Non carious tooth lesions

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NoN CariouS TootH LesionS
(NCTL / NCCL)
Presented by: D r Ab h isek Gur ia
Dept. of Conservative Dentistry & Endodontics

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Contents
 Introduction
 Definition
 Classification (Grippo)
Atrition
 Definition
 Classification
 Proximal surface attrition
 Occlusal surface attrition
 Etiology and Clinical features
 Treatment modalities
 The Dahl concept
 Schools of thought to increase the
V.D.
 Endodontic considerations
 Treatment strategies for Dentinal
hypersensitivity
 Nerve desensitization
 Anti-inflammatory agents
 Covering or plugging dentinal
tubules
 Restorative materials
 Periodontal surgery
 Lasers
5/11/2020 Management of Non-carious lesion

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Management of Non-carious lesion
Abrasion, Erosion, Abfraction
 Definition
 Etiology and pathogenesis
 Clinical features
 Monitoring of lesion progression
 Restorative decision making
 Perimolysis
Fracture line/tooth crack
 Etiopathogenesis
 Classification
 Characteristics
 Distribution
 Clinical diagnosis
 Radiographic examination
 Management of peg laterals
 Management of palatogingival groove
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 Localized Non Hereditary Enamel
Hypoplasia
Hypocalcification
 Localized Non Hereditary Dentin
Hypoplasia
 Localized Non-hereditary Dentin
Hypocalcification
 Amelogenesis Imperfecta
 Dentinogenesis Imperfecta
 Definition
 Etiology
 Conclusion
 References
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Introduction
Non carious tooth tissue loss (NCTL):
 Surface loss due to a disease process other than dental
caries. (Pual A Brunton ,Decision making in Operative Dentistry )
 25% of tooth destruction does not originate from a
carious process.(Marzouk)

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Etiology of NCTL
1. Attrition
2. Abrasion
3. Erosion
4. Abfraction
5. Localized Non- Hereditary Enamel Hypocalcification
6. Localized Non- Hereditary Dentin Hypolpasia
7. Localized Non- Hereditary Dentin Hypocalcification
8. Fracture lines
9. Amelogenesis imperfect
10. Dentinogenesis imperfecta
• John O Grippo,Marvin Simmering,JADA 2004 135;1109-1118
• Osborne-Smith KL, Burke FJ, Wilson NH. Int Dent J. 1999 Jun;49(3):139-43. Review

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Attrition
• Mechanical wear of the incisal or occlusal surface as a
result of functional or parafunctional movements of
mandible (tooth to tooth contacts) (Sturdevant)
• Surface tooth structure loss resulting from
direct frictional forces between contacting
teeth. (Marzouk)
• It also includes the proximal surface wear at the contact
area because of the physiologic tooth movement

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Etiology
1. Bruxism
2. Developmental enamel defect
3. Physiologic

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A) Proximal surface attrition (proximal surface facets)
 Results from surface tooth
structure loss and flattening ,
widening of the proximal contact
areas.
 Mesiodistal dimension of the teeth is
decreased, leading to drifting , with
the possibility of overall reduction in
the dental arch.

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B) Occluding surface attrition ( OCCLUSAL WEAR)
 It is the loss ,flattening, faceting or reverse cusping of the
occluding elements.
 It leads to loss of vertical dimension of the tooth .
A) If the LOSS IS SEVERE & accomplished in a relatively short
time
No chance for the alveolar bone to erupt occlusally to compensate for the
occlusal tooth loss
Loss of VD
overclosure during mandibular functional movements
strain areas on stomato-gnathic system.

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B) If the loss occurs over a long period-
• The alveolar bone can grow occlusally, bringing the teeth to their
original occlusal termination.
• Vertical dimension loss will be confined to teeth but not imparted to
face.
• Deficient masticatory capabilities
• Cheek biting
• Decay
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Clinical presentation
• Flattened occlusal surfaces.
• The degree of wear in both arches is normally equal.
• Sometimes there may be presence of peripheral, ragged,
sharp enamel edges .
• The presence of hypertrophic masseter is a warning
sign of the impact of bruxism .
• TMJ problems can be elicited especially by the over
closure situation

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A. When surface attrition is SLOWER & compensated by,
intrapulpal deposition of secondary & tertiary dentin, then
there will be no pulpal exposure.
B. At other times, the attrition is faster than the intrapulpal
dentine deposition, leading to direct pulpal exposure.

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Treatment modalities
• Pulpally involved teeth →endodontic therapy /extraction
depending upon their restorability .
• Para functional activities ,( bruxism)-- be controlled with
protecting occlusal splints.

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 Myofunctional, TMJ/ any other symptoms in the stomato-
gnathic system -----diagnosed and resolved (modifying the
occlusal splint).
 Occlusal equilibration : should be performed by :
1. Selective grinding of tooth surfaces that includes
rounding and smoothening the peripheries of the
occlusal tables.
2. By creating adequate overlap between the working inclines
to prevent further cheek biting.
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Any exposed sensitive
dentin should be
protected and actual
carious lesion be
obliterated .
Periodontium be
examined and any
pathology be treated
.
Restorative
modalities can than
be initiated.

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 Restorations are only needed in the following situations:
 Noticeable loss of vertical dimension
 Or a progressive loss of tooth structure is observed
compromising the tooth strength .
 Caries ,if present
 Defect contributes to a periodontal problem.
 Worn tooth contour, (usually proximal ) which is not
conducive to the maintenance of periodontium .
 A tooth is cracked or endodontically treated.
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Procedure
• Amount of V.D. lost is estimated .
• It gives an estimate up to what should be the height of the
worn clinical crowns be increased .
Management of Non-carious lesion5/11/2020

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 The additional V.D. that the stomognathic system can
accommodate without untoward effects is estimated.
 Composite temporary restorations are most frequently used
 Permanent restoration should be done in a cast alloy
 These restorations should be cemented only temporarily for
an extendedperiod of time ,until it is established that no
untoward symptoms would occur.

