ABNORMALITIES OF TEETH

Environmental and Developmental Alterations

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1. ??
2. ?
3. --?

:
1. Oral pathology, Neville et al(Saunders), 3rd ed., 2009
2. .
3. British Dental Journal 2003: (195)243-248.

2
 ENVIRONMENTAL ALTERATIONS OF TEETH
Developmental tooth defects
Turners tooth
Hypoplasia caused by antineoplastic therapy
Fluorosis
Syphilitic hypoplasia
Postdevelopmental structure loss
Tooth wear
Internal and external resorption
Discolorations of teeth
Intrinsic stains
Extrinsic stains
Localized disturbances in eruption
Primary impaction
Ankylosis
3
 Enamel development
Three stages:
1. Matrix formation: protein laid down

2. Mineralization: minerals deposition, majority of

original prot. removed-- diffuse, opaque white, soft
enamel

3. Maturation: final mineralization-- translucent, hard

enamel
Amelogenesis imperfecta
Enamel hypoplasia

4
 Enamel development
No remodeling after initial formation
Timing of ameloblastic damage has a great
impact on location & appearance of the
defect
Development of crown : from 14th week of
gestation to 12 months of age in deciduous
dentition; 6 months to 15 y/o in permanent
dentition
Neonatal ring on deciduous enamel and
deposition with a rate of 0.023mm/day

5
 See Box 2-2

Factors associated with enamel defects

Systemic
1. Birth-related trauma: premature birth
2. Chemicals: antineoplastic C/T, fluoride, tetracycline
3. Chromosomal abnormalities: trisomy 21
4. Infections: chicken pox, CMV, syphilis
5. Inherited diseases: Vit.D-dependent rickets
6. Malnutrition: Vit. A deficiency
7. Metabolic disorders: hypoparathyroidism, maternal
diabetes
8. Neurologic disorders: cerebral palsy

6
 See Box 2-2

Factors associated with enamel defects

Local
1.Local acute mechanical trauma
2. Electric burn
3. Irradiation
4. Local infection: periapical inflammatory
disease

7
 Clinical and Radiographic Features
Environmental enamel defects:
1.Hypoplasia: pits, grooves or large
area of missing enamel
2. Diffuse opacities: variation in
translucency, normal thickness,
white opacity without clear
boundary
3. Demarcated opacities: increased
opacity, a sharp boundary with
adjacent normal enamel, normal
thickness
Ref. 1
8
 Turners hypoplasia, Turners tooth
Permanent teeth
Periapical inflammatory
disease of the overlying
deciduous tooth, less
frequently in anterior teeth

Traumatic injury- not rare

-45% children sustain injury
to their deciduous teeth.
-23% corresponding
permanent teeth Turners hypoplasia secondary
development disturbed. to previous trauma

Ref. 1
9
 Turners teeth
Ref. 1,2
10
 Hypoplasia caused by antineoplastic therapy

Under 12 y/o, esp. under 5y/o

Age at treatment, forms of therapy

Chemotherapy-
Less alteration than radiation
Increased number of enamel hypoplasia and
discolorations, slight smaller tooth size, radicular
hypoplasia

11
 Radiotherapy-
0.72 Gy related to mild defects in enamel, dentin (
2Gy)
Dose, radiation field

12 From: Radio-oncological dept of KMUH

 Ref. 1

Developmental radicular hypoplasia and

microdontia caused by radiotherapy
13
 Hypodontia, microdontia, radicular hypoplasia,
enamel hypoplasia, mandibular hypoplpasia,
reduced in vertical development of lower 1/3 of face

Mandibular hypoplpasia may caused by

Radiation impaired root development reduced
alveolar bone growth

Cranial radiation altered pituitary gland function

growth failed

14
 *Dental fluorosis
1901, Dr. Frederick S. McKay: Colorado brown stain
1909, Dr. F.L. Robertson in Bauxite, Arkansas Modified from : Map_of _USA
_highlighting_Colorado.png

