Transcript Un-carious defects of teeth. Classification after Patrikeev. Pathomorphology, clinic and

Un-carious defects of teeth.
Classification after Patrikeev.
Pathomorphology, clinic and
diagnostics of defects which are
developed before and after cut of
teeth. Treatment.
Lecturer: as. Yavors’ka-Skrabut I.M.
Therapeutic dentistry department

Environmental Alterations of Teeth

Developmental Alterations of Teeth
ENVIRONMENTAL ALTERATIONS OF
TEETH
Developmental tooth defects
Turner’s 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
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
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
See Box 2-2
Factors associated with enamel defects
Systemic1. 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
See Box 2-2
Factors associated with enamel defects
Local1.Local acute mechanical trauma
2. Electric burn
3. Irradiation
4. Local infection: periapical
inflammatory disease
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
Turner’s hypoplasia, Turner’s 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,
Turner’s hypoplasia secondary
23% permanent teeth
to previous trauma
development disturbed
Turner’s teeth
Hypoplasia caused by antineoplastic
therapy
Under 12 y/o, esp. under 5y/o
Age at treatment, forms of therapy
ChemotherapyLess alteration than radiation
Increased number of enamel hypoplasia and
discolorations, slight smaller tooth size,
radicular hypoplasia
Radiotherapy0.72 Gy related to mild defects in enamel,
dentin Dose, radiation field

