Management of Non carious

lesions of teeth

Contents • Introduction• Attrition• Abrasion• Erosion• Abfraction• Localized Non- Hereditary Enamel Hypoplasia• Localized Non- Hereditary Enamel

Hypocalcification• Localized Non- Hereditary Dentin Hypoplasia• Localized Non- Hereditary Dentin

Hypocalcification

• Fracture lines• Amelogenesis imperfecta• Dentinogenesis imperfecta• Conclusion • References

Introduction

• Non carious tooth tissue loss is defined as surface loss due to a disease process other than dental caries. (Pual A Brunton ,Decision making in Operative Dentistry )

• Although decay is the usual cause of tooth destruction necessitating operative procedures , it has been estimated that 25% of tooth destruction does not originate from a carious process .

The etiology of the non carious tooth surface lesions include : ( 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) • Attrition

• Abrasion

• Erosion

• Abfraction

• Localized Non- Hereditary Enamel Hypocalcification

• Localized Non- Hereditary Dentin Hypolpasia

• Localized Non- Hereditary Dentin Hypocalcification

• Fracture lines• Amelogenesis imperfecta• Dentinogenesis imperfecta

Attrition• Defined as the mechanical wear of the incisal or

occlusal surface as a result of functional or

parafunctional movements of mandible (tooth to tooth contacts) Sturdevant.

• It is an age dependent ,continuous process usually physiologic (Marzouk)

• It also includes the proximal surface wear at the contact area because of the physiologic tooth movement

Attrition can predispose to or precipitate any of the following :

A) Proximal surface attrition (proximal surface

facets)

• Results from surface tooth structure loss and flattening , widening of the proximal contact areas.

• Surface area proximally increases in dimension , which is susceptible to decay.

• Mesiodistal dimension of the teeth is decreased, leading to drifting , with the possibility of overall reduction in the dental arch.

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 there would be no chance for the alveolar bone to erupt

occlusally to compensate for the occlusal tooth loss, & therefore the vertical loss might be imparted to the face

overclosure during mandibular functional movements &

strain areas on stomato-gnathic system.

Leading to

a. if the loss occurs over a long period- the alveolar bone can grow occlusally, bringing the teeth

to their original occlusal termination.

i.e vertical dimension loss will be confined to teeth but not imparted to face.

Deficient masticatory capabilities

Cheek biting- vertical overlap between the working inclined planes

will be lost, which will cause surrounding cheek, lip, tongue to be fed between the teeth.

Decay- because the underlying dentin will be exposed & thereby becomes more susceptible to decay.

Clinical presentation :

• Attrition in its purest form is seen as 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 ( will overstretch the joint ligaments ).

• Severe occluding surface attrition → predominantly horizontal masticatory movement of the mandible → extreme strain on the muscles of stomatognathic

system .

• When surface attrition is SLOWER & compensated by, intrapulpal deposition of secondary & tertiary dentin, then there will be no pulpal exposure.

• At other times, the attrition is faster than the intrapulpal dentine deposition, leading to direct pulpal exposure.

Treatment modalities The treatment must involve several

modalities ,which should be chosen and initiated in the following sequence:

• Pulpally involved teeth →endodontic therapy /extraction

depending upon their restorability . • Para functional activities ,( bruxism)-- be controlled

with protecting occlusal splints.

• Myofunctional , TMJ/ any other symptoms in the stomato-

gnathic system -----diagnosed and resolved (modifying the

occlusal splint).

• Occlusal equilibration : should be performed by :

Selective grinding of tooth surfaces that includes rounding and smoothening the peripheries of the occlusal tables.

And by creating adequate overlap between the working inclines to prevent further cheek biting.

• 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.

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.

Procedure • The most involved treatment modality is regaining

the lost vertical dimension .

• Verify and reverify its necessity i.e. one should make sure that alveolar bone did not grow occlusally at the same pace at which attrition occurred .

• 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 .

• The additional V.D. that the stomognathic system can accommodate without untoward effects is estimated.

• Hence , if a substantial increase in the dimension is to be considered (>2mm), it is wise to build a temporary restoration or removable occlusal splint that can be easily adjusted through subsequent addition or removal of material .

• Composite temporary restorations are most frequently used.

• Permanent restoration should be done in a cast alloy material to preserve the remaining the tooth structure and to assure the integrity of the supporting tissues. .

• A fully adjustable articulator ,hinge axis determination ,use of pantographic tracings and face bow records are essential for such cases .