1930, H.V. Churchill: high concentration of fluoride of

Bauxite(13.7ppm) and Colorado
Permanent dental stain but resistance to caries
1931, Dr. H. Trendley Dean: association between fluoride, dental
fluorosis and prevalence of caries among children => 1st water
fluoridation clinical trial in Grand Rapids, Michigan
1.0 ppm reduced caries by 50~70% and associated with low and
mild mottled enamel
0.7~1.2 ppm water fluoridation was recommended after 1962,
currently 0.7ppm is recommended due to increased dental
fluorosis
15
 Dental fluorosis
Retention of the amelogenin protein in enamel structure
hypomineralized enamel
permanent hypomaturation
increased surface and subsurface porosity
alters light reflection and create white, chalky area

16 Ref. 1
 Dental fluorosis
Critical period for clinical dental fluorosis is the 2nd
and 3rd year of life, dose dependent
Caries resistant

Ref. 2
17
 Syphilitic hypoplasia
Congenital syphilis
Hutchinsons incisors &
mulberry molars

Ref. 2
18
 POSTDEVELOPMENTAL LOSS OF TOOTH
STRUCTURE

Begin from enamel surface (tooth wear):

Attrition, abrasion, erosion, abfraction

Begin from dentin, cemental surface: internal

or external resorption

19
 Attrition
Tooth to tooth contact during occlusion and
mastication, some are physiologic
Accelerated by: poor quality or absent enamel,
premature contact, intraoral abrasives, erosion,
grinding habits
Incisal, occlusal and interproximal surfaces

20 Ref. 1
 Abrasion
Pathologic loss of tooth structure or restoration
secondary to the action of an external agent (ex.
Toothbrush, hair grips, toothpicks, chewing tobacco,
biting thread, dental flossing)
Toothbrush abrasion: horizontal buccal cervical notches
of exposed radicular cementum and dentin with smooth
surface.
Greater on prominent teeth ( canines, premolars , and
teeth adjacent to edentulous area) and side of the arch
opposite to the dominant hand
Demastication- when tooth wear is accelerated by
chewing an abrasive substance between opposing teeth
(both attrition and abrasion)
21
 Abrasion

22 Ref. 1
 Improper use of hair grips

Abrasion

Long-term use of tobacco pipe

23 Ref. 1
 Erosion
Chemical process, exposure to acidic foods or drinks,
medications (chewable Vit. C, aspirin), involuntary
regurgitation (ex. esophagitis, pregnancy), voluntary
regurgitation (ex. psychologic problems, bulimia)
Perimolysis- dental erosion from gastric secretion
Facial surface of maxillary anteriors affected-dietary
source
Posterior teeth extensive loss of occlusal surface, and
palatal surface concave dentin surrounded by an
elevated enamel rim- regurgitation of gastric secretion

24
 Erosion

concave dentin surrounded

by an elevated enamel rim

25 Ref. 1
 Erosion

A bulimia patient

26 Ref. 1
 Abfraction
Repeated tooth flexure caused by occlusal stresses
(tensile stress)
concentrate at the cervical fulcrum
may produce disruption in the chemical bonds of
enamel crystal
cracked enamel can be lost or removed by erosion or
abrasion
Wedge-shaped cervical defects, deep, narrow V-shaped,
not allow toothbrush to contact base; if the defect, often
affect a single tooth
Almost exclusively on facial surface and more often in
bruxism, higher in mandibular dentition
27
 Abfraction

28 Ref. 1
 Treatment and prognosis of tooth wear

Resolve pain and sensitivity

Identify the cause of tooth
structure loss
Protection

29
 INTERNAL & EXTERNAL RESORPTION
Internal resorption- by cells located in pulp, rare
Follows injury to pulp tissues, physical trauma or caries,
continue as long as vital pulp remains, may result in
communication of the pulp and PDL
External resorption- by cells in PDL, common

30 Ref. 1
 Factors associated with
external resorption

31 Ref. 1
 Clinical and Radiographic Features

Internal resorption-
Inflammatory resorption- dentin
replaced by inflamed granulation
tissue
Pink tooth of Mummery: internal
resorption involved coronal pulp
Balloonlike enlargement of the
canal
Replacement, or metaplastic
absorption- pulpal dentinal walls
are replaced by bone or
cementum-like bone