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 An acrylic splint( as a stabilization splint) may be necessary

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Restorative treatment
 Tooth wear can be followed and re-evaluated during
recall examinations.
 Less severe anterior wear can be treated with
adhesive composite resin.
(Strassler HE, Kihn PW, Yoon R. Conservative treatment of the worn dentition with adhesive composite resin.
Contemp Esthet Restor Pract. 1999)

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When the wear is more severe, a number of treatment
modalities are available.
1. Bonded porcelain veneers have been used to treat incisal wear.
(Ibsen RL, Ouellet DF. Restoring the worn dentition. J Esthet Dent. 1992;4:96-101.)
1. In some cases, the incisal edges can be restored to the original
vertical dimension with direct composite resin.
(Strassler HE, Kihn PW, Yoon R. Conservative treatment of the worn dentition with adhesive composite
resin. Contemp Esthet Restor Pract. 1999)
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 Hemmings and coworkers reported on the restoration of
severe anterior wear with composite restoration including re-
establishment of the occlusal vertical dimension.
 They reported a 89.4% success at 30 months.
(Hemmings KW, Darbar UR, Vaughan S. Tooth wear treated with direct composite restorations
at an increased vertical )dimension: results at 30 months. J Prosthet Dent. 2000;83:287-293.
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 Adhesive cast metal restorations have also been used to
replace missing tooth structure.
( Nohl FS, King PA, Harley KE, et al. Retrospective survey of resin- retained cast-
metal palatal veneers for the treatment of anterior palatal tooth wear. Quintessence
Int. 1997)
 In cases where the occlusion is severely altered by attrition,
the only treatment choice may be a reconstruction with crowns
and bridges.
(Stewart B. Restoration of the severely worn dentition using a systematized
approach for a predictable prognosis. Int J Periodontics Restorative Dent.
1998;18:46-57.)
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The Dahl concept
 Dahl and his coworkers (1975)
described the use of a partialbite
raising appliance‘ to create inter-
occlusal space in an 18-year-old
patient with severe localised
attrition.
 The removable appliance was cast in
cobalt-chromium, placed on the palatal
aspects of the upper anterior teeth,
and worn 24 hours a day.

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 The creation of inter- occlusal space significantly reduced the amount
of tooth preparation required, especially on the already compromised
palatal surface.
 Teeth were restored with full coverage porcelain bonded
crowns
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2 schools of thought to increase the V.D.
 Addition of increments : gradual increments by
progressively adding to the hard splint at 1mm /week, until
the patient reaches the increased V.D. for restorative
purposes----time consuming
 The second approach ----taking the patient immediately to
needed increase in V.D.----considerably lesser adjustments
are made ,lesser time consuming

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Anterior Bite plane
 Used in the reduction of overbite.
 Occurs by altering the rate of eruption
of posterior teeth relative to the
eruption of lower incisors that are in
contact with the bite plane.
 Overbite reduction by this method ---
most successful in actively growing
patients

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Endodontic considerations
In certain cases intentional endodontic therapy has to be performed
 Hypererupted teeth
 Pulpal involvement
For location of calcified canal
 Use of magnification
 staining the pulp chamber floor with 1%methylene blue dye .
 searching for canal bleeding points .
 Performing the sodium hypochlorite ―champagne bubble test are helpful in locating
calcified.
 Long ,thin Ultrasonic tips can also be used

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Dentinal hypersensitivity
Dentin Hypersensitivity is a condition characterized by short , sharp
pain arising from exposed dentin in response to stimuli typically
thermal , evaporative , tactile, osmotic or chemical and which cannot
be ascribed to any other form of dental defect or pathology .
( Holland et al 1997)

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THEORIES
1. The transduction theory
2. Direct neural stimulation theory
3. The hydrodynamic theory

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Treatment strategies for Dentinal
hypersensitivity ( DCNA 53,2009; 47-60)
1. Nerve desensitization
 Potassium nitrate
2 .Anti-inflammatory agents
 Corticosteroids
3. Covering or plugging dentinal tubules
• calcium hydroxide
• sodium fluoride

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• Sodium monoflourophosphate
• Stannous fluoride
• Oxalates
• Strontium chloride
 Protien precipitants
 formaldehyde
 glutaraldehyde
• Flouride iontophoresis
• Resins and Adhesives
4) Restorative materials
5) Periodontal surgery
6) Lasers
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Nerve desensitization
 Potassium nitrate
 5% concentration in a low abrasive tooth paste was able to
desensitize dentin for up to 4 weeks compared to a control
paste . (Tarbet et al )
 In bio adhesive gels at a concentration of 5% and 10% has
also been shown to be effective in reducing dentinal
hypersensitivity .(Freschoso SC,Menendez M,2003)

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Anti inflammatory agents:
Corticosteroids
 glucocorticoids to the cavity preparation may reduce
dentinal hypersensitivity by their effect on pain
mediators
 Lawson and Huff found that paramethasone had a
significant desensitizing action.
 Furseth and Mjor reported complete obturation of dentinal
tubules after corticosteroid application to exposed dentin –
reduce dentin permeability.
 However there is a little experimental evidence to support
or refute the use of such agents

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Sodium fluoride
 Treatment of exposed root surface with
fluoride toothpaste (1.1%) and conc.
fluoride solutions(0.2%) is very efficient.
(Minkow B,1975;Kerns D G 1991)
 Mechanism- precipitated fluoride
compound mechanically blocking the
exposed dentinal tubules. (Tal et al)

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Sodium monoflourophosphate
• Tooth pastes containing sodium monoflourophospshates have
been shown to be effective in managing dentinal
hypersensitivity. (Hernandez F,Mohammed C,1972)
• Its mechanism of action is unclear (,Scherman A et al 1992)

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Stannous fluoride
 Stannous fluoride in aqueous solution or in glycerin gelled
with carboxymethylcellulose
(Miller JT et al 1969)
 Mode of action : induction of high mineral content which
creates a calcific barrier blocking the tubular openings on
the dentine surface .
(Furseth R ,1970)

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Fluoride iontophoresis
• It is the process of influencing ionic motion by an electric
current and has been used as a desensitizing procedure in
conjunction with sodium fluoride .
(Mc Fall WT,1986)
 Studies report that there is a immediate reduction in
sensitivity after treatment with iontophoresis, but the
symptoms gradually return over the next six months
(Kern DA et al 1989 )

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Procedure

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Oxalates
 potassium oxalates have both tubule obturation properties and
inhibitory effects caused by potassium ions on nerve activity
(Pashly DH ,1986)
 Oxalate ion reacts with calcium to form insoluble calcium
oxalate crystals that bind tightly to dentin and obturate
dentinal tubules (TrowbridgeHO,1990)
 Three types of oxalates are available :
1. 6% ferric oxalate (Sensodyne Sealant )
2. 30% di-potassium oxalate( Butler Protect )
3. 3% monohydrogen monopotassium oxalate

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Strontium chloride
 strontium ions have the capacity to reduce sensory nerve
activity, but less effectively than potassium ions.
(MarkowitzK , kim S 1990).
 Dentifrices containing 10% strontium chloride (Sensodyne) -
widely used as desensitizing agents and were one of the
first agents to be marketed for that purpose.

