NON CARIOUS TOOTH DEFECTS

GUIDED BY
DR.P.KARUNAKAR
DR.UMRANA FAIZUDDIN
DR.ASHISH JAIN
Presented by:
A.Sarika
 CONTENTS
Introduction
Etiology
Attrition
Abrasion
Erosion
Abfraction
Localized non hereditary enamel hypoplasia
Localized non hereditary enamel hypocalcification
Localized non hereditary dentin hypoplasia
Localized non hereditary dentin hypocalcification
Amelogenesis imperfecta
Dentinogenesis imperfecta
Discoloration
Trauma
Conclusion
References
 INTRODUCTION
T
O
O
T
H

S
T
R
C
T Physiological
U
R
E

L
O Pathological 25% of tooth destruction
is caused by these non-
S
carious lesions.
S
 Non carious tooth defects

Developmental Acquired

Hereditary Non hereditary Tooth wear Resorption

Trauma
 INCIDENCE
Non carious lesions

 unique to modern man

 copper age & middle age

( 2050-2080 BC & 110-1400 AD)

 children as well as adult

teeth.

 incidence :increasing with age.

One study:1,753 children are examined at 12 years of age and then again at 14
years of age.
Erosion was present in 56% at 12 years of age and 64% at 14 years of age.

Terminology

 Eccles : “Tooth substance loss” used to encompass terms such as

attrition, abrasion, erosion.

 Later smith& knight(1984) : “ Tooth wear” so as to include all these

conditions & their combination.

 They also proposed a tooth wear index

 Etiology

entire etiology of NCCLs has

not been determined toothpaste/
tooth brush
 there is overwhelming abrasion
evidence that the cause is
multifactorial
occlusal
forces
,

low pH.
Tooth wear:

 The term tooth wear is used in general to describe the process of

attrition, abrasion, erosion and abfractions.

 It is a common problem and estimated prevalence indicates that up to

97% of the population is affected.
SCOR BUCCAL/LINGUAL INTERPROXIMAL/OCC CERVICAL
E LUSAL
0 No loss of enamel No loss of enamel No change in
surface surface contour
1 Change in enamel Change in enamel Minimal loss of
surface surface contour

2 Loss of 1/3rd of enamel Loss of enamel fissure Defect < 1mm

surface exposing dentin

3 Loss of more > 1/3rd of Exposure of dentin 1-2mm deep

enamel defect
Surface
4 Complete loss of Substantial loss of 2-3mm deep
enamel surface, dentin; no exposure of defect
exposure of dentin pulp
5 Pulp exposure Pulp exposure Pulp exposure
 SIMPLIFIED SCORING CRITERIA FOR TOOTH WEAR INDEX

SCORE CRITERIA

0 No wear into dentin

1 Dentin just visible or dentin exposed for less

than 1/3rd of surface
2 Dentin exposure greater than 1/3rd of surface

3 Exposed of pulp or secondary dentin

 Consequences of tooth wear
 Change in appearance of teeth
 Exposure of dentin normally covered by enamel
 Dentin Hypersensitivity
 Loss in occlusal vertical dimension
 Loss in posterior occlusal stability resulting in
 Mechanical failure of teeth or restorations
 Hypermobility and drifting
 Pulpitis and loss of vitality
 Exposure of pulp
 ATTRITION:

Definition: It is defined as physiological wearing away of tooth as a result

of tooth to tooth contact as in mastication.
-Shafer
It may be defined as surface tooth structure loss resulting from direct
frictional forces between contacting teeth.
-Marzouk
 Etiology:

 usually physiologic.
 Any contacting tooth surface is subjected to the attrition process,
beginning from the time it erupts in the mouth and makes contact with
reciprocating tooth surface.
 Accelerated by parafunctional movements
 Men > women
 Certain occupation.
Clinical features of attrition:
The first manifestation:
 appearance of a small facet on cusp tip or ridge or a slight flattening of
incisal edge.

In severe cases:
 “a reverse cusp” situation might be created in place of the cusp tips and
inclined planes.
Although every person has some signs and symptoms of attrition in
their dentition, attrition can predispose to or precipitate any of the
following
proximal surface attrition (proximal surface faceting)
occluding surface attrition (occlusal wear)
 Proximal surface attrition:

 It results from surface tooth structure loss and flattening widening of

proximal areas.

surface area proximally: increased Mesio-distal dimensions of teeth

susceptible to decay is increased are reduced, resulting in overall
reduction of the arch length.

