surfaces of maillay anterior teeth green stsins Brown ane block stains typically are sce Orange inthe cervical zone of teeth, either a8 thin Tne slong the Tobecco, tea cafe Brown Lingual surfaces of mandibular anterior teeth Gingival nemortnage Green “wpicaly seen in conjunction with poor thee, hemonfagic and edematous gingiva, Restorative materials Blackegray ‘Adjacent to large lass ll amalgam ‘estrations or deep lingual metalic restorations. ee sem = Seine Figen onan Peete cae Sts outs paw cal ope nor Not carmen in citon—_Ppr ae ce o eh camet pa ow pape ‘Shoveolakto ed sapling Stones wo ‘pro wer maga fom ros i, fonlad rest wpe me ar reins sd pling (eo. ne att tues Valor tou niente ig Troe Ghana nc as te eng ong Creme nae Peles ag prove gin ‘eapaldungee Gert ene mh pees hegre naar erat tnd Peles les an ‘ea oug fetter Ch tes dese alg ‘atari er) ling 2 Intrinsic sources: amgelogenesis and denitogenesis imperfecta, flurorsis medications. A, Deposits of systemically circulating substances during tooth development is defined as endogenous or intrinsic staining B. Tetracycline should not be prescribed for children younger than 7 years except in unusual circumstancesE Biliary atresia: a blockage in the tubes (ducts) that carry bile from the liver tothe gallbladder . Congenital condition occurs, ‘a. Appear as fluorescent yellow. Exposure to sunlight, though, causes a change in color, and the teeth become brownish or grayish over time. . Since sunlight affects final tooth color, anterior teeth Bh incompatibiity/erythroblastosis fetalis - cause endogenous staining in primary teeth due to red blood call hemolysis resulting from maternal antibody destruction of fetal REC. Due to the biiubin the teeth appear green to brown. — only primary teeth are affected, Congenital porphyria a. errors of porphyrin metabolism, autosomal ~ recessive walt is associated with photosensitivity, vesiculobullous skin eruption, red urine and splenomegaly Appear red to brown because of deposition of porphyrin in the developing teeth ©. Clincal:fluroesce red with ultraviolet light Liver disease, bilary atresia (green) and neonatal hepatts(yellowish-brown) may produce discoloration of the primary dentition ‘snot uncommon to have greater discoloration inthe front or ‘when the bile duets inside or outside the liver do not develop normally. + Figure 16-47 Tetacjeine stn Not the yotow exer Cataoy ofthe postr txt an te 1a clr of be startet, a ‘hich onto of endogenous tearyelne hs ooained (Cause oF Sram ‘Srunanc Coton CCunteat Presextamion Congenital eywopoietic porphyria Reds-brown Red fluorescence on expasure to Wood's ultraviolet ht. Hypebilrbinemia ‘Green "wicaly during the neonatal period of conditions Groysh blue ‘ke erythroblastosis fetalis and biliary atresia Dertinogenesisimperteta Grey Radiographic appearance of shell teth with normal ‘Blish-beown thickness enamel and thin dentin. “anslucent or opalescent Fotos ‘Occurs ding 2nd and 3rd years of He with ‘exposure to furide levels > part per milion. Medications ‘Tetraqtine expose