REVIEW

Resin bonding to cervical sclerotic dentin: A review

Franklin R. Taya,*, David H. Pashleyb

aPaediatric Dentistry and Orthodontics, Faculty of Dentistry, University of Hong Kong, Prince Philip DentalHospital, 34 Hospital Road, Hong Kong, ChinabDepartment of Oral Biology and Maxillofacial Pathology, Medical College of Georgia, Augusta, GA, USA

Received 10 July 2003; accepted 15 October 2003

KEYWORDSSclerotic cervical

dentine; Resin; Adhesive

Summary Several reports have indicated that resin bond strengths to noncarioussclerotic cervical dentine are lower than bonds made to normal dentine. This isthought to be due to tubule occlusion by mineral salts, preventing resin tag formation.The purpose of this review was to critically examine what is known about the structureof this type of dentine. Recent transmission electron microscopy revealed that inaddition to occlusion of the tubules by mineral crystals, many parts of wedge-shapedcervical lesions contain a hypermineralised surface that resists the etching action ofboth self-etching primers and phosphoric acid. This layer prevents hybridisation of theunderlying sclerotic dentine. In addition, bacteria are often detected on top of thehypermineralised layer. Sometimes the bacteria were embedded in a partiallymineralised matrix. Acidic conditioners and resins penetrate variable distances intothese multilayered structures. Examination of both sides of the failed bonds revealed awide variation in fracture patterns that involved all of these structures. Microtensilebond strengths to the occlusal, gingival and deepest portions of these wedge-shapedlesions were significantly lower than similar areas artificially prepared in normal teeth.When resin bonds to sclerotic dentine are extended to include peripheral sounddentine, their bond strengths are probably high enough to permit retention of class Vrestorations by adhesion, without additional retention.q 2004 Elsevier Ltd. All rights reserved.

Introduction

The efficacy of current adhesive systems is oftenevaluated based upon their ability to bond to sounddentine. Although many dentists bond to sounddentine, a variety of pathological dentin substratesare encountered in the clinical practice, whichinclude carious and sclerotic dentin. It is ironic

that our current knowledge on the variability ofclinical bonding substrates is so limited comparedwith the progress achieved in adhesive technology.This review examined the ultrastructure and bond-ing characteristics of one type of abnormal bondingsubstrate–noncarious sclerotic dentine. Essentially,it compared the obstacles in bonding to sound vs.sclerotic dentine. It will be seen that there is atremendous difference in substrate morphology aswell as that of the resin–dentine interfaces createdby bonding to such substrates. The recent introduc-tion of contemporary self-etching primers and

0300-5712/$ - see front matter q 2004 Elsevier Ltd. All rights reserved.doi:10.1016/j.jdent.2003.10.009

Journal of Dentistry (2004) 32, 173–196

www.intl.elsevierhealth.com/journals/jden

*Corresponding author. Tel.: þ86-852-28590251; fax: þ86-852-23933201.

E-mail address: kfctay@hknet.com

the timely all-in-one adhesives are redefiningadhesive dentistry. Because these simplifiedadhesive systems are easy to use, we have placedextra emphasis on the interfaces created by theseagents on sclerotic cervical dentine.

Noncarious cervical sclerotic dentine

Noncarious cervical sclerotic lesions was describedby Zsigmondy in 18941 as angular defects, and byMiller in 19072 as ‘wasting of tooth tissue’ that wascharacterised by a slow and gradual loss of toothsubstances resulting in smooth, wedge-shapeddefects along the cemento-enamel junction. Themultifactorial etiology of these cervical lesions hasbeen extensively reviewed.3–9 There is increasingevidence of the possible role of eccentric occlusalstress in the pathogenesis of these hard tissuedefects.10 – 18 Recent studies on simulation ofwedge-shaped cervical lesions using various finiteelement analytical models of cuspal flexure con-firmed the contribution of stress induction in theseso-called ‘abfraction lesions’.19 – 22 Unrestored,angular, wedge-shaped lesions demonstratedsevere stress concentration that varied with thelocation of the teeth in the oral cavity, with thehighest stress contractions around the maxillaryincisors and premolars. These stresses were onlypartially relieved after these lesions were restored.

Sclerotic dentine is a clinically relevant bondingsubstrate in which the dentine has been physiologi-cally and pathologically altered, partly as thebody’s natural defense mechanism to insult, andpartly as a consequence of colonisation by the oralmicroflora. Partial or complete obliteration of thedentinal tubules with tube- or rod-like scleroticcasts is commonly observed.23 –28 Depending on thedegree of clinical sensitivity of the lesion, variouslevels of tubular patency were observed, with mostdentinal tubules being occluded within the insensi-tive transparent dentine regions.25,27,29 –34

In the absence of undercut retention, cervicalsclerotic dentine was found to be more difficult toadhere to than normal dentin both in vitro and invivo, even with increased etching time.35–39 Recentstudies showed that the sclerotic casts thatobliterated the dentinal tubules were still presentafter acid-conditioning of the sclerotic dentine,resulting in minimal or no resin tag formation.Furthermore, the zone of resin-impregnated sclero-tic dentine was found to be thinner than thoseobserved in normal dentine.25,27,40 –43

Due to the thinness of hybrid layers in scleroticdentine, and the complexity of the resin-bonded

interface, regional tensile bond strength to cervicalsclerotic root dentine with some contemporaryadhesives was found to be 20–45% lower than thosebonded to artificial wedge-shaped lesions created innormal cervical root dentine.40,42 This was attrib-uted to: (a) the presence of sclerotic casts withindentinal tubules that precluded optimal resininfiltration into the dentinal tubules, and/or (b)the presence of a surface hypermineralised layerthat is more resistant to acid-etching. It waspostulated that an adhesive strategy that involvedmicromechanical interlocking by the formation of aresin–dentine interdiffusion zone combined withresin-tag formation into the dentinal tubules wouldbe less effective when applied to the hyperminer-alised sclerotic dentine.42,44 Contrary to thesefindings, a recent study suggested that phosphoricacid-etching was detrimental to the bonding ofsclerotic dentine, and that sclerotic dentine thatwas treated with a hydrophilic primer exhibitedbetter marginal adaptation of resin composites thansimilarly primed normal dentine.45 These authorsrecommended that the layer of sclerotic dentine bepreserved for optimal bonding in cervical lesions.

Scanning electron microscopy of such surfaces,even with the use of field emission-type micro-scopes, does not provide sufficient detail to under-stand the complex subsurface structures, or toreveal how well these structures are demineralisedduring etching.28,43 This information is bestobtained using transmission electron microscopy(TEM). In this review, extensive TEM examinationswere used to evaluate biologic variations insclerotic cervical dentine. This is not an exhaustivereview of the literature on noncarious cervicallesions or in resin-bonding to sclerotic dentine.Rather, it is an attempt to summarise a number ofstudies that provide a rationale for why resin bondsto sclerotic, noncarious, wedge-shape cervicallesions are lower than those made to normaldentine at those same sites. This review will bedivided into two sections. In Section 1, microstruc-tural changes that exist in noncarious, scleroticcervical dentine will be summarised. This isfollowed by a review on the application of adhesiveresins to this altered bonding substrate.