• These restorations should be cemented only temporarily for an extended period of time ,until it is established that no untoward symptoms would occur.

• An acrylic splint ( as a stabilization splint) may be necessary to protect the dentition from further damage due to attrition and this is frequently the only treatment required to prevent further tooth tissue loss .

• Can also be used as a diagnostic aid ( esp. if an increase in the vertical dimension is planned subsequently )

Stabilization splint

The splint would need to be relined with cold cure acrylic resin to improve the retention of the appliance and occlusal adjustments will typically be required

Restorative treatment • tooth wear can be followed and re-evaluated during

recall examinations.• When the wear requires restorative intervention, 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):

• When the wear is more severe, a number of treatment modalities are available.

• 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.)

• 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)  

• 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.

• 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.)

The Dahl concept• In this approach, space is created by placing restorations intentionally ‘high’ – i.e. in supra-occlusion – allowing axial

tooth movement that, over time, re-establishes complete

occlusion.• This principle was known prior to the publication of Dahl’s

work in 1975. For example, the anterior bite platforms of

removable orthodontic appliances have long made use of this effect (Cousins AJ, Brown WA, Harkness EM, 1969).• Dahl and his coworkers (1975) were, however, the first to

describe how it may be used in the management of the worn dentition. They described the use of a ‘partial bite 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.

• After a period of eight months sufficient space was created

to restore the worn upper anterior teeth.

• once sufficient inter-occlusal space had been created. However, 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

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 a needed increase in V.D.----considerably lesser

adjustments are made ,lesser time consuming

•To ensure that the patient is able to tolerate the increase in the vertical dimension , it is necessary to wear the appliance for at least 6- 8 weeks

(12 hours /day ,generally evenings and nights)

• At this time if the muscles of mastication are flaccid and show no tenderness to palpation and the TMJ’s are free from pain , palpation and opening clicks , then it is usually safe to proceed , to the restorative care .

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 .

• Overbite reduction should be evident within first two months of fitting the appliance .

• It is important to increase the thickness of bite plane slowly with progressive additions of cold cure acrylic as the overbite reduces .

Endodontic considerations• In certain cases intentional endodontic therapy has to be

performed in hyper erupted teeth or drifted teeth, worn that have to reduced drastically, that pulp is certain to be involved.

• Careful examination of the color changes in pulp chamber floor ,along with aids like magnification and transillumination can help safely locate the canals .

• Additional aids like: 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

Treatment strategies for Dentinal hypersensitivity

( DCNA 53 ,2009; 47-60)There are a number of treatment options for

managing dentinal hypersensitivity . Can be broadly be categorized into :1. Nerve desensitization Potassium nitrate

2 .Anti-inflammatory agents Corticosteroids

3. Covering or plugging dentinal tubules• calcium hydroxide• sodium fluoride

• Sodium monoflourophosphate• Stannous fluoride • Oxalates• Strontium chloride

Protien precipitants formaldehyde glutaraldehydeFlouride iontophoresis

Resins and Adhesives

4) Restorative materials 5) Periodontal surgery6) Lasers

Nerve desensitization Potassium nitrate • A number of studies have reported the efficacy of

potassium nitrate for managing dentinal

hypersensitivity .

• Tarbet et al demonstrated that potassium nitrate at a concentration of 5%in a low abrasive tooth paste was able to desensitize dentin for up to 4 weeks compared to a control paste .

• 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)

Anti inflammatory agents Corticosteroids

• It has been suggested that application of anti-inflammatory drugs such as 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 ,thus

reducing dentin permeability. • However there is a little experimental evidence to support or refute the use of such agents .

Covering or plugging dentinal tubules .

Calcium hydroxide • It has little or no effect on the dentine sensory nerve

activity (Trowbrdge H ,Edwall L ,1982)

• However it is thought that it induces peritubular dentin remineralization and less hypersensitive dentin .(Mjor IA 1967)

• Levin and colleagues found that application of Ca(OH)2 paste to hypersensitive exposed dentine resulted in an immediate decrease of dentinal hypersensitivity in over 90%of treated teeth .

Sodium fluoride

• Many clinical studies have shown that the treatment of

exposed root surface with fluoride toothpaste (1.1%) and conc. fluoride solutions(0.2%) is very efficient in managing dentinal hypersensitivity. (Minkow B,1975;Kerns D G 1991)

• Tal et al suggested that the probable desensitizing effects of fluorides are related to precipitated fluoride compound mechanically blocking the exposed dentinal tubules.

