• Influenced by environmental forces
– Defects of tooth development
– Post‐development loss of tooth structure
– Discoloration of teeth
– Localised disturbance of eruption
• Idiopathic or appear hereditary in nature

• Enamel development
– Matrix formation
– Mineralization
– Maturation
• Initially‐
– Dull, white & relatively soft
– Hard, translucent

– Ameloblasts are extremely sensitive to external
stimul
• Primary hereditary abnormalities in enamel
unrelated to other disorders are amelogenesis imperfecta
• Unique ‐ no remodelling after initial
formation
• Abnormalities permanently etched
• Timing of damage is critical (neonatal ring)

• SYSTEMIC
– Birth trauma‐Breech/hypoxia/labor/multiple/preterm
– Chemicals‐chemo/Fl/Pb/tetracycline/thalidomide
– Trisomy 21‐chromosomal
– Infections‐chickenpox/CMV/GI/measles/rubella/
syphillis ‐ hutchinsons incisors, mulberry molars /
tetanus
– Inherited diseases
– Malnutrition‐Vit A/D deficiency
– Metabolic disorders
-Neurologic disorders cerebral palsy/ MR

• LOCAL
– Trauma‐gunshot/fall/V. accidents/ mutilation
– Electrical burns
– Irradiation
– Local infection‐ Acute neonatal maxillitis/
periapical inflammatory disease

• Almost all visible environmental enamel
defects can be classified into one of three
patterns:
• Hypoplasia
• Diffuse opacities
• Demarcated opacities
• Masked by poor illumination, saliva, plaque
• Dental operatory light
• Small defects – plaque disclosing solution

• Diffuse opacities‐ variation in translucency
Affected enamel
– normal thickness
– Increased white opacity
– no clear boundary

• Demarcated opacities‐
– Decreased tanslucence
– Increased opacity
– Sharp boundary with adjacent normal enamel
– Thickness normal
– Color is white, cream ,yellow or brown

ENVIRONMENTAL ALTERATIONS OF
TEETH

• Exanthematous fevers during first 2 yrs‐
– Horizontal rows of pits,diminished enamel
• Ant teeth and first molars
• Bilaterally symmetrical
• Location correlates with dev stage
– Similar pattern in cuspids, bicuspids and 2nd
molars ‐ 4‐5 years of age

• Frequently seen
• Affects permanent teeth secondary to PA
inflamn of overlying primary
• Altered tooth is called Turner's tooth
• Vary from focal areas of white, yellow, or
brown discoloration to extensive hypoplasia
(crown)
– Most frequently in the permanent bicuspids

• Traumatic injury to deciduous
– Max central incisors most common – dilaceration
of crown/root may result
– Up to 45% of children sustain injuries to primary
– May give rise to product mimicking complex

• Ingestion of Fl ‐ significant enamel defects
• Caries resistance
• Permanent hypomaturation with increased surface & subsurface
porosity due to retention of enamel proteins
• Critical period during the 2nd‐3rd yrs
– When ant teeth are forming
– If Fl levels > 1 ppm
• Prevalence increasing

• Areas of lusterless white opaque enamel, may have zones of
yellow to dark‐brown discoloration
(mottled enamel)
• Severity is dose dependent
• Defect must be bilaterally symmetric
• Cosmetic treatment as most problems are aesthetic in nature

• Tooth structure loss after formation
– Enamel surface on crowns
– Dentin/cemental surfaces

– Also called ‘tooth surface loss’
– Aging‐physiologic
– Pathologic‐destruction
(functional/aesthetic/dental sensitivity)

• Attrition
• Abrasion
• Erosion
• Abfraction
• External/Internal Resorption

• Loss of tooth structure by tooth‐tooth contact
during occlusion and mastication
• Mild degree is physiologic
• Increases with age, severe change ‐pathologic
• Destruction accelerated by
– poor quality or absent enamel (flurosis,
environmental /hereditary enamel
hypoplasia,dentinogenesis imperfecta)
– premature contacts (edge‐to‐edge occlusion)
– intraoral abrasives, erosion, and grinding habits

• Can occur in both deciduous and permanent
• Most frequently, incisal & occlusal surfaces
• Lingual of ant max teeth & labial of ant mand
teeth
• Wear facets‐
– Large, flat, smooth, shiny
– Interproximal contact points‐ vertical movement
– Shortening the arch length
– Pulp exposure /dentin sensitivity rare‐slow
process
(apposition of secondary dentin)
• Early diagnosis and intervention e g mouth