Microstructural changes in scleroticdentine

Tubular occlusion

In dentine sclerosis, tubular obliteration withrhombohedral, whitlockite crystallites (Fig. 1A)

F.R. Tay, D.H. Pashley174

has been well documented at an ultrastructurallevel.27,31,34,46 –48 A high degree of variation couldbe observed even within a single lesion. While sometubules may be completely devoid of, or sparselyoccluded with crystallites, others may be heavilyobliterated with crystallites and/or peritubulardentine (Fig. 1B). Toward the surface of the lesion,these crystallites were reduced in size and formedcolumns of agglomerates that completely plug thetubular orifices. They were often referred to assclerotic casts (Fig. 2A). At an ultrastructural level,these tiny, electron-dense crystallites were sur-rounded by a tube-like membranous structure26,27

that probably represented a mineralised form of thelamina limitans of the dentinal tubule (Fig. 2B).

Hypermineralised surface layer in shinysclerotic lesions

Unlike tubular occlusion, the presence of a surfacehypermineralised layer in natural cervical scleroticwedge-shaped lesions has only been elucidatedthrough the use of microradiography30 and FTIRphotoacoustic spectroscopic analysis.32 Although ithas been speculated that the hypermineralised

Figure 1 (A) SEM micrograph of the body of a scleroticlesion showing a dentinal tubule that was heavilyoccluded with whitlockite crystallites (pointer). Theadjacent tubules were almost completely obliteratedwith peritublar dentine. (B) A higher magnification viewof the rhombohedral whitlockite crystallites (pointers)that were present within another dentinal tubule in thesclerotic lesion. P: peritubular dentine; I: intertubulardentine.

Figure 2 (A) SEM micrograph of sclerotic casts thatblocked the dentinal tubular orifices (pointer) along thesurface of a shiny sclerotic lesion. (B) TEM micrographtaken from an undemineralised section of the surface of abonded sclerotic lesion. Tubules were obliterated withsclerotic casts that consisted of electron-dense crystal-lites. They were surrounded by a tube-like sheath(pointer). A thin, electron-dense, hypermineralisedlayer was also evident along the surface of the lesion(open arrow) (from Tay et al., 2000,57 with permission).

Resin bonding to cervical sclerotic dentin: A review 175

layer is devoid of collagen fibrils,37 the ultrastruc-tural features of this layer were only verifiedrecently. Fig. 3A is a toluidine blue-stained,undemineralised thin section taken from the dee-pest part of a wedge-shaped defect that is leastaccessible to tooth brushing. In the preparation ofthe specimen, the surface of the lesion was notcleaned and was fixed in Karnovsky’s fixative priorto the embedding protocol for TEM preparation. Asurface layer of stained, unmineralised filamentousbacteria could be seen, beneath which was anapproximately 15 mm thick hypermineralised layer.

Mineralised bacteria could vaguely be discernedwithin this layer. The corresponding undeminera-lised TEM image (Fig. 3B) shows that both themineralised plaque zone and the surface layer ofthe lesion are hypermineralised with respect to theunderlying sclerotic dentine. At a higher magnifi-cation (Fig. 4), plate-like minerals could be recog-nised within intermicrobial matrix.

The ultrastructure of the surface hyperminer-alised layer is highly variable within the deepestpart of the wedge-shaped lesions. This can bebetter discerned using demineralised TEM sec-tions. It is interesting to observe that such alayer is still retained after complete deminerali-sation of the underlying sclerotic dentine. Fig. 5Ashows a thick, continuous, dense hyperminera-lised layer that contained two different speciesof bacteria. One species was trapped within thislayer, while the other was found to grow on thesurface of this layer. The hypermineralised layerin Fig. 5B, on the other hand, consists of severalthin, discontinuous layers that were sandwichedamong different species of bacteria. This suggeststhat changes in the microecology of the oralenvironment may have resulted in the colonisa-tion of different species of bacteria at sequentialperiods. Each colony of bacteria was, in turn,mineralised prior to the deposition of the nextcolony. It is pertinent to point out that bothspecimens, from which Fig. 5A and B were taken,were brushed cleaned with a mixture of chlor-hexidine and pumice prior to laboratory proces-sing. Both appeared as clean, highly shiny lesionswhen examined under magnification lens.

Figure 3 (A) Light microscopic image of an undeminer-alised section taken from the deepest part of anuntreated noncarious cervical sclerotic lesion. B: stained,unmineralised bacteria; HM: hypermineralised surfacelayer of the lesion; SD: intact sclerotic dentine; Pointers:mineralised bacteria ghosts. (B) Corresponding unstainedTEM micrograph of the undemineralised section. Thehypermineralised nature of the surface layer (HM) couldbe recognised by comparing its electron density with theunderlying sclerotic dentine (SD) (from Tay et al., 2000,57

with permission).

Figure 4 (A) Undemineralised TEM micrograph of abacterium (B) within the hypermineralised layer (HM).The intermicrobial matrix (i.e. the material betweenadjacent bacteria) was mineralised and contained plate-like crystallites (pointer) (from Tay et al., 2000,57 withpermission).

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The presence of colonising bacteria on thesurface of sclerotic wedge-shaped lesions isconsistent with the report of Spranger.6 Themicroecology beneath bacterial plaque changesover time depending on the metabolism of themicroorganisms. This results in substantial pHfluctuations along the tooth surface.49 Bacterialproducts may trigger gingival inflammation withan increased rate of sulcular fluid flow, which inturn, provides nutrition for the microorganisms. Ifa plentiful supply of fermentable carbohydrates isavailable, the microbes release organic acids thatwill lower the plaque pH and tend to deminer-alise the underlying dental hard tissue. When thecarbohydrate source is depleted, the local pHrises due to salivary buffering, and remineralisa-tion of the dental hard tissue and mineralisationof the dental plaque can proceed. In the absenceof carbohydrates, these bacteria may remainviable for prolonged periods,50 utilising glyco-gen-like intracellular polysaccharide as a metab-olisable source of carbon during periods ofnutrient deprivation.51 They may also metaboliseamino acids and other nitrogenous substrates,creating ammonia and other basic chemicals thatmay elevate plaque pH and promote mineralis-ation and, perhaps, hypermineralisation.52

Along the occlusal wall of the wedge-shapedlesions, both the surface bacterial layer and thehypermineralised layer are usually thinner, withthe latter between 1 and 2 mm thick. Similarly, thegingival wall of a wedge-shaped lesion, which isusually more accessible to tooth brushing, is usuallydevoid of bacteria. However, a very thin surfacehypermineralised layer may sometimes be observed.Such a layer, if present is around 200–300 nm thickand may be readily discerned in undemineralisedsections by its increased electron density, as well asthe characteristic arrangement of the crystallites,which will be discussed in Section 3.3.

