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Abnormalities of the Teeth Advanced Oral Pathology

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1 Abnormalities of the Teeth Advanced Oral Pathology

2 Environmental Effects on Tooth Structure Development

3 Environmental Effects on Tooth Structure Development
Visible environmental enamel defects can be classified into one of three patterns: Enamel hypoplasia – pits, grooves, or larger areas of missing enamel Diffuse opacities of enamel – variations in translucency or normal thickness; increased white opacity with no clear boundary with adjacent normal enamel Demarcated opacities of enamel show areas of decreased translucence, increased opacity, and a sharp boundary with adjacent enamel; normal thickness

4 Environmental Effects on Tooth Structure Development
Common pattern, occurs as result of systemic influences (such as exanthematous fevers) which occur during the first two years of life; horizontal rows of pits or diminished enamel on anterior teeth and first molars; enamel loss is bilateral Similar pattern in cuspids, bicuspids, and second molars when the inciting event occurs at age 4-5

5 Enamel Hypoplasia associated with exanthematous fevers

6 Turner’s Hypoplasia (1)
Secondary to periapical inflammatory disease of the overlying deciduous tooth Enamel defects vary from focal areas of white, yellow or brown to extensive hypoplasia involving the entire crown. Most frequently affects permanent bicuspids Traumatic injury to deciduous teeth also causes Turner’s teeth (45% of children sustain injuries to primary teeth)

7 Turner’s Hypoplasia (2)
Trauma can displace the already formed hard tooth substance in relationship to the remaining soft tissue for root formation causing dilaceration (a bend in the tooth root) Severe trauma early in tooth development can cause disorganization of the bud resembling a complex odontoma. Severe trauma later on can lead to partial or total arrest of root formation.

8 Turner’s Hypoplasia

9 Turner’s Hypoplasia

10 Hypoplasia Caused by Antineoplastic Therapy
Degree and severity related to age, form of therapy (chemotherapy/radiotherapy) and dose Defects include hypodontia, microdontia, radicular hypoplasia, enamel hypoplasia and discolorations Radiotherapy effects more severe than chemotherapy alone but sometimes used together Dose of radiation as low as 0.72 Gy can cause mild defects in enamel/dentin Mandibular hypoplasia due to direct radiation, alveolar deficiency or pituitary effects.

11 Hypoplasia Caused by Antineoplastic Therapy

12 Dental Fluorosis Critical period is age 2-3, if fluoride levels greater than 1 part per million are ingested Fluoride comes from several sources besides water: adult-strength fluoride toothpastes, fluoride supplements, infant foods, soft drinks, and fruit juices Severity is dose dependent (higher intakes during critical periods associated with more severe fluorosis)

13 Dental Fluorosis

14 Dental fluorosis

15 Syphilitic Hypoplasia
Mulberry molars – constricted occlusal tables with disorganized surface anatomy resembling surface of a mulberry Anterior teeth called Hutchinson’s incisors, have crowns shaped like straight-edge screwdrivers; incisal taper & notch Treatment - Most are cosmetic problems; treatment includes acid-etched composite resin restorations, labial veneers, and full crowns

16 Hutchinson’s triad

17 Syphilitic Hypoplasia
Moon’s (mulberry) molars Hutchinson’s incisors

18 Postdevelopmental Loss of Tooth Structure: Attrition
Loss of tooth structure caused by tooth-to-tooth contact during occlusion and mastication. Pathologic when it affects appearance and function. Process can be accelerated by poor quality or absent enamel, premature edge-to-edge occlusion, intraoral abrasives, erosion, and grinding habits.