Developmental radicular hypoplasia and
microdontia caused by radiotherapy
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
*Dental fluorosis
1901, Dr. Frederick S. McKay: Colorado brown stain
1909, Dr. F.L. Robertson in Bauxite, Arkansas
1930, H.V. Churchill: high concentration of fluoride of
Bauxite(13.7ppm) and Colorado
1931, Dr. H. Trendley Dean: association between fluoride,
dental fluorosis and prevalence of caries among children
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
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
Dental fluorosis
Critical period for clinical dental fluorosis
is the 2nd and 3rd year of life, dose
dependent
Caries resistant
Syphilitic hypoplasia
•Congenital syphilis
•Hutchinson’s incisors &
mulberry molars
POSTDEVELOPMENTAL LOSS OF
TOOTH STRUCTURE
Begin from enamel surface (tooth wear):
Attrition, abrasion, erosion, abfraction
Begin from dentin, cemental surface:
internal or external resorption
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
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)
Abrasion
Improper use of hair grips
Abrasion
Long-term use of tobacco pipe
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 affecteddietary source
Posterior teeth extensive loss of occlusal
surface, and palatal surface concave dentin
surrounded by an elevated enamel rimregurgitation of gastric secretion
Erosion
concave dentin surrounded
by an elevated enamel rim
Erosion
A bulimia patient
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
Abfraction
Treatment and prognosis of tooth
wear
Resolve pain and sensitivity
Identify the cause of tooth
structure loss
Protection
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
Factors associated with
external resorption
Clinical and Radiographic
Features
Internal resorptionInflammatory resorptiondentin replaced by inflamed
granulation tissue
Pink tooth of Mummery: internal
resorption involved coronal pulp
Balloonlike enlargement of the
canal
Replacement, or
metaplastic absorptionpulpal dentinal walls are
replaced by bone or
cementum-like bone
Clinical and Radiographic Features
External resorptionMoth-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)
Histopathologic Feature
• Increased cellularity, vascularity and collagenization
• Numerous multinucleated dentinoclasts
• Inflammatory cells infiltration
Treatment and prognosis
Internal resorptionRemoval 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 resorptionIdentification and elimination the accelerating
factor
ENVIRONMENTAL
DISCOLORATION OF TEETH
Extrinsic- surface
accumulation of
exogenous pigment
Intrinsic-secondary to
endogenous factors
that result in
discoloration of
underlying dentin
Extrinsic stains
Bacterial- Chromogenic bacteria, green, blackbrown, 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
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, reddishbrown coloration, red fluorescence when
exposed to a Wood’s UV light
Present both in dentin and enamel in
deciduous teeth, but only dentin affected in
permanent teeth
Erythropoietic porphyria
Hyperbilirubinemia
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
Intrinsic stains
MedicationsTetracycline (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
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
Treatment and prognosis
Extrinsic stains- polishing
Intrinsic stains- bleaching,
bonded restoration, crowns
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
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
Classification :
Partially erupted or full bony impaction
according to angulation: Mesioangular, distoangular,
vertical, horizontal or inverted
Eruption sequestrum
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
The risks associated with intervention:
Transient or permanent sensory loss
Alveolitis
Trismus
Infection
Fracture
TMJ injury
Periodontal injury
Injury to adjacent teeth
ANKYLOSIS
Infraocclusion, secondary retention,
submergence, reimpaction,
reinclusion
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
DEVELOPMENTAL ALTERATIONS OF
TEETH
NUMBER
Hypodontia
Hyperdontia
SIZE
Microdontia
Macrodontia
STRUCTURE
Amelogenesis imperfecta
Dentinogenesis
imperfecta
Dentin dysplasia I & II
Regional odontodysplasia
SHAPE
Gemination, Fusion,
Concrescence
Accessary cusps
Dense in dente
Ectopic Enamel
Taurodontism
Dilaceration
Hypercementosis
Supernumerary roots
Missing teeth
1.6-9.6% , excluding 3rd molars, female
predominance
Hypodontia: missing one or more teeth
Oligodontia: missing 6 or more teeth
Anodontia: total missing
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
Hypodontia
Ectodermal dysplasia
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
Gardner’s syndrome
Mesiodens
The most common in
supernumerary.
Premaxillary area , usually
between upper central
incisors
Cone-shaped crown &
short root
One or two in number
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
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.
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
Gardner’s 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
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
Microdontia
True:
1.General -pituitary dwarfism
2. Single -peg lat., 3rd molar
Relative microdontia
Macrodontia
True macrodontia :
1. Generalized-pituitary gigantism
2. Localized- single, hemifacial hypertrophy
Relative macrodontia: small jaw, child
Gemination, Fusion, Concrescence
Gemination
single tooth germ
division
single root & root canal +
2 complete or incomplete
separated crowns
tooth no.: normal
twinning
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
Concrescence
Fusion after root
formation
Cementun united
Traumatic injury
or crowding
Pre-extraction xray check
Talon cusp
Eagle’s talon
Lingual projection
from the cingulum area
of ant. teeth
Most contain a pulp
horn
Both in deciduous &
permanent dentition
Dens evaginatus
( central tubercle, occlusal tuberculated premolar;
Leong’s 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
Dens evaginatus
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
Shovel-shaped incisors
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
Dens invaginatus, coronal type II
Dens invaginatus
Radicular type
Hertwig’s sheath invagination
Food deposition→ caries → pulp infection
Restorated as soon as possible
Taurodontism
“Bull-like “ teeth
Bi- or trifurcation
near the apex
Pulp chamber :
greater apicoocclusal height and
no constriction at the
cervical of the tooth
Syndromes associated with taurodontism
Hypercementosis
Supernumerary roots
Any tooth may develop accessary
roots
No tx required, but critical important in
endodontic procedure
Dilaceration
Angulation, sharp
bend of root or crown
Trauma during
tooth is forming
Pre-extraction xray check
Amelogenesis imperfecta
(Hereditary enamel dysplasia; Hereditary brown
enamel; Hereditary brown opalescent teeth)
Defects in-Formative stage→hypoplastic 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
Amelogenesis imperfecta
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
Hypoplastic type
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
Hypoplastic type
2.Hypomaturation
normal thickness of enamel,
but mottled surface; cloudy
white, yellow or brown, opaque
in color
softer than normal
same density as dentin
Hypomaturation type
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
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
Hypocalcified type
Tricho-dento-osseous syndrome
Hypoplastic-Hypomaturation type
Dentinogenesis imperfecta
(Hereditary opalescent dentin)
Classification of DI : (Shields)
Type I : DI + OI (osteogenesis imperfecta) COL1A1,
COL1A2
Type II : Isolated DI. (1/8000)
DSPP
Type III: DI of the Brandywine type *
DSPP
A racial isolate in Maryland,
DI + multiple pulp exposures in deciduous teeth
Osteosclerosis imperfecta
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.
Dentinogenesis imperfecta
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
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
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.
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
Dentin dysplasia
Hereditary, autosomal dominant.
Normal enamel but atypical dentin
formation with abnormal pulp
morphology
Type I (radicular type): “Rootless teeth”
Type II (coronal) DSPP (dentin
sialophosphoprotein) gene mutation
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”.
Dentin dysplasia, type I
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.
Dentin dysplasia,
type II (coronal)
“Lava flowing around boulders”.
Dentin dysplasia
Large pulp stones
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
Radiographic features
1. Radiodensity ↓, “ghost appearance”
2. Large pulp, thin enamel & dentin
Histologic features
1. Dentin↓
2.Widening of the predentin layer,
3. Interglobular dentin and an irregular
tubular pattern of dentin ↑
4.Calcification of the reduced enamel epi.
Enameloid conglomerates
Odontogenic epithelium
Regional
odontodysplasia
Summary
ENVIRONMENTAL ALTERATIONS OF
TEETH
Developmental tooth defects
Turner’s 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
Summary
DEVELOPMENTAL ALTERATIONS OF
TEETH
NUMBER
Hypodontia
Hyperdontia
SIZE
Microdontia
Macrodontia
STRUCTURE
Amelogenesis imperfecta
Dentinogenesis
imperfecta
Dentin dysplasia I & II
Regional odontodysplasia
SHAPE
Gemination, Fusion,
Concrescence
Accessary cusps
Dense in dente
Ectopic Enamel
Taurodontism
Dilaceration
Hypercementosis
Supernumerary roots