Sodium monoflourophosphate

• Tooth pastes containing sodium monoflourophospshates have been shown to be effective in managing dentinal

hypersensitivity (Hernandez F,Mohammed C,1972)

• It does not appear to act by occluding dentinal tubules since scanning electron microscopic studies have failed to

demonstrate any visual changes to the dentinal surface treated with it .(Addy M ,1983)

• Any tubule occlusion which might occur does not appear to be permanent .(Tarbet WJ et al ,1983)

• Its mechanism of action is unclear (,Scherman A et al 1992)

Stannous flouride

• Stannous fluoride in aqueous solution or in glycerin gelled with carboxymethylcellulose is effective in controlling dentinal hypersensitivity.

(Miller JT et al 1969)

• Mode of action appears to be through induction of high mineral content which creates a calcific barrier blocking the tubular openings on the dentine surface .

(Furseth R ,1970)

• Alternatively ,it may precipitate on the dentine surface leading to occlusion of the exposed dentinal tubules

Flouride 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 )

This method has gained popularity but more controlled studies are required .(Gillian DG et al 1990)

Oxalates

• It has been shown that 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 :• 6% ferric oxalate (Sensodyne Sealant )• 30% dipotassium oxalate( Butler Protect )• 3% monohydrogen monopotassium oxalate

Strontium chloride

• It has been proposed that the ions occlude dentinal tubules by binding to the tooth substance and stimulating reparative dentin formation.

• It has also been suggested that 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.

• Cohen found that 67% of the subjects using a strontium chloride containing toothpaste reported complete relief of dentinal hypersensitivity within a 2 month period.

• Protein precipitants (Formaldehyde and glutaraldehyde )

• Claims have been made that Formaldehyde and glutaraldehyde through their ability to precipitate salivary proteins in the dentinal tubules, can be used to manage dentinal hypersensitivity .

• 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)

• Given that these agents are very strong fixatives ,they should

be used with extreme caution too ensure they do not come in

contact with vital gingival tissues.

Resins and Adhesives

• The rationale for the use of resins and adhesives is to seal the dentinal tubules and hence to preclude the transmission of pain causing 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)

• Copeland reported successful treatment of dentinal hypersensitivity for up to 18 months in 89% of

hypersensitive teeth treated by Scotchbond.

• A combination product consisting of an aqueous solution of 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)

• The glutaraldehyde intrinsically blocks dentinal tubules counteracting the hydrodynamic mechanism that leads

to dentinal hypersensitivity • In summary, resin restorations have been used to cover

areas of denuded dentin. This would seem to be a rational treatment strategy.

Bioactive glass: • NovaMin is the brand name of a

particulate bioactive glass that is used in dental care products 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.

Lasers • There are a number of reports that suggest that laser

treatment may be useful in the treatment of, dentinal hypersensitivity although definitive trials are lacking(Cooper LF et al ,1988).

• A recent review of the literature by Kimura and colleagues reported that effectiveness of laser treatment of dentinal hypersensitivity ranged from 5% to 100%.

• In a clinical and SEM study, Kumar and Mehtas (2005) found that Nd:YAG laser irradiation in combination with 5% sodium fluoride varnish has higher efficacy in the management of DH

than either treatment alone. • Slutzky-Goldberg (2008)and colleagues have

demonstrated that CO2 laser treatment resulted in decreased permeability of dentinal tubules as shown by a dye penetration test.

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.

• Generally this approach is reserved for situations where there has been significant prior loss of cervical tooth structure or as a last resort for a tooth which does not respond to other less invasive

desensitizing protocols.

Part- 2

• 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 ) .

Abrasion

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 .

Iatrogenic causes:

• Dentures with porcelain teeth opposing natural teeth.

• Extremely rough occluding surface of the restoration

enhancing its abrasive capability .

• ill fitting dentures and clasps ,producing a constant wear of the affected surfaces.

Tooth brush abrasion 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 .

The clinical signs and symptoms of an abrasion are :

• 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 .

Treatment modalities 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. Judiciously tooth brushing with a dentifrice i.e. incorporating

correct method of tooth brushing .

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

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 .

If restoration is not indicated for a lesion, then :

• Edges of the defect should be eradicated to a smooth, non- demarcating pattern relative to adjacent tooth surface.

• Tooth surface then should be treated by fluoride solution to improve caries resistance

If the involved teeth→ extremely sensitive:• Desensitize the exposed dentin before

restoration .