19 Attrition Can occur in deciduous and permanent dentitions
Most frequently, incisal and occlusal surfaces involved Large flat wear facets found in relationship corresponding to pattern of occlusion Interproximal contact points also affected Over time, interproximal loss can result in shortening of arch length

20 Postdevelopmental Loss of Tooth Structure: Attrition

21 Postdevelopmental Loss of Tooth Structure: Abrasion
Pathologic loss of tooth structure secondary to the action of external agent Most common source is tooth brushing with abrasive toothpaste and horizontal strokes. Also pencils, toothpicks, pipe stems, bobby pins, chewing tobacco, biting thread, inappropriate use of dental floss

22 Abrasion Variety of patterns, depending on the cause
Toothbrush abrasion presents as horizontal cervical notches on buccal surface of exposed radicular cementum and dentin; degree of loss greatest on prominent teeth Thread-biting, pipe stem, bobby pins etc., produce rounded or V-shaped notches in incisal edges of anterior teeth Dental floss, toothpicks result in loss of interproximal radicular cementum and dentin

23 Abrasion

24 Abrasion Abrasion from partial clasp Abrasion from improper flossing

25 Postdevelopmental Loss of Tooth Structure: Erosion
Loss of tooth structure by chemical reaction, not that associated with bacteria (caries) Secondary to presence of acid or chelating agent Source can be dietary (e.g., vinegar, lemons), internal (gastric secretions – perimolysis), or external (e.g., acids, industrial, atmosphere) “If it is not abrasion or attrition, it must be erosion”

26 Erosion Commonly affects facial surface of maxillary anteriors and appears as shallow spoon-shaped depressions in cervical portion of the crown Posterior teeth exhibit loss of occlusal surface, where dentin is destroyed more rapidly than enamel, resulting in concave depression of dentin surrounded by elevated rim of enamel Erosion limited to facial surfaces of maxillary anterior dentition is usually associated with dietary acid.

27 Erosion Tooth loss confined to incisal portions of anterior dentition of both arches indicates environmental source. Erosion on palatal surfaces of maxillary anterior teeth and occlusal surfaces of posterior teeth of both dentitions probably caused by regurgitation of gastric secretions.

28 Erosion Fizzy Drinks Are Major Cause of Teen Tooth Erosion Thu Mar 11, 7:06 PM ET LONDON (Reuters) - Fizzy drinks are the major cause of tooth erosion in British teenagers but many parents are not aware of the problem, researchers said on Friday.    The sodas and pop drunk by up to 92 percent of UK 14-year-olds wear away the enamel protective coating on teeth. Dental erosion weakens teeth and can cause thinning or chipping of the tooth edges. "This research identifies fizzy drink as by far the biggest factor in causing dental erosion among teenagers," said Dr Peter Rock, of Birmingham University. "Drinking fizzy drinks only once a day was found to significantly increase a child's chances of suffering dental erosion," he added. Drinking four or more glasses of fizzy drinks a day raises a 12-year-old's chances of suffering from tooth erosion by 252 percent. Heavy consumption in 14-year-olds increased the risk to 513 percent, according to research published in The British Dental Journal. Unlike tooth decay, which results from high levels of sugar, erosion is caused by acidic substances in the drinks. Even diet versions are harmful. Drinking milk and water, instead, reduces the risk. "Erosion is a growing problem among British teenagers, yet many parents don't understand the difference between decay and erosion," said Professor Liz Kay of the British Dental Association. "Parents need to is the acidity of certain products that cause erosion," she added in a statement.

29 Erosion

30 Postdevelopmental Loss of Tooth Structure: Abfraction
Loss of tooth structure resulting from repeated tooth (enamel & dentin) flexure produced by occlusal stresses Disruption of chemical bonds at cervical fulcrum leads to cracked enamel that can be vulnerable to abrasion and erosion

31 Abfraction Wedge-shaped defects limited to cervical area
Deep, narrow, V-shaped Sometimes single tooth or subgingival More common in mandibular dentition and among those with bruxism

32 Abfraction

33 Treatment of Postdevelopmental Loss of Tooth Structure
Early diagnosis and intervention to restrict severity of tooth loss Patient education Mouth guards Limit (redirect) tooth brushing & flossing Replacement of lost posterior teeth and avoidance of edge-to-edge occlusion Composite resins, veneers, onlays, full crowns

34 Internal & External Resorption
Internal resorption is caused by cells located in dental pulp. Rare, usually follows injury to pulpal tissues. External resorption is caused by cells in the periodontal ligament. Most patients are likely to have root resorption on one or more teeth.