The interproximal space is reduced, interfering with

physiology of dental papilla, leading to periodontitis.
 Occlusal surface attrition:

flattening, faceting and or reverse cusping of occluding elements leading

to loss of the vertical dimension of the tooth.
Short period Loss of vertical dimension
Time
factor
Long period No loss of vertical dimension
Effects:
 Deficient masticatory capabilities
 Blunting of the cusps needs more force to shear food items.
 Cheek biting and gingival irritation
 Decay
 Hypersensitivity
 Tmj problems
 ATTRITION INDEX

SCORE CLINICAL FEATURE

0 No wear

1 Minimal wear

2 Noticeable flattening parallel to occluding

planes
3 Flattening of cusps & grooves

4 Total loss of contour & or dentin exposure

 Treatment modalities for attrition:
Pulpally
involved teeth Periodontium

Myo-functional Exposed dentinal

, TMJ disorders surfaces

Occlusal
equilibrium
Restorative modalities

Lost tooth structure due to attrition is at high stress concentration areas.

metal-based restorations should be used in following situations,
 Noticeable loss of vertical dimension
 Reshaping of remaining tooth structure not enough in creating physiological
mandibular movements.
 Decay superimposed with attrition
 Proximal tooth wear which leads to lack of maintenance of periodontium.
 A tooth cracked or endodontically
Bruxism: (Night grinding; bruxomania)
Bruxism is the habitual grinding of the teeth, either during sleep or as an
unconscious habit during working hours.
Etiology:
Meklas in 1971 reviewed bruxism and described causes as
Local
occlusal disturbances
unrecognized tension
transition from deciduous to permanent dentition.
Systemic
Malnutrition
Endocrine disturbances
Hereditary factors
Psychological factors
Bruxism (emotional disturbances )
children as nervous manifestation and related to biting or chewing of toys.
Occupational factors
Athlete's engaged in physical activities
Watchmakers
Habitual gum chewers
Clinical features seen in bruxism:
Effects of bruxism are divided into six groups (Glaros & Rao)
Effects on dentition:
When the habit is firmly established severe wearing or attrition of teeth may occur, not
only occlusal wear, but also interproximal wear.
Effects on periodontium:
Loss of integrity of periodontal structures
Loosening or drifting of teeth
Gingival recession with alveolar bone loss
Effects on masticatory muscles
Bruxism may result in hypertrophy of masticatory muscles, which may interfere with
maintenance of resting position
Causes trismus, and alter occlusion and the opening and closing patterns of the jaws.
Effects on TMJ:
TMJ disturbances may be produced as a result of continuous tooth impact without
normal periods of rest.
head pain
psychologic and physiologic effects
 ABRASION:
Definition:

Abrasion is defined as the pathological wear of tooth substance through some abnormal
mechanical process.
-Shafer

Surface loss of tooth structure resulting from direct friction forces between teeth and
external objects, or from frictional forces between contacting teeth components in the
presence of an abrasive medium.
-Marzouk

Wearing away of the tooth substance because of grinding, rubbing or scraping caused by
external mechanical means, like in repeated contact of the teeth with foreign object or
substances.
-Vimal K. Sikri
Etiology:
Abrasion is a pathologic process
Most common cause:
faulty oral hygiene practice like
brushing (horizontal) technique, and
frequency; time and forces applied during brushing.
Oral hygiene products :
• hardness and shape of tooth bristles,
• flexibility and length of the tooth brush handle affecting the
grip of the tooth brush, and
• the grittiness, pH and amount of dentifrice used.
• Tooth powder is generally five times more abrasive than its
dentifrice counterparts.
 Ill fitting clasps of partial dentures are also known to induce localized abrasion lesions.

 Cervical abrasive wear on the proximal surfaces of teeth is often caused by friction from
objects such as tooth picks, interproximal brushes etc.

 Occupation of the patient- carpenters, shoe makers, tailors- notching of the maxillary
central incisors may be seen.
 Tooth brush abrasion:

Robinson stated that the most common cause of abrasion of tooth surface is the use
of abrasive dentifrice.
 This progresses quickly when the gingiva recedes.
The extent, depth and rate of formation depend on
 The size of the abrasive: larger and more irregular
 The direction of brushing strokes: Horizontal directions are the most detrimental.
 The percentage of abrasives : higher the percentage is, the more abrasion
 The type of abrasives: Silica abrasives are more abrading than phosphate and
carbonate ones.
• The diameter of brush bristles: greater the diameter, the more the abrasion.
• The type of bristles : Natural bristles are more abrasive than synthetic (mylar) ones.
• The forces used in brushing: more the force, the more abrasion there will be.
• The type of tooth tissues being abraded.
• Generally, enamel is quite hard and not easily abraded therefore it serves as a
protection for the underlying dentin, which is abraded 25 times faster.
• Cementum is the softest of all tissues and shows an abrasion rate of 35 times
higher than enamel.
 Clinical features of abrasion:

 Males are comparatively more affected than females.

 Premolars and canines are more susceptible to abrasion probably because they
are placed slightly protruded in the dental arch.
 Right-handed individuals show a preponderance of lesions on the left side and
vice versa.
 Morphology of abrasion lesions:
Abrasion lesions are of varying morphology and may be classified as :

Notch/V- shaped defects: where oblique occlusal and cervical walls intersect at a
certain depth with no definite axial wall in between them.

C-shaped defects(C): where cross section of the defect is C-shaped with rounded floors.

Under cut concave (UC): where occlusal and cervical walls intersect with a definite axial
wall in between them.

Divergent box (DB): where a definite axial wall is present with the occlusal and cervical
walls diverging towards the surface.
Lesions may show varying grades of depths like
-shallow: 0.1- 0.5 mm in depth.
-deep: more than 0.5 mm in depth.
-exposure: pulp is exposed.

