Presented by :

Dr. Sayak Gupta

Introduction
What & when ?
Lesions -
Attrition
Abrasion
Abfraction
Erosion
Disturbances affecting structure of teeth
Discolourations
Malformations
Hereditary disturbances of teeth
Trauma
Crack tooth syndrome
References
Conclusion
 what when

Tooth tissue Miller

loss for reasons 1907
other than
caries, trauma
or operative
procedures
 Wasting disease

Attrition Abrasion Erosion

Wear

Physiological Pathological
Pathological tooth wear

Pulp exposure
Loss of vitality
Exposure of tertiary dentin
Exposure of dentin on buccal / lingual surface
Notched cervical surface
Cupped incisal / occlusal surface
Wear of one arch more
Inability to make contact in excursion of mandible
Restoration projecting above tooth surface
Persistent sensitivity
Decrease in length – out of proportion to width
Predisposing factors for tooth substance loss

 Developmental anomalies
 Malocclusion / posterior tooth loss
 Parafunctional habits
 Restorative materials
 Diet
 Systemic disease
 Natural wear & tear
Etiology of tooth substance loss
Endogenous MULTIFACTORIAL
Parafunction
Occlusion
Degluttion Stress / abfraction
Exogenous
Mastication Endogenous
Habits Parafunction
combined combined Degluttion
Occupation
Dental appliance multifactorial Exogenous
Mastication
Dental hygiene
Friction / wear Habits
erosion combined
Occupational
Dental appliance
Endogenous
Plaque
GCF
Gastric juice
Exogenous
Diet
Occupation
Drugs / alcohol
 surface tooth structure loss resulting from direct
frictional forces between contacting teeth.

Continuous
Age dependant
Physiologic
Affects ?
Accelerated by ?
 Attrition can predispose the following

Proximal surface attrition (Proximal surface faceting)

Occluding surface attrition (occlusal wear)

Deficient masticatory capabilities of the teeth

Cheek biting (cotton roll cheeks)

Decay

Tooth sensitivity

TMJ problems
 Modes to detect attrition
Broca method
Photographic & plainimetric method
3 D digital imagery

ATTRITION INDEX ( mod. By Richard & Brown )

0 – No wear
1 – Minimal wear
2 – Noticeable flattening parallel to occlusal plane
3 – Flattening of cusps & grooves
4 – Total loss of contour & / or dentin exposure when identifiable
Tooth wear in general with erosion as one of its
component
Ratings Explanation
Satisfactory
R ( romeo ) No visible wear or change in anatomic form
S ( sierra ) Limited wear & change in anat. Form
Considerable wear & change in anat. Form
M ( mike) but no treatment

Not acceptable
T ( tango ) Considerable wear & change in anatomic form
Further damage to tooth & surrounding tissue
Excessive wear , extreme change in anat form
V ( victor ) Esthetics , function.. Pain on chewing. Damage
To the tooth & surrounding tissue
 Tooth wear index
Score / surface Criteria

B / L/ O / I No loss of enamel surface characteristics

0 C No change of contour

B/L/O/I Loss of enamel surface characteristics

1 C Min.loss of contour

B/L/O Loss of enamel exposing dentin ( < 1/3 of surface )

I Loss of enamel just exposing dentin
2 C Defect less than 1mm deep

B/L/O Loss of enamel exposing dentin ( > 1/3 of surface )

3 I Loss of enamel & dentin but not exposing pulp
C Defect 1-2 mm deep

B /L/O Complete loss of enamel or pulp exposure

4 I Exposure of pulp / secondary dentin
C Defect > 2mm deep / pulp or secondary dentin exposure

B – buccal / L – lingual / O – occlusal / I – incisal / C - cervical

 Pulpally involved teeth
Parafunctional activities
Myofunctional, TMJ, or any other symptoms in
the stomatognathic system
Occlusal equilibration
Exposed sensitive dentinal areas
Actual carious lesions
Restorative modalities
 loss of vertical dimension
 Extensive loss of tooth structure
 Reshaping tooth structures not conducive
 Decay or any other cavitating lesion .
 Worn tooth contour (usually proximally)
 A tooth cracked or endodontically treated.