35 Internal Resorption Internal resorption presents as a uniform, well-circumscribed symmetrical radiolucent enlargement of pulp chamber. When it affects the coronal pulp, crown can display pink discoloration (pink tooth of Mummery)

36 External resorption External resorption presents with a “moth-eaten” loss of root structure in which radiolucency is less well-defined and demonstrates variations in density. Most cases of external resorption involve apical or mid-portions of root

37 Internal & External Resorption
Cervical pattern of external resorption is often rapid (invasive resorption) Multiple idiopathic root resorption – involves several teeth, underlying cause not obvious Treatment involves the removal of all soft tissue from sites of dental destruction. For external resorption, determine if an accelerating factor is present, and eliminate it.

38 Internal & External Resorption
Internal resorption Internal resorption External resorption-- embedded tooth

39 Environmental Discoloration of Teeth

40 Environmental Discoloration of Teeth: Extrinsic
Arise from surface accumulation of exogenous pigment Bacterial stains – occur most frequently in children Excessive use of tobacco, tea, coffee Foods that contain abundant chlorophyll Restorative materials, especially amalgam Medications Stannous fluoride and chlorhexidine Extrinsic stains can be removed by polishing with fine pumice, (sometimes with added 3% hydrogen peroxide); recurrence is likely unless the associated cause is altered

41 Environmental Discoloration of Teeth: Extrinsic
Amalgam stain Tobacco stain

42 Environmental Discoloration of Teeth: Intrinsic
Secondary to endogenous factors that discolor underlying dentin Congenital erythropoietic porphyria (Günther’s disease) is an AR disorder of metabolism that results in increased synthesis and excretion of porphyrins Hyperbilirubinemia due to jaundice, erythroblastosis fetalis (hemolytic anemia of newborns secondary to blood incompatibility, usually Rh factor), biliary atresia (sclerosing process of the biliary tree), and chlorodontia (green discoloration).

43 Environmental Discoloration of Teeth: Intrinsic
Localized red blood cell destruction (pink discoloration arising from hemoglobin breakdown within necrotic pulp tissue when blood has accumulated in the head) Lepromatous leprosy (pink discoloration secondary to infection-related necrosis and the rupture of numerous small blood vessels within the pulp Medications (tetracycline) Intrinsic stains are difficult to treat. Possible treatments include full crowns, external bleaching of vital teeth, internal bleaching of nonvital teeth, bonded restorations, composite build-ups, and laminate veneer crowns.

44 Intrinsic Coloration of Teeth
Porphyria Hyperbilirubinemia Tetracycline Stain

45 Localized Disturbances in Eruption

46 Localized Disturbances in Eruption
Eruption – the continuous process of movement of a tooth from developmental location to functional location Impacted – teeth that cease to erupt due to physical obstruction Embedded – teeth that cease to erupt due to lack of eruptive force Ankylosis – teeth that cease to erupt due to anatomic fusion of tooth with alveolar bone

47 Localized Disturbances in Eruption
Primary impaction of deciduous teeth is extremely rare. Most commonly involves second molars often due to ankylosis. Primary impaction of permanent teeth most frequently affects third molars. Lack of eruption is most often related to crowding and insufficient maxillofacial development. Impacted teeth are frequently diverted or angulated, eventually losing their potential to erupt; mesioangular, distoangular, vertical, horizontal and inverted

48 Localized Disturbances in Eruption
Treatment includes long-term observation, orthodontic-assisted eruption, transplantation, or surgical removal Risks associated with both intervention and nonintervention Surgical removal of impacted teeth is the procedure most frequently performed by OMFS

49 Localized Disturbances in Eruption
Ankylosis – cessation of eruption after emergence Usually develops between ages 7-18; peak 8-9; prevalence est % Fails to respond to orthodontic therapy Failure to treat can result in tilting, carious destruction, and periodontal disease When successor tooth present, best treated with extraction and space maintenance

50 Localized Disturbances in Eruption
Primary tooth impaction Mesioangular impaction Ankylosis

51 Developmental Alterations of the Teeth

52 Developmental Alterations in the Number of Teeth
Anodontia – total lack of tooth development. Rare; most cases occur in hereditary hypohidrotic ectodermal dysplasia Hypodontia – lack of development of one or more teeth. Uncommon in deciduous teeth, usually involves mandibular incisors. More common in permanent teeth, third molars most affected. More frequent in females than males Oligodontia – lack of development of six or more teeth