• Loss of tooth structure secondary to the
action of an external agent
• Variety of patterns – cause related
• Most common source is
– Toothbrushing
– Acids
– Thread biting
– Bobby pins
– Inappropriate use of dental floss

• Toothbrush –
– Horizontal cervical notches
• buccal of exposed radicular cementum & dentin
• Sharply defined margins
• Hard, smooth surface
• Most commonly affects cuspids and premolars
• Acids –rounded & shallow
• Limit tooth‐brushing to 1/day

• Loss of tooth structure caused by a chemical
reaction
• Typically secondary to the presence of an acid
• May proceed to pulp exp/dentin sensitivity

• Sources
– Dietary (e.g. lemons, soft drinks, or vinegar)
– Internal (e.g., gastric secretions)
– External (e.g., acidic industrial atmosphere such as wine tasting or poorly monitored swimming pools)

• Secondary to gastric secretions ‐ perimylolysis
• Seen in anorexia nervosa or bulimia

• Affects facial of max ants
• Shallow spoon‐shaped depressions in cervical
portion of crown
• Post teeth ‐ extensive loss of occlusal and
edges of restorations may be above level of
tooth

• Post enamel loss‐extensive dentinal loss
• Buccal cusps replaced ‐ slope like depressions
from ling cusp to CEJ
• When limited to facial surfaces of max
anteriors ‐ dietary sources of acid

• When located on palatal of max anteriors and
occlusal of posteriors ‐ regurgitation of gastric
acid
– Voluntary – psychologic problems, anorexics,
bulimics , occupations requiring low body wt
– Involuntary‐ hiatal hernia,esophagitis,alcoholism,
pregnancy

• Loss of tooth structure from flexural forces
– Occlusal stress
• Dental research – cause and effect
relationship not yet established
• Teeth flex under pressure
• Hypothesis ‐ Enamel at CEJ
– undergo this pattern of destruction
– separating the enamel rods

• Occlusion, causes
– Tension on one side of the tooth
– Compression on the other side of the tooth
• This causes V‐shaped depressions on tension
side and C‐shaped depression on the
compression side

• This theory is not satisfactory ‐
– Occlusion of many teeth causes tension and
compression on either side
– Consequently,abfraction should be more frequent

• Not evident clinically ( >> frequency)
• Research ‐ identify the role of this pattern of
tooth destruction
• Wedge shaped cervical defect
• Deep & narrow
• Single tooth, subgingival, facial surface &
more in bruxers
• mandibular dentition ‐ lingual orientation of
the teeth

• Destruction through resorption by cells in the
dental pulp
• Relatively rare
• Most cases follow trauma to pulp or cariesrelated
pulpitis
• Continue as long as vital pulp tissue is present
• Often results in communication with the PDL

-within teeth

-dentinoclasts at work

Two types:
• Inflammatory resorption
• Replacement/metaplastic resorption
• Uniform, well‐circumscribed symmetric
radiolucent enlargement of the pulp chamber
or canal, resorbed dentin replaced by inf
granulation tissue
• Coronal pulp ‐ Pink tooth of Mummery
• Endo therapy removes vital pulp tissue prior
to perforation into PDL

-hard to save the tooth

• Resorption by cells in the periodontal ligament
• Extremely common (orthodontic therapy)
• Upon close exam, all patients are most likely
to have root resorption on one or more teeth
• Typically presents as a "moth‐eaten" loss of
tooth structure where lucency is less well
defined
• Most involve the apical/midportions of the
tooth -- ortho cause

• Extrinsic Stains
– Arising from the surface accumulation of
exogenous pigment
• Intrinsic Stains
– Secondary to endogenous factors

• Bacteria ‐ common cause of surface staining
– Chromogenic bacteria ‐ green or black‐brown to orange.chlrophyll containing foods
– Most frequently in children and usually on the labial of max ant teeth in the gingival one third
• Extensive use of tobacco, tea, or coffee
• Stains from beverages ‐ ling surf of anteriors, usually more idespread and less intense
• Large number of medications
– Doxycycline‐yellow/brown stain
• Most frequently due to stannous fl & chlorhexidine
• Can be removed by careful polishing of teeth