Depression abrasion:
This is seen in pipe smoking, where one can see an abraded depression on the
occluding surfaces of teeth at a latero-anterior portion of the arch, coinciding with intra
oral location of the pipe stem. Probing or stimulants (hot, cold or sweets) on the lesion
can elicit sensitivity or pain.
Treatment modalities for abrasion:

Diagnose the cause of abrasion and take necessary steps to eliminate the etiological factor

 In case of tooth brush abrasion, patient should be advised or educated about the
brushing technique and the tooth brush, dentifrice to be used.

 Prevent the patient from practicing causative habits. The objective should be to
prevent any further destruction of the tooth.

 Lesions on non-occluding surfaces not exceeding 0.5mm in dentin does not require
any restoration. The edges of the defect should be smoothened.
 If the lesion is > 0.5mm into dentin (V-shaped), then it should be restored.
Desensitization of the hypersensitive teeth by fluoride solution application (8- 30%
sodium or stannous fluorides for 4- 8 minutes).

 If the abrasive lesion involves an anterior tooth or facially conspicuous area of a

posterior tooth, at a non occluding tooth surface, restoration can be done with
direct tooth colored materials
 EROSION:
Definition:

Erosion can be defined as the loss of tooth structure resulting from

chemico- mechanical acts in the absence of specific microorganisms.
-Marzouk

Loss of tooth substance by chemical process that does not involve known
bacterial action.
-Shafer

Defects arising because of dissolution of tooth structure subsequent to

chemical attack of either endogenous or exogenous origin, or combined chemico-
mechanical attack.
-Vimal K Sikri
Depending upon the source of chemicals, usually acids, erosion may be intrinsic or
extrinsic.
Intrinsic erosion:

 Gastric acid contacting the teeth during recurrent vomiting,

regurgitation or reflux.
 psychosomatic disorders eg: Nervous vomiting,
self induced anorexia nervosa, bulimia etc.
 somatic disorders like pregnancy, gastric dysfunction,
chronic constipation, duodenal and peptic ulcers etc.
 Excess of acid salts present in the saliva ( fermentation process).
 Acidity from a local acidosis in periodontal tissues ( traumatic occlusion).
 Intrinsic erosion is most likely seen on lingual surfaces of anterior teeth especially
maxillary teeth because of the accumulation of vomitus on the dorsum of tongue
first reaches and is in prolonged contact with these surfaces.
 Extrinsic erosion:

 Extrinsic erosion is a consequence of exogenous acids

found as a contaminant in the work atmosphere
 eg: acid battery factories.
 Chlorinated swimming pools.
 Medications like iron tonics, aspirin, hydrochloric acid
replacements, oral hygiene products etc.
 The most commonly consumed, potentially
damaging acidic diets are rich in fruits, fruit acids,
and phosphoric acids in juices, lemons vinegar and
beverages
 STUDIES

 High (1977) described an unusual pattern of dental erosion in a 23 year old male and
attributed it to the subject’s bizarre habit of holding a gulp of cola in his mouth until
all the carbonation had dissipated

 Levine (1973) based on his results warned against excessive consumption of fruits
and juices.
 Shaw (1987) highlighted the potential erosive effects of acidic juices when given for
prolonged periods of time in some form of comforter or feeder.
Several factors may actually vary the erosive response in individuals consuming acidic
fluids.
- manner in which the fluids consumed
- tooth surfaces that come in contact with the fluid
- duration of contact with the teeth
- pH, buffering effect and content of calcium and phosphate in the drink.
- swallowing habits
- access to saliva
- soft tissue movements.
- roughness of individual food consumed.
- prolonged contact of an acid with tooth surface increases its damaging potential.
Role of saliva:
 Saliva plays an important role in modifying the
erosive effects of dietary foods and beverages by the following mechanisms.
 Dilution and clearance of an erosive agent from the oral cavity
 Neutralization and buffering of dietary acids
 Formation of a pellicle layer on the surface of enamel which protects it from
demineralization by dietary acids.
 Both quantity and quality of saliva are known to control the extent of dental erosion.
 Clinical features of erosion:

 Dental erosion is believed to be a result of demineralization

of the inorganic matrix of the tooth.
 Eroded enamel appears smooth and polished, perikymata on it are usually
absent and the eroded area may or may not be discolored.
 According to Mannerberg (1961), two erosive phases are seen on enamel
Manifest erosion:
 Actively occurring and appears in micrographs as a hollowed out pitted
surface resembling honey comb.
 The pits characterize ends of enamel prisms that have been dissolved below
the level of interprismatic matrix

latent erosion:
 It is an inactive stage and here the prisms are much less obvious.
 Manifest erosion is more common than latent erosion and is seen more
frequently in females and young individuals.
• Extensive loss of buccal and occlusal tooth structure.

• Raised amalgam restorations .

• Occlusal view of maxillary dentition exhibiting concave

dentin depressions surrounded by elevated rims of enamel
Multiple cupped out depressions corresponding to the cusp tips.