Desensitization:• 8-10%sodium/stannous fluorides for 4-8 minutes.

• Iontophoresis- --using an electrolyte containing fluorides( galvanic energy supplied to the tooth in the presence of electrolyte, drives ions deep into the dentin)

Restoring cervical abrasions

In many instances no treatment is necessary but restoration is

indicated when :

• Caries ,if present .

• Sensitivity is present.

• Lesion is esthetically objectionable .

• If the defect contributes to a periodontal problem

• The area to be involved in the design of a removable partial denture.

• When the depth of defect is found to be close to pulp

• Or a progressive loss of tooth structure is observed

compromising the tooth strength .

Restorative materials :

• Glass ionomer restorative material.

• Resin modified glass ionomer.

• Polyacid-modified resin composites.

• Resin composites.

Restoration

• 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 )

As a result materials with low elastic modulus such as :

Microfilled composites (Heymann and others ,1991 :Levitch

and others ,1994 ) Flowable resins (Unterbink ,Liebenberg ,1999: Li and

others 2006 ) 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 .

Two-year clinical evaluation of four polyacid-modified resin composites and a resin-modified glass-ionomer cement in Class V abrasion/erosion lesions. Ermiş RB.. Quintessence Int. 2002 Jul-Aug;33(7):542-8

• The aim of the study was to compare the clinical performances of four polyacid-modified resin composites (F2000, Dyract AP, Compoglass F, and Elan) and one resin-modified glass-ionomer cement (Vitremer) in Class V abrasion/erosion lesions.

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. No statistically significant differences were found among the materials after 2 years for any evaluation category

Discussion

• It is generally well accepted that glass-ionomer cements have an inhibitory effect on secondary caries, and the release of fluoride is considered to be one of the major benefits associated with glass-ionomer cements,

• However, it bas been demonstrated that polyacid-modified resin composites may not be recharged again with fluoride as are glassionomer cements.

comparative analysis of techniques of restoring cervical lesions- (Quintessence Int 1993:24:553-

559.)• The clinical significance of this investigation is that two of the

techniques tested, ie, the sandwich technique and the glass-ionomer cement restoration, have definite potential to successfully restore cervical lesions, from the standpoint of marginal leakage.

• While glass-ionomer cement may not have as good esthetic properties as resin materials, the sandwich technique does not have universal application, because it requires space and hence may not be the technique of choice in relatively shallow cavities.

• When the lesion is relatively shallow and esthetic demands necessitate the use of a resin material, the all-composite restoration would be a compromise in terms of marginal seal.

• This result should be kept in mind when cervical lesions are to be restored with these materials.

The success of modern-day restorative materials depends, on the ability to stop marginal leakage. Within the limitations of this study, the following conclusions may be drawn:

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 restorafions.

3. The dentina! adhesive used with the composite resin did not always provide a leak-free seal at the gingival margins of the restorations.

4.Composite resin restorations inserted over a glassionomer liner demonstrated significantly less leakage than when the liner was not used.

5. In general, the use of the sandwich technique or glass-ionomer restorative material alone provided the most effective seals in cervical wedge-shaped cavities, compared to the all-composite restoration.

6. There was no significant difference between the marginal leakage of glass-ionomer cement and sandwich technique restoration

5-year clinical performance of resin composite versus resin modified glass ionomer restorative system in non-carious cervical lesions.Franco Eb, Benetti A , SK Ishikiriama,SL Santiago ,JRP Lauris

AIM: To comparatively assess the 5-year clinical performance of a resin composite system with a resin-modified glass ionomer restorative in non-carious cervical lesions.

METHOD AND MATERIALS: One operator placed 70 restorations (35 resin modified glass ionomer restorations 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.

Erosion • Loss of surface tooth structure by chemical action in

the continued presence of demineralizing agents(acids). (Sturdevant- 5 th edition)

• It is one of the most predominant oral pathologic changes .

• 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 .

Chemical factors :

• Ingested acids : citric acids (lemon and citrus fruits ) 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)

The latter defective surfaces are associated with gastro esophageal reflux .(GERD)

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

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 aconcave 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

• A similar appearance is found in patients with eating disorders-

Anorexia ( is an eating disorder characterized by immoderate food restriction and irrational fear of gaining weight, as well as a distorted body self-perception)

Bulimia nervosa (is an eating disorder characterized by 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 ( a chronic condition characterized by effortless regurgitation of most meals following consumption) have all been closely associated with dental erosion .

• 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)

• It has been reported that 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)

• As reported by Lussi ,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 )

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.

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 sought to evaluate 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.

Mean ph values for each beverage

• Coca cola 2.49• Diet Coke 3.12• Gatorade 2.93 • Red Bull 3.24• Starbucks Frappucino 6.59• Tap water 7.12

•  Coca-Cola Classic produced the lowest mean pH, while Starbucks Frappucino produced the highest pH of any of the drinks except for tap water.

• 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.

• Buffering capacity is the measure of total no. of acid molecules and determines the actual hydrogen ion availability for interaction with tooth surface (Boulton R,1980)

• 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 .

Monitoring tooth wear

• Recognizing how the appearance of teeth change with tooth wear ,can be helpful in assessing the activity.

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 .

• 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 .

(Beatrice K,Edmond L ,J Contemp.Dental practise ,1999)

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

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

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.

• 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 erosio. Journal of Contemp.Dental Practice 1999)

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.

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 .

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.

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 .

Abfraction

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 . (Grippo JO,1991: Levitch LC , Bader JD, Heymann HO ,1994 )

• 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. (Lee WC, Eakle WS, J Prosthet Dent 52(3): 374-

380, 1984.)

• 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.

( 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.

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.

Restoration

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

• Aesthetics demands are a concern .

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 .

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

Part- 3

Fracture lines The cause of these fractures may include :

• Physical trauma• Occlusal prematurities• Repetitive heavy and stressful chewing• Resorption weakened teeth• 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.

Five types of longitudinal fractures have been described (American Association of Endodontists,2008 ):

(1) Craze line: affect only the enamel, originate on the occlusal surface, are typically from occlusal forces or and are asymptomatic .

2) Fractured cusp: occur on the cusps and cervical margins of the root and 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

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

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

• 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”

• This has been described as acute pain that results during the mastication (or release) of small hard food substances and also exacerbates with cold.

(Cameron CE,JADA,1964 : American Association of Endodontists,2008)

• However, the signs and symptoms of a cracked tooth may also be consistent with an irreversible pulpitis or necrosis.

• In summary there are 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 )

Characteristics of tooth infarctions

Problems in diagnoses :

• 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 ,radiogarphs are not very diagnostic .

• 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 )

Distribution • Molars and premolars are the teeth are

almost exclusively involved

• Teeth with restorations are most likely to develop infarctions

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 ( if rebound pain occurs on release ,it is very likely that one of the two teeth ,maxillary or mandibular ,has an infarction )

Clinical test for detecting infarction :• The patient bites onto the moist cotton roll and on release the pain will often be quite noticeable .

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.

• Act of chewing is also implicated

• 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.

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

Removal of the restoration and highlighting with the dye to detect infarction

• Use of optic light source to identify an infarction .

•Note that the beam of light does not cross the infarction

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 .

Use of tooth Slooth to test biting sensitivity to differentiate between pain from infarction and pain from micro leakage related to a restoration

• Significant response to biting ….when pain is experienced release of biting pressure (rebound pain ) /relief pain

• Pain …….with the release of pressure ……due to fluid movement as the crack rapidly closes .

• Cold stimulus application and Electric pulp testing(EPT ) :

Gives information about the pulpal status ,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

Radiographic examination

• 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 .

• 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.

• 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 .

• 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

Treatments designed to bind the infarcted segments of teeth together .,that includes the use of adhesives , full coverage crowns .

Localized Non Hereditary Enamel Hypoplasia DEFINITION CAUSE CLINICAL

PRESENTATIONTREATMENT

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

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

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

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 .

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-

c) 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

Direct tooth colored resinous material (composite material) is inserted with /without tooth preparation

Localized Non Hereditary Enamel Hypocalcification

DEFINITION CAUSE CLINICAL

PRESENTATION

TREATMENT

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.

If diagnosis is made early in tooth’s life ,while the uncalcified enamel is still intact an attempt at remineralization should be made .

4. If extensive- these lesions predispose to attrition and abrasion.5. Enamel chipped if lesion involves the entire surface of a tooth .

Can be done using-A)fluoride applications B)fluoride iontophoresis C)strict prevention of plaque accumulation in these areas .

CLINICAL PRESENTATION TREATMENT

Vital bleaching

Laminated veneering

Composite

Crowns

Localized Non Hereditary Dentin HypoplasiaDEFINITION CAUSE CLINICAL

PRESENTATIONTREATMENT

Odontoblasts are the specialized cells ,any disturbance in their function- deficient or complete absence of dentin matrix deposition

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 eugenolCalcium hydroxide Zinc phosphate cement

Leads to the development of localised non-hereditary dentin hypoplasia

During tooth preparation for a restoration , these defects may get exposed

Polycarboxylate cement VarnishesGlass ionomer cement

LOCALIZED NON-HEREDITARY DENTIN HYPOCALCIFICATION

DEFINITION CAUSE CLINICAL PRESENTATION

TREATMENT

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

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 eugenolCalcium hydroxide Zinc phosphate cement

During tooth preparation for a restoration , these defects may get exposed

Polycarboxylate cement VarnishesGlass ionomer cement

Amelogenesis imperfecta DEFINITION CLINICAL

PRESENTATIONTREATMENT

developmental alterations in the structure of enamel in the absence of a systemic disorder

HYPOPLASTIC AI-•Thin enamel• Open contact•Enamel is glossy•Enamel can look wrinkled.• Signs of severe occlusal wear• Missing teeth.•Delay in eruption.

AIM OF TREATMENT-•Reducing tooth sensitivity•Improving esthetics•Correcting or maintaining vertical dimension•Restoring masticatory function

4 MAIN TYPES-1)Hypoplasia2)Hypocalcification 3)Hypomaturation4)Hypomaturation –hypoplasia with taurodontism Small yellowish teeth

exhibiting hard, glossy enamel with numerous open contacts points and anterior open bite

Temporary phase –undertaken during primary or mixed dentition Transitional phase –when all the permanent teeth have erupted Permanent phase – occurs in adulthood

CLINICAL PRESENTATION TREATMENT

HYPOCALCIFIED- •Enamel is usually stained (yellow/Black)• Enamel chips easily ,very soft in consistency

Reducing tooth sensitivity-topical fluoride products ,CPP-ACP products , dietary modification

Maintaining good oral hygiene

•stains become darker with time•Enamel- worn easily in life with all signs and symptoms of severe attrition

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

CLINICAL PRESENTATION TREATMENT

HYPOMATURATION AI• Affected teeth ---normal in shape , but exhibit mottled, opaque white brown –yellow discoloration .• Enamel is softer than normal ,tends to chip from underlying

Restoring masticatory function • Performed by full veneering ,includes procedures - 1)metallic 2) Cast ceramic restorations

diffuse yellow white dentition

Dentinogenesis imperfecta DEFINITION CAUSE CLINICAL

PRESENTATIONTREATMENT

Autosomal dominant disorder with variable expressivity

Caused by mutation in the DSPP gene.

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

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

Primary teeth are normally more severely affected than permanent teeth

Atypical color of teeth → dentin showing through the relatively translucent opalescence enamel

In patients without cracks and rapid attrition of enamel, intracoronal restorations and veneers used.

Classification : (Witkop)Type I : dentin mineralization defects are coupled with osteogenesis imperfecta

External bleaching (notably prolonged night guard vital bleaching ) with carbamide peroxide has been reported with excellent results

a CLINICAL PRESENTATION

TREATMENT

Type II: Hereditary Opalescent dentin Type III: Brandy wine type (Shell teeth )

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

In anterior teeth → stainless steel crowns with composite facings may be given

At a later stage porcelain crowns are suggested .

Loss of pulp chamber radiographically

Splinting between these teeth- to avoid root fracture.

MANAGEMENT OF NON CARIOUS LESIONS

ATTRITION- dentinal hypersentivity using F ions, acrylic splints, treatment of bruxism, restorative treatment with composite 7 cast metal

ABRASION- proper tooth brushing, use of RMGIC, sandwich technique, composite restorationEROSION- F

application, splints, composite, antacid tablets, reduction in acidic drink consumtion.

ABFRACTION- Use of RMGIC, sandwich technique,occlusal adjustments,

LN ENAMEL HYPOPLASIA- Odontomy/ reshaping, composite restoration

LN ENAMEL HYPOCALCIFICATION- F Remineralisation, Vital bleachingLaminated veneering,Composite Crowns

LN DENTIN HYPOPLASIA/ HYPOCALCIFICATION- intermediary bases-Zinc oxide eugenol, Calcium hydroxide ,Zinc phosphate, Polycarboxylate cement Varnishes,GIC

FRACTURES- Bind the infarcted segment & stabilized with adhesives/crowns

AMELOGENESIS IMPERFECTA- F application,composite & crowns

DENTINOGENESIS IMPERFECTA- Veneers, crowns, bleaching

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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