6
January/February 2010 Australasian Dental Practice 117 116 Australasian Dental Practice January/February 2010 clinical | EXCELLENCE clinical | EXCELLENCE W hen patients present with an extensively worn dentition, the dentist must have an understanding of what is causing the wear to be successful in treatment. Tooth wear can be caused by a number of factors, but usually one factor may predominate. Communication between the dentist and patient is essential in establishing an etiology of the wear. Usually patients are aware of a problem and must be informed on how to prevent further damage and what treatment options are available. This article will review the etiology of gastroesophageal reflux disease (GERD) and a conservative, aesthetic treatment solution. The first time a patient is examined, it is difficult for the dentist to determine if the rate of wear is excessive. The only way to tell is if the patient has been a patient of record for a number of years. What constitutes “normal” wear rates? Various published articles have conflicting values. One study reports a normal loss of enamel between 20 microns and 38 microns per year. 1 Another study reports a wear of 65 microns in 6 months. 2 Non-carious tooth wear is a normal physiologic process that occurs in many patients throughout life. 3 If the rate of wear is such that it is the source of concern to the patient, or if it is likely to prejudice the survival of the teeth, then the rate is considered to be pathological, and action must be taken to minimize the damage. 4,5 Erosion is defined as “the progressive loss of tooth substance by chemical processes that do not involve bacterial action”. 6 Acid reflux appears as one of the most common causes of dental erosion. Erosion can be divided into extrinsic and intrinsic factors. The extrinsic factors include acid from bev- erages and foods, vigorous tooth brushing and some oral medications. Intrinsic erosion is often caused by vomiting, gastric reflux, pregnancy, quality and quantity of saliva, and alcoholism. 7 It was reported that patients with low unstimulated flow rates of saliva were found to have an increased risk for development of cervical lesions. 8 Since saliva rinses away and buffers acids on tooth surfaces, low sali- vary flow rates may be an initiating factor in dental erosion. It has also been reported that anorexics and bulimics develop xerostomia and their saliva may have a lower buffering and remineralizing capacity. 9 Most individuals experience gastroesophageal reflux at some time in their lives. GERD, however, is a clin- ical condition that occurs when the reflux of stomach acid into the esophagus is severe enough to impact the patient’s life and/or damage the esophagus. 10 A relationship between GERD and dental erosion has been described in a number of publications. 11-15 In most patients, GERD is due to a transient relaxation of the sphincter that keeps the lower end of the esophagus closed when he or she is not swal- “Dentists need to familiarize themselves with the consequences of gastroesophageal reflux disease (GERD) and know how to treat it...” Treating worn dentition caused by Gastroesophageal Reflux Disease By Bob Margeas Figure 1. Figure 2. Figure 3. Figure 4. Figure 5. Figure 6. Figure 7. Figure 8.

Treating Worn Dentition

Embed Size (px)

Citation preview

Page 1: Treating Worn Dentition

January/February 2010 Australasian Dental Practice 117116 Australasian Dental Practice January/February 2010

clinical | EXCELLENCE clinical | EXCELLENCE

When patients present with an extensivelyworn dentition, the dentist must have anunderstanding of what is causing the

wear to be successful in treatment. Tooth wear canbe caused by a number of factors, but usually onefactor may predominate. Communication betweenthe dentist and patient is essential in establishing anetiology of the wear. Usually patients are aware ofa problem and must be informed on how to preventfurther damage and what treatment options areavailable. This article will review the etiology ofgastroesophageal reflux disease (GERD) and aconservative, aesthetic treatment solution.

The first time a patient is examined, it is difficultfor the dentist to determine if the rate of wear isexcessive. The only way to tell is if the patient hasbeen a patient of record for a number of years. Whatconstitutes “normal” wear rates? Various publishedarticles have conflicting values. One study reports anormal loss of enamel between 20 microns and 38microns per year.1 Another study reports a wear of65 microns in 6 months.2 Non-carious tooth wear isa normal physiologic process that occurs in manypatients throughout life.3 If the rate of wear is suchthat it is the source of concern to the patient, or if itis likely to prejudice the survival of the teeth, thenthe rate is considered to be pathological, and actionmust be taken to minimize the damage.4,5