Extensive loss of enamel and dentin on the Buccal surface of maxillary bicuspids.
( pt had sucked chronically on tamarinds )
Palatal surfaces of maxillary dentition in which

the exposed dentin exhibits a concave surface

and a peripheral white line of enamel

Perimylosis (decalcification of the teeth caused by exposure to gastric acid in patients

with chronic vomiting, as may occur in anorexia or bulimia)

• Loss of lingual enamel and dentin due to acid regurgitation aggravated by circular
movements of tongue.

• Associated with stress reflux syndrome

The other substances that can corrode teeth.

• chewable vitamin C tablets

• aspirin tablets
• aspirin powders
• use of the amphetamine drug Ecstasy
• have been associated with corrosion on the occlusal surfaces of posterior teeth.
• Active wear → smooth and unstained ,clean surfaces.
→ erosion of tooth around the existing restoration .
(Restoration is resistant to acid,remains unchanged ,
but the tooth is gradually dissolved leaving the restoration proud)
• Inactive wear — stained .
 Treatment modalities:

 Proper diagnosis of the cause of erosion is the first step

 A complete analysis of diet, occlusion, habits, vomiting, and environmental
factors should be taken into consideration.
 The cause should be identified and be should eliminated.
 There should not be any rush to attempt restorative modalities, except in
extremely symptomatic or disfiguring lesions.
 Tooth colored materials such as GIC or composite, capable of chemico-phyiscal
bonding to tooth structure can be used with minimum or no tooth preparation.
 ABFRACTION

Tooth structure loss due to excessive buccal or lingual occlusal load that
contributes to the erosive process through either compression or tension in the
cervical areas of the tooth just above the bony support.

Grippo in 1991, originated the term abfraction to describe the pathologic

loss of both enamel and dentin caused by biomechanical loading forces.
 Some authors explain the formation of cervical, wedge shaped defect by
the heavy force in eccentric occlusion resulting in flexuring (elastic
bending) of the tooth.

• When the tooth is loaded in long axis ,the forces are dissipated with
minimal stress on enamel and dentin .

• If the direction of force changes laterally ,teeth are flexed towards both the
sides .
 Changes in stress pattern continuously in
the same area
compresssive ↔ tensile
(esp. ,underneath the enamel)reaches to the
fatigue limit.
Rupture of chemical bond between
hydroxyapetite crystals is termed as
Abfractures .

This occurs most commonly in the cervical regions of the tooth where the flexure may
lead to breaking away of extremely thin enamel rods ,as well as microfractures of
cementum and dentin .
 Microfractures can foster loss of tooth structure from tooth brush abrasion and
from acids in the diet or plaque or both .

 The resulting defect has a smooth surface .

• Also known as idiopathic erosion.

• Abfraction has a possibility of being the initial factor and the dominant progressive
modifying factor in producing cervical lesions.

• Stresses that concentrate to produce abfractions in teeth usually are transmitted by

occlusal loading forces.
 Theories explaining abfraction

• Stress on enamel causes concentration of stress at CEJ and generates tensile pull
that breaks the enamel prisms and increases susceptibility to chemical erosion
Tensile stress from mastication and malocclusion are the primary etiologic factor for
cervical tooth breakdown. Once micro fracture occurred water and other small
molecules penetrate the broken hydroxyapatite chemical bonds and makes the tooth
susceptible for chemical erosion and toothbrush
• Biomedical engineering factors like piezoelctricity at the cervical region and stress
corrosion are the prime etiologic factors in non carious cervical lesion progression
 Clinical features

• The lesion is typically wedge shaped with sharp line angles

• Affects buccal/labial cervical areas of teeth
• Deep, narrow V-shaped notch
• Commonly affects single teeth with excursive interferences or eccentric occlusal
loads
 Monitoring abfraction lesions

• A novel method of determining the activity of abfraction lesions over time ----
Scratch test .
• A no.12 scalpel blade is used to superficially scratch the tooth surface .
• Visual observation gives an indication of rate of tooth structure loss
• Loss of scratch definition or loss of the scratch altogether signifies active tooth
structure loss.
 Restoration

• when clinical consequences (e.g. dentin hypersensitivity ) have developed or likely

to be developed .
• Aesthetics demands are a concern .

Occlusal adjustments

 Occlusal adjustment may involve

• Altering cuspal inclines,
• Reducing heavy contacts
• Removing premature contacts.
Occlusal splints
Aimed at reducing the amount of nocturnal bruxism and non axial tooth
loading when constructed properly
COMBINED LESIONS
1- Attrition- abfraction.

 Attrition- abfraction is the joint action of stress and friction when teeth
are in tooth-to-tooth contact, as in bruxism or repetitive clenching.
2- Abrasion-abfraction.