32 Ref. 1
 Clinical and Radiographic Features
External resorption-
Moth-eaten loss of tooth
structure, less well-defined and
variation in density in
radiography
Most involved apical or
midportions of root,
occasionally, begin from
cervical (invasive cervical
resorption)

33 Ref. 1
 Histopathologic Feature
Increased cellularity, vascularity and collagenization
Numerous multinucleated dentinoclasts
Inflammatory cells infiltration

34 Ref. 1
 Treatment and prognosis
Internal resorption-
Removal of all soft tissue from site of resorption
Endodontic treatment before perforation in internal
resorption
Placement of calcium hydroxide paste for remineralization
Surgical exposure and restoration
Extraction

External resorption-
Identification and elimination the accelerating factor

35
 ENVIRONMENTAL DISCOLORATION
OF TEETH
Extrinsic- surface
accumulation of
exogenous pigment

Intrinsic-secondary to
endogenous factors
that result in
discoloration of
underlying dentin
36 Ref. 1
 Extrinsic stains
Bacterial- Chromogenic bacteria, green, black-brown,
orange coloration
Frequently in children, labial surface of maxillary ant. in
gingival third
Iron- formation of ferric sulfide
Tobacco
Food and beverage- chlorophyll
Gingival hemorrhage- Hb. breakdown to biliverdin
Restorative material ex. Amalgam
Medications- iron, iodine, silver nitrate, chlorhexidine,
stannous fluoride

37
 Intrinsic stains
Amelogenesis imperfecta
Dentinogenesis imperfecta
Dental fluorosis
Erythropoietic porphyria
autosomatic recessive disorder of porphyrin metabolism,
increased synthesis and excretion of porphyrins and
their related precursors
Porphyrin deposition in teeth, reddish-brown coloration,
red fluorescence when exposed to a Woods UV light
Present both in dentin and enamel in deciduous teeth,
but only dentin affected in permanent teeth

38
 Erythropoietic porphyria

Hyperbilirubinemia
39 Ref. 1
 Intrinsic stains
Hyperbilirubinemia- bilirubin, breakdown product of
RBC, jaundance (yellow-green discoloration),
erythroblastosis fetalis, biliary atresia
Biliverdin deposition, green discoloration of teeth
(chlorodontia)
Ochronosis() -alkaptonuria(), blue-
black discoloration
Trauma- coronal discoloration, pulp necrosis
Localized RBC breakdown

40
 Intrinsic stains
Medications-
Tetracycline (bright yellow to dark brown),
chlortetracycline (gray-brown), oxytetracycline
(yellow) , minocycline hydrochloride
Time of administration dose, duration
Avoid from pregnancy up to 8 yrs of age

41 Ref. 1
 Minocycline hydrochloride
Tx for Acne
Blue-gray from incisal 3/4,
to dark green or black in
roots, also affect
developed teeth
Skin, nail, sclera,
conjunctiva, thyroid, bone
discoloration in
susceptible individuals Stained alveolar bone

42 Ref. 1
 Treatment and prognosis

Extrinsic stains- polishing

Intrinsic stains- bleaching, bonded

restoration, crowns

43
 LOCALIZED DISTURBANCES IN ERUPTION

PRIMARY IMPACTION- Teeth cease

to eruption before emergence

ANKYLOSIS -Cease of eruption after

emergence and anatomic fusion of
tooth cementum or dentin with
alveolar bone

44
 Impaction
3rd molars, maxillary canines, mandibular premolars,
mandibular canines, maxillary premolars, maxillary central
incisors, maxillary lateral incisors, and mandibular second
molars; usually angulated or diverted

Factors associated with impaction:

Crowding and deficient maxillofacial development
Overlying cysts or tumors
Trauma
Reconstructive surgery
Thickened overlying bone or soft tissue
A host of systemic disorders, diseases or syndromes

45
 Ref. 1

Classification according to angulation:

Mesioangular, distoangular, vertical, horizontal or
inverted

46
 Treatment and Prognosis
Choice of treatment:
Long-term observation
Orthodontically assisted eruption
Transplantation
Surgical removal