Erosion is defined as “the progressive loss oftooth substance by chemical processes that do notinvolve bacterial action”.6 Acid reflux appears asone of the most common causes of dental erosion.Erosion can be divided into extrinsic and intrinsicfactors. The extrinsic factors include acid from bev-erages and foods, vigorous tooth brushing and someoral medications. Intrinsic erosion is often causedby vomiting, gastric reflux, pregnancy, quality andquantity of saliva, and alcoholism.7 It was reportedthat patients with low unstimulated flow rates ofsaliva were found to have an increased risk fordevelopment of cervical lesions.8 Since saliva rinsesaway and buffers acids on tooth surfaces, low sali-vary flow rates may be an initiating factor in dentalerosion. It has also been reported that anorexics andbulimics develop xerostomia and their saliva mayhave a lower buffering and remineralizing capacity.9

Most individuals experience gastroesophageal refluxat some time in their lives. GERD, however, is a clin-ical condition that occurs when the reflux of stomachacid into the esophagus is severe enough to impactthe patient’s life and/or damage the esophagus.10 Arelationship between GERD and dental erosion hasbeen described in a number of publications.11-15

In most patients, GERD is due to a transientrelaxation of the sphincter that keeps the lower endof the esophagus closed when he or she is not swal-

“Dentists need to familiarizethemselves

with the consequences ofgastroesophageal

reflux disease(GERD) and know how to

treat it...”

Treating worn dentition caused by Gastroesophageal Reflux Disease

By Bob Margeas

Figure 1. Figure 2.

Figure 3. Figure 4.

Figure 5. Figure 6.

Figure 7. Figure 8.

Page 2: Treating Worn Dentition

In order to efficiently treat tooth ero-sion, a comprehensive understanding ofthe effects of tooth wear must be obtained.Potential results of tooth wear can berelated to functional, aesthetic, and sensi-tivity concerns.24

• Functional: Patients tend to have diffi-culty with mastication, broken teeth,and failing restorations;

• Aesthetic: As the dentition undergoeswear and fracture, the patient’s generalappearance may change as he or shereveals less teeth during speech and theirnatural smile. In some instances, thesmile line may be reversed entirely; and

• Sensitivity: While most patients withexcessive tooth wear often experiencereduced sensitivity as a result of exposeddentin, some patients have reported pre-operative hypersensitivity.Minimally invasive treatments are proce-

dures that restore form, function andaesthetics with minimal removal of soundtooth structure.25-27 As a person ages, so dotheir teeth and previously placed restora-tions. Eventually, teeth that have been

restored will break down and need to havethose restorations replaced.28,29 Fortunately,restorative materials and procedures are con-stantly evolving. The conservative nature ofthe initial restoration will allow more toothstructure to work with at the time that asecond restoration may be needed.

Case presentationA 55-year-old patient was referred to thepractice with a severe (grade III) general-ized loss of enamel and dentin. The patientwas aware that his teeth were becomingthinner and was concerned that some of theanterior teeth may fracture (Figure 1). Thepatient was not aware of any systemicproblems or that they had severe symptomsof acid reflux. Prior to proceeding withdental treatment, the patient was referred toa gastroenterologist for a full diagnosticexam. Following the diagnostic exam,which included the monitoring of acidregurgitation and pH while the patientslept, a final diagnosis of GERD was ren-dered. The patient was treated with agastric secretion suppressor medication

(Prilosec) that inhibits the hydrogen/potas-sium ATPase enzyme system in the gastricparietal cells of the lining of the stomach. Itis considered a gastric acid pump inhibitorsince it works by blocking the final step ofacid production.

Examination resultsNo abnormalities, asymmetry or temporo-mandibular dysfunction were evident uponextraoral examination. Intraoral examina-tion revealed deep erosive lesions withsevere lack of enamel on all functionalcusps and the cervical areas of severalteeth. Severe wear of the maxillary incisaledges was observed and excessive “cup-ping” was noted on the palatal aspects ofthe maxillary anterior teeth (Figures 2-6).Aesthetic evaluation revealed a normalsmile line with a previously restoreddiastema that was discoloured. There wasno evidence of periodontal disease and thepatient’s oral hygiene was satisfactory.