• Congenital erythropoietic porphyria
(Gunther's disease) ‐ autosomal recessive
disorder of porphyrin metabolism
– Diffuse discoloration noted as a result of
depostion of porphyrin , also in urine
– Affected teeth ‐ marked reddish‐brown coloration
red fluorescence exposure to wood’s UV light
• Alkaptonuria‐blue/black (ochronosis)
• Parkinson’s‐ blue discoloration of dentition

-autosomal recessive disorder of porphyrin metabolism
– Diffuse discoloration noted as a result of
depostion of porphyrin , also in urine
– Affected teeth ‐ marked reddish‐brown coloration
red fluorescence exposure to wood’s UV light

– Deciduous teeth affected during neonatal period
– Two most common causes are erythroblastosis
fetalis and biliary atresia
– Results in chlorodontia‐yellow/green (billiverdin)

• Several medications incorporated into
developing teeth
• Most infamous is tetracycline
– Vary from bright yellow to dark brown
– In uv light, show a bright yellow fluorescence
– Can cross the placental barrier
– Must be avoided during pregnancy and up to age
8 years
• Minocycline hydrochloride‐ acne, Rh arthritis
• Long‐term use in adults can result in
significant objectionable discoloration

– Vary from bright yellow to dark brown
– In uv light, show a bright yellow fluorescence
– Can cross the placental barrier
– Must be avoided during pregnancy and up to age
8 years

-TOOTH NOT EMERGED

• Failure to erupt before emergence
• Partial/full
• Angulation with dentition
• Associated factors include:
– Crowding/insufficient dev
– overlying cysts or tumors
– trauma
– reconstructive surgery
– thickened overlying bone/soft tissue
– systemic disorders/disorders

• Impaction of deciduous is extremely rare
– 2nd molars
• Mand 3rd molars most often followed by max
3rd molars & cuspids
• Long‐term observation, orthodontic eruption,
transplantation, & surgical removal

• Eruption continues to compensate for
masticatory wear and growth of jaws
• Cessation of eruption after emergence is
ankylosis

 

-TOOTH EMERGED, but NOT REACH THE PLANE OF OCC

• Pathogenesis is unknown‐ anatomic fusion of
cementum/dentin with alv. bone
• May be secondary to many factors:
– local metabolism,trauma,injury,chemical/thermal
irritation,local failure of bone & abnormal
pressure of tongue

• Occur at any age, but most obvious during the
first 2 decades of life (most cases 7‐18)
• Occlusal plane of the involved tooth is below
adjacent dentition
• Primary mand 1st ,2nd ,max 1st , 2nd molars
• Mandibular primary 10 times more affected
• Sharp, solid sound on percussion
– Detected only when >20% of root is fused

• Radiographically, absence of PDL space
• Fail to respond to orthodontic forces
• Ankylosis of primary molars is best treated
with extraction and space maintenance

• Variations in number of teeth are common
• Anodontia ‐ total lack of tooth development
• Hypodontia ‐ lack of development of one or
more teeth
• Oligodontia (subdivision of hypodontia)‐ lack
of development of six or more teeth

• Development of an increased number of teeth
• Additional teeth‐ supernumerary
– Single‐tooth hyperdontia more frequent in the
permanent‐ 90% in ant max‐ mesiodens,
distomolars/distodens, paramolar
• Supernumerary teeth‐supplemental/
rudimentary( conical, tuberculate &
molariform)
• Dental transposition ‐ usually hypodontia

• Multiple supernumerary teeth (nonsyndromic)
occur most frequently in the mand premolar
region

• Maxillary anterior incisor region – most
common (mesiodens),4th max molar, 4th mand
molar,premolar, canine & lateral incisors

• Accessory teeth at or shortly after birth ‐
natal teeth and arising within first 30
days of life neonatal teeth
– Represent prematurely erupted portions of
the deciduous dentition, not
supernumerary teeth
– 85%‐mand incisors,11% max incisors 4%
posterior
• Surgical removal

• Complete anodontia is rare
– Occurs in the presence of hereditary
hypohidrotic ectodermal dysplasia
• Uncommon in deciduous dentition (<1%
of the population)
• Missing teeth in the permanent dentition
common
– 3rd molars most commonly affected
– Followed by second premolars and lateral
incisors

• More common in females than in males.
• Multiple missing teeth may be a
component of several syndromes
• Replaced via prosthetics

• > F, Strong associationhypodontia
• Used only when the teeth are physically
smaller than usual
• Relative microdontia‐ macrognathia
• Diffuse true microdontia is uncommon
– Occur isolated in Down’s syndrome or pituitary
dwarfism
• Isolated microdontia within an otherwise
normal dentition does occur
• The maxillary lateral incisor 3rd molar

• >M,relative macrodontia‐ micrognathia
• Often is seen in association with hyperdontia
• the term "macrodontia" should be applied only when eeth are physically larger than usual
• Incisors/canines also 2nd premolars/3rd molars
• Diffuse macrodontia is rare
• Has been associated with pituitary gigantism

• Double teeth are two separate teeth
exhibiting union by dentin and maybe their
pulps
• Caused by fusion of
– Two adj tooth buds
– Splitting of one tooth bud into two

-more in max. , both dentition
• a single enlarged tooth or joined
tooth in which the tooth count is normal
when the anomalous tooth is counted as one
– 1 crown, bifid pulp chamber, 1 root and 1 pulp
canal

-a single enlarged tooth or joined
(double) tooth in which the tooth count
reveals a missing tooth when the anomalous
tooth is counted as one
– 2 crowns, 2 separate pulp chambers and 1 root
• > mand.
• Both primary and permanent dentitions
• Higher frequency in the anterior maxillary
region

• Root surface (cemental) fusion of two fully
formed teeth ‐ without confluence of the
dentin
• Posterior & maxillary region
• 2nd molar with adjacent impacted 3rd molar
– Large carious coronal loss
– Apices overlying horizontal/distoangular
impactions
• Significant difficulties in extraction
• May result in surgical separation/procedure

– Posterior maxillary teeth ( molars)
–Increased M‐D diameter in permanent dentition/
also present in deciduous dentition
– Cusp/small indented pit/fissure – max 1st molar
– Palatal aspect of Mesio‐lingual cusp
– Predominantly in whites, 90% prevalence
– Protostylids – mand perm & deciduous molar

– Well‐delineated additional cusp located on the surface of an anterior tooth and extends at least half the distance from the cemento‐enamel junction to the incisal edge
– Frequent in permanent teeth, rare in deciduous, M=F
– Max. laterals > centrals >> mand. Incisors >max. canines
– Forms a three‐pronged formation resembling an eagle's tail

– Asians, Native americans ,inuits, arabs
– Associated with ‘Rubinstein, taybi’ syndrome (strongly), Sturge ‐Weber syndrome

– More frequently in oriental groups
– Cusp‐like elevation of enamel located in the
central groove or lingual ridge of the buccal cusp
of permanent premolar /molar teeth
– Bilateral,>> mandibular premolar
– Shovel‐shaped incisors, scooped/hollowed
– Results in occlusal problems and is prone to
fracture

• Deep surface invagination of the crown or
root lined by enamel
• Most likely due to defect in enamel organ
• Most often ‐ permanent maxillary lateral and
central incisors
• May resemble a tooth within a tooth
• Opening may become carious
• A small preventive restoration advised

• Presence of enamel in unusual locations
• Widely known are enamel pearls
• Hemispherical structures of enamel
• Most frequent q ‐ roots of max molars, mand
molars ‐ second most frequent
• Majority at furcation area or near CEJ
• Precludes normal periodontal attachment
• Less resistant to breakdown rapid loss of
attachment likely

• Enlargement of the body & pulp chamber of a
multi‐rooted tooth
• Apical displacement ‐ pulp chamber and
bifurcation
• Diagnosis made by radiograph
• Maybe bilateral

-BULL TOOTH

• Affects the permanent dentition more
frequently
• May be associated with several syndromes
–Down’s
– Klinefelter’s
– Ectodermal dysplasia,
– Amelogenesis imperfecta (hypomaturation)

• Non‐neoplastic deposition of excessive
cementum along the root
• X‐ray: thickening or blunting of the roots
• Normal PDL space is observed
• May be isolated or may involve multiple teeth

• Associated with local factors like trauma,
inflammation
• Systemic factors
–Acromegaly
– Paget’s disease of bone
– Arthritis
– Calcinosis
– Goiter