The risks associated with nonintervention:

Crowding dentition
Resorption and worsening of the periodontal status
of adjacent teeth
Development of pathologic conditions, ex infections,
cysts or tumors
47
 The risks associated with intervention:
Transient or permanent sensory loss
Alveolitis
Trismus
Infection
Fracture
TMJ injury
Periodontal injury
Injury to adjacent teeth

48
 ANKYLOSIS
Infraocclusion, secondary retention,
submergence, reimpaction, reinclusion

49 Ref. 1
 ANKYLOSIS
Clinical And Radiographic Features
Pathogenesis is unknown, may be secondary to many
factors and result in PDL barrier deficiency.
May occur at any age, any tooth
Most affect 8~9yr-old children and D , E , D , E
PDL absent
Occlusal, periodontal problems, impaction of the
underlying teeth

Treatment and Prognosis

Variable : extraction, orthodontics, segmental
osteotomy

50
 DEVELOPMENTAL ALTERATIONS OF TEETH
NUMBER SHAPE
Hypodontia Gemination, Fusion, Concrescence
Hyperdontia Accessary cusps
Dens in dente
SIZE Ectopic Enamel
Microdontia Taurodontism
Macrodontia Dilaceration
Hypercementosis
STRUCTURE Supernumerary roots
Amelogenesis imperfecta
Dentinogenesis imperfecta
Dentin dysplasia I & II
Regional odontodysplasia

51
 Missing teeth
1.6-9.6% (excluding 3rd molars) in permanent dentition, F:M=1.5:1
Hypodontia: missing one or more teeth
Oligodontia: missing 6 or more teeth
Anodontia: total missing
Teeth 8 > 5 > 2 > 1
Deciduous mandibular incisors
Gene mutation, ex: PAX9, MSX1, AXIN2 gene, He-Zhao
deficiency(maps to chromosome 10q11.2 )
AXIN2 mutation: associated with the development of
adenomatous polyps of colon, and colorectal carcinoma
Ectodermal dysplasia
orofaciodigital syndrome
52
 Hypodontia

53 Ref. 1
 Ectodermal dysplasia

Ref. 2

Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

 Supernumerary teeth, hyperdontia
Mesiodens
4th molar
Paramolar
Distomolar, distodens
deciduous - lat. incisors
86% single supernumerary
multiple & impaction
cleidocranial dysostosis
Gardners syndrome

55
 Mesiodens
The most common in
supernumerary.
Premaxillary area , usually
between upper central
incisors
Cone-shaped crown & short
root
One or two in number

56 Ref. 1
 Ref. 2

57 Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

 Cleidocranial dysostosis
1.Skull: flat appearance, sutures remain open

2.Jaws: underdeveloped, high narrow palate

3.Teeth: prolonged retained deciduous teeth,

delayed eruption of permanent teeth

4.Clavicles: complete or partial absent

58
59 Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
60 Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
63 Ref. 3
 Gardners syndrome

1.multiple polyposis of the large intestine

2.osteoma of the bone
3.multiple epidermoid cysts or sebaceous cysts of the
skin
4.desmoid tumors
5.impacted supernumerary & permanent teeth

64
 Predeciduous dentition
Neonatal teeth: within 30 days
Natal teeth: newborns
Most are prematurely erupted deciduous teeth
Removal only if mobile and at risk of aspiration

65 Ref. 1
66 Ref. 1
 Microdontia
True:
1.General -pituitary dwarfism
2. Single -peg lat., 3rd molar
Relative microdontia
Ref. 1

67
 Macrodontia
True macrodontia :
1. Generalized-pituitary gigantism
2. Localized- single, hemifacial hypertrophy
Relative macrodontia: small jaw, child

68 Ref. 1
 Ref. 2
69
 Gemination, Fusion, Concrescence

70
 Gemination
single tooth germ
division
single root and root canal +
2 complete or incomplete
separated crowns
tooth no.: normal
twinning

71 Ref. 1
 Fusion
Union of 2 separate tooth germs
Contact of tooth germ before calcified
Confluent of the dentin
Complete- form a single tooth
Incomplete- after calcified begins
Tooth no. : less one