 Abrasion-abfraction is the loss of tooth substance caused by friction from an

external material on an area in which stress concentration due to loading forces
may cause tooth substance to break away.
Such a synergistic tooth-destructive effect may be observed cervically when
toothbrushing abrasion exacerbates abfraction to produce wedge-shaped lesions.
The critical roles of both tooth brushing abrasion and occlusal loading of an
anatomically vulnerable zone may be one reason why such lesions are limited
almost exclusively to the buccal and labial cervical areas of teeth
 3) Erosion-abfraction

 Corrosion-abfraction is the loss of tooth substance due to the synergistic action of

a chemical corrodent on areas of stress concentration. This physicochemical
mechanism may occur as a result of either sustained or cyclic loading and leads to
static stress corrosion or cyclic stress corrosion
4) attrition-corrosion
 Attrition-corrosion is the loss of tooth substance due to the action of a corrodent
in areas in which tooth-to-tooth wear occurs.

 This process may lead to a loss of vertical dimension, especially in patients with
GERD or gastric regurgitation. An occlusal or incisal pattern of wear develops.
5) Abrasion-corrosion
 Abrasion-corrosion is the synergistic activity of corrosion and friction from an
external material.
 This could occur from the frictional effects of a toothbrush on the superficially
softened surface of a tooth that has been demineralized by a corrosive agent.
 Teeth that are out of occlusion could be affected by this mechanism and develop
cervical lesions, since they frequently extrude, thus exposing the vulnerable
dentin.
 Similarly, gingival recession may expose the cementum and dentin to this
odontolytic process.
6) Biocorrosion-abfraction
 Biocorrosion (caries)-abfraction is the pathological loss of tooth structure
associated with the caries process, where an area is micromechanically and
physicochemically breaking away due to stress concentration.

 A common site for this synergistic activity is the cervical area of the tooth, where it
may be manifested as root or radicular caries.

 The combined mechanisms of static stress corrosion and cyclic (fatigue) stress
corrosion can account for the rapid odontolytic progression of these types of
carious lesions.
 Localized Non Hereditary Enamel Hypoplasia

 During enamel formation , AMELOBLASTS are injured/irritated ,their

metabolic product i.e enamel matrix, would not be properly formed resulting in
formation of either hypoplastic or hypomineralized enamel.
 When the teeth erupt, these defects will be apparent in the crown portion of

teeth (tooth) which is called as localized non hereditary enamel hypoplasia

causes
 Localized disorders- These include periapical infections of the preceding
deciduous tooth (Turner’s hypoplasia ), traumatic intrusion of the preceding
deciduous tooth etc

a. Systemic disorders:
 Exanthematus diseases
 NutritionaL deficiencies(especially vitamins A,C and D)
 Hypocalcemia
 Microbial process e.g . (syphilis)
 Fluorides :
Metabolizing fluorides in excessive amounts could poison the ameloblasts and
disturb their activities to variable degrees, leading too slightly mottled enamel or a
completely disfigured crown in its enamel
 Clinical presentation

Isolated pits to widespread linear defects, depressions,

or loss of a segment in the enamel .

These defective areas will have different color from the

surrounding enamel.

In contrast with the caries and erosion and abrasion lesions, enamel hypoplasia
does not progress

If defects are minimum ( narrow lines /isolated pits /shallow depressions) - then
selective odontomy/esthetic reshaping can be performed .
If odontomy and esthetic reshaping of the tooth enamel can’t produce a
pleasing functional effect, then-

Direct tooth colored resinous material (composite material) is inserted with

/without tooth preparation
 Localized Non Hereditary Enamel Hypocalcification

Hypomineralized enamel results when normal amount of enamel matrix fails to

achieve full mineralization and is a usual consequence of damage to ameloblasts .

causes

1.childhood fever,
2.Trauma / Flourosis- during developmental stages of tooth formation
 Clinical presentation

1.Appear chalky
2.soft to indentation.
3.Stainable.
4. If extensive- these lesions predispose to attrition and abrasion.
5. Enamel chipped if lesion involves the entire surface of a tooth .

• If diagnosis is made early in tooth’s life ,while the uncalcified enamel is still
intact an attempt at remineralization should be made can be done using-
A)fluoride applications
B)Fluoride iontophoresis
• C)strict prevention of plaque accumulation in these areas .
 Treatment

Vital bleaching

Laminated veneering

Composite

Crowns
 Localized Non Hereditary Dentin Hypoplasia

 Odontoblasts are the specialized cells ,any disturbance in their function- deficient
or complete absence of dentin matrix deposition Leads to the development of
localised non-hereditary dentin hypoplasia
Cause:
It appears to be a hereditary disease, transmitted as an autosomal dominant
characteristics

CLINICAL PRESENTATION

 There would be NO apparent destruction to be diagnosed or treated ,till the

time the lesion is covered with enamel.
 During tooth preparation for a restoration , these defects may get exposed
Various intermediary bases that can be used are :
Zinc oxide eugenol
Calcium hydroxide
Zinc phosphate cement
Polycarboxylate cement
Varnishes
Glass ionomer cement
 Localized non hereditary dentin hypocalcification

In hypocalcification, there is failure of union of many globules,the dentin will be

present in substance ,but would be softer ,more penetrable , and less resilient

CAUSE
a) Systemic disorders

b) Localized disorders
c) Fluorides

There would be NO apparent destruction to be diagnosed or treated ,till the time

the lesion is covered with enamel
Various intermediary bases that can be used are :
Zinc oxide eugenol
Calcium hydroxide
Zinc phosphate cement
Polycarboxylate cement
Varnishes
Glass ionomer cement
 AMELOGENESIS IMPERFECTA

Developmental alterations in the structure of enamel in the absence of a systemic

disorder

4 MAIN TYPES
1)Hypoplasia
2)Hypocalcification
3)Hypomaturation
4)Hypomaturation
–hypoplasia with taurodontism
 HYPOPLASTIC
Thin enamel
Open contact
Enamel is glossy
Enamel can look wrinkled.
Signs of severe occlusal wear
Missing teeth.
Delay in eruption.