!
The surface loss of tooth
structure resulting from direct
frictional forces between the
teeth and external objects, or
from frictional forces between
contacting teeth components in
the presence of an abrasive
medium.
 The direction of brushing strokes
The size of the abrasive
The percentage of abrasives in the
dentifrice
The type of abrasive
The diameter of brush bristles
The type of bristles
The forces used in brushing
The type of tooth tissues being abraded
Clinical signs & symptoms

Linear in outline
Peripheries : very angular
Surface : extremely smooth and
polished
Surrounding walls : V-shape
Probing or stimulating elicits pain.

Other forms of abrasion

Iatrogenic tooth abrasions
Pica-syndrome
Certain professional habits
Chewing tobacco
Toothpick, interdental stimulator, or other solid plaque control modes
Pipe smoking or “depression abrasion ”
Diagnose
Correct or replace the iatrogenic dental work
Prevent practicing the causative habits
Lesions multiple, shallow
Involved teeth extremely sensitive
Restorative treatment
“loss of tooth structure resulting from
chemico-mechanical action in the
absence of specific microorganisms”
Etiology

Salivary flow

Ingested acid
Salivary citrates
Excessive tensile stresses at
the tooth clinical cervix
Refused acids
Chelating microbial metabolic products
Secreted acids
Acid fumes
Mechanical
 Erosion ( watson & burke 2000 )

Extrinsic Intrinsic

Gastric reflux
Environmental
sphincter incompetence
Diet
inc gastric pr.
Medication
inc gastric vol.
Life style
Vomiting
psycosomatic
GI disorders
drug induced
Regurgitation
Rumination
 Nomenclature & classification

Etiology Extrinsic
environment
diet
medication
lifestyle
Intrinsic
Idiopathic

Superficial
Clinical severity of tooth surface Generalized
localized

Pathogenecity Manifest / active

Latent / inactive

Palatal / occlusal surface of max .

localization
Buccal / occlusal surface of mand.
No demarcation
The lesion surface is glazed
Does not affect occluding surfaces
Erosion rate
P-D organ
Adjacent gingiva and periodontium
Tooth sensitivity
Carious lesions
 Complete analysis of diet, occlusion,
habits, chronic vomiting and
environmental factors
Eliminate the causes
Treatment symptomatic
Preoperative study models or
photographs
restorative modalities
Gippo -
wedge shaped defects in the
cervical region of the tooth and
are hypothesized to be the result
of tensile stresses concentrated in
this cervical area.
 Etiology
Mechanism of formation

Characteristics

Size of lesion
Typical wedge shaped lesion
Direction of lateral forces
Is always at or near the fulcrum
Classification for treatment
Localized

Tooth surface loss

Generalized

Category 1 : Appearance satisfactory

Category 2 : Appearance not satisfactory
no increase in occlusal ht. req.
Category 3 : Appearance not satisfactory
increase in occlusal ht. req.
i ) sufficient space present
ii ) insufficient space present
Indications for treatment

Associated pathology

Sensitivity

Loss of occlusal stability

Esthetics
Principles of treatment

Eliminate etiology
Denture support
Desensitizing agents
Localized area
Large area
Occlusal functional problem
Extensive case : young
: old
Multiple crown & full mouth rehabilitation
Crown lengthening
Lost occlusal surface
Intrusion / overruption
Increasing the vertical dimension
Category 1

Counseling
Restoration of edentulous space
Control of habits ( bruxism )
Elimination of occlusal interference
Routine restorative procedures

Category 2

Same as above
Counseling
Restoration
monitoring
Category 3

Increase in occlusal vertical dimension

Space obtained by 3 ways

Type of restoration

Metal ceramic or gold full coverage posterior rest.

Short crown height
Occlusal build up
Anterior teeth
Stage I : (Secretary stage) : Enamel matrix formation.
Stage II : : Initial mineralization
Stage III : Enamel maturation

quantitative

Defects
qualitative

maturation
Environmental Enamel Hypoplasia
Localized Non-Hereditary Enamel Hypoplasia
Localized Non-Hereditary Enamel Hypocalcification
Localized Non-Hereditary Dentin Hypoplasia
Localized Non-Hereditary Dentin Hypocalcification
incomplete or defective formation of the organic
enamel matrix of teeth.

hereditary

environmental
Trauma
Nutritional Deficiency
Ingestion Of Chemicals
Congenital Syphilis
Hypocalcemia
Birth Injury, Prematurity, Rh Hemolytic Diseases
Local Infection Or Trauma
Exanthematous Diseases
Idiopathic Causes
Defects are of minimum size
Defect is at the occluding or contacting area
The lesions are discolored
Lesion is completely disfiguring
No sufficient amount of enamel
Any alteration or change in the
colour of the teeth either due to
surface stains or deposits or factors,
which could have created changes in
one or more of tooth tissues during
the development.

intrinsic
Stains

extrinsic
 Amelogenesis imperfecta Bacterial stains
Dentinogenesis Tobacco
imperfecta Foods and
Dental fluorosis beverages
Erythropoietic porphyria Gingival
Hyperbilirubinemia hemorrhage
Localised red cell break Restorative
down materials
Medication Medications
 surface staining, calculus or any other surface deposits.

Clinical Features :
Chromogenic bacteria
Tobacco products
Foods
Dental restorative materials
Medications
Sulfur, silver nitrate or manganese
Copper or nickel
Cadmium
Stannous fluoride
Chlorhexidine
 changes in one or more of the tooth tissues.

Clinical Features

Enamel hypoplasia and hypocalcification.

Dentin non-vitality

Pulp-root canal system pulpal necrosis

Internal resorption
Congenital erythropoetic porphyria
(Gunther's disease) Biliary Atresia

Erythroblastosis Fetalis Medications

Congenital hypothyroidism.
Significant internal hemorrhage.
Neonatal hepatitis.
Proper scaling and polishing.
Intrinsic discoloration
Intrinsic discoloration due to discoloring changes in the pulp-root
canal
Non-vital bleaching
Laminated veneer or porcelain fused to metal or cast ceramic
veneering
Internal resorption
Internal hemorrhage
Microform

Macroform

Properly alligned
Malaligned
Insufficient quality enamel
Amelogenesis imperfecta is a heterogenous group of hereditary disorders of
enamel formation affecting both deciduous and the permanent dentition.

Hypoplastic type of Amelogenesis imperfecta

Types
Hypocalcification type of Amelogenesis imperfecta

Hypomaturation type of Amelogenesis imperfecta

 Enamel thickness far below normal.
Teeth exhibit either complete absence
of enamel or very thin layer of enamel on
some focal areas.
Open contact
Small teeth, with short roots, very
limited pulp chambers and root canal
dimensions
Delay in eruption
Sometimes the enamel is glassy
(prismless)
There may be some discoloration,
usually yellow
The enamel could look wrinkled
All signs of severe occlusal wear
 It may be chalky at early stages of
life.
The enamel chips easily.
The enamel can be very soft in
consistency (cheesy).
Although teeth will have normal
forms when they erupt, they have dull
surfaces readily stainable by age. The
stains become darker with time.
The enamel is worn away very easily
in life with all signs and symptoms of
severe attrition (may be to the gum line
 Affects both deciduous and the permanent
teeth
Sex predilection
Color of the teeth chalky white yellow or
even dark brown
Contact points mostly open
Sometimes the tooth is completely devoid
of enamel
Enamel may have a cheesy consistency
On rare occasions the enamel may look
almost normal except the presence of few
grooves and wrinkles on its surface
Does not increase the susceptibility of
teeth to dental caries.
The mildest form of hypomaturation
“Snow-capped teeth”.
Hypoplastic type

Hypocalcific type
 Early diagnosis
Only two modalities can be used in
most cases.
Selective odontotomy and
esthetically reshaping the teeth
Full veneering
 inherited disorder of dentin formation, which affects the
deciduous as well as the permanent dentition and it usually
exhibits an autosomal dominant mode of transmission.

Type I : Dentinogenesis imperfecta, which occurs in patients

afflicted with Osteogenesis Imperfecta (OI).
Type II : Dentinogenesis Imperfecta, which is not associated with
Osteogenesis Imperfecta.
Type III : Dentinogenesis Imperfecta Type III or the
“Brandywine type” is a rare condition and is inherited as an
autosomal dominant trait.
 Type I : Dentinogenesis imperfecta,
which occurs in patients afflicted with
Osteogenesis Imperfecta (OI).

Inherited as an autosomal dominant trait.

It involves the deciduous teeth more
Teeth have an opalescent color
Patients exhibit Osteogenesis Imperfecta
 Type II : Dentinogenesis Imperfecta, which is not associated
with Osteogenesis Imperfecta.

hereditary opalescent dentin

Most common type
Inherited as an autosomal dominant trait
Involves deciduous and
permanent teeth with equal
frequency.
The color may be from grey, brown,
yellow-brown to violet
Most of them exhibit a
translucent hue.
The enamel, although intact, is
easily chipped because of the
defective dentino-enamel junction.
 The crowns are overcontoured.
The roots are short and slender.
There are signs and symptoms of
extensive attrition.
The dentin is devoid of tubules.
The dentin contains a lot of interglobular
dentin.
The decay process, if initiated, will spread
laterally.
Root canal and pulp chamber space is
obliterated.
Dentin hardness and resilience is almost
half that of normal dentin
 Type III : Dentinogenesis Imperfecta

“Brandywine type”
Inherited as an autosomal
dominant trait.
It is commonly seen in a racial
isolate area in the state of
Maryland.
It affects both dentitions.
Is same as type I and type II
variants, however it often exhibits
multiple pulp exposures and
periapical lesions in deciduous
teeth.
• The Type I and Type II diseases “bulb
shaped” or “bell shaped” crowns
• The roots of the teeth are thin and
spiked
• Depending on the age varying degrees
of obliteration of the coronal as well as
the radicular pulp chamber.
• The cementum, periodontal ligament
and the alveolar bone radiographically
appear normal.
• type III similar to those of the type I
and type II
• “shell” teeth.
• These teeth frequently exhibit multiple
pulp exposure and associated periapical
pathology.
 Early diagnosis
 Two possible treatment modalities
 Selective odontotomy and permanent full veneering
 Metal and ceramic crowns are given.
 Not suitable candidates for playing the role of abutments
 Trauma

Ellis Classification

Class 1 : simple fracture of the tooth crown involving little or no dentin

Class 2 : extensive fracture of the tooth crown involving considerable dentin
but no pulp
Class 3 : extensive fracture of the crown involving considerable dentin and
exposing the pulp
Class 4 : A non vital traumatized tooth with or without loss of crown
structure
Class 5 : Tooth loss as a result of trauma
Class 6 : fracture of the tooth root , with or without loss of crown structure
Class 7 : displacement without fracture of crown or root
Class 8 : fracture of crown enmasse
Class 9 : cracked tooth
Class 10 : cyclic incomplete dislocation of the tooth
CLASSIFICATION OF FRACTURED TEETH

WHO classification from 1978

(code no corresponding to the international classification of diseases; )

873.60 Enamel fracture

873.61 Crown fracture involving enamel and dentin
873.62 Crown fracture involving pulp
873.63 Root fracture
873.64 Crown root fracture
873.66 Luxation
873.67 Intrusion or extrusion
873.68 Avulsion
873.69 Other injuries
 Treatment

Accurate & detailed diagnostic data

Tooth vitality
Incomplete tooth development / early stages of passive tooth eruption

Class 1 Class 2

Class 3
Class 4
Class 5

Class 6 : cervically horizontal

midradicularly horizontal
apically horizontal
vertical root fracture

Class 7
Class 8
Class 9 : Crack tooth syndrome

Class I - involving enamel

Class II – involving enamel & dentin without pulp
Class III – involving pulp
Class IV – root fracture

Etiology

Morphologic
Masticatory accidents
Habits
Systemic causes
Cyclic thermal stress
Iatrogenic
Trauma from occlusion
External trauma
Diagnosis

Visible crack
Radiographic diagnosis
Bite on hard objects
Extensive restoration removed
Crack stained
Fibre optic transillumination
Operating microscope
Tooth slooth crack detector
Probing of sulcus
History of onset
Digital manipulation
Wedging along margin of restoration
Bright mouth light in a dark room
Cold application
EPT
Analgesic ineffective
Tender on percussion when periapical involvment
Treatment

Immediate therapy :
splint
stabilize
relieve occlusion
RCT if indicated
coronal restoration removed
periodontal defect corrected

Permanent restoration :
reinforcing – protecting cast / cast based restoration
foundation

Class 10
 Retention of a resin modified glass ionomer adhesive in non carious cervical lesions-
Follow up.
J dent. 2005 aug 33 (7); 541 -547. (van dijken jw )

3yr clinical evaluation of a compomer & a resin composite as a cl v filling material

Oper dent 05. may 30 (3), 275 – 81.( Gallo jr., Burgess jo )

Attrition , abrasion, erosion – a review .

JADA 04. aug, 138 (8) : 1109 – 18.