Mineral distribution

Minerals present within the hypermineralised layerare larger in size compared with those within theunderlying sclerotic dentin (Fig. 6A). Unlike crystal-lites within the underlying dentine that are randomlyarranged, those that are found in the hyperminer-alised layer are longitudinally aligned along the c-axis of the crystallites. This is clearly demonstratedin Fig. 6B. Orientation of the crystallites along theirc-axis in the surface hypermineralised layer isanalogous to the induction of cellular orientationby low-level electrical currents53 and the alignmentof filler particles within resin composites under

Figure 5 Variation in the ultrastructure of the hyper-mineralised layer in noncarious cervical sclerotic lesions.(A) This demineralised TEM micrograph showed a hyper-mineralised layer (HM) within the deepest part of awedge-shaped lesion that was about 14 mm thick.Bacteria colonies were trapped inside this layer (openarrow). Another species of bacteria (arrowhead) accu-mulated along the surface of the hypermineralised layer.Dentinal tubules were not occluded with sclerotic castsand were also filled with bacteria (pointer) (from Kwomget al., 2002,42 with permission). (B) Another deminer-alised TEM micrograph showing a complex, intact, hybridstructure that consisted of several discontinuous, hyper-mineralised layers (pointers) that were sandwichedamong different colonies of bacteria (A, B, C and D).The entire complex is about 18 mm thick. SD: scleroticdentine.

Resin bonding to cervical sclerotic dentin: A review 177

the application of an electric field.54 Dentine is onlymildly piezoelectric compared with bone.55 How-ever, piezoelectric potentials have been reported tobe generated when teeth are subjected to parafunc-tional loading.6 Some have speculated that polaris-ation of the remineralised crystallites caused bypiezoelectric potentials created during eccentrictooth flexure results in their attraction and repulsionby dipole interaction. Dipole interaction competeswith randomisation caused by Brownian motionand alignment occurs as the dipole interactionpredominates.56

STEM/EDX analysis

Hypermineralisation implies that the density of themineral within the surface layer of the defect ishigher than that of the underlying sclerotic dentine.This is confirmed by a qualitative STEM/EDX linescan of the calcium and phosphorus distributionlongitudinally across the surface layer of thedefect into the underlying sclerotic dentine(Fig. 7A and B). Also evident in the line scan is thepresence of a region of decreasing calcium andphosphorus counts along the top 500 nm of thehypermineralised layer that is attributed to partial

Figure 6 (A) Crystallites (pointer) with the hyperminer-alised layer (HM) were plate-like and were aligned alongthe c-axis. They were also larger than those (arrowhead)present within the underlying sclerotic dentine (SD). (B)The characteristic orientation of crystallites along theirc-axis was also evident in a thick hypermineralised layertaken from the deepest part of another wedge-shapedlesion. The lesion surface was etched by a self-etchingprimer, with blunting and rounding of the partiallydissolved crystallites.

Figure 7 (A) Brightfield STEM image showing thelocation of a line scan that was performed across thesurface hypermineralised layer of a noncarious cervicalsclerotic lesion (from Tay et al., 2000,57 with permission).(B) Qualitative energy dispersive line scans showing thedistribution of calcium and phosphorus alongthe adhesive, the surface hypermineralised layer of thelesion and the underlying intact sclerotic dentine (fromTay et al., 2000,57 with permission).

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demineralisation by a self-etching primer (ClearfilLiner Bond 2V; Kuraray Medical, Inc., Tokyo, Japan)that was used to bond to sclerotic lesions.57

QuantitativeenergydispersiveX-ray spectraof theelemental content of crystallites present within (a)the surface hypermineralised layer, (b) the under-lying intertubular dentine, and (c)within the dentinaltubules of the wedge-shape defect are shown inFig. 8.57 As the analysis was performed using 70 nmthick undemineralised sections, this enabled esti-mation of the calcium/phosphate ratio of these

crystallites without additional ZAF correction.The Ca/P ratios of the crystallites within thehypermineralised layer and the underlying dentineapproach the theoretical value of 1.67 calculated forhydroxyapatite.58 The larger apatite crystallitesobserved in the surface hypermineralised layer aresimilar to larger apatite crystallites reported inremineralised carious dentin59,60 and cementum.61

Conversely, the Ca/P ratio of crystallites fromthe sclerotic casts within the dentinal tubules isslightly lower than the calculated value of 1.50 for

Figure 8 Energy spectra from different locations of a noncarious cervical sclerotic lesion. (a) Spectrum showingcomposition of crystallites within the surface hypermineralised layer. (b) Spectrum of crystallites within the underlyingintact sclerotic dentine. (c) Spectrum of crystallites occupying the lumen of a dentinal tubule. Spectra were obtainedusing a 7 nm probe for 200 live seconds at 200 kV. The relative concentration of Ca, P and Mg, and the calculated Ca/Pratios are shown in the table beneath the spectra (modified from Tay et al., 2000,57 with permission).

Resin bonding to cervical sclerotic dentin: A review 179

tricalcium phosphate.58 The additional presence ofabout 5% magnesium suggests that these crystallitesare whitlockite (Mg substituted b-tricalcium phos-phate).

Status of the collagen fibrils withinthe surface hypermineralised layer

An intriguing question that has remained unan-swered is whether the surface hypermineralisedlayer is devoid of collagen.36 Using special stainingfor collagen, it can be seen that the supportingmatrix for the crystallites within the hyperminer-alised layer consists of a bed of denatured collagen(Fig. 9A). The transition from denatured collagen(gelatin) to intact collagen with cross-banding isevident at the base of the hypermineralised layer,where some of the collagen fibrils are observed tounravel into microfibrillar subunits.57 Thistransition from banded collagen to denaturedmicrofibrils is further illustrated beneath a layerof bacteria in Fig. 9B, in which unraveling ofcollagen fibrils created a network of microfibrillarstrands that no longer showed cross-banding.

It is possible that colonisation of bacteria alongthe surface of the wedge-shaped defect results inthe production of acidic and enzyme by-productsthat demineralise and denature the collagen fibrils(Fig. 9B). Diffusion of the enzymes from thedemineralised surface downwards probablyaccounts for the transition from completelydenatured collagen to unraveled microfibrils andfinally intact collagen within the underlying sclero-tic dentine. The loss of phosphoproteins62 andsubsequent remineralisation of the surface bed ofdenatured collagen under the possible influence ofpiezoelectric charges generated from eccentricflexural deformation6 may result in the character-istic orientation of the crystallites within thedenatured microfibrillar matrix of the surfacehypermineralised layer.