• Abnormal angulation or bend in the root
• Majority arise following injury that displaces
the calcified portion of the tooth germ
• Some idiopathic
• Permanent max incisors most frequently
affected
• Complications in extractions or endo

􀂉Increased number of roots on a tooth
􀂉More frequently on 3rd molar teeth
􀂉Complications in extractions/ endodontic
therapy

• Hereditary condition ‐ alterations in the
enamel in the absence of systemic disease
• Frequency from 1:8000 and 1:700
• More than 14 different subtypes

-Enamel alteration WITHOUT systematic diseases

• Alterations in the enamel may arise at any of
the following stages:
– Formation of matrix i.e. amount of enamel
formed: Hypoplastic
– Mineralization of matrix i.e. degree of
calcification: Hypocalcified
– Maturation of the enamel : Hypomaturation

• Generalized: pinpoint pits
• Localized: horizontal row of pits in the middle
3rd of the facial surface
• Incisal edge or occlusal surface is not affected
• Crown prep like teeth on x‐ray

• Matrix is laid down and begins to mineralize
normally, but crystals do not mature
• Teeth appear normal in shape but have a
mottled, opaque white‐brown‐yellow
discoloration
• Enamel is soft and chips off, can be pierced
with tip of an explorer
• X‐ray: enamel looks like dentin

• Matrix here is laid down normally but
abnormal calcification / mineralization takes
place
• Soft enamel that is easily lost
• Yellow‐brown or orange enamel
• Easily stained & teeth show very rapid calculus
formation
• X‐ray: density of enamel is similar to dentin

• 2 types:
– Hypomaturation ‐ hypoplastic (No
hypertaurodontism, mild manifestation of the
syndrome)
– Hypoplastic ‐ hypomaturation type (syndromal)

• Both probably associated with ‘Tricho dento
osseous syndrome’
– Kinky hair
– Osteosclerosis of mastoid process & base of skull
– Brittle nails

• Hereditary disturbance in the formation of
dentin
• Also called hereditary opalescent dentin when seen in association with osteogenesis imperfecta
• only called ____ when Isolated cases absence of systematic disease

• Most cases in US traced to whites from
around the English Channel
• Autosomal dominant condition
•Severity of alterations depends on the age :
– Deciduous most severely affected
– Followed by the perm incisors and 1st molars
– 2nd & 3rd molars least altered

• Teeth exhibit a blue to brown discoloration
with distinctive translucence
• Enamel strips of easily from the underlying
dentin

• X‐ray: Bulbous crowns, cervical constriction,
thin roots, early obliteration of root canals and
pulp chambers
• “Shell teeth” may be seen ‐ extremely large
pulp chambers and very thin dentin
– Maybe a new variant of DI

• Short roots ‐ malformation of root dentin
• Autosomal dominant pattern
• Enamel and coronal dentin are normal
• X‐ray: deci teeth more severely affected with
little or no pulp and very short roots
• Perm teeth: range from little or no pulp to
crescent or chevron‐shaped pulp chambers

-‘Stream flowing through boulders’ presentation

• Similar to DI
• Autosomal dominant inheritance pattern
• Blue to amber to brown translucence of teeth
• X‐ray‐ bulbous crowns, cervical constriction,
thin roots and early obliteration of pulp
chamber
• Pulpal enlargement /apical extension‐thistle
tube, flame shaped pulp , both dentition
• Numerous pulp stones

• “Ghost teeth”: Uncommon condition
found in both dentitions
• Localized developmental abnormality
involving enamel, dentin and pulp
• Non‐hereditary

• Idiopathic mostly but some associated with
vascular nevi of the head and neck
• No racial predilection
• Female predominance
• Bimodal peak : eruption of prim teeth‐2 to 4
yrs and perm dentition‐7‐11 yrs

• Several contiguous teeth affected usually
in the maxillary anterior
• Involvement of the prim teeth is typically
followed by perm teeth being affected
• Failure of eruption

• Teeth that erupt have small irregular, brown to
yellow, rough surfaced crowns
• X‐ray: extremely thin enamel and dentin
surrounding an enlarged pulp ‐ pale wispy
image of teeth‐ “ghost teeth”
• Densities of enamel and dentin appear fuzzy