• Small yellowish teeth exhibiting hard, glossy enamel with numerous open
contacts points and anterior open bite
HYPOCALCIFIED-
•Enamel is usually stained (yellow/Black)
• Enamel chips easily ,very soft in consistency stains become darker with time
•Enamel- worn easily in life with all signs and symptoms of severe attrition

HYPOMATURATION
• Affected teeth ---normal in shape , but exhibit mottled, opaque white brown –
yellow discoloration .
• Enamel is softer than normal ,tends to chip from underlying diffuse yellow white
dentition
AIM OF TREATMENT-
•Reducing tooth sensitivity
•Improving esthetics
•Correcting or maintaining vertical dimension
•Restoring masticatory function

Temporary phase –undertaken during primary or mixed dentition

Transitional phase –when all the permanent teeth have erupted
Permanent phase – occurs in adulthood
Reducing tooth sensitivity-
topical fluoride products ,CPP-ACP products ,
dietary modification
Maintaining good oral hygiene

Correcting or maintaining vertical dimension –

Placement of GIC ( sensitivity ,if any ) on grossly worn down molars followed by
placement of composite restorations ,assist in restoring the occlusal vertical
dimension
Esthetic improvements
Bonding direct or indirect resin composite restorations

Restoring masticatory function

• Performed by full veneering ,includes procedures -
1)metallic
2) Cast ceramic restorations
 DENTINOGENESIS IMPERFECTA

Autosomal dominant disorder with variable expressivity

Primary teeth are normally more severely affected than

permanent teeth

Classification : (Witkop)
Type I : dentin mineralization defects are coupled with osteogenesis imperfecta
Type II: Hereditary Opalescent dentin
Type III: Brandy wine type (Shell teeth )
 CAUSE

Caused by mutation in the DSPP gene.

CLINICAL PRESENTATION

Teeth affected vary in color from yellow brown –brownish ,violet /grey with a typical
translucency and opalescence.

Atypical color of teeth → dentin showing through the relatively translucent

opalescence enamel

Enamel tends to chip and fracture off from the tips of teeth → exposed
dentin , leaving the occlusal surface of posterior teeth flat .
 Treatment

 Early diagnosis and care (preventing loss of enamel and subsequent loss
through attrition).

 In patients without cracks and rapid attrition of enamel, intracoronal

restorations and veneers used.

 External bleaching (notably prolonged night guard vital bleaching ) with

carbamide peroxide has been reported with excellent result
• In anterior teeth → stainless steel crowns with composite facings may be
given at a later stage porcelain crowns are suggested

• Splinting between these teeth- to avoid root fracture.

 discoloration

• Classified from etiologic aspect as

1. Extrinsic : due to surface staining , calculus or any other surface deposits

2. Intrinsic : created from changes in one or more of the tooth tissues

• Discoloring changes in enamel include hypoplasia and hypocalcification

• Discoloring changes in dentin may result from non – vitality resulting in
disintegration of the dentinal tubules contents or from pigmentation and
staining which is due to external sources e.g. corrosion products of metallic
restorations,medications,microbial metabolites,etc

• Tetracycline coloration

• Discoloring changes in the pulp root canal system can result from pulpal necrosis
 Treatment modalities

• By scaling and polishing with abrasives

• Intrinsic discoloration in enamel and dentin can be treated by Vital bleaching

,laminated veneering ,composite veneering and porcelain fused to metal and
cast ceramic crowns as in localized non hereditary enamel hypoplasia and
hypocalcification.
• In intrinsic discoloration due to discoloring changes in pulp-root canal system
first endodontic therapy should be instituted and then proceed with following
treatment sequence

a. non-vital bleaching

b. If no pleasant result are there it may be necessary to resort laminated veneer or

porcelain fused to metal or cast ceramic veneering restorations
• Separation and/or loss of tooth structure as a result of trauma frequently occurs
necessitating dental treatment
• According to Ellis classification ,injury to natural teeth can be classified into:

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

Treatment
Smoothing of edges and peripheries
esthetic reshaping
If relatively large surface areas are involved :
anterior GIC restoration
posterior metallic restoration
Class II :Extensive fracture of tooth crown involving considerable dentin but no pulp.