Summary of the microstructural changesin noncarious sclerotic cervical dentine

Sclerotic dentine is an abnormal bonding sub-strate that exhibits a high degree of variabilityboth in terms of occlusion of the dentinal tubulesas well as the thickness of the surface hypermi-neralised layer. The latter, in particular isinvariably associated with bacteria. It is possiblethat bacteria are involved in the pathogenesis ofthe hypermineralised layer. That is, dentine mayfirst require demineralisation before it can behypermineralised. Also, mineral crystallites can-not accumulate without a scaffold. The presence

of bacteria, apart from demineralising the den-tine, also denatures the existing collagen matrix,resulting in a bed of denatured collagen. Thismay act as a scaffold upon which the deminer-alised dentin may be subsequently remineralised.The formation of the hypermineralised layer isprobably also enhanced by the presence of highconcentrations (10 ppm) of fluoride ions.63 –65 Asdenaturing of the collagen fibrils probablyremoves some of the restrictions on the size of

Figure 9 (A) TEM micrograph from a demineralisedspecimens, showing that the supporting matrix of thehypermineralised layer (HM) consisted of a bed ofdenatured collagen microfibrils(arrow). These subunitsof collagen were formed by unraveling of collagen fibrils(arrowhead). Within the underlying sclerotic dentine(SD), intact banded collagen fibrils could be seen(pointers) (from Tay et al., 2000,57 with permission). (B)A thin hypermineralised layer (HM) beneath a layer ofbacteria (B) showing the transition from intact, bandedcollagen fibrils into denatured collagen (gelatine),appearing ultrastructurally as microfibrillar strands (poin-ter). SD: sclerotic dentine.

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crystallite formation, this may enable largercrystallites to be formed during the process ofremineralisation. The unique arrangement of thecrystallites further suggests the complex role ofparafunctional stress on the formation of thesurface hypermineralised layer in these naturalwedge-shaped lesions.15,23 The presence of bac-teria, mineralised bacterial matrices, hypermi-neralised surfaces and mineral occluded tubulesmakes sclerotic cervical dentine a unique multi-layered bonding substrate. This implies thatbonding studies that attempt to generate hyper-mineralised dentine in vitro by immersing par-tially demineralised dentine in a remineralisingsolution containing a high fluoride content66,67 donot simulate the actual bonding conditions thatclinicians are likely to encounter when bonding tononcarious cervical sclerotic dentine.

Bonding adhesive resins to scleroticdentine

Current dentine adhesives employ two differentmeans to achieve the goal of micromechanicalretention between resin and dentine.68 –70 The firstmethod, the total-etch or etch and rinse technique,attempts to remove the smear layer completely viaacid-etching and rinsing. The second approach, theself-etch technique, aimsat incorporating the smearlayer as a bonding substrate.

Total-etch technique

Most self-priming, single-bottle adhesives availableto-date attempt to bond to dentine that is etchedwith inorganic or organic acids. Following rinsing ofthe conditioners, retention is accomplished bymeans of resin-infiltration into the exposed, demi-neralised collagen matrix to form a hybrid layer ofresin-impregnated dentine.69 –71 Systems containinghydrophilic primer resins solvated in acetone orethanol were found to produce higher bond strengthwhen acid-conditioned dentine was left visibly moistprior to bonding.72 Pioneered by Kanca,73 thistechnique is often referred to as ‘wet bonding’.The benefit of wet bonding stems from the ability ofwater to keep the interfibrillar channels within thecollagen network from collapsing during resin-infiltration.74,75 These channels, which are about20 nm wide when fully extended, (Fig. 10) must bemaintained open to facilitate optimal diffusion ofresin monomers into the demineralised intertubulardentine.76,77

Self-etch technique

Recent developments in dentine bonding havereintroduced the concept of utilising the smearlayer as a bonding substrate, but with improvedformulations that could etch through the smearlayer and beyond, into the underlying dentinematrix. Failure to etch beyond the smear layer,exemplified by some of the early adhesives that wereapplied directly to the smear layer, resulted in weakbonds due to the complete absence of a hybrid layerin underlying intertubular dentine.78,79 Contempor-ary self-etch adhesives have been developed byreplacing the separate acid-conditioning step withincreased concentrations of acidic resin monomers.Two-step self-etching primers combine etching andpriming into a single step. The primed surfaces aresubsequently covered with a more hydrophobicadhesive layer that is light-cured. In the presenceof water as an ionising medium, these adhesives thatetch through smear layers and bond to the under-lying intact dentine.80,81 The recent introduction ofsingle-step (all-in-one) self-etch adhesives rep-resents a further reduction in bonding steps thateliminates some of the technique sensitivity andpractitioner variability that are associated with theuse of total-etch adhesives.82 –84

When applied to sound dentine, the milder self-etch adhesives produce a hybridised complex(Fig. 11) that consists of a surface zone of hybridisedsmear layer and a thin, subsurface hybrid layer in theunderlying intertubular dentine.85 –87 Despite thepresence of a hybrid layer that was generally below2 mm thick, high initial bond strengths have

Figure 10 Dentine collagen fibrils from a hybrid layerthat was produced using a total-etch technique. Inter-fibrillar channels (pointers) must be maintained open foroptimal resin infiltration. This is achieved using a wetbonding technique.

Resin bonding to cervical sclerotic dentin: A review 181

been reported for sound dentine.88 –91 The moreaggressive self-etch adhesives completely dissolvesmear plugs and demineralise dentine to the extentthat is comparable with phosphoric acid-etching.87

There has been some concern that mild self-etchadhesives may not be able to penetrate throughthick smear layers, such as those produced clinicallyby rough diamond burs.85 –92 The use of adjunctivephosphoric acid pre-conditioning has beensuggested as a means to improve bonding of self-etching primers to sound dentine with thick smearlayers.93 –96

Problems in bonding to sclerotic dentine

Irrespective of the use of a total-etch or a self-etchtechnique, bonding to pathologically altered sub-strates such as sclerotic dentine from noncariouscervical lesions generally led to compromisedbonding.40 – 42,57 Reduced bonding efficacy wasattributed to a combination of factors that includethe obliteration of dentinal tubules with scleroticcasts, the presence of an acid-resistant hypermi-neralised layer, and the presence of bacteria on thelesion surface. The presence of the hyperminer-alised layer, bacteria and the tubular mineral castsin sclerotic dentin are analogous to the presence ofthe smear layer and smear plugs in sound dentine,being potential diffusion barriers for primer andresin-infiltration. The concern that a self-etchingprimer may not etch through the superficial layers

on sound dentine may likewise be applicable tosclerotic dentine. Acid pre-conditioning prior tothe application of a self-etching primer may thus bea viable technique when bonding to scleroticdentine.42 It has been shown that the hybrid layermorphology after self-etching or wet bonding inuninstrumented sclerotic dentine is substantiallydifferent from those observed in sound, abradeddentine.

Obstacles in bonding to acid-etched,sound dentine

Adhesive strategies that rely mostly on microme-chanical retention are hampered by obstacles thatjeopardise effective infiltration of resin into dentaltissues.97 In abraded sound dentine, the smear layeris effectively removed in adhesive systems thatutilise a separate acid-conditioning and rinsing step(Fig. 12). In order to achieve optimal resin-infiltra-tion, acid-etched demineralised dentine must besuspended in water to prevent collapsing of theinterfibrillar spaces. This is effectively accom-plished using the wet bonding technique. Interfacialstrength is dependent upon the ability of resins toengage the leading edge of demineralised inter-tubular dentine.98 –102 The collagen matrix may thusbe viewed as a diffusion barrier or obstacle forresin-infiltration in acid-etched dentine.