The pulps of numerous teeth werenearly exposed, particularly in the anteriorregion. Occlusal analysis revealed a Class I

January/February 2010 Australasian Dental Practice 119

lowing food or liquids, which allows acidand food particles to reflux into the esoph-agus.10 GERD is characterized by thechronic, intermittent, unrestricted move-ment of stomach acids into the esophagus.This is defined as regurgitation and shouldbe distinguished from vomiting since itinvolves a passive or effortless return ofthe stomach contents into the mouthversus a physiological response to astimuli controlled by the autonomicnervous system.13-15 The four major symp-toms of GERD are heartburn(uncomfortable, rising, burning sensationbehind the breast bone); epigastric and ret-rosternal (non-cardiac) pain; regurgitationof gastric acid or “sour stomach” contentsinto the mouth; and difficult and/orpainful swallowing.13-15 GERD can beeffectively managed with medication orlifestyle changes. Surgery is an option insevere cases.

The frequent regurgitation of stomachacids into the mouth results in continuousundesired contact of these acids with theteeth in the oral cavity. This can lead todental erosion. Dentists need to familiarizethemselves with the consequences ofGERD and know how to treat it. Erosion isdifferent from abrasion in cause andappearance. As stated previously, erosion isa non-bacterial, chemical dissolution ofhard tooth surfaces, whereas abrasion iscaused by mechanical wear of tooth struc-ture by external agents. The appearance ofthe lesions is different in that tooth surfacesaffected by erosion have a spoon-shapedappearance, while abrasive lesions appearsharp, flat and angular. Moreover, sinceerosion does not affect metal or plasticdental restorations as does abrasion, theseremain as prominent elevated plateaus.16

Dental erosion can be the result of var-ious systemic conditions, which oftenmakes the etiology difficult to identify.These conditions include upper gastroin-testinal disorders with an acid diet (43%);upper gastrointestinal disorders (25%); anacid diet (24%); eating disorders (6%); andunknown causes (2%).16 Unfortunately, thecause of dental erosion often goes undiag-nosed, or the presence of other factors suchas abrasion and attrition make diagnosismore difficult to determine.17

Bargen and Austin were the first to iden-tify and report a relationship betweendental erosion and gastrointestinal distur-bances in a case report of a woman who

presented with chronic vomiting.18 The ero-sion was primarily evident on the palatalsurfaces of the anterior maxillary teeth.

Eccles and Jenkins found a relationshipbetween erosion of the lingual surfaces ofanterior teeth and GERD.19,20 They sug-gested the following grading system forerosion: grade I = loss of enamel surfacetexture with no dentin involvement; gradeII = erosion involving dentin for less thanone third of the areas of the tooth surface;and grade III = dentin erosion involvingmore than one third of the tooth surface.Bartlett et al reported that there was astrong relationship between palatal dentalerosion and GERD, even in those patientswith no symptoms of reflux.13-15

The damage caused to the dentition byGERD depends on the severity of the case.In the majority of cases, the occurrence of pathological reflux was noted to occur during the day. These findings areconsistent with many other studies. Ifregurgitation of the gastric juice occurs atnighttime, however, when salivary flow isat its lowest, the potential for damage tothe teeth increases significantly.21

Several authors have reported a highincidence of erosion in patients with psy-chological and psychiatric disorders andthose taking certain medications such astranquilizers or beta-blocking agents.10

These medications produce a reduction ofsalivary secretion rates that contributes todental erosion.22 While other investigatorswere unable to determine a significant rela-tionship between the use of anticonvulsantdrugs and dental erosion,23 evidence sug-gested that this type of medicationdecreased the pressure of the loweresophageal sphincter, making such individ-uals more likely to suffer from reflux.22,23

It has not been determined if the qualityof oral hygiene has an effect on the severityof dental erosion.23 It has been reported,however, that mechanical factors such asocclusal wear, abrasive tongue action andtooth brushing can potentiate the destruc-tive nature of the acids.23 Ideally, therestoration of eroded tooth structure shouldoccur following appropriate diagnosis andcontrol of the etiology and it should be ori-ented towards the reestablishment offunction and aesthetics. Other researchersemphasize the importance of early inter-vention before the progressive erosionmakes it an almost impossible task or afull-mouth rehabilitation is necessary.23

118 Australasian Dental Practice January/February 2010

clinical | EXCELLENCE

Figure 9. Figure 10. Figure 11.

Figure 12. Figure 13. Figure 14.

Figure 15. Figure 16. Figure 17.

Page 3: Treating Worn Dentition

molar relationship. There was minimal tono overjet and almost 100% overbite. Dueto the severe wear of the teeth, it is possiblethat the vertical dimension of occlusionwas lost, but it would only be possible toconfirm if the patient had previously takencephalometric x-rays from years ago thatwe could compare with today.