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Protein precipitants
(Formaldehyde and glutaraldehyde)
 Have ability to precipitate salivary proteins in the
dentinal tubules.
 However this effect has been questioned since various
formulations have been found to have little or no effect
on dentinal hypersensitivity(Addy M,Mostafa P,1988)

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Resins and Adhesives
• rationale – they seal the dentinal tubules and hence to
preclude the transmission of pain stimuli to the pulpal
nerve fibers.
• This mode of treatment is performed on localized
hypersensitive dentin.
• Resin-based materials have been reported to successfully
reduce dentinal hypersensitivity.(Kakaboura A ,2005)

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 Copeland reported successful treatment of dentinal
hypersensitivity for up to 18 months in 89% of
hypersensitive teeth treated by Scotchbond.
 5% glutaraldehyde and 35% hydroxyethyl methacrylate
(Gluma Desensitizer) has been reported to be an effective
desensitizing agent for up to 9 months. ( Kakaboura A ,2005)
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Bioactive glass:
 NovaMin - for remineralisation of teeth, treating
hypersensitivity.
 The active ingredient is called Calcium Sodium
Phosphosilicate.
 NovaMin is an ionic form of calcium, phosphorus, silica, and
sodium which are necessary for bone and tooth
mineralization.

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Lasers
 Nd:YAG laser irradiation in combination with 5% sodium
fluoride varnish has higher efficacy in the management of
DH than either treatment alone. (Kumar and Mehtas ,2005)
 Slutzky-Goldberg (2008) demonstrated that CO2 laser
treatment resulted in decreased permeability of dentinal
tubules as shown by a dye penetration test.

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Restorative materials
• The use of restorative materials is generally an invasive
solution to the problem of hypersensitivity.
• Commonly used materials include composite resins and
glass ionomer restorations.

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Abrasion

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 Abnormal tooth surface loss resulting from direct
frictional forces between the teeth and external objects
or from frictional forces between contacting teeth
components in the presence of abrasive medium.
(Sturdevant 5 th edition)
 It occurs most frequently on the cervical neck of the teeth.
 The labial or buccal surfaces. (tooth brush abrasion )
 Labial or buccal and lingual surfaces( in case of poorly fitted
clasps and artificial dentures ) .
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Causes of abrasion :
• Traumatic occlusion .
• Improper brushing technique .
• Occupational (Habits such as holding bobby pins in between the
teeth .)
• Tobacco chewing /tobacco pipe .
• Vigorous use of tooth picks between the adjacent teeth.
• Excessive mastication of coarse foods .

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 Tooth brushabrasion results in a
horizontal cervical notches on the
buccal surfaces of exposed radicular
cementum and dentin .
 Notching in right central incisor
caused by improper use of bobby
pins .

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clinical signs and symptoms
 The surface of the lesion is extremely smooth and polished and it
seldom has any plaque accumulation or caries activity in it .
 The surrounding walls tend to make a V shape ,by meeting at an
acute angle axially.
 Peripheries of the lesion are angularly demarcated from the adjacent
tooth surface.
 Probing or stimulating the lesion can elicit pain .
 Hypersensitivity may be intermittent in character appearing and
disappearing at occasional or frequently repeated periods .

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 Diagnose the cause of the presented abrasion.
 A detailed history is to be taken considering various factors such as:
• Oral hygiene techniques ( use of abrasive tooth cleaning techniques and
materials)
• Habits- pipe smoking, chewing tobacco, professional habits
• Iatrogenic causes,if any.
 Avoidance or counteraction of the causes which may lead to its
production.
 Instituting proper oral hygiene measures.
 incorporating correct method of tooth brushing .

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 Have the habit of chewing tobacco ,toothpick , etc
discontinued . If successful in breaking the habit proceed
with the restorative treatment as planned.
 Correcting or avoiding ill fitting metal clasps and dentures
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 Abrasive lesions at non-occluding tooth surfaces should be:
• Evaluated critically for the need for restoring them.
• If the lesions are multiple, shallow( not exceeding 0.5 mm in
dentin) and wide → no need to restore them .
• If there is involvement of cementum / enamel only → no need
to restore .
• If lesion is wedge (V) shaped and exceeds 0.5 mm into dentin →
restoration is performed .

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 If restoration is not indicated for a lesion, then :
1. Edges of the defect should be eradicated to a smooth, non-
demarcating pattern relative to adjacent tooth surface.
2. Tooth surface then should be treated by fluoride solution
to improve caries resistance
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Restoring cervical abrasions
 Indicated when
1. Caries ,if present .
2. Sensitivity is present.
3. Lesion is esthetically objectionable .
4. If the defect contributes to a periodontal problem
5. The area to be involved in the design of a removable partial denture.
6. When the depth of defect is found to be close to pulp
7. Or a progressive loss of tooth structure is observed compromising the
tooth strength .

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Restorative materials :
• Glass ionomer restorative material.
• Resin modified glass ionomer.
• Polyacid-modified resin composites.
• Resin composites.

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Biomechanics

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 High modulus restorative materials are unable to flex in the
cervical regions when the tooth structure is deformed under
occlusal load and ,therefore the restorative materials can
be displaced from the cavity .
(Heymann HO ,Sturdevant Jr ,Baynes S ,JADA,122(2) 41- 57 )
 An intermediate material with reduced elastic modulus may
function as a stress absorbing layer and improve marginal
sealing .
(Kemp-Scholte CM ,Davidsson,CL complete marginal seal of class V resin composite restorations affected by
increased flexibility .JDR 1990 ;69:1240 -3 )
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 As a result materials with low elastic modulus such as :
1. Microfilled composites (Heymann and others ,1991 :Levitch and others ,1994 )
2. Flowable resins (Unterbink ,Liebenberg ,1999: Li and others 2006 )
3. Glass ionomer cements (Loguercio and others ,2003:Burgess and others ,2004)
Have been used in restoring cervical lesions ,with the aim of
absorbing the stresses generated during the polymerization
shrinkage of composites and mechanical loading in which the
teeth are subjected during function .
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Literature
 Two-year clinical evaluation of four polyacid- modified resin
composites and a resin-modified glass-ionomer cement
(Vitremer) in Class Vabrasion/erosion lesions. (Ermiş RB.. Quintessence Int.
2002 Jul- Aug;33(7):542-8)
Result
• Retention levels at 2 years were 90% for F2000, 90% for
Dyract AP, 89% for Compoglass F, 84% for Elan, and 95% for
the Vitremer restorations.