Treatment
 In anterior, provisional restoration can be
 Class IV and in posterior amalgam restoration

Class III : extensive fracture of crown , involving

considerable dentin and exposing the pulp

Treatment
 Pulp and root canal treatment
Class IV :

A traumatized tooth which becomes non vital with/without

loss of crown structure

Treatment
 If tooth crown is intact - Endodontic therapy
a. If tooth crown is fracture-pulp or root canal therapy
b. If tooth crown is discolored – non vital bleaching or laminated veneering
c. If toth is discolored beyond any bleaching then should be veneered with cast
alloy based or cast ceramic restoration
Class V :
Tooth lost as a result of trauma

Treatment
 Accidental tooth loss or fracture beyond any
restorative capability should be replaced with a prosthesis like
o Provisional fixed bridge
o Pontic
o Electrochemically etched ,non noble alloy based bridge
Class VI :
Fracture of tooth root with or without loss of tooth structure
Root fracture can be
a. Cervically horizontal :
Treatment –endodontic therapy
b. midradicularally horizontal :
Treatment –endodontic treatment and/or splinting
c. Apically horizontal:
Treatment-
vital tooth –should be left without interference
non vital tooth-endodontic therapy and splint, when surgery is not feasible
d. Vertical root fracture
Treatment-unfavorable prognosis ,
single rooted teeth-extraction
Multirooted teeth -hemisectioning
Class VII :

Displacement (dislocation) of tooth(teeth) without

fracture of crown or root

Treatment:

After proper reduction of tooth and/or replacing in its socket should be splinted

Class VIII :

fracture of crown en masse with broken crown pieces

Treatment

Endodontic treatment pulp chamber should be filled with resin and two pieces should be
brought together and kept under pressure until primer and composite resin sets
Class IX :
Incomplete fracture of tooth
Treatment:
Relieve tooth from eccentric occluding contacts.
Orthodontic band
If any sign of pulpitis-endodontic therapy
Firstly, endodontic therapies should be considered to treat the deformities like
1) Attrition-Composite resin
2) Abrasion-glass ionomer cement
3) Erosion –metallic restorations
4) Abfraction-composite resins
5) Enamel hypoplasia and calcifications-selective odontomy,flouride
application
6) Dentin hypoplasia and calcificatons-intermediary basing
7) Amelogenesis and dentinogenesis imperfecta-Odontomy and full veneer
8) Discolouration –abrasives
9) Trauma-splinting
Randomized Clinical Trial of Two Resin-Modified Glass Ionomer Materials:
1-year Results
J Perdigão, M Dutra-Corrêa, SHC Saraceni, MT Ciaramicoli, and VH Kiyan .
Operative Dentistry: November/December 2012, Vol. 37, No. 6, pp. 591-
601.

Aim of the study: is to compare the different properties of two resin modified
GIC Fuji II i.e., a traditional RMGIC restorative material; Ketac Nano a nano
filled RMGIC restorative material.

CONCLUSIONS

The one-year retention rate was statistically similar for the three adhesive
materials.
Enamel marginal deficiencies and color mismatch were more prevalent for
Ketac Nano.
Surface texture of Fuji II LC restorations deteriorated quickly.
One year comparative clinical evaluation of EQUIA with resin-modified glass
ionomer and a nanohybrid composite in noncarious cervical lesions

Vaid DS, Shah NC, Bilgi PS. One year comparative clinical evaluation of
EQUIA with resin-modified glass ionomer and a nanohybrid composite
in noncarious cervical lesions. J Conserv Dent 2015;18:449-52.

Aims: Comparative evaluation of EQUIA with a resin-modified glass ionomer

cement (RMGIC; GC Gold Label glass ionomer light cured universal
restorative cement) and a nanohybrid composite (Tetric N-Ceram) in
noncarious cervical lesions (NCCLs).
Conclusions: EQUIA, resin-modified glass ionomer, and nanohybrid composite
performed equally at 1-month, 6 months, and 1-year follow-up periods
Santamaria MP, Queiroz LA, Mathias IF, Neves FLS, Silveira CA, Bresciani E, Jardini
MAN, Sallum EA. Resin composite plus connective tissue graft to treat single
maxillary gingival recession associated with non-carious cervical lesion: randomized
clinical trial. J Clin Periodontol 2016; 43: 461–468.

Four Classes emerged:

Class A -, gingival recession presented a visible CEJ and
intact root surface;
Class A+, gingival recession presented a NCCL(step) and a visible CEJ;
Class B-, gingival recession associated with an unidentifiable CEJ without a
surface discrepancy;
Class B+, gingival recession associated with an unidentifiable CEJ with a
surface discrepancy
Tooth allocated to the CTG+RC group. (A) Pre-operative view; (B) lateral view showing the
cervical step; (C) after flap elevation and rubber dam isolation; (D) restoration was
performed following the manufacturer’s instructions; (E) final restoration
view; (F) lateral restoration view; (G) after connective tissue graft was sutures, the flap
was coronally advanced and sutured; (H)final view after 1 year of follow-up.
 conclusion