53 Developmental Alterations in the Number of Teeth
Hyperdontia – development of increased number of teeth. Additional teeth are supernumerary. Prevalence 1-3%. More common in males and usually develops by age 20. Maxilla is most common site (90%) for single tooth hyperdontia, especially incisor region (mesiodens) Most single supernumerary teeth are unilateral. Nearly 75% of supernumerary teeth in anterior maxilla fail to erupt Non-syndromic multiple supernumerary teeth occur mostly in mandible.

54 Hypodontia (oligodontia)
Example of pedigree

55 Hypodontia in Ectodermal Dysplasia

56 Developmental Alterations in the Number of Teeth
Mesiodens – supernumerary tooth in maxillary anterior incisor region Distomolar/Distodens – accessory fourth molar Paramolar – posterior supernumerary tooth situated lingually or buccally to a molar tooth Dental transposition – normal teeth erupted in an inappropriate pattern Natal teeth – teeth present in newborns; teeth arising during the first 30 days of life; (85% mandibular incisor region)

57 Hyperdontia (supernumeray teeth)
Mesiodens Cleidocranial dysplasia Supernumeray premolar

58 Transposition (canine-first premolar)

59 Treatment of Developmental Alterations in the Number of Teeth
Hypodontia – often no treatment required for individual missing teeth; prosthetic replacement for multiple missing teeth. Hyperdontia – early removal of accessory tooth; delayed in therapy can delay eruption of adjacent teeth or cause displacement. Natal teeth – may be removed if they are loose; if stable, they should be retained; Riga-Fede disease (ulceration of ventral tongue associated with breast-feeding) can often be treated without removal of the teeth.

60 Natal teeth (Riga-Fede syndrome)

61 Supernumerary teeth Mesiodens Mesiodens Supernumerary premolar

62 Supernumerary teeth

63 Supernumerary teeth in cleidocranial
dysplasia syndrome

64 Developmental Alterations in the Size of Teeth

65 Developmental Alterations in the Size of Teeth (1)
Microdontia – small teeth. Can also be related to tooth size relative to jaw size. More common in females. Isolated microdontia within otherwise normal dentition is not uncommon (peg-shaped lateral %). Diffuse microdontia occurs in some hereditary disorders and sometimes associated with hypodontia. Increased in Down’s, pituitary dwarfism & a few other syndromes. Macrodontia – larger than average teeth. More common in males. Typically only a few teeth are abnormally large. Diffuse macrodontia may occur in pituitary gigantism. It can be associated with hyperdontia.

66 Microdontia “peg-shaped” laterals “paramolar”

67 Developmental Alterations in the Size of Teeth (2)
Macrognathia – normal sized teeth widely spaced in larger than normal jaw. Treatment – not necessary except for esthetic reasons

68 Developmental Alterations in the Shape of Teeth

69 Developmental Alterations in the Shape of Teeth
Double teeth – two separate teeth exhibiting union by dentin and sometimes pulps (fusion). May result from fusion of two tooth buds, or partial splitting of one into two. Concrescence – union of two teeth by cementum without confluence of dentin. Gemination – single enlarged tooth or joined (double) tooth in which tooth count is normal when this tooth is counted as one. Fusion – single enlarged tooth or joined (double) tooth in which the tooth count is short one when this tooth is counted as one.

70 Concrescence

71 Gemination / Fusion Fusion Gemination

72 Treatment of Developmental Alterations of Shape of Teeth
Extraction of deciduous double teeth may be necessary Shaping with/without placement of full crowns May require surgical removal with prosthesis Concrescence requires no therapy unless interfering with eruption

73 Developmental Alterations in the Shape of Teeth: Accessory Cusps
Cusp of Carabelli – accessory cusp located on palatal surface of mesiolingual cusp of maxillary molar. Very common in Caucasians (up to 90%), rare in Asians. Talon cusp (anterior dens evaginatus) – well defined additional cusp located on surface of anterior tooth extending at least half the distance from the cemento-enamel junction to the incisal edge (<1-8%). Usually projects from the lingual surface. Dens evaginatus – cusp-like elevation of enamel located in central groove or lingual ridge of buccal cusp of permanent premolar or molar teeth. Rare in whites; 15% Asians.