Figure 12 Application of Clearfil Liner Bond 2V (Kur-aray) to sound dentine (from an artificial wedge-shapedlesion) that was etched with 40% phosphoric acid for 15 s.The smear layer was completely removed. The hybridlayer (H) was about 5 mm thick. Arrow: base of hybridlayer; A: filled adhesive containing nanofillers; D: sounddentine (from Kwong et al., 2000,27 with permission).

Figure 11 The etching effect of a self-etching primer(Clearfil SE Bond, Kuraray) through a thick smear layerproduced in sound dentine. The substructure of the smearlayer consisted of loose, globular subunits (arrow) andchannels that were filled with water prior to resin (R)infiltration (asterisk). The hybridised complex consistedof a hybridised smear layer (Hs) and a thin hybrid layer(Ha) in intact dentine (D).

F.R. Tay, D.H. Pashley182

Obstacles in bonding to acid-etchedsclerotic dentine

Unlike sound dentine, application of the sameadhesive strategy to sclerotic dentine results insubstantial variation in both hybrid layer and resintag morphology. Potential obstacles of resin-infil-tration into uninstrumented natural lesions includethe hypermineralised surface layer, an additionalpartially mineralised surface bacterial layer andintratubular mineral casts that are comparativelymore acid-resistant.23,25,27 As these inclusions varyconsiderably along the occlusal, gingival, and thedeepest part of a wedge-shaped lesion, variation inthe ultrastructure of the resin–sclerotic dentineinterfaces are possible in these different regions.While it is reasonable to assume that the extent oftubular occlusion (Fig. 13A) would vary according tothe severity of dentine sclerosis,103 both thesuperficial bacterial and hypermineralised layersare found to vary from site to site, being thickeralong the deepest part of the wedge-shapedlesions.42 The surface hypermineralised layer wasusually thinner in gingival and occlusal surfacesthan in the apical or deepest part of the wedge-shaped defects, and was often partially or com-pletely dissolved when phosphoric acid is applied tosclerotic dentine (Fig. 13A). As a result, thethickness of the hybrid layers in the gingival andocclusal sites were similar to those seen in acid-etched sound dentin and remained fairly consistentat about 5 mm. Bacteria, if present, tended to betenaciously attached to the dentine surfaces and inthe dentinal tubules, and were retained even afterrinsing (Fig. 13B).

Thicker diffusion barriers were found within thedeepest part of wedge-shaped lesions that ham-pered the penetration of acids through the under-lying intact sclerotic dentine. As a result,alterations in hybrid layer morphology and thick-ness were seen in these regions. Considering thatthe mean thickness of the hybrid layer was about5 mm in sound dentine as well as the gingival/oc-clusal aspects of natural sclerotic lesions, hybridlayer morphology in the deepest part of the wedge-shaped lesions may be described as ‘erratic’ inappearance.

One example is shown in Fig. 14A. The surfacehypermineralised layer from the deepest part of awedge-shaped lesion was about 3 mm thick and wastrapped within the resin–sclerotic dentine inter-face. The phosphoric acid apparently etchedthrough the hypermineralised layer and created ahybrid layer of about 2 mm thick within theunderlying intact sclerotic dentine. Rhombohedral

whitlockite crystallites from the sclerotic casts mayalso be identified within dentinal tubules in theunderlying sclerotic dentine.

Fig. 14B is a stained, demineralised TEM micro-graph taken from the deepest part of another acid-etched, wedge-shaped natural sclerotic lesion.The surface obstacle layers were either absent orcompletely dissolved. Within the 50 mm wide regionof the micrograph, the thickness of the hybrid layer

Figure 13 (A) Application of One-Step (Bisco) to acid-etched sclerotic dentine (SD). This stained undeminer-alised section was taken from the gingival aspect of awedge-shaped lesion. Remnants of a very thin, electron-dense, hypermineralised layer (arrowhead) could be seenon the surface of the hybrid layer (H). Some tubules wereoccluded with sclerotic casts (pointers). Others werepatent (arrows) and filled with adhesive resin (A). (B)Stained, undemineralised TEM section showing appli-cation of a filled adhesive to the occlusal aspect of anacid-etched, sclerotic lesion. Bacteria (pointers) weretrapped on the hybrid layer (Hd) surface and in thetubules. Other tubules were filled with sclerotic casts(arrows).

Resin bonding to cervical sclerotic dentin: A review 183

in sclerotic dentine changed abruptly from 2 to5 mm. This aspect of uneven etching may alsobe seen in areas in which the acid etches laterallywithin the subsurface sclerotic dentine,producing lateral hybrid layer extensions thatare separated from areas above that are notinfiltrated with resin. This feature is distinct fromincompletely resin-infiltrated hybrid layers that areobserved in air-dried, acid-etched sound dentine.

These ‘eccentric’ hybrid layers in abnormal dentinsubstrates have never been observed in bondedsound dentine.

Unlike sound dentine in which the morphology ofthe hybrid layer remains fairly consistent as long asa wet bonding technique is used, extensive vari-ations are found in different specimens or locationswithin cervical sclerotic lesions. Fig. 15A and B are

Figure 14 (A) Undemineralised section taken from thedeepest part of a wedge-shaped natural lesion that wasetched with 40% phosphoric acid and bonded usingClearfil Liner Bond 2V. Hh: hybridised hypermineralisedlayer that contained bacteria remnants (pointer). Hd:hybridised sclerotic dentine that was about 2 mm thick. A:adhesive containing nanofillers; SD: sclerotic dentine. (B)Demineralised TEM micrograph of an ‘erratic’ hybridlayer from the apex of a wedge-shaped lesion that wasetched with 40% phosphoric acid and bonded usingClearfil Liner Bond 2V. The thickness of the hybrid layervaried from 2 mm (pointers) to 5 mm (Hd). A lateralextension of the hybrid layer could be seen below an areathat was not infiltrated with adhesive resin (asterisk). A:adhesive; SD: sclerotic dentine.

Figure 15 (A) Undemineralised TEM micrograph fromthe deepest part of an acid-etched, natural lesion. Thehybrid layer (Hd) in intact sclerotic dentine (SD) was 5 mmthick. This was reduced to 2 mm thick beneath thehypermineralised layer (HM). The separation of thehypermineralised layer (arrow) was an artefact producedduring specimen processing. A: filled adhesive. (B)Demineralised TEM micrograph of an ‘erratic’ hybridlayer from the apex of a wedge-shaped lesion that wasetched with 40% phosphoric acid and bonded usingClearfil Liner Bond 2V. The thickness of the hybrid layervaried from being absent (arrow) when a hyperminer-alised layer (HM) was present, to 5 mm (Hd) where thelatter was thin and was eroded by bacteria (B). A:adhesive; SD: sclerotic dentine.