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Discussion
• GIC have an inhibitory effect on secondary caries,
and the release of fluoride is considered to be one
of the major benefits associated with GIC
• Polyacid- modified resin composites may not be
recharged again with fluoride as are GIC

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Comparative analysis of techniques of restoring
cervical lesions- (Quintessence Int 1993:24:553- 559.)
• Aim - the sandwich technique and the GIC restoration, from the
standpoint of marginal leakage.
• While GIC may not have as good esthetic properties as resin materials
• the sandwich technique does not have universal application, because it
requires space : not the technique of choice in shallow cavities.

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Result
1. The acid-etch technique was effective in reducing marginal
leakage along the tooth - composite resin interface in enamel.
2. None of the techniques studied consistently provided a complete
seal at the gingival aspect of cervical restorations.
3. Composite resin inserted over a GIC liner demonstrated
significantly less leakage than when the liner was not used.
4. The use of the sandwich technique or GIC alone provided the most
effective seals in cervical wedge-shaped cavities, compared to the
all- composite restoration.
5. There was no significant difference between the marginal leakage
of GIC and sandwich technique restoration

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5-year clinical performance of resin composite versus
RMGIC in non-carious cervical lesions.
Franco Eb, Benetti A, SK Ishikiriama,SL Santiago ,JRP Lauris
METHOD AND MATERIALS: One operator placed 70
restorations (35 RMGIC and 35 resin composite restorations) in
30 patients under rubber dam isolation.
CONCLUSIONS : After 5 years of evaluation, the clinical
performance of resin modified glass ionomer restorations was
superior to resin composite restorations.

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Erosion
• Def- Loss of surface tooth structure by chemical
action in the continued presence of demineralizing
agents(acids). (Sturdevant- 5th edition)
• There is no convincing etiology ,and multiple factors
have been theorized for its pathogenesis:
Mechanical factors:
The action of the muscles of lips and cheeks , and of
tooth brush against affected surfaces .

72
Chemical factors :
• Ingested acids : citric acids esp. if use in large amounts , can precipitate or
initiate erosive lesion
• Secreted acids : the acidity of crevicular fluid has been correlated to
cervical erosion
(Bodecker CF. Local acidity: a cause of dental erosion- abrasion.Ann Dent 1945)
• Acid fumes : acid vapours from nitric acid and sulphuric acids, acting in the
mouths of workers in the factories ,where these acids are largely used or
manufactured ( Miller)
• Refused acids : as a result of chronic , frequent regurgitation ,the stomach‘s
hydrochloric acid can hit the teeth at specific locations ( atypical pattern of
erosion affecting buccal surfaces of lower posterior teeth)

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Clinical presentation
• Extensive loss of buccal and
occlusal tooth structure
• Raised amalgam restoratins.
• Occlusal view of maxillary dentition
exhibiting concave dentin
depressions surrounded by
elevated rims of enamel

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• 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 )

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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

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• A similar appearance is found in patients with eating disorders-
• Anorexia - immoderate food restriction and irrational fear of
gaining weight, as well as a distorted body self-perception
• Bulimia nervosa - consuming a large amount of food in a short
amount of time followed by an attempt to rid oneself of the food
consumed, typically by vomiting
• Rumination - effortless regurgitation of most meals following
consumption
• Chronic alcoholism produces a similar pattern of erosion,
although usually more generalized.
• ( ND Robb and BGN Smith, Anorexia and bulimia nervosa (the eating disorders): conditions of
interest to the dental practitioner, J Dent (1996)

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• Any food substance with a critical pH value of less than 5.5
can become a corrodent and demineralize the teeth.
( Stephan RM, JADA 1940) ,( Gray JA, J Dent Res 1962) , (Zero DT. Cariology. Dent Clin North
Am 1999)
• Holding ,swilling or retaining acidic drinks and foods in the
mouth prolongs the acid exposure on the teeth increasing the
risk of erosion .
(Mossazzez R ,Smith BGN,Barlett DW,Oral Ph and drinking habit during the ingestion of
carbonated drink in a group of adolescents with dental erosion ,J Dent 2000)

78
• The corrosive potential of an acidic drink does not depend
exclusively on its ph value, but also is strongly influenced by
its buffering capacity of the acid and by the frequency and
duration of ingestion.
(Lussi A. Dental erosion: clinical diagnosis and case histor taking. Eur J Oral Sci 1996 )

79
 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.

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The potential effects of pH and buffering capacity
on dental erosion.
Owens BM. Gen Dent. 2007 Nov-Dec;55(6):527-31
• This in vitro study evaluated five different soft drinks (Coca-
Cola Classic, Diet Coke, Gatorade sports drink, Red Bull high-
energy drink, Starbucks Frappucino coffee drink) and tap
water (control) in terms of initial pH and buffering capacity.
• Initial pH was measured in triplicate for the six beverages.
The buffering capacity of each beverage was assessed by
measuring the weight (in grams) of 0.10 M sodium hydroxide
necessary for titration to pH levels of 5.0, 6.0, 7.0, and 8.3.

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Mean ph values for each beverage
• Coca cola
• Diet Coke
• Gatorade
• Red Bull
• Starbucks Frappucino
• Tap water
2.49
3.12
2.93
3.24
6.59
7.12

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• Red Bull had the highest mean buffering capacity
(indicating the strongest potential for erosion of
enamel), followed by Gatorade, Coca-Cola Classic,
Diet Coke, and Starbucks Frappucino.

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• Beverages with high buffering capacities compete with
natural buffering characteristics of saliva and resist ph
changes as a result .
• Greater the buffering capacity , more time it takes for saliva
to restore the pH value ,which causes beverage pH to decline
to a sustained level --------- prolonged periods of oral acidity
---- thus increasing the erosive potential .

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Monitoring tooth wear
Most effective way to monitor wear is :
• comparing the dated study casts to the clinical
conditions of teeth over time .
• It can also be used as a part of preventive regime .

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• 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 .