74 Talon cusp (anterior dens evaginatus)

75 Cusp of Carabelli / Dens Evaginatus

76 Treatment of Accessory Cusps
Talon cusps on mandibular teeth often require no therapy, talon cusps on maxillary teeth should be removed Cusps of Carabelli require no treatment, unless deep groove is present, then it should be sealed Dens evaginatus often results in occlusal problems, so should be removed Shovel-shaped incisors – deep fissures should be restored

77 Dens Invaginatus Deep surface invagination of crown or root that is lined by enamel Coronal dens invaginatus may be large, resembling a tooth within a tooth (dens in dente), or it may be dilated and disturb tooth formation resulting in anomalous tooth development (dilated odontome) Radicular dens invaginatus is rare, formation of strip of enamel extending along root surface; altered enamel forms a surface invagination into dental papilla

78 Dens invaginatus

79 Treatment of Dens Invaginatus
Minor cases of coronal dens invaginatus do not require removal of the tooth Opening of invagination should be restored to prevent caries Large coronal dens invaginations often disrupt normal coronal development and should be removed Complications of radicular dens invaginatus rare

80 Ectopic Enamel Ectopic enamel – presence of enamel in unusual places.
Enamel pearls – hemispheric structures projecting from the surface of the root, found mostly on the roots of maxillary molars. Cervical enamel extensions – located on buccal surface of root overlying bifurcation. Buccal bifurcation cyst – inflammatory cyst developed along buccal surface over the bifurcation Treatment: Enamel pearls – good oral hygiene, sometimes removal with caution. Buccal bifurcation cyst – surgical removal, periodontal treatment.

81 Ectopic Enamel

82 Taurodontism Enlargement of body and pulp chamber of multirooted tooth with apical displacement of pulpal floor and bifurcation region ( %) Increased apico-occlusal height and bifurcation near apex Unilateral or bilateral; Affects permanent teeth more often than deciduous teeth Normal (cynodont), Mild (hypotaurodontism), moderate (mesotaurodontism), severe (hypertaurodontism) No specific treatment; Prosthodontic, endodontic considerations.

83 Taurodontism

84 Hypercementosis Non-neoplastic deposition of excessive cementum continuous with the normal radicular cementum Thickness or blunting of root radiographically, localized or generalized. Local or systemic factors; loss of antagonist tooth, occlusal trauma, inflammation, Paget’s disease, acromegaly, etc. Significant generalized hypercementosis in persons with Paget’s disease No specific treatment

85 Hypercementosis

86 Dilaceration Abnormal angulation or bend in root (or commonly the crown) During tooth development, it is thought to arise following displacement injury or less frequently secondary to the presence of an adjacent cyst or tumor Treatment - minor dilaceration in permanent teeth requires no therapy; grossly deformed teeth should be removed; extraction of deciduous teeth when eruption is delayed.

87 Dilaceration

88 Supernumerary Roots Increased number of roots
No treatment necessary, but detection of extra root critical for endodontic therapy or exodontia

89 Developmental Alterations in the Structure of Teeth

90 Amelogeneis Imperfecta
Group of conditions that demonstrate developmental alterations in enamel structure in the absence of a systemic disorder Development of enamel has three major stages: (1) Elaboration of the organic matrix; (2) Mineralization of the matrix; and (3) Maturation of the enamel At least 14 subtypes related to above with a variety of inheritance and clinical patterns

91 Amelogeneis Imperfecta
Witkop classification combines inheritance and clinical patterns Type I hypoplastic; generalized/localized, smooth/pitted/rough, AD, AR. X-linked Type II hypomaturation; pigmented/non-pigmented, diffuse/snow capped; AD, AR, X-linked Type III Hypocalcified; diffuse AD/AR Type IV Hypomaturation-hypoplastic or hypoplastic-hypomaturation with taurodontism; AD

92 Amelogeneis Imperfecta
Hypomineralized form Hypoplastic form

93 Hypoplastic Amelogenesis Imperfecta
Inadequate deposition of enamel matrix Generalized pattern – pinpoint sized pits scattered across surface of teeth Localized pattern – horizontal rows of pits, linear depression or one large area of hypoplastic enamel Autosomal dominant smooth pattern – smooth surface, enamel is thin, hard, and glossy X-linked dominant smooth pattern – alternating zones of normal and abnormal enamel related to active X chromosomes Rough pattern – thin, hard, rough enamel Enamel agenesis – total lack of enamel formation

94 Hypoplastic Amelogenesis Imperfecta

95 Hypomaturation Amelogenesis Imperfecta
Enamel matrix laid down appropriately and begins to mineralize, but there is defective maturation of enamel’s crystal structure; normal shape but abnormal mottled, opaque white-brown color Pigmented pattern (AR) – surface enamel is mottled and brown X-linked pattern – deciduous are opaque white; permanent are yellow-white that darken with age Snow-capped pattern – zone of white opaque enamel on incisal or occlusal surface of the crown

96 Hypocalcified Amelogenesis Imperfecta
Enamel matrix laid down appropriately but no significant mineralization occurs (very soft enamel) Normal shape but enamel soft and easily lost Teeth yellow-brown to orange Unerupted teeth and anterior open bite fairly common

97 Hypocalcified Amelogenesis Imperfecta

98 Hypomaturation/hypoplastic Amelogenesis Imperfecta
Enamel hypoplasia combined with hypomaturation. Hypomaturation-hypoplastic pattern – primary defect is enamel hypomaturation; mottled yellow-white to yellow-brown. Hypoplastic-hypomaturation pattern – primary defect is enamel hypoplasia (thin enamel). Both patterns seen in tricho-dento-osseous dysplasia syndrome

99 Treatment of Amelogenesis Imperfecta
Depends on severity; Problems include aesthetics, sensitivity, vertical dimension, caries, open bite, delayed eruption and impaction Where enamel is very thin, full coverage needed as soon as possible Less severe cases, aesthetics are main consideration. Full crowns or facial veneers

100 Dentinogenesis Imperfecta
Hereditary developmental abnormality of the dentin (Hereditary opalescent dentin, Capdepont’s teeth) May be seen alone (type II) or in conjunction with osteogenesis imperfecta (type I—opalescent teeth) All teeth in both dentitions affected Blue/brown discoloration, dentin demonstrates accelerated attrition “Shell teeth” – normal-thickness enamel, extremely thin dentin, enlarged pulps (Brandywine variant; Shield’s type III) Treatment Entire dentition at risk Most need full dentures by age 30

101 Dentinogenesis Imperfecta
Radiographic features of type I or II

102 Dentinogenesis imperfecta

103 Dentinogenesis imperfecta III (“Shell teeth”, Brandywine variant, Shield's type III)

104 Dentin Dysplasia Dentin dysplasia type I (rootless teeth); 1/100,000; Loss of organization of root dentin leads to shortened root length; crowns appear normal; periapical pathology related to caries/exposure of threads of pulp tissue Dentin dysplasia type II (coronal dentin dysplasia); thistle tube shape of pulp chamber; features of dentinogenesis imperfecta (bulbous crowns, cervical constriction, thin roots, early obliteration of pulp, blue to amber-brown coloration); pulp stones in enlarged pulp chambers Treatment - preventive care, good oral hygiene

105 Dentin Dysplasia Type I Type I

106 Dentin Dysplasia Type II

107 Regional Odontodysplasia (Ghost Teeth)
Idiopathic, localized developmental abnormality (segment or region of jaw) with adverse effects on formation of enamel, dentin & pulp. Maxilla more common (2.5:1) with predilection for anterior teeth; deciduous & permanent involvement or permanent alone Extremely thin enamel and dentin surrounding an enlarged radiolucent pulp Treatment is try to retain altered teeth to allow for appropriate development and preservation of surrounding alveolar ridge. Severely affected and infected teeth should be removed. Unerupted teeth covered with removable partial prosthesis until skeletal growth period has passed

108 Regional Odontodysplasia

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