Treatment planThis case could have been treated a numberof different ways. Orthodontics was anoption given to the patient to allow roomfor restorative material in the anteriorregion. This would be the most conserva-tive treatment option. It would allow theanterior teeth to be restored and the poste-

120 Australasian Dental Practice January/February 2010

00Figure 18. Figure 19.

Figure 20. Figure 21.

Figure 22. Figure 23.

Figure 24. Figure 25.

Figure 26. Figure 27.

Page 4: Treating Worn Dentition

rior conservatively restored withoutchanging the vertical dimension. The teethwould be moved anteriorly and intruded toallow us room to restore. However, thepatient did not want to proceed with ortho-dontics. The anterior teeth were very thinwith severe notching and not enoughoverjet to restore functionally. If the teethwere prepared for full coverage crowns,they would be severely compromised andthe risk of fracture would be high. The pos-terior teeth could be treatment planned forpartial coverage restorations fabricatedfrom gold, porcelain or composite. Sinceorthodontics was not an option, the verticaldimension of occlusion needed to bealtered to restore the case properly. Consid-ering the findings and the patient’s concernof possible fracturing of the anterior teeth, aminimal invasive treatment plan was pre-sented. This would consist of fabricatinglingual veneers made indirectly out of com-posite resin and composite onlays for theposterior mandibular molars. Theserestorations would be fabricated indirectlyby the dentist from a diagnostic wax upusing a silicone die material (Bisco, orMach 2 Parkell) and a clear polyvinylmaterial (RSVP, Cosmedent).

Diagnostic impressions were made out

of a polyether material (Impregum, 3MESPE) so that the silicone die materialwould not adhere to it when the models arefabricated. If you use a polyvinyl material,the silicone die material will adhere to theimpression and cannot be removed. Themodels were sent to the laboratory so aKois Deprogrammer could be fabricated tofacilitate mounting the case in centric rela-tion. The patient wore the appliance for 3weeks and then bite registration impres-sions were made with the appliance inplace to capture the jaw position. Once thecasts were mounted on a Panadent articu-lator, wax was added to the lingual of theanteriors (Figure 7) to restore the toothstructure that was missing. By adding thewax to the lingual of the anteriors, this willopen the articulator so the posteriors canbe waxed (Figure 8) to the new verticaldimension. The minimal amount ofopening was achieved so the teeth could berestored properly.

Once the wax up was completed,polyvinyl impressions (RSVP, Cosme-dent) were made so that we would have amatrix to form the new restorations in theposterior. The polyether impressions wereinjected with the silicone die material(Figure 9) and allowed to set for 2 minutes.

The silicone die material was thenremoved from the impression and hybridcomposite was added to form the lingualveneers (Figure 10). This was done free-hand and only enough material to replacewhat was missing was added. This is whatdetermined the new vertical dimension. Aclear polyvinyl matrix could have beenused for fabricating these restorations. Thecomposite was light cured and then placedin a Triad unit for final light curing (Figure11). This should make the restorationsstronger, due to the heat and light. Therestorations were finished and polishedusing finishing disks and polishing points(Figure 12). The restorations were firstmicro-etched with 50 micron aluminumoxide powder and then etched with hydro-fluoric acid (Figure 13) for 90 seconds andsilanated. The restorations would then beadhesively bonded with resin cement. Therestorations were tried in for fit (Figure 14)and cleaned in an ultrasonic bath with ace-tone. The teeth were isolated with anExpandex retractor (Parkell) and micro-etched using aluminum oxide powder(Figure 15). The teeth were etched for 20seconds (Figure 16) with ultra-etch (Ultra-dent) and then rinsed and air dried. Afourth generation bonding system (All

122 Australasian Dental Practice January/February 2010

clinical | EXCELLENCE

00Figure 28. Figure 29.

Figure 30. Figure 31.

Page 5: Treating Worn Dentition

Bond II, Bisco) was utilized for its excel-lent bond strength. The two- part primerwas mixed in a dispensing well andapplied in numerous coats to the moist sur-face (Figure 17). This was followed by anapplication of the unfilled D/E resin(Bisco). The restoration was treated withD/E resin and Insure resin cement (Cosme-dent). The adjacent teeth were protectedfrom the etch and adhesive by using Teflontape. The restorations were seated one at atime and light cured for 40 seconds on thelingual and facial. Figure 18 shows the firstthree restorations placed. The same proce-dure was followed for the remaininganterior restorations.