86
 Diminish the frequency and severity of acid challenge.
• ↓ the amount and frequency of acidic foods or drinks
• Acidic drinks should be drunk quickly rather than sipped.
• Use of straw reduces erosive potential
 Treating the underlying medical disorder or disease.
• GERD ,anorexia ,bulimia → refer to a physician
/psychologists
Protocol for the prevention of
progression of erosion
(Beatrice K,Edmond L ,J Contemp.Dental practise ,1999)

87
 Enhance the defense mechanisms of body:
• Saliva provides buffering capacity→ increases with
salivary flow rate.
• Saliva supersaturated with Ca, P → inhibits
demineralization of tooth structure.
• Stimulation of salivary flow → sugarless lozenge,
candy/gum is recommended

88
 Enhance acid resistance, remineralization and
rehardening of the tooth surfaces.
• Daily use topical flouride at home
• Fluoride application in office- 2-4 times a year
,flouride varnish recommended.
 Decrease abrasive forces.
• Use a soft bristled toothbrush and brush gently.

89
• No brushing should be done immediately after
consuming acidic food and drink as teeth will be
softened.
• Rinsing with water is better than brushing after
consuming acidic foods and drinks.
(Gandara, B.K; E.L Truelove ,Diagnosis and management of dental erosion. Journal
of Contemp.Dental Practice 1999)

91
Improve chemical protection
• Neutralize acids in mouth ---dissolving sugar free antacid
tablets 5 times a day ,particularly after an intrinsic or
extrinsic acid challenge.
• Dietary components- hard cheese ( provides Ca and PO4),
held in
 mouth after acidic challenge.

92
Mechanical protection
• By application of composites and direct
bonding
where appropriate – to protect exposed dentin
• Occlusal guard /Acrylic splint in the form of stabilization
splint
necessary to protect dentition from further damage
due to erosion .

93
 Monitor stability
• by use of casts /photos to document tooth wear
status.
• Regular recall examinations to review diet, oral
hygiene methods, compliance with medications, topical
flouride and splint usage.

94
Restoration
• Metallic restorations should be the choice of material
,if restoration indicated .
(more resistant to erosion )
• Tooth colored materials may also be used with minimal
or no tooth preparation, with the assumption that
restoration may require periodic replacement .

96
NoN CariouS TootH LesionS
(NCTL / NCCL)
Presented by: D r Ab h isek Gur ia
Dept. of Conservative Dentistry & Endodontics
SHDCH , Hassan
Sem - 14
Date of Presentation : 26/02/T20

97
Contents
 Introduction
 Definition
 Classification (Grippo)
Atrition
 Definition
 Classification
 Proximal surface attrition
 Occlusal surface attrition
 Etiology and Clinical features
 The Dahl concept
 Schools of thought to increase the
V.D.
 Endodontic considerations
 Treatment strategies for Dentinal
hypersensitivity
 Nerve desensitization
 Anti-inflammatory agents
 Covering or plugging dentinal
tubules
 Restorative materials
 Periodontal surgery
 Lasers

98
Abrasion, Erosion, Abfraction
 Definition
 Etiology and pathogenesis
 Monitoring of lesion progression
 Restorative decision making
 Perimolysis
Fracture line/tooth crack
 Etiopathogenesis
 Classification
 Characteristics
 Distribution
 Clinical diagnosis
 Radiographic examination
 Management of palatogingival groove
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99
Hypoplasia
Hypocalcification
 Localized Non Hereditary Dentin
Hypoplasia
 Localized Non-hereditary Dentin
Hypocalcification
 Amelogenesis Imperfecta
 Dentinogenesis Imperfecta
 Definition
 Etiology
 Conclusion
 References
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100
Abfraction
 Def- The pathological loss of tooth substance caused by the
biomechanical loading forces that result in flexure and failure of
enamel and dentin at a location away from the loading.(Grippo)
 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.

101
 Loss of tooth surface at the cervical areas caused
by tensile and compressive forces during tooth
flexure
Milosevic, 1998

102
Etiopathogenesis

103
 The size and the development of abfractive lesions are
proportional to the direction, magnitude, frequency, duration,
and location of the static and cyclic loading forces causing the
stress.

104
 Enamel prisms and orientation of dentinal tubules.
 The cervical region depicts parallel prisms and tubules, which result in
less resistant dental tissue than in the occlusal/incisal regions.
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105
 Stress-strain pattern by finite element analysis.
 Stress distribution was performed using maximum principal stress,
identifying areas with tensile stress (positive) and/or compressive
stress (negative).

106
 Microfractures can foster loss of tooth structure from
 tooth brush abrasion
 from acids in the diet or plaque or both .
 The resulting defect has a smooth surface .
 Also known as idiopathic erosion.
(Lee WC, Eakle WS, J Prosthet Dent 52(3): 374 -380, 1984.)
 Stresses that concentrate to produce abfractions in teeth usually
are transmitted by occlusal loading forces.
( Whitehead SA, Wilson NHF, Watts DC. J Esthet Dent 2000),(Pintado MR, DeLong R, Ko C, Sakaguchi RL,
Douglas WH. Correlation J Prosthet Dent 2000)
 Occlusal interferences, premature contacts, habits of
bruxism and clenching all may act as stressors.

107
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

108
Types
1. Hairline Abfractions
2. Striation Abfractions
3. Saucerized Abfractions
4. Semilunar Abfractions
5. Cusp tip invagination Abfractions
Grippo. J of Esth Dent. 1991

109
Passive treatment
Active treatment
Passive treatment
 Monitoring
 Prevention
The form of the preventive treatment will be dependent on
the aetiology

110
Active treatment
 Restorative – for Sensitivity, Aesthetics, Function,
 Orthodontic – for Aesthetics, Function
 Prosthodontic – for Aesthetics, Function, Space loss in
the vertical dimension.

111
Monitoring abfraction lesions
• A novel method of determining the activity of abfraction
lesions over time ----Scratch test .
( Kaidonis JA.The tooth wear :view of anthropologists ,Clin Oral Investig 2008)
• 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.

112
Restoration
• When clinical consequences (e.g. dentin
hypersensitivity ) have developed or likely to be
developed .
• Aesthetics demands are a concern .

113
Tyas recommended the RMGIC should be the first preference
(Tyas MJ,the class V lesion –aetiology ,restoration,Aust. Dental Journal.1995)
• In esthetically demanding cases,
• RMGIC/GIC liner laminated with resin composite.
Vandelwalle and Vigil ( Gen Dent 1997)
• Recommended the use of microfilled resin composite(low modulus
of elasticity ) as it will flex with tooth and not compromise
retention .