F.R. Tay, D.H. Pashley184

demineralised, stained TEM micrographs takenfrom the deepest part of the same natural lesion.Whereas a thin hypermineralised layer and thepresence of bacteria did not prevent the pen-etration of acid or resin into the underlyingsclerotic dentine, the thickness of the hybrid layerwas greatly reduced in the presence of a thickhypermineralised layer (Fig. 15A). In some areas,the hybrid layer in sclerotic dentine is reduced tothe extent that it is almost nonexistent (Fig. 15B).These thick hypermineralised layers serve asobstacles to diffusion and prevent the penetrationof even phosphoric acid. Reduced hybrid layerthickness may have no correlation with reducedregional microtensile bond strength in naturalsclerotic dentine.40,42,57 However, the presence ofthin hybrid layers should clearly be differentiatedfrom the total absence of hybrid layer formation inthe bonding substrate. Under such circumstances,the adhesive will be bonding directly to thediffusion barriers that impede acid-etching. Theresultant bond strength will depend on the strengthof the attachment of such obstacles to theunderlying sclerotic dentine. It is remarkable thatthese morphological fluctuations are continuousand vary within a very small region of a lesion that iscovered by these micrographs. Such extremevariations in hybrid layer morphology are probablyresponsible for the large standard deviations inmicrotensile bond strength measurements of bond-ing to sclerotic dentine. It is likely that thesesegregated areas of deficient hybrid layer for-mation act as weak links, or stress raisers, thatcontribute to the initiation of adhesive failures inbonded sclerotic dentine.

Obstacles to bonding in sound dentin treatedwith a self-etching primer alone

The use of two-step and single-step self-etchadhesives represents an alternative means toacquire micromechanical retention in dentine.They are attractive in that they may be used ondry dentine and, after mixing, require only oneprimer application, which is subsequently air-dried rather than rinsed. The latest single-stepself-etch adhesives further incorporates allthe resin monomers, photoinitiator and tertiaryamine accelerator into a single bottle (iBond,Heraeus Kulzer, Hanau, Germany) and eliminatesan additional mixing step. Despite the physicalappearance of thin hybrid layers and short,hybridised smear plugs in a two-step self-etchadhesive (Fig. 16), high initial bond strength hasbeen reported. This suggests that there is nocorrelation between hybrid layer thickness and

bond strength as along as a uniform deminerali-sation front is created in sound intertubulardentine.89,98,104,105

There was concern, in normal dentine, thatthick and rough smear layers may interfere withdiffusion of self-etching primers into the under-lying intact dentine. This may be due to thephysical presence of thick smear layers as adiffusion barrier, or their ability to buffer theacidic monomers, making the pH too high todemineralise the underlying intertubular dentine.Recent studies showed that mildly aggressive self-etching adhesives penetrated through smearlayers up to 3–4 mm thick and still retainedsufficient acidity to demineralise the underlyingintertubular dentine to a depth of 0.4–0.5 mm.106

This suggests that either the buffering capacity ofthe smear layer is weak, or the smear layer doesnot impose much of a physical barrier to theprimer compared with the underlying mineraliseddentine matrix. The looseness of the surfaceportion of the smear layer and/or the presenceof diffusion channels between its constituents mayfacilitate diffusion of the self-etching primerthrough the smear layer.107 Disaggregation of thesmear layer into globular subunits108 furtherprovides microchannels for diffusion of the self-etch adhesives. These microchannels, in theory,should be more permeable to resin monomersthan the interfibrillar spaces (ca. 20 nm) ofdemineralised intertubular dentine.

Figure 16 Demineralised TEM micrograph of the appli-cation of Clearfil Liner Bond 2V to sound dentine (artificialwedge-shaped lesion). To achieve effective bonding, aself-etching primer must not only create a hybridisedsmear layer (Hs), but also a hybrid layer in the underlyingintact sound dentine (Ha). The dentinal tubule was sealedby a hybridised smear plug (Hp). R: adhesive resin; D:sound dentine.

Resin bonding to cervical sclerotic dentin: A review 185

Obstacles in bonding to self-etching primertreated sclerotic dentine

The smear layers in sound, cut dentine do notimpose much of a restriction to the bonding ofcontemporary self-etch adhesives because of theirloose organisation. Unless they are instrumented,shiny sclerotic cervical lesions are free of smearlayers. In lieu of smear layers, other diffusionbarriers in shiny cervical sclerotic lesions includethe much denser surface hypermineralised layer, aswell as the more loosely arranged, partially miner-alised bacterial clusters. Some of the hyperminer-alised layers in sclerotic dentine are so thick thatthey restrict the penetration of strong inorganicacids such as phosphoric acid that usually etches5 mm or beyond into sound dentine. Being lessacidic in nature, a mild self-etching primer such asClearfil Liner Bond 2V (Kuraray) etches only 0.5 mminto sound dentine that are covered with smearlayers. As sclerotic dentine is highly variable in itsultrastructure, different morphologic expressionsof the resin–dentine interfaces can be anticipatedwhen a mild self-etching primer is applied to thisabnormal bonding substrate. This may be classifiedinto three categories, depending on the in terms ofits thickness and continuity of the surface hypermi-neralised layer at different locations of the wedge-shaped lesion.

Sclerotic dentine with a thin hypermineralisedlayer (<0.5 mm thick)

Thin hypermineralised layers are usually locatedalong the gingival and occlusal aspects of wedge-shaped lesions. Fig. 17A represents a straightfor-ward situation in which a very thin hypermineralisedlayer is present, without bacteria, along the occlusalaspect of a natural wedge-shaped lesion. This layermay be recognised by the characteristic arrange-ment of the partially dissolved crystallite remnants.The difference in hybrid layer morphology thatresults from uneven etching is readily apparent. Onthe left side, the effect of the self-etching primer isrestricted to the surface layer alone, producing a0.1 mm thick, hybridised hypermineralised layer. Onthe right, the primer etched beyond the surfacelayer to form an additional layer of hybridiseddentine that was about 0.5 mm thick.

A similar uneven etching effect may be seen inthin hypermineralised layers that contain additionalsurface bacterial attachments (Fig. 17B). Thiscomplicates etching by the fact that the self-etching primer must first infiltrate through thematrix between the bacteria, and then through thehypermineralised layer in order to demineralise

the underlying intact sclerotic dentine. Unlike thehypermineralised layer that consists of denselyarranged crystallites, the intermicrobial matrix ismore easily penetrable by the self-etching primer.The hybridised complex, thus consisted of threecomponents: the hybridised intermicrobial matrix,the hybridised hypermineralised layer and the layer

Figure 17 (A) Demineralised TEM micrograph of thegingival aspect of a wedge-shaped lesion that was treatedwith Clearfil Liner Bond 2V (A). Uneven etching wasevident. On the left, only a hybridised hypermineralisedlayer (Hh) was produced, within which were plate-likecrystallite remnants (pointers). On the right, a 500 nmthick layer of hybridised sclerotic dentine (Hd) wasformed beneath. SD: sclerotic dentine. (B) The bondedinterface from the occlusal aspect of a sclerotic lesionthat contained a thin hypermineralised layer but heavysurface bacterial deposits. The hybridised complexconsisted of: (1) a hybridised intermicrobial matrix(Him); (2) a hybridised hypermineralised layer; and (3) ahybridised layer of intact sclerotic dentine. (Hd). Thelatter was absent on the right side of the micrograph(arrows). SD: sclerotic dentine.