72 Ref. 1
 Concrescence

Fusion after root

formation
Cementun united
Traumatic injury or
crowding
Pre-extraction x-ray
check

73 Ref.2
 Talon cusp
Eagles talon
Lingual projection from
the cingulum area of ant.
teeth Ref. 2

Most contain a pulp horn

Both in deciduous &
permanent dentition

74
 Dens evaginatus
central tubercle, occlusal tuberculated premolar;
Leongs premolar; evaginated odontome;
occlusal enamel pearl
An accessory cusp or a globule of enamel on
central groove or buccal cusp of premolars or
molars; unilateral or bilateral.
15% in Asians, rare in whites

75
 Dens evaginatus

76 Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

 Ref. 1

Shovel-shaped incisors
-Predominent in Asians, Native Americans, Inuit
77
 Dens in dente
(Dens invaginatus; Dilated composite odontome)
Tooth within a tooth, incidence 5%
Invagination of the enamel organ into
dental papilla before calcification

Coronal type: 3 types

maxillary lateral incisors are common

78 Ref. 1
 Dens invaginatus, coronal type II

Ref. 1

79
 Dens invaginatus
Radicular type
Hertwigs sheath invagination

Ref. 1
Food deposition caries pulp infection
Restorated as soon as possible

80
 Taurodontism

Bull-like teeth
Bi- or trifurcation
near the apex
Pulp chamber :
greater apico-occlusal
height and no
constriction at the
cervical of the tooth

81 Ref. 1
 Syndromes associated with taurodontism

82 Ref. 1
 Hypercementosis
LOCAL FACTORS
Abnormal occlusal trauma
Adjacent inflammation
Unopposed teeth

SYSTEMIC FACTORS
Acromegaly and puitary gigantism
Arthritis
Calcinosis
Pagets disease
Rheumatic fever
Ref. 1
Thyroid goiter
Vitmin A deficiency(possible)
83
 Supernumerary roots
Any tooth may develop accessary roots
No tx required, but critical important in
endodontic procedure

84 Ref. 1
 Dilaceration
Angulation, sharp
bend of root or crown
Trauma during tooth
is forming

Pre-extraction x-ray
check

85 Ref. 2
 Amelogenesis imperfecta
(Hereditary enamel dysplasia; Hereditary brown enamel;
Hereditary brown opalescent teeth)

Defects in--
Formative stagehypoplastic type defective
formation of matrix
Calcification stage hypocalified defective
mineralization of formed matrix
Maturation stage hypomaturation enamel
crystallites remain immature
Genes mutation : AMELX, ENAM, MMP-20, KLK4, DLX3

86
 Amelogenesis imperfecta

Ref. 1
87
 1.Hypoplastic type
Thin enamel with pitted, rough or smooth &
glossy surface; yellowish to brown
undersized, squared crown, lack of contact
flat occlusal surface & low cusps, attrition

88
 Hypoplastic type

89 Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

 Hypoplastic type

90 Ref. 1
 2.Hypomaturation

normal thickness of enamel, but

mottled surface; cloudy white,
yellow or brown, opaque in color
softer than normal
same density as dentin

91
 Hypomaturation type

Ref. 1
92
 3.Hypocalcified type
normal thickness of enamel, density less than
dentin
normal size & shape when erupt, abrade or
fracture away rapidly
permeability increase, darkened & stained

4.Hypomaturation-hypocalcified
with taurodontism

93
 Hypocalcified type

Ref. 1
94
 Tricho-dento-osseous syndrome

Hypoplastic-Hypomaturation type with taurodontism Ref. 1

95
 Dentinogenesis imperfecta
(Hereditary opalescent dentin)
1: 8,000
Classification of DI : (Shields)

Type I* : DI + OI (osteogenesis imperfecta) COL1A1,

COL1A2
Type II : Isolated DI. DSPP
Type III : DI of the Brandywine type * DSPP
A racial isolate in Maryland,
DI + multiple pulp exposures in deciduous teeth
*osteogenesis imperfecta with opalescent teeth
96
 Blue sclera

M Greenwood, J G Meechan,:General medicine and surgery for dental

practitioners Part 8: Musculoskeletal system. British Dental Journal 2003 (195)
243 - 248 ,
 Clinical features
type I : deciduous severe than permanent
teeth;
type II: equally affected;
type III: both dentitions affected.
Gray to brownish violet or yellowish brown
color, with translucent or opalescent hue.
Enamel lost early through fracture, esp. on the
incisal & occlusal surface, and dentin attrition
rapidly.
Caries rate is not increased.