114
Occlusal adjustments
 Occlusal adjustment may involve (Piotrowski BT
JADA 2001 and Ichim IP Dent Mater 2007):
• 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

115
Fracture lines
The cause of fractures may include :
i. Physical trauma
ii. Occlusal prematurities
iii. Repetitive heavy and stressful chewing
iv. Resorption weakened teeth
v. Iatrogenic dental treatment
 It has been suggested that the determination of a fractured
tooth is often more of a prediction rather than a definitive
diagnosis based on a collective analysis of subjective and
objective findings.

116
• Five types of longitudinal fractures have been described
(American Association of Endodontists,2008 ):
(1) Craze line:
 Affect only the enamel,
 originate on the occlusal/labial surface
 typically from occlusal forces and are asymptomatic .

117
2) Fractured cusp:
 occur on the cusps and cervical margins
of the root
 can have acute pain to mastication and
cold.
3) Cracked tooth :
 occurs on the crown and may extend into
the root ,
 develop from damaging occlusal forces or
weakened tooth structure

118
 (4) Vertical root fracture:
 occur and originate only in the roots,
 have variable but a lesser degree of
signs and symptoms
 caused by wedging forces within the
roots (i.e. root canal obturation or posts)

119
5) Split tooth:
 a fracture through the crown and roots,
 developing from damaging occlusal forces or weakened
tooth structure,
 separating the tooth into two segments, with the tooth
typically being painful to mastication

120
• Cracked teeth are thought to occur as a result of
parafunctional habits or from weakened tooth structure
• The symptoms that develop subsequent to these cracks have
been termed as ―cracked tooth syndrome
• acute pain that results during the mastication (or release) of
small hard food substances and also exacerbates with cold.
(Cameron CE,JADA,1964 : American Associationof Endodontists,2008)
• However, the signs and symptoms of a cracked tooth may
also be consistent with an irreversible pulpitis or necrosis.

121
two main groups of cracked teeth :
A) Tooth infarctions:
(incomplete tooth fractures extending partially through a tooth )
that includes :
 Craze lines
 Cuspal fractures
 Cracked teeth
B) Vertical root fractures :
(that occur in endodontically treated teeth )

122
Characteristics of tooth infarctions
Problems in diagnosis :
• Infarctions typically originate internally and extend
peripherally → not likely to be identified by percussion until
the fracture extends to involve the periodontal ligament .
• The fractures are incomplete, tend to present in a mesial
distal orientation and are generally centered on the occlusal
table ,radiographs are not very diagnostic .

123
• Also difficult to differentiate masticatory pain /pain from
infarction /pain from microleakage associated with restorations .
• Infarctions ….not readily visualized without magnification (unless
they are at least 20um )

124
Distribution
 Molars and premolars are the teeth are almost exclusively
involved
 Teeth with restorations are most likely to develop
infarctions

125
Pain characteristics
• Occurs when there is release of
pressure from biting (rebound
pain or relief pain )
• Can be duplicate diagnostically
by having the patient bite on a
moist cotton roll

126
Etiology
• Excessively large and incorrectly designed
restorations .
• Use of pins for supporting large restorations ,esp. self
threading and friction locked )
• Abrasion ,erosion ,caries ,along with age changes in dentin.

127
 Biting onto hard objects ,bruxism and clenching , wedging
effect of the cusp in the opposing fossa
 Use of both high speed handpieces and course diamond
burs can lead to infarctions
 Acute trauma to the teeth.

128
Clinical examination
• Begins with the chief complaint i.e. pain on chewing ,elevated
sensitivity to cold food and sweets
• Absence of carious etiology …trigger a suspicion of infarction
• Visual examination by …….Transillumination and …..Dyes
(methylene blue)
• Any existing restoration in the tooth should be removed
to reveal the infarction lines

129
 Removal of the restoration and
highlighting with the dyeto
detect infarction
 Use of optic light source to
identify an infarction .
 Note that the beam of light
does not cross the infarction

130
Biting test :
• Biting on rubber wheels, cotton tip applicators ,moist cotton,
commercial biting appliances like tooth slooth.
• Tooth slooth …….. Differentiates biting pain from restorations
with microleakage /pain from infarction……pressure is placed
first onto the restoration followed by tooth cusps .

131
 teeth with infarctions respond to a lower threshold to cold
and EPT as compared to the non cracked teeth.
 Cameron suggested the use of thin sharp explorer tip to
probe around the cervical circumference of the suspected
teeth….the click of the explorer‘s tip and the patient‘s
response can provide a clue

132
Radiographic examination
 radiographs are not very diagnostic .
 Even cone beam volumetric tomography (CBVT) scans
cannot consistently visualize these fractures, the coronal-
apical progression of fractures cannot always be objectively
assessed until the tooth has been extracted.

133
Treatment
 Aims :
 Preventing the separation of the hard tissue entities ,
 Keeping the bacteria's from colonizing the space
caused by infarction
It is not clear whether all the teeth with infarction
require root canal therapy, it depends on the extent of
the fracture .

134
 Orthodontic band was placed to bind the crown
together .
 After 3 weeks the tooth was completely
asymptomatic and the patient chose to restore it
with a crown

135
Localized Non Hereditary Enamel
Hypoplasia
DEFINITION CAUSE Clinical presentation Treatment
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
a) Systemic disorders
b) Localized disorders
c) Fluorides
• Isolated pits to
widespread linear
defects,
• depressions, or loss
of a segment in the
enamel .
In contrast with the
caries and erosion and
abrasion lesions,
Enamel hypoplasia
does not Progress
Exanthematus diseases
NutritionaL
Deficiencies
(especially vitamins
A,C and D)
Hypocalcemia
Microbial process
e.g . (syphilis)
These defective
areas will have
different color
from the
surrounding enamel
If defects are
minimum ( narrow
lines /isolated pits
/shallow
depressions) -
then selective
odontomy/esthetic
reshaping can be
performed .

136
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CAUSE Clinical presentation Treatment
b) Localized disorders-
These include periapical infections of
the preceding deciduous tooth
(Turner‘s hypoplasia ),
traumatic intrusion of the
preceding deciduous tooth etc
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 preparationc) 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

137
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
1.Childhood fever,
2.Trauma / Flourosis
During developmental
stages of tooth
formation
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
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 .