F.R. Tay, D.H. Pashley186

of hybridised dentine. In this micrograph, the layerof hybridised dentine was about 0.5–0.8 mm on theleft, but was completely absent on the right. Thisillustrates the kind of biological variation that maybe expected along the entire lesion surface. Thefeatures are not the rare, one of a kind phenom-enon that is observed only in one single lesion.Fig. 18A and B are high magnifications of similarfeatures observed in another specimen. There weretaken from the same 1 mm £ 1 mm section of thegingival aspect of a bonded sclerotic lesion.

Sclerotic dentine with a thick, continuoushypermineralised layer (>0.5 mm)Thicker hypermineralised layers are found along theocclusal aspects and sometimes within the deepestpart of wedge-shaped, sclerotic lesions. As theetching effect of a self-etching primer is limited, itcannot etch beyond the hypermineralised layer intothe underlying sclerotic dentine (Fig. 19A). At ahigher magnification, the crystallites within thebonded hypermineralised layer are shorter andmore sparsely arranged, when compared with theunderlying unaffected hypermineralised layer(Fig. 19B). This partially demineralised zone wasabout 0.5 mm in depth. Porosities created for resininfiltration within this zone are reminiscent of acid-etched, aprismatic enamel. It has been shown thatbonding to the surface hypermineralised layer aloneresulted in relatively high bond strength.42 Theultimate strength of the entire bonded assembly,however, depends on the strength of the attach-ment of the hypermineralised layer to the under-lying sclerotic dentine.

Partial demineralisation of the surface hypermi-neralised layer also occurs in the presence ofbacteria inclusions. In Fig. 19C, an unstainedundemineralised TEM micrograph, silhouettes ofthe unstained bacteria could be seen above thepartially demineralised, hypermineralised layer.The depth of demineralisation within this layer iscomparable to the action of this self-etching primeron sound dentine, and was about 0.5 mm thick. It isreasonable to assume that a layer of hybridiseddentine cannot be formed in the underlying dentinewhen the surface hypermineralised layer is thickerthan 0.5 mm. It appears that the self-etching primercan easily diffuse through the intermicrobialmatrix. When such a complex is subjected to tensilestress, it remains to be seen whether bond failurewould occur between the resin infiltrated bacteria,the partially infiltrated hypermineralised layer, orbetween the base of the hypermineralised layer andthe underlying dentine.

Sclerotic dentine with a thick, discontinuoushypermineralised layer (>0.5 mm)These thick hypermineralised layers are found alongthe apex ordeepest part of wedge-shaped lesions. Aspreviously described, they consist of thin, discon-tinuous hypermineralised layers that are dispersedamong several different colonies of bacteria. Thesehypermineralised layers are probably intercon-nected to form a three-dimensional structure(Fig. 20A). It is highly unlikely that a self-etchingprimer can etch through a discontinuous hypermi-neralised layer that is 10–15 mm thick. At a highermagnification, Fig. 20B shows the demineralisation

Figure 18 (A) The hybridised complex of Clearfil LinerBond 2V to sclerotic dentine in this micrograph consistedof only the hybridised intermicrobial matrix (Hm) andhybridised, partially dissolved, hypermineralised layer(Hh). Crystallite remnants, arranged in a parallel orien-tation, were observed within the latter. No hybridiseddentine was found within the underlying sclerotic dentine(SD). (B) This micrograph was taken from the samesection as Fig. 18A. An additional layer of hybridisedsclerotic dentine (Hd) could be observed. B: bacteria; A:filled adhesive; SD: sclerotic dentine.

Resin bonding to cervical sclerotic dentin: A review 187

front represented by the scalloped electron-denseedge of the partially demineralised intermicrobialmatrix. It is anticipated that bond failure occurswithin the porous regions of this thick layer that isoccupied by bacteria but not infiltrated withadhesive resin.

Summary of obstacles in bonding to sound vs.sclerotic dentine

Potential deterrents to resin-infiltration followingtotal-etching or self-etching in sound and scleroticdentine are summarised schematically in Fig. 21.27

The left side of the figure illustrates the response tobonding with a self-etching primer adhesive systemalone, while the right side illustrates the response topre-etching sclerotic dentine with 40% phosphoricacid prior to bonding with the same self-etchingprimer (Clearfil Liner Bond 2V). The thickness of thehybrid layer is fairly consistent both for self-etch andwet-bonded, acid-etched sound dentine, but is muchthicker in the latter group. Conversely, applicationof the same adhesive strategy to sclerotic dentineresults in substantial variation in the hybrid layermorphology in both treatment techniques. Absenceof a hybrid layer in some parts of a lesion suggeststhat both treatment protocols are ineffective incompletely overcoming the diffusion barriers insclerotic dentine. This situation is comparable tothe early generation dentine adhesives that weredirectly applied to the smear layers in sounddentine.78 Similar to the junction between thepartially infiltrated smear layer and the underlyingintact sound dentine,109 areas devoid of hybrid layerformation are potential weak links that may beresponsible for the lower bond strengths observedwhen boning to sclerotic dentine.

Although reduction in hybrid layer thicknessmay not affect micromechanical retention, spora-dic absence of the hybrid layer and resin tagsindicate that both treatment techniques are

Figure 19 (A) Undemineralised TEM micrograph takenfrom the gingival aspect of a Clearfil Liner 2-treatedsclerotic lesion. There was only partial demineralisation(pointer) of the hyperminerlised layer (HM), with thelatter still attached to the underlying sclerotic dentine(SD). Dentinal tubules were heavily obliterated withsclerotic casts (arrow). A: filled adhesive. (B) A highermagnification of Fig. 19A, showing the crystallites

(pointer) within the partially demineralised zone of thesurface hypermineralised layer (HM). The ample poros-ities thus created within this layer for micromechanicalretention of the adhesive is comparable to that of acid-etched aprismatic enamel. SD: sclerotic dentine.C. Undemineralised TEM micrograph taken from thegingival aspect of a Clearfil Liner 2V-treated scleroticlesion. The self-etching primer diffused through theunstained bacteria layer (B) and partially demineralised(pointer) and infiltrated the superficial portion of thehypermineralised layer (HM). The basal portion of thehypermineralised layer appeared to be firmly integratedwith the underlying sclerotic dentine (SD). A: filledadhesive.

F.R. Tay, D.H. Pashley188

inadequate in overcoming diffusion barriers insclerotic dentine. Physical removal of the super-ficial obstacle layers with a bur may improveintertubular retention. In highly sclerotic lesionshowever, this may be offset by moving thebonding interface pulpward into an area wherebonding requires increasing contribution from

intratubular resin infiltration. Moreover, the for-mation of a smear layer that consists of acid-resistant hypermineralised dentine chips andwhitlockite crystals derived from the scleroticcasts also creates additional diffusion barriers forboth total-etch and self-etch adhesives.