98
 Dentinogenesis imperfecta

Ref. 1

99
 Dentinogenesis imperfecta

Histology:
1.pulp chamber obliterated
with dentin
2.flatten D-E junction
3.atypical granular dentin,
enlarged tubles, poor
calcification
water contents: 50% above
normal

100 Ref. 1
 Radiographic features

Partial or total
obliteration of the pulp
chamber & root canal by
continued formation of
dentin, in both dentitions.
Short and blunted roots

Normal cementum, PDL &

supporting bone

Ref. 1
101
 Shell teeth
Initial reported in the Brandywine population
Normal thickness of enamel associated with
extremely thin dentin and dramatically enlarged
pulps (due to insufficent and deffective dentin
formation)
Short roots.

102 Ref. 1
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
 Dentin dysplasia
Hereditary, autosomal dominant. Normal
enamel but atypical dentin formation with
abnormal pulp morphology
1:100,000

Type I (radicular type): Rootless teeth

Type II (coronal) DSPP (dentin
sialophosphoprotein) gene mutation

104
 Type I (radicular type)
Radiographically:
deciduous teeth affected more severely, little or no pulp,
short or absent roots.
If disorganization late---normal pulp chambers, with a
large pulp stone.
periapical lesions (R-L) no obvious cause.

Histologic features
Normal coronal enamel& dentin.
In root: tubular dentin and atypical osteodentin
surrounded with normal dentin --- appearance of Lava
flowing around boulders.
Ref. 1
105
 Dentin dysplasia, type I

Ref. 1

106
 Type II (coronal)
Normal root length in both dentitions.
Primary dentition similar to DI:
bulbous crowns, cervical constriction
thin roots , early obliterated pulp.
Permanent teeth : normal coloration,thistle
tube-shaped or flame-shaped pulp chamber
with pulp stones.

107 Ref. 1
 Dentin dysplasia, type II
(coronal)

108 Ref. 1
 Lava flowing around boulders.

Dentin dysplasia

Large pulp stones

109 Ref. 1
 Regional odontodysplasia
(odontodysplasia; odontogenic dysplasia;
odontogenesis imperfecta; ghost teeth)
One or several teeth in a localized area
Maxi. > Mand.; both dentitions
most in ant. area
Delayed or total failure eruption
Irregular appearance
Defective mineralization
110
 Radiographic features
1. Radiodensity , ghost appearance
2. Large pulp, thin enamel & dentin

Histologic features
1. Dentin
2.Widening of the predentin layer,
Ref. 1
3. Interglobular dentin and an irregular
tubular pattern of dentin
4.Calcification of the reduced enamel epi.

111
 Enameloid conglomerates Odontogenic epithelium

Regional
112 Ref. 1 odontodysplasia
 Summary

ENVIRONMENTAL ALTERATIONS OF TEETH

Developmental tooth defects
Turners tooth
Hypoplasia caused by antineoplastic therapy
Fluorosis
Syphilitic hypoplasia
Postdevelopmental structure loss
Tooth wear
Internal and external resorption
Discolorations of teeth
Intrinsic stains
Extrinsic stains
Localized disturbances in eruption
Primary impaction
Ankylosis
113
 Summary

DEVELOPMENTAL ALTERATIONS OF TEETH

NUMBER SHAPE
Hypodontia Gemination, Fusion, Concrescence
Hyperdontia Accessary cusps
Dens in dente
SIZE Ectopic Enamel
Microdontia Taurodontism
Macrodontia Dilaceration
Hypercementosis
STRUCTURE Supernumerary roots
Amelogenesis imperfecta
Dentinogenesis imperfecta
Dentin dysplasia I & II
Regional odontodysplasia

114