138
Treatment
 Vital bleaching
 Laminated veneering
 Composite
 Crowns

139
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
It appears to be a
hereditary
disease,
transmitted as an
Autosomal dominant
characteristics
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
During tooth
preparation for a
restoration , these
defects may get
exposed

140
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
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
cementDuring tooth
preparation for a
restoration , these
defects may get
exposed

141
Amelogenesis Imperfecta
 Amelogenesis – enamel formation; imperfecta – improper

142
Amelogenesis Imperfecta
 Relatively rare group of inherited disorders
characterized by abnormal enamel formation
 AI can be inherited as an x-linked, autosomal recessive
(AR), or Autosomal dominant (AD) condition.
 AI classified into four main types based on the enamel
defects

143
Types
Type Clinical Appearance Enamel
Thickness
Radiographic
Appearance
Inheritance
Hypoplastic
(Type I)
Crowns size varies
from small to normal,
small teeth may lack
proxmial contacts,
color varies from
normal to opaque white
– yellow brown
Varies from thin
and smooth to
normal
thickness with
grooves, furrows
and/or pits
Enamel has
normal to slightly
reduced contrast/
thin
Autosomal
dominant,
recessive, or X-
linked
Hypomaturation
(Type II)
Varies from creamy
opaque to marked
yellow/brown,
surface of teeth soft
and rough, dental
sensitivity
Normal
thickness with
enamel that
often chips and
abrades easily
Enamel has
contrast similar to
or more than
dentin, unerupted
crowns have
normal
morphology
Autosomal
dominant,
recessive, or X-
linked

144
Types
Type Clinical Appearance Enamel Thickness Radiographic
Appearance
Inheritance
Hypocalcified
(Type III)
Opaque white to
yellow-brown, soft
rough enamel surface,
dental sensitivity and
open bite common,
heavy calculus
formation common
Normal thickness
with enamel that
often chips and
abrades easily
Enamel has
contrast similar to
or less than
dentin, unerupted
crowns have
normal
morphology
Autosomal
dominant,
recessive
Hypomaturation/
Hypoplasia/
(Type IV)
White/Yellow- Brown
mottled,
teeth can appear
small and
lack proximal contact
Reduced,
hypomineralized
areas and pits
Enamel contrast
normal to slightly
> dentin, large
pulp chambers
Autosomal
dominant

145
Management of Hypoplastic AI Types
 involves the use of bonding procedures to protect the malformed
teeth from caries and improve esthetics.
 Hypoplastic teeth usually have reasonably well mineralized enamel,
pitted, making them suitable for restorative therapies involving
bonding to the enamel

146
 Orthodontic therapy may be used to partially close the
interdental spaces prior to restoration
 Composite resin or porcelain veneers can be bonded to the anterior
teeth when the incisor shape, size and/or color requires
modification.
 However, if the enamel is extremely thin and malformed the teeth
can require full dental coverage with crowns.

147
Treatment of Hypomaturation and
Hypocalcified AI Types
 full coverage restorations should be placed.
 Esthetic anterior restorations can be made using a variety of
techniques.
 Open face stainless steel crowns with composite inserts
 composite restorations can greatly reduce tooth sensitivity and provide
reasonable esthetics.

148
 Resin crowns can be placed on permanent incisors soon after they
begin to erupt during the mixed dentition (about age 7 – 10 years).
 As the gingival margin becomes exposed during continued tooth erupt
the resins are easily modified by adding resin to the gingival margin of
the tooth.
 Ultimately, custom fabricated crowns can be placed on the dentition.

149
Dentinogenesis imperfecta
 It is a hereditary mesodermal defect
 It may be associated with
“Osteogenesis imperfecta”, also a
mesodermal defect.
 There is a wide range of difference in
manifestation of the lesions or
defects.
 It is classified in 3 types

150
Types
 Type I – Dentinogenesis imperfecta with Osteogenesis Imperfecta
 Autosomal dominant trait
 Clinical appearance varies greatly
 Type II - Dentinogenesis imperfecta without Osteogenesis imperfecta
 Also called as hereditary opalescent dentin
 Autosomal dominant trait
 Most common dominantly inherited disorder
 Type III - Brandywine type
 This is a racial isolate in Maryland
 Inherited as autosomal dominant trait

151
Types
Type Clinical Appearance Radiographic Appearance
Type I Clinical appearance varies
greatly
Deciduous teeth are mostly
affected
Partial or precocious obliteration of the pulp
chamber
Type II Both dentitions are equally
effected
Partial or precocious obliteration of the pulp
chamber
Type III Both dentitions are involved Variable
Changes similar to type I and II
In Brandywine population characteristic “Shell
teeth” are present

152
Clinical features
 Colour - gray to brownish violet or yellowish brown
 translucent or opalescent hue
 Enamel may be lost early through fracturing away because of
abnormal DEJ
 With the early loss of enamel the abnormal dentin undergoes
rapid attrition
 Teeth are prone for fracture

153
Histological feature
 The appearance of enamel is normal
 The pulp chamber is usually obliterated by the
continuous deposition of dentin.
 The dentin is composed of irregular tubules,
 Dentinal tubules are larger in diameter and
less in number
 Some times tubules may be absent
 Dentin often shows large areas of uncalcified
matrix

154
 The water content is greatly increased, as much as 60% above
normal
 Inorganic content is less than that of normal dentin
 Micro-hardness of dentin closely corresponds to that of cementum

155
Radiographic Features
 The Type I and Type II diseases are radiographically similar and
they often exhibit “bulb shaped” or “bell shaped” crowns of the
teeth with abnormally constricted cervical areas.
 The roots of the teeth are thin and spiked.
 varying degrees of obliteration of the coronal as well as the
radicular pulp chamber.
 The cementum, Pdl and the alveolar bone radiographically appear
normal.

156
 The type III - similar to those of the type I and type II,
 although in many cases the affected teeth exhibit extremely large
pulp chambers surrounded by a thin shell of dentin and enamel.
 Because of their typical appearance the affected teeth are often
called “shell” teeth.
 These teeth frequently exhibit multiple pulp exposure and associated
periapical pathology.

157
Management
 Any possible success for treatment depends upon early di-
agnosis and care.
 Only two treatment modalities : selective odontotomy and
permanent full veneering.
 Metal and ceramic crowns are given.
 These teeth are not suitable candidates for playing the role of
abutments for any bridge work since the roots are small and they
also tend to fracture under frictional stress.
 In case of severe generalized attrition, complete denture
prosthesis may be necessary.