Sclerotic dentine located at the apex of wedge-shaped natural lesions is derived from deepdentine. Consequently, resin tag formation shouldplay an important role in achieving strong immedi-ate bond strength in the sclerotic cervical lesion.However, resin tag formation is sporadic regardlessof the conditioning methods. Absence of intratub-ular infiltration may even be observed in some ofthe occlusal parts of natural lesions that wereetched with phosphoric acid, where the thicknessof intertubular infiltration is comparable to that

Figure 20 (A) Bonding of Clearfil Liner Bond 2V to athick, discontinuous layer of hypermineralised dentine(HM). The presence of a segregated piece of hyperminer-alised tissue (arrow) suggested that the discontinuouslayers are probably interconnected three-dimensionally,with the porous regions occupied by different colonies ofbacteria. Dentinal tubules (pointer) within the scleroticdentine (SD) were patent and were arranged parallel tothe surface. (B) A higher magnification of a similar lesion.The action of Clearfil Liner Bond 2V was limited to thesuperficial part of this porous layer. The demineralisationfront was represented by the electron-dense, scallopedjunction of the partially demineralised intermicrobialmatrix (arrows). Other discontinuous layers of hypermi-neralised tissues could be seen (pointers) that may beconnected outside the plane of this section.

Figure 21 A schematic representation of the potentialdeterrents to resin-infiltration during total-etching orself-etching in sound and sclerotic dentine. The left sideillustrates the responses to bonding with a self-etchingprimer adhesive system alone, while the right sideillustrates the responses to pre-etching sclerotic dentinewith 40% phosphoric acid prior to bonding with the sameself-etching primer adhesive (Clearfil Liner Bond 2V)(modified from Kwong et al., 2000,27 with permission).

Resin bonding to cervical sclerotic dentin: A review 189

present in sound dentine. Similar to the results ofFerrari et al.110 and Prati et al.,41 lateral branchesof resin tags were rarely observed when bondedsclerotic dentine were examined by TEM.42,57 Thisis likely to be caused by the acid-resistant natureof the mineral-dense sclerotic casts that occludethe dentinal tubules. It has been suggested that20% of the strength of an interfacial bond wascontributed by resin-infiltration derived from resintag formation and another 20% from hybridisationof the intertubular dentine.111,112 Regional tensilebond strength from cervical sclerotic root dentinewas found to be 20–45% lower than those obtainedfrom artificial lesions prepared in sound rootdentine.40,42 This reduction may be due to theabsence of resin tags and incomplete hybridisationin sclerotic dentine.

Regional microtensile bond strengthevaluation

Microtensile bond strength measurements compar-ing resin bonds to the occlusal, gingival and theapex or deepest part of natural lesions andartificially wedge-shaped defects created in soundcervical dentine were reported by Kwong et al.42

using the microtensile bond test.113 Lesions wererestored with Protect Liner (Kuraray) and ClearfilAP-X resin composite (Kuraray) following treatmentwith Clearfil Liner Bond 2V, with or withoutphosphoric acid pre-conditioning of the lesions.Using the nontrimming technique developed byShono et al.114 beams with a mean area of0.46 ^ 0.03 mm2 were prepared and stressedto failure. The use of a nontrimming technique(Fig. 22) facilitated preparation of a series of slabs,thus allowing more than one beam to be harvestedfrom each lesion.113

The mean tensile bond strengths of bondsproduced by the self-etching primer alone to naturallesions (48.7 MPa) were 26% lower (Fig. 23) thanthose from artificial lesions (65.8 MPa) when all ofthe bonds were pooled, and the result was statisti-cally significant ðp , 0:001Þ: Similarly pooled data onbonds made using the self-etching primer withadjunctive phosphoric acid pre-conditioning tonatural lesions (53.1 MPa) were 24% lower ðp ,

0:005Þ than those produced from artificial lesions(69.8 MPa). Pooled data, however, showed nosignificant difference among the bonds made byself-etching or total-etching to either sound dentineðp ¼ 0:415Þ or sclerotic dentine ðp ¼ 0:314Þ: Of thethree factors (substrate, conditioning method andlocation) tested, only the difference in the type of

substrate (i.e. sound dentine vs. sclerotic dentine)was found to have a significant influence on bondstrength ðp , 0:05Þ: Multiple comparison testsshowed that there was no difference in self-etchingor total-etching sclerotic dentine except for thegingival aspect of the lesions, in which higher bondstrengths were obtained for total-etching (Fig. 23).

These results are comparable to those ofYoshiyama et al.40 in that lower bond strengthswere found in natural sclerotic lesions, and to thework of Phrukkanon et al.115 showing that bondingof a self-etching primer to sound dentine isindependent of the tubular orientation. The orien-tation of dentinal tubules in the occlusal or upperwall of wedge-shaped lesions is approximatelyparallel to the surface, while their orientation inthe gingival wall is perpendicular to the preparedsurface.116,117 Many believed that resin tag for-mation would be more prominent in surfaces where

Figure 22 Schematic representation of the protocolemployed for regional microtensile bond strengthevaluation.

F.R. Tay, D.H. Pashley190

the tubules are oriented perpendicular to thesurface rather than parallel. However, measure-ment of microtensile bond strengths of self-etchingprimers and total-etch adhesives to these walls inwedge-shaped cavities prepared in normal dentinerevealed significantly higher bond strengths todentine in which the bonded surfaces were orientedparallel to the tubules (i.e. occlusal walls).116,117

Double-etching of dentin by phosphoric acidfollowed by a self-etching primer adhesive hasbeen shown to increase bond strengths to enamelbut to lower bond strengths in dentine,118 that maybe caused by incomplete infiltration of the adhesiveinto the phosphoric acid-etched dentine.119 UsingClearfil Liner Bond 2, Ogata et al.120 found thatmultiple applications of the primer to wedge-shaped lesions increased bond strength due to theweak acidity of the primer. Although this has notbeen tested in sclerotic dentine, the same resultwould be expected. That is, multiple applicationsof weakly acidic agents using constant agitation,should improve bonding.

TEM examination of the failed bonds exhibited bybonds created in sclerotic dentine revealed a widevariation in the mode of failure that included all ofthe different structural components that are pre-sent within the resin–sclerotic dentine interfaces.42

The complexity of failure modes indicates that

reduced bond strength in sclerotic dentine is notrelated to any single factor. Similar to otherbiological variations, it is possible that each factorcontributes to a variable degree in different lesions.The summation of all these factors, however, leadsto an overall reduction in bond strength.

The presence of a partially mineralised bacterialzone in sclerotic lesions is analogous to thepresence of a smear layer on sound, abradeddentine. This zone is porous, allowing easy pen-etration of acids and primers to form a zone ofhybridised intermicrobial matrix. The presence of ahