• Attrition is mechanical wear of the incisal or occlusal
surface as a result of functional or parafunctional
movements of mandible ( tooth- to- tooth contact .
• Is a continuous, age dependentprocess, which is
• Seen in both deciduous and permanent
dentition.(rare in decidous not retained for a
longer period of time).
• Seen in children those who have Dentinogenesis
and Amelogenesis imperfecta.
• Men exhibit more severe attrition than women.
a) Proximal surface attrition
b) Occluding surface attrition
Proximal surface attrition :
• Widening of proximal contact areas.
• Decreased mesio-distal width of teeth.
• Interproximal space will be decreased in
Occluding surface attrition :
• Loss, flattening, faceting and /or reverse cusping
of occluding elements.
• Loss of vertical dimension of tooth.
• Cheek biting and gingival irritation occurs.
• coarseness of diet ,chewing tobacco or bruxism,
occupation –person exposed to an atmosphere
of abrasive dust.
• Appearance of small polished facet on a cusp tip
or ridge or a slight flattening of incisal edge.
• Gradual reduction of cusp height & flattening of
occlusal inclined plane with aging.
• Tooth sesitivity
• TMJ problem elicited especially in the
• In some older patients, the enamel of the cusp
tips or incisal edges is worn off, resulting in
cupped-out areas because the exposed, softer
dentin wears faster than surrounding enamel.
• Sometimes these areas are an annoyance
because of food retention or the presence of
peripheral, ragged, sharp enamel edges.
• Advanced attrition – enamel may worn away
results in an extrinsic yellow or brown staining of
exposed dentin from food or tobacco.
• May progress to complete loss of cuspal
• Abrasion is an abnormal tooth surface loss
resulting from direct friction forces between the
teeth and external objects or from frictional
forces between contacting teeth components in
the presence of an abrasive medium.
• It is the pathologic wearing away of tooth
substance through some abnormal
mechanical process .
Mainly due to :
• Improper brushing technique
• Abrasive dentrifices & Hard tooth brush
• Habits such as holding a pipe stem by the teeth,
opening of bobby pins with the teeth (resulting
notching of incisal edges of maxillary CI )
• In carpenters, tailors, shoe makers who holds
nail, tacks and pins between the teeth
• Improper use of tooth picks and dental floss
• Pipe smokers, Chewing tobacco
• Tooth brush abrasion is more common, occuring
• Usually occurs on exposed root surfaces of teeth
and in sometimes incisal and occlusal surfaces.
• Abrasion caused by dentrifices appears as “v”
shaped or wedge shaped ditch on the root side
of CEJ in teeth with gingival recession.It also
involving cervical enamel and dentin.
• Abrasion more common on left side of mouth in
right handed people.
• Canines and premolars are most affected.
• Exhibit sharp margins and sharp internal angles.
• Many teeth are affected.Usually on the facial
surfaces of maxillary left canine to molar region
in right handed person and vice versa
• Modern dentrifices are not sufficiently abrasive
to damage intact enamel severely, can cause
wear cementum & dentin,particularly in
horizontal direction rather than vertical direction .
• Pipesmoking “depression abrasion” which is an
abraded depression on the occluding surfaces of
teeth at a latero-anterior of arch coinciding with
intraoral location of pipestem.
• Results from intrusion and abrasion of the tooth.
• Chewing tobacco cause generalized occlusal
• Pica-syndrome, which is due to the habit
• Erosion is the wear or loss of tooth surface by
• It is the irreversible loss of dental hard tissue
that does not involves bacteria.
• Dissolution of mineralised tooth structures
occurs upon contact with acids that are
introduced in to oral cavity from intrinsic (eg ,
gastroesophageal reflux ,vomiting ) or
extrinsic sources (eg,acidic beverages , citrus
• Topographically, the extent of erosive lesion can
range from a fine unnoticeable line at CEJ to
substancial tooth substance loss making an hour-
glass shape out ofa tooth.
Saliva as a modifying factor
Netrualisation of acid
• Erosion lesion generally present as broad,
shallow, saucer- shaped defects involving
enamel and dentin.
• No sharp line angles and the margins of the
defects are not well defined.
• Surface appears smooth and polished
• Occurs on facial or lingual surfaces.But usually
on the lingual surfaces of maxillary anteriors.
• Exogeneous agents such as lemon juice (by
lemon sucking) , cause crescent or dished
defects ( rounded as opposed to angular) on the
surfaces of exposed teeth.
• Endogenous agents cause generalized erosion
on the lingual, incisal and occlusal surfaces.
Erosive lesion is pathognoic in following situations :
• No demarcation between lesion & adjacent tooth
• Erosion usually does not affect occluding
surface, except in advanced situations.
• Erosion rate is similar for enamel, dentin,
cemetum & sometimes for restorative materials.
• Adacent periodontium and gingiva are sound
• Tooth sensitivity to physical, chemical &
mechanical stimuli .
• No carious lesion present.
Rate of erosion in active lesion was esteemed to
be 1micron per day.
• Abfraction is the pathological loss of tooth
substance due to biomechanical loading forces
that result in flexure and ultimate fatigue of
enamel and dentin at a location away from
• It has been proposed that the predominant
causative factor of some cervical, wedge-
shaped is a strong(heavy) eccentric occlusal
force resulting in microfractures or abfractures.
• Such microfractures occurs as the cervical
areas of the tooth flexes under such loads.
• With each bite , occlusal forces causes teeth to
• Constant flexing ; enamel to break from the
crown usually on the buccal surface.
• Parafunctional habits such as bruxism and
clenching is also a cause of abfraction.
• Forces could be static ,such as produced by
swallowing & clenching or cyclic as those
generated during chewing action.
• Abrasive lesions were caused by flexure &
ultimate material fatigue of susceptible teeth at
locations away from the point of loading. The
breakdown was dependent on the magnitude ,
duration ,direction , frequency & location of the
Clinical features :
• Appears as wedge-shaped defects on the facial
• With sharp margins and internal line angles.
• In the initial stages the enamel surface is rough
and shows striations or grooves.
• Later stages the defects progresses deeper in
dentin two or more grooves may be visible on
a)Incomplete Fracture Not Directly Involving Vital Pulp
• Also called Greenstick fracture.
• This condition is very sensitive, yet the patient can
specify only which side of the mouth rather than the
a)Complete Fracture Not Involving (Not into) Vital
• Not associated with pain, unless the gingival border
of the fractured segment is still held by periodontal
• Restorative treatment is indicated.
c)Fracture Involving (into) Vital Pulp
• Always result in pulpal infection and
• If tooth is restorabe, immediate root canal
therapy is indicated, otherwise it must be
• Ellis classification :
• Class 1 : Fracture of enamel, involving
little or no dentin.
• Class 2 : Fracture of enamel and dentin,
but no pulp.
• Class 3 : Fracture of enamel, dentin and
• Class 4 : Tooth becomes non-vital with or
without loss of crown.
• Class 5 : Traumatically avulsed tooth.
• Class 6 : Frature of root wit or withot
• Class 7 : Displacement of tooth without
NON HEREDITORY ENAMEL
• Occurs when ameloblasts are injured during enamel
formation, resulting in defective enamel formation
(diminished form or calcification or both ).
• Usually seen on anterior teeth and first molars in the
form of opaque white or light brown areas with
smooth, intact, hard surface or of pitted or grooved
enamel, which is usually hard & discoloured.
• Nutritional deficiencies (vit.A,C & D)
• Exanthematous diseases (Measels,chicken
• Congenital syphilis
• Birth injury,prematurity, Rh hemolytic disease
• Local infection or trauma
Clinical features :
• In mild condition, few small grooves, pits,or
fissures on the enamel surface.
• In severe condition, rows of deep pits arranged
horizontally across the surface of tooth.
• Enamel hypoplasia due to congenital syphilis is
not of pitting variety, instead almost
pathognomic appearance.It involves maxillary &
• The anterior teeth affected are called
“Hutchisons teeth”& molar are called “Mulberry
Molars” (Moon’s molars,Fournier’s molars).
• Enamel Hypoplasia due to local infection or
truama seen in single tooth, commonly
permanent max. incisors or max. or mand.
Premolars called Turner’s teeth and the
condition is called Turner’s Hypoplasia.
• Occurs as mild brownish discolouration of the
enamel to a sever pitting and irregularity of the
• Due fluoride ingestion during the time of tooth
formation result in mottled enamel.
• Depending upon the level of fluoride in the
1)Questionable changes charecterizd by
white flecking or spotting of enamel.
2)Mild changes manifested by white opaque
areas involving more of tooth surface
3) Moderate & severe changes showing
pitting and brownish staining of the
4) Corroded appearance of the teeth
Moderately or severly affected teeth may
Non Hereditary Enamel Hypocalcification
• Destruction of ameloblast interfere the formation
• Also interfere with mineralization of matrix.
• Clinical features :
• Affected area will not be defective.
• Chalky and soft to indendation and will be
• If extensive it changed to attrition & abrasion.
• Enamel can be chipped if the lesion involves
Non Hereditary Dentin Hypoplasia
• Odntoblast are disturbed by enironmental
• Result in defective dentin deposition.
Non Hereditary Dentin Hypocalcification
• Have same cases as Hypoplasia.
• Dentin is softer, more penetrable, and less
resilient. Eg. Interglobular dentin
• Mostly the lesion is unnoticed.
• Extrinsic : Surface staining due calculus.
• Intrinsic : Changes in one or more of tooth
• 1)Discolouration in enamel –Hypoplasia &
• 2) Discolouration in dentin – Due to non
vitality resulting in disintegration of dentinal
tubules or from pigmentation or staining.
• 3) Tetracycline discolouration
• 4) Discolouration in pulp
• Either in micro or macro forms.
• Usually hereditary in origin.
• Most common type is one or two teeth become
smaller called peg teeth.
• Commonly upper laterals are involved
• Enamel is defective in form or calcification as a
result of hereditary and has an appearance
ranging from essentially normal to extremely
• Also called Hereditary enamel dysplasia or
Hereditary brown enamel or Hereditary brown
• In radiographically, the overall shape of the teeth
may or may not be normal depending upon the
amount of enamel present on the tooth and the
amount of occlusal & incisal wear.
• Enamel appear totally absent or when present
appear as thin layer, chiefly over the tips of cusp
and on interproximal surface.
• No treatment except for the improvement of
• Is a hereditary condition in which only the dentin
• Normal enamel is weakly attached and lost
• Affecting both decidous and permanent detition.
• Affected teeth are gray to yellowish brown and
have broad crowns with constriction of cervical
area resulting a ‘tulip’shape
• Radiographically, teeth appear solid, lacking
pulp champers and root canals.
• Enamel is easily broken leading to exposure of
• Dentinogenesis imperfecta 1
• Dentinogenesis imperfecta 2
Dentinogenesis imperfecta type 1
• Also called Opalescent dentin or Capdepont
teeth or Den. Imperfecta with out Osteogenesis
imperfecta. Or Shields type II.
• Affects only the teeth, no bone fractures.
• Blue grey or amber brown or opalescent.
• On X-rays teeth as bulbous crowns, roots
are narrow and pulp champers and root canals are
smaller than normal or completely obliterated.
• Enamel split from dentin when subjected to
Dentinogenesis imperfecta 2
• Also called Shields type III or Brandywine type
• Crowns of the deciduos and permanent teeth
wear rapidly after eruption.
• Multiple pulp exposure may occur.
• X-rays of decidous teeth show large pulp
Champers and root canals & reduced in size as
• Permanent teeth have pulpal spaces that are
• Non-carious lesions require clinical attention if
any of the following factors exist :
3)Risk of tooth fracture
6)Poor periodontal health
• 1) Dentin desensitization
• Used in situations where minimal amount
of dentin is exposed (less than 1mm) &
patient experiences hypersesitivity.
• This managed by any of the method
suggested for dentin desensitization such
• Fluoride varnishes or fluride iontophoresis
• Dentin bonding agents
• Use of desensitization tooth pastes
Indicated in following situations
• Considerable loss enamel and dentin
• Esthetic is compromised
• Deep lesion affecting the strength of the tooth
and pulpal integrity
• Caries beginning in the cervical lesion
• Significant sensitivity of the exposed dentin
• Class v non carious lesion with any of the
permanent restorative material presently
• Of these, Amalgam, direct gold, cast gold inlays
• Currently composite resins and glass ionomer
cements are used.Because they are adhesive
and do not require extensive cavity preparation.
• Composite resin restorations :
a) To o th pre paratio n :
• No cavity preparation is necessary for class v
non carious lesions.Shape of the defect is
amendable for filling .However enamel margin
beveled to increase the surface area for bonding
& to produce esthetic .
b) Pum ice pro phylaxis :
• Clean the surface of any debris or plaque.
c)Shade se le ctio n
d) Iso latio n
e )Acid e tching & de ntin bo nding
f)Co m po site re sin place m e nt
g )Finishing & po lishing
• New variety introduced in 1990s
• Combines the durability of composite & fluoride
releasing ability of GIC.
• Available as a single component light curable
material in a syringe.
• Steps is same as that of composite restoration
• Indicated for class V cavities.
• Glass IonomerCements :
• Chemically cured GIC have an excellent track
record for restoring class V noncarios defects.
• Nowadays resin-modified GIC are referred.
• ENDONTIC THERAPY:
• When cervical tooth loss is extensive reslting in
pulpal involvement, endodontic therapy is
necessary followed by post placement & full
coverage in the form of crown
• Required when non-carios cervical defects are associated
with gingival recession and mucogingival problems.
• Diet councilling
• Use of sodium bicarbonate mouth rinse
• Use of fluoride mouth rinse & xylitol gum
• Psychiatric consultation
• Correct brushing technique
• Correct occlusal stresses
• Provide mouth guards
• Correct abnormal oral habits
Management of Attrition
• Pulpally involved tooth should be
extracted or undergo endontic therapy.
• Para-functional activities, notably bruxism,
controlled with proper discluding-
protecting occlusal splints.
• Occlusal equilibration – by selective
grinding of tooth surfaces (include
rounding and smoothening the
perepheries of occlusal tables.
• Restorative modalities- Metallic restoration
Management of Abrasion
• Remove the cause.
• Treated with fluoride solution to improve
its caries resistance.
• Lesion is exceeding 0.5mm into dentin, it
should be restored.
• Tooth is sensitive then desensitize the
exposed dentin before starting restorative
treatment. (Desensitization by 8-30% Na
or Stannous fluoride for 4 to 8 min )
• Restoration by Direct tooth coloured
materials(in anterior) & metallic restoration
Management of Erosion
• Remove the cause.
• If restoration is the choice of treatment,
metallic restoration is ndicated because it is
resistant to erosion.
Management of Enamel Hypoplasia
• Bleach the affected teeth with an agent such as
• This carried out periodically,since the teeth continue
• Lighteningof discolourations of teeththroughthe
applicationof chemical agents tooxidizetheorganic
• BleachingAgents :
Mechansm of Action :
• Low mol. Wt of H2O2 allows it to easily diffuse
through enamel & dentin.
• Here it breaks down in to water and releases
perhydroxyl ions and nascent oxygen.
• Due to its great oxidative power it breaks up
large macromolecule stains into smaller stains.
• These reflect less light and tooth appear
lighter.The free oxygen opens the c-ring of
pigment molecules converting them into
colourless hydroxyl compound.
Non Hereditary Enamel Hypocalcification
• Mineralization of tooth enamel should be
made using fluoride application, fluoride
• Vital bleaching,laminated
veneering,composite veneering, and
porcelian fused to metal and cast ceramic
Non heritary dentin hypoplasia and
• Intermediary bases
Management of Malformation
• Malaligned teeth is repositioned
• Porcelain fusedto metal or cast ceramic
Management of Dentinogenesis
• Cast metal crown or on posterior teeth and
jacket crown on anterior teeth.
• Filling are not usually permanent because
of softness of dentin.
• With increasing dental awareness and
improved dental care, more and more
people are retaining their teeth for a longer
period of time.
• When loss of enamel and dentin at the
CEJ becomes significant, resulting in loss
of function and esthetic, restoration of
these defects becomes necessary.
• Composite resins and GIC are used
extensively for restoration of non-carious