• Because of improved caries prevention, greater awareness of the importance of

preserving all masticatory units, and change in the life style and dietary habits, we
might face increased frequency of non carious lesions
• Depending on the degree of tooth wear, restorative treatment can range from
placement of bonded composites in a few isolated areas of erosion, to full mouth
reconstruction in the case of the devastated dentition.
• Regardless of the type of restorative therapy provided, prevention of the
progression of tooth wear should be the basis of management.
• This will increase the likelihood of successful, long-term outcomes of the
restorative treatment.
• The patient should be monitored at regular intervals to determine compliance and
success of treatment.
• Thus, apart from regular monitoring of the aetiology and development of these
lesions, improved measures of prevention and therapy still need to be introduced.
 REFERENCES
1) Art and science of operative dentistry- Sturdevant 5 th edition
2) Operative Dentistry- Modern Theory and Practice: Marzouk
3) Nisha grag-textbook of operative dentistry
4) Vimal sikri- textbook of operative dentistry
5) Role of erosion in tooth wear :aetiology ,prevention and management ---
IDJ(2005) 55,277-284.
Randomized Clinical Trial of Two Resin-Modified Glass Ionomer Materials:
1-year Results
J Perdigão, M Dutra-Corrêa, SHC Saraceni, MT Ciaramicoli, and VH Kiyan .
Operative Dentistry: November/December 2012, Vol. 37, No. 6, pp. 591-
601.

Aim of the study: is to compare the different properties of two resin modified
GIC Fuji II i.e., a traditional RMGIC restorative material; Ketac Nano a nano
filled RMGIC restorative material.

CONCLUSIONS

The one-year retention rate was statistically similar for the three adhesive
materials.
Enamel marginal deficiencies and color mismatch were more prevalent for
Ketac Nano.
Surface texture of Fuji II LC restorations deteriorated quickly.
 Periodontal treatment

maximum coronal root coverage (MRC) :

If the MRC is apical to the CEJ, then a Class 5 restoration should be accomplished first,
with the apical margin of the restoration at or just apical to the MRC.
Access and Isolation of NCCLs
 Surgical retraction

Gingivoplasty Conventional flap surgery

Miniflap
Class 5 restorative materials:

Nonesthetic materials
Amalgam
Gold foil (direct, not widely used)
Gold inlay (indirect, not widely used)

Esthetic materials
Resin composite (with dentin bonding system)
Resin composite (with glass-ionomer liner—sandwich technique)
Flowable resin composite
Glass ionomer
RMGI
Compomer
Porcelain inlay (not widely used)
 AMALGAM

There is no need to create sharp internal line angles or to remove sound dentin for axial
depth greater than 1 mm.
The cavosurface margins should be as close to 90 degrees as possible.
Cavosurface bevels are contraindicated in preparations for amalgam or glass
ionomer because of the low edge strength of these materials.
Composites:
incremental resin composite placement is recommended
 Beveling of enamel margins is recommended when it would expose the ends of
the enamel rods .
 Beveling the gingival margin that ends on cementum is not recommended.
 Resin composites

 For small restorations, the resin composite may be inserted and cured in one
increment unless esthetic considerations call for layering to achieve appropriate
shading.
 For restorations that are moderate to large in size,
 first increment of resin composite should be placed from about the midpoint of
the gingival floor to the incisal or occlusal cavosurface margin and light
polymerized.
 The second increment can then fill the remainder of the preparation.
 Flowable resin composite

flowable resin composite as a liner has not been shown to improve clinical
performance

Glass ionomer and RMGI

A review of Class 5 restorations concluded that glass-ionomer materials (both

conventional and resin-modified) showed the highest retention rates
 Glass-ionomer sandwich technique

• Glass ionomer is used to replace the missing dentin, reduce leakage, improve the
potential for tissue attachment for subgingival restorations, and potentially
increase retention.
• A veneer of resin composite is placed to enhance esthetics, increase color stability,
• improve marginal performance, provide a smoother surface, and increase abrasion
resistance.
• In one clinical study using the sandwich technique, a 100% retention rate was
reported after 3 years
 Compomer

marginal integrity of compomers has been worse than that of resin

composites in long-term clinical trials
• USPHS criteria

1. retention,
2. color match,
3. marginal staining,
4. marginal adaptation,
5. surface texture, and
6. Postoperative sensitivity.
 One-year comparative evaluation of Ketac Nano with resin-modified
glass ionomer cement and Giomer in non carious cervical lesions:
A randomized clinical trial

Priyadarshini BI, Jayaprakash T, Nagesh B,Sunil CR, Sujana V, Deepa VL.

J Conserv Dent 2017;20:204-9.

Restorative retention Marginal Marginal Color match Surface

material staining adaptation texture
NS NS NS 0.0022 0.0077
Fuji II LC
Giomer 0.0050 NS NS NS NS
Ketac Nano NS 0.0025 NS 0.0053 NS
• High retention rates were seen with RMGIC and Ketac Nano when compared to
Giomer, which were statistically significant

• Marginal discoloration was found to be high for Ketac Nano which was
statistically significant with Giomer and RMGIC
Surface roughness and color mismatch was statistically high for RMGIC

• Giomer showed statistically significant difference in surface finish with RMGIC

and color match with RMGIC and Ketac Nano
Thank you

Thank you