158
Palatogingival groove (PGG)

159
Palatogingival groove (PGG)
 Radicular groove (1908): A developmental anomaly that begins
near the tooth cingulum and extends from the CEJ in apical
direction along the root with a wide range of depths and
lengths. (Black)

160
History
 1958, Oehlers first reported radicular invagination of a
maxillary lateral incisor in a Chinese female
 1968, Lee et al. proposed the term PGG

161
Other names
 Distolingual groove,
 Corono-radicular groove,
 Radicular lingual groove,
 Vertical developmental radicular groove,
 Cingulo-radicular groove,
 Developmental radicular anomaly,
 Interruption groove,
 Palatoradicular groove

162
Etiology
a) consequence of an alteration in growth, such as an infolding of
the inner enamel epithelium and epithelial sheath of Hertwig,
b) variant of dens invaginatus
c) alteration of a genetic mechanism
d) attempt to form another root.

163
Clinical charracteristics
 Prevalance -2-18%
 Commonly lateral incisor
 high prevalence in Sino-Americans and low prevalence in Sub-
Saharan Africans and Sahul-Pacific people
 Clinically, patients with a pathologic lesion related to PGG often
complain of dull intermittent or acute pain,
 mobility of the teeth, pain on percussion,
 Pus discharge, sinus tract formation and gingival swelling

164
 They can also present with no symptoms.
 In most cases, the patient had no history of dental caries, trauma, or
discoloration of the teeth.
 Pulp vitality was retained or lost contingent upon pulpal nerve
involvement.
 Cases with advanced lesions along deep grooves frequently show no
response to thermal or EPT
 Funnel shaped hollow grooves with an accumulation of plaque and
calculus, along with loss of epithelial attachment, pocket formation, and
bleeding on probing.
 Observed bilaterally in the oral cavity.
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165
Classification

166
Relationship between PGG and
periodontal/pulpal health
 Hypothesis 1-
 Al-Rasheed et al. studied the association between PGG and
periodontal health by investigating the plaque index (PI),
bleeding index (BI), and pocket depth (PD)
 They reported that teeth with an apical groove showed PI and
BI of 100%;
 In several case reports, PGG cases presented as a combined
type of primary periodontal lesion with secondary involvement
of the pulp

167
 Hypothesis 2
 some authors have insisted that the pulpal and periodontal
lesions are unrelated with different etiologies that simply
coincide in time.
 the root apex, accessory foramina, lateral canals, and dentinal
tubules as possible communication channels between periodontal
defects
 pulpal tissues, and speculated that bacteria and necrotic debris
from a primarily infected root canal could extend into the apical
base of the fissure groove with subsequent coronal progression
along the groove.
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168
 Hypothesis 3
 irritants and microorganisms from the periodontal pocket could
progress along the hollow, funnel-shaped PGG surface, advancing
to the periodontal breakdown and root surface contamination
 resulting in retrogenic pulp necrosis even though PGGs do not
reach the apex and are not very deep.

169
Diagnosis
 Radiographically, teardrop-like radiolucency can be observed in
cases with primary pulpal infection and pear shaped radiolucency
can be observed in the coronal aspect with apical periodontal
widening

170
 CBCT can provide accurate, sensitive information to assess and
plan the treatment

171
Treatment of PGG
1. Basic principle for treatment
a) complete eradication of microbials
b) permanent and thorough sealing of the root groove that
communicates between the root canal and the periodontium
c) periodontal regeneration and complete healing of the
periodontium.

172
Treatment interventions needed in cases of relatively
shallow PGG (Kerezoudis et al 2003)
1. surgical removal of granulation tissue and irritants
2. a gingivectomy and apically positioned flap
3. surgical exposure and flattening of the groove by grinding,
with or without application of guided tissue regeneration
4. positioning a restoration in the groove
5. orthodontic extrusion of the tooth.

173
2. Treatment of mild PGG
 ‘Saucerization’ to the level of the crestal bone with a rotary
cutting and polishing instrument

174
3. Treatment of complex PGG
 granulation tissue removal through a flap,
 Saucerization with or without the guided tissue regeneration,
 Intentional extraction of a problematic tooth to achieve
complete removal of the groove and subsequent reimplantation
(intentional replantation),

175
4. Various regenerative materials currently used to fill the
groove
 Dragoo et al. indicated that any subgingival restoration material
should include the following characteristics:
(i) biocompatibility, (ii) a dual-cure set, (iii) adhesiveness, (iv)
radiopacity, (v) compactness, (vi) surface hardness, (vii)
insolubility in oral fluids, (viii) absence of microleakage, (ix) low
coefficient of thermal expansion, and (x) low cure shrinkage.
 In addition, convenience of use and rapid setting that does not
interfere with hemostasis are important properties in clinical
circumstances

176
 Several materials, including amalgam,
glass ionomer cement (GIC), composite
resin, and calcium silicate based-cement
such as mineral trioxide aggregate
(MTA), have been selected for PGG
treatment.

177
5. Various regenerative materials currently
used to fill intrabony defects
 GTR membrane
 Bone graft
 PRF
 enamel matrix derivative (EMD, Emdogain,
Straumann, Basel, Switzerland)

178
Prognosis
Depends on several factors:
 The location of the groove,
 severity of the accompanying periodontal disease,
 accessibility to the defect area, and
 type of groove (shallow/deep or long/ short)

179
5/11/2020

180
Conclusion
 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.

181
References
1. Art and science of operative dentistry- Sturdevant 5 th edition
2. Operative Dentistry- Modern Theory and Practice: Marzouk
3. Shafer‘s Textbook of Oral Pathology- Shafer, Hine, Levy
4. Abfraction : separating fact from fiction --ADJ 2009
5. Fracture necrosis :Diagnosis ,Prognosis assesment and Treatment Recommendations –
Louis H Berman,Sergio Kettler
6. Non carious cervical lesions and abfractions :A re – evaluation –JADA 2003 ;134:845—850
7. Role of erosion in tooth wear :aetiology ,prevention and management ---IDJ(2005) 55,277-
284
8. Erosion –Chemical and biological factors of importance –IDJ (2005 ) 55 285-290
9. Removable Orthodontic Appliances—K.G.Isaacson
10. Quintessentials 3 – Decision–Making in Operative Dentistry Brunton, Paul A.

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