Download 02. Un-carious defects of teeth

Un-carious defects of teeth.
Classification. Pathomorphology,
clinic and diagnostics of defects
that are developed before and
after eruption of teeth. Treatment.
Therapeutic dentistry department
Uncarious lesions of teeth
Developmental
Alterations of
Teeth
Post-eruptive
Alterations of
Teeth
Developmental Alterations of Teeth
I. Lesions that occur in the stage of
dental follicle development, before
eruption:
1. hypoplasia;
2. hyperplasia of enamel (enamel
pearls);
3. endemic fluorosis;
4. developmental disturbances and
disorders of eruption;
5. genetic disturbances of tooth
development.
Posteruptive Alterations of Teeth
II. Lesions that occur after teeth have
been erupted:
1. tooth wear: attrition, abrasion,
wedge-shaped defect;
2. erosion;
3. necrosis of hard tooth tissues;
4. hyperesthesia;
5. trauma of teeth;
6. fluorosis;
7. discolorations of teeth:
intrinsic stains
extrinsic stains
DEVELOPMENTAL DISTURBANCES AND
DISORDERS OF ERUPTION
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
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
Premature eruption
Neonatal teeth: within 30 days
Natal teeth: newborns
Most are prematurely erupted deciduous teeth
Removal only if mobile and at risk of aspiration
Disturbances in tooth form
may present as dilacerated teeth, double teeth,
dens invaginatus and enamel pearls
Anhidrotic
ectodermal
dysplasia
showing
conical teeth,
giving an
undesirable,
Dracula-like
appearance.
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
Cementum 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 invaginatus
( 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 invaginatus
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
Enamel pearls
Enamel pearl.
There is a small
mass of enamel
at the root
bifurcation
Supernumerary roots
Any tooth may develop accessory
roots
No rtg required, but critical important
in endodontic procedure
Dilaceration
Angulation, sharp
bend of root or
crown
Trauma during
tooth is forming
Pre-extraction xray check
DISTURBANCES IN THE NUMBER
OF TEETH
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
Hypodontia
Congenital absence of lateral incisors with
spacing of the anterior teeth.
Supernumerary teeth, hyperdontia
Mesiodens
Paramolar
Supplemental teeth
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.
DISTURBANCES OF TOOTH SIZE
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
Disturbances in the structure of teeth
Disturbances of enamel
■ Genetic disturbances
- Amelogenesis imperfecta.
■ Local disturbances:
- Infection.
- Trauma.
- Idiopathic.
■ Generalised disturbances:
- Infections.
- Fluorosis.
- Neonatal events, e.g.
premature birth, rhesus
incompatibility.
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
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
ACQUIRED DISTURBANCES OF
ENAMEL FORMATION
Factors associated with enamel defects
Local1.Local acute mechanical trauma
2. Electric burn
3. Irradiation
4. Local infection: periapical
inflammatory disease
Acquired disturbances of enamel formation
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
Acquired disturbances of enamel
formation
Most acquired enamel defects result in areas of
HYPOPLASIA, which may be due to either a defect
in matrix production or a defect in mineralisation.
Localized - only a single tooth is affected
Generalized - several teeth are affected
Turner’s hypoplasia, Turner’s tooth
Permanent teeth
Periapical
inflammatory
disease of the
overlying
deciduous tooth,
less frequently in
anterior teeth
Traumatic injurynot rare
-45% children
sustain injury to
their deciduous
teeth, 23%
permanent teeth
development
disturbed
Turner’s hypoplasia secondary
to previous trauma
Turner’s teeth
Generalized defects are sometimes referred
to as chronological hypoplasia
The overwhelming majority of chronological
hypoplasia are the result of disturbances in
the first 10 months of life and the teeth
usually affected are:
■ The first permanent molars.
■ Upper central incisors.
■ Lower lateral incisors and canines.
Chronological hypoplasia due to metabolic upset.
Unlike the hereditary types of amelogenesis imperfecta,
defects are linear and thought to correspond to a short
period of amelogenesis disturbed by a concurrent
severe illness
Syphilitic hypoplasia
•Congenital syphilis
•Hutchinson’s incisors &
mulberry molars
Congenital syphilis; Hutchinson's teeth. The
characteristics are the notched incisal edge and the
peg shape tapering from neck to tip.
Disturbances in the structure of teeth
Disturbances of dentine
This genetic disorder is characterised by defective dentine
matrix production and two types have been described.
Dentinogenesis imperfecta type 1 occurs in association with
osteogenesis imperfecta, in which there is defective bone
formation. It is very uncommon.
Dentinogenesis imperfecta type 2 is the commonest form. It
has the following features:
■ Both the permanent and primary dentition are affected.
■ The teeth have a normal shape on eruption but appear
amber–brown or purple–blue in colour.
■ The enamel shears away from the poorly formed dentine
which quickly wears away.
■ The pulps become obliterated with abnormal dentine.
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
Developmental Structural Abnormalities
Involving Both Enamel and Dentin
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
On one side of the midline the
deciduous incisors have poor root
formation with thin radicular dentine
and enamel. A poorly organised
spotty calcification is present at the
site of the permanent successors.
Odontogenesis
Imperfecta
Shell teeth
Initial reported in the Brandywine population
Normal thickness of enamel associated with
extremely thin dentin and dramatically enlarged
pulps (due to insufficient and defective dentin
formation)
Short roots.
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.
ENDEMIC DENTAL FLUOROSIS
Acceptable measures
of fluorine in water
according to hygienic
standards is –
0,8-1,2 (1,5) mg/l.
Fluorosis is the term
given to changes in
the enamel which are
associated with
excess ingestion of
fluoride
Fluorosis. Moderate effects from an
area of endemic fluorosis. Irregular
patchy discolouration.
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
POSTERUPTIVE DEFECTS
II. Lesions that occur after teeth have been
erupted:
1. tooth wear: attrition, abrasion, wedgeshaped defect;
2. erosion;
3. necrosis of hard tooth tissues;
4. hyperesthesia;
5. trauma of teeth;
6. fluorosis;
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
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
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
Treatment and prognosis of tooth
wear
Resolve pain and sensitivity
Identify the cause of tooth
structure loss
Protection
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, jaundice (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
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
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
TRAUMA
Uncomplicated crown fracture
Complicated crown fracture
Crown-root fracture
Root fracture