To fabricate the posterior restorations, aclear silicone impression tray, fabricatedfrom the diagnostic wax up was utilized(Figure 19). This would be filled withcomposite resin and placed over the sili-cone die material. In order to make thecomposite resin more flowable, a Calsetcomposite heater (Addent) was used(Figure 20). The composite was injectedinto the clear matrix and placed on the sil-icone die material (Figures 21-22). Theclear impression tray was seated over thesilicone die material and light cured for 40

seconds. The tray was removed and therestorations are shown on the silicone die(Figure 23). These restorations were thenseparated, finished and polished and readyto be bonded on the posterior teeth.

Rubber dam isolation was used in theposterior for ideal moisture control. Theteeth were etched with a microetcher first(Figure 24) and then etched with phos-phoric acid. The same bonding protocolwas utilized as the anterior restorations. Inorder to keep the etch from the adjacentteeth when bonding, a Brasseler serratedsaw blade (Figure 25) was inserted inter-proximally because the contacts were notbroken. A clear matrix would not gothrough the contacts. The restorations werethen bonded individually (Figure 26) andthe resin cement cleaned up. Figure 27shows the lower right quadrant bonded toplace prior to removing the rubber dam.

Once all of the posterior restorationswere bonded to place, final equilibrationwas necessary. A composite platform wasfabricated and placed on the lingual of theupper anterior teeth similar to a Koisdeprogrammer (Figure 28). This wasretained mechanically due to the diastemawithout any adhesive. The patient lightly

124 Australasian Dental Practice January/February 2010

An Easy Approach toPredictable AnteriorDirect and Indirect

RestorationsPresented by

Marcos Vargus (Peru) andBob Margeau (USA)

Unique combined course. Compositeand veneer lecture and hands-on coursewith two world experts. This course will

provide dentists with high end resultswithin realistic practical timing.

Melbourne23 June - Lecture

Sydney25 June - Lecture

26 June - Hands-on (25 max)27 June - Hands-on (25 max)

For more info or to register, seewww.dentaled.com.au

Figure 32. Figure 29.

Figure 34. Figure 35.

clinical | EXCELLENCE

00

Page 6: Treating Worn Dentition

occluded on the platform for about 15 min-utes to allow the muscles to relax. Theplatform was then slightly modified(Figure 29) to allow the first tooth to touch.This would represent the initial contact incentric relation. Equilibration was thencarried out until even simultaneous con-tacts were present on all the posterior teethand cuspids. The final equilibration toremove any interference on the lingual ofthe anteriors when chewing, was accom-plished with the patient chewing gum inthe posterior and 200 micron articulatingpaper placed in the anterior. Only thestreaks and aberrant lines are necessary toremove. These are areas of friction withinthe envelope of function.

The patient elected to have the diastemaclosed and all the cervical lesions wererestored with direct composite resin(Renamel microfill, Cosmedent). Thefinal results are shown in Figures 30-35.

ConclusionThis case could have been treatment plannedseveral ways. The patient in this case under-went a procedure with no tooth removal.The conservative nature of the treatmentthat was rendered will allow future restora-tions to be accomplished without worryingabout previous destruction due to treat-ment. The restorations are easily repairedand should provide years of service.

About the authorDr Bob Margeas graduated from the Uni-versity of Iowa College of Dentistry in1986 and completed his AEGD residencythe following year. He is currently anAdjunct Professor in the Department ofOperative Dentistry at the University ofIowa. He is Board Certified by the Amer-ican Board of Operative Dentistry and is aFellow of the Academy of General Den-tistry. He offer hands on courses at theKios Centre as well as his own centre inIowa. Dr Margeas has written numerousarticles on aesthetic implant dentistry andhe lectures and presents hands-on courseson those subjects. He serves on the Edito-rial Advisory Board of Inside Dentistry,Functional Aesthetics & Restorative Den-tistry, and is a contributing editor toDentistry Today and Oral Health inCanada. Dr Margeas maintains a privatepractice focusing on comprehensiverestorative and implant dentistry in DesMoines, Iowa.

References1. Lambrechts P, Braem M, Vuylsteke-Wauters M, Van-herle G. Quantitative in vivo wear of human enamel. JDent Res 1989;68(12):1752-1754.2. Xhonga FA. Bruxism and its effect on the teeth. J OralRehabil 1977;4(1):65-76.3. Flint S, Scully C. Orofacial age changes and related dis-ease. Dent Update 1988;15(8):337-342.4. Smith BG, Knight JK. An index for measuring the wearof teeth Br Dent J 1984;156(12):435-438.5. Watson IB, Tulloch EN. Clinical assessment of cases oftooth surface loss. Br Dent J 1985;159(5):144-148.6. The glossary of prosthodontic terms. The Academy ofProsthodontics. J Prosthet Dent 1994;71(1):41-112.7. Levitch LC, Bader JD, Shugars DA, Heymann HO, Non-car-ious cervical lesions. J Dent. 1994;22(4):195-207.8. British Soft Drinks Association 1998 report.9. Hurst PS, Lacey LH, Crisp AH. Teeth, vomiting anddiet: A study of the dental characteristics of seventeenanorexia nervosa patients. Postgrad Med J1977;53(620):298-305.10. Ibarra G, Senna G, Cobb D, Denehy G, Restoration ofEnamel and dentin erosion due to gastroesophogeal refluxdisease: A case report. Pract Procd and Aes Dent.2001;13(4): 297-304.11. Jarvinen V, Meurman JH, Hyvarinen H, Rytomaa II,Murtomaa H, Dental erosion and upper gastrointestinaldisorders. Oral Surg Oral Med Oral Pathol1988;65(3):298-303.12. Taylor G, Taylor S, Abrams R, Mueller W. Dental ero-sion associated with asymptomatic gastroesophageal reflux.ASDC J Dent Child 1992;59(3):182-185.13. Bartlett DW, Evans DF, Smith BG. The relationshipbetween GERD disease and dental erosion: Review J OralRehabil 1996;23(5):289-297.14. Bartlett DW, Evans DF, Anggiansah A, Smith BG. Astudy of the association betweenGERD and palatal dentalerosion. Brit Dent J 1996;181(4):125-132.15. Bartlett DW, Smith BGN. Clinical investigations ofGERD: Part1 Dent Update 1996;23(5):205-208.16. Bouquot JE,Seime RJ. Bulimia nervosa: Dental perspec-tive. Pract Periodont Aesthet Dent 1997;9(6):655-663.17. Cardoso AC,Canabarro S, Myers SL. Dental erosion:Diagnostic-based noninvasive treatment. Pract PerioAesthe Dent 2000;12(2):223-228.18. Bargen JA, Austin LT, Decalcification of teeth as aresult of constipation with long continued vomiting:Report of a case J Am Dent Assoc 1937;24:1271.19. Eccles JD, Jenkins WG. Dental erosion and diet J Dent1974;2(4):153-159.20. Eccles JD. Tooth surface loss from abrasion, attrition,and erosion. Dent Update 1982;9(7):373-381.21. Smith BG, Robb ND. Dental erosion in patients withchronic alcoholism. J Dent 1989;17(5):219-221.22. Meurman JH, Toskala J, Nuutinen P, Klemetti E. Oraland dental manifestations in GERD. Oral Surg Oral MedOral Pathol 1994;78(5):583-589.23. Gilmour AG, Beckett HA. The voluntary reflux phe-nomenon. Brit Dent J 1993;175(10):368-372.24. Cortellini D, Parvizi A, Rehabilitation of severelyeroded dentition utilizing all-ceramic restorations. PractProced Aesth Dent 2003;15(4):275-282.25. Christensen GJ. The advantages of minimally invasivedentistry. J Am Dent Assoc 2005;136(11):1563-1565.26. White JM, Eakle WS. Rationale and treatmentapproach in minimally invasive dentistry. J Am Dent Assoc2000;131(9):1250,1252.27. Rainey JT. Understanding the applications of micro-dentistry. Comped Contin Ed Dent2001;22(11A):1018-1025.28. Brantley CF, Bader JD, Shugars DA,Nesbit SP. Doesthe cycle of rerestoration lead to larger restorations?1995;126(10):1407-1413.29. Lutz F, Krejci I, Besek M. Operative Dent: The missingclinical standards. Pract Periodont Aesth Dent1997;9(5):541-548.

126 Australasian Dental Practice January/February 2010

00