abnormalities of the teeth advanced oral pathology

Abnormalities of the Teeth

Advanced Oral Pathology

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


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

Enamel Hypoplasia associated with exanthematous fevers

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)

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.

Turner’s Hypoplasia

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Turner’s Hypoplasia

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.

Hypoplasia Caused by Antineoplastic Therapy

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)

Dental Fluorosis

Dental fluorosis

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

Hutchinson’s triad

Syphilitic Hypoplasia

Hutchinson’s incisors

Moon’s (mulberry) molars

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.

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

Postdevelopmental Loss of Tooth Structure: Attrition

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

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

Abrasion

Abrasion

Abrasion from improper flossing

Abrasion from partial clasp

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”

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.

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.

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 understand...it is the acidity of certain products that cause erosion," she added in a statement.

Erosion

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

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

Abfraction

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

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.

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)

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


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.


External Resorption

Internal resorption

Internal resorption

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External resorption--

embedded tooth

Environmental Discoloration of Teeth

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

Environmental Discoloration of Teeth: Extrinsic

Tobacco stain

Amalgam stain

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).

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.

Intrinsic Coloration of Teeth

Hyperbilirubinemia

Tetracycline Stain

Porphyria

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


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


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


Ankylosis – cessation of eruption after emergence

Usually develops between ages 7-18; peak 8-9; prevalence est. 1.3-8.9%

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


Primary tooth impaction Mesioangular impaction

Ankylosis

Developmental Alterations of the Teeth

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


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.

Hypodontia (oligodontia)

Example of pedigree

Hypodontia in Ectodermal Dysplasia


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)

Hyperdontia (supernumeray teeth)

Mesiodens

Cleidocranial dysplasia

Supernumeray premolar

Transposition (canine-first premolar)

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.

Natal teeth (Riga-Fede syndrome)

Supernumerary teeth

Mesiodens

Supernumerary premolar

Mesiodens

Supernumerary teeth

Supernumerary teeth

Supernumerary teeth in cleidocranial

dysplasia syndrome

Developmental Alterations in the Size of Teeth

Developmental Alterations in the Size of Teeth (1)(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 0.8-8.4%). 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.

Microdontia

“peg-shaped” laterals

“paramolar”

Developmental Alterations in the Size of Teeth (2)(2)

Macrognathia – normal sized teeth widely spaced in larger than normal jaw.

Treatment – not necessary except for esthetic reasons

Developmental Alterations in the Shape of Teeth

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.

Concrescence

Gemination / Fusion

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Gemination

Fusion

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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

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.

Talon cusp (anterior dens evaginatus)

Cusp of Carabelli / Dens Evaginatus

Dens EvaginatusCusp of Carabelli

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

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

Dens invaginatus

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

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.

Ectopic Enamel

Taurodontism Enlargement of body and pulp chamber of

multirooted tooth with apical displacement of pulpal floor and bifurcation region (2.5-3.2%)

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.

Taurodontism

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

Hypercementosis

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.

Dilaceration

Supernumerary Roots

Increased number of roots No treatment necessary, but detection of

extra root critical for endodontic therapy or exodontia

Developmental Alterations in the Structure of Teeth

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

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

Amelogeneis Imperfecta

Hypoplastic form

Hypomineralized form

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

Hypoplastic Amelogenesis Imperfecta

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

HypocalcifiedAmelogenesis 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

Hypocalcified Amelogenesis Imperfecta

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

Treatment ofAmelogenesis 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

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

Dentinogenesis ImperfectaRadiographic features of type I or II

Dentinogenesis imperfecta

USC.edu

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

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

Dentin Dysplasia

Type I

Type I

Dentin Dysplasia

Type II

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

Regional Odontodysplasia

abnormalities of the teeth advanced oral pathology

Documents

abrasion slide

turners hypoplasia slide

attrition slide

dentin slide

dental fluorosis slide

primary teeth slide

severe fluorosis slide

enamel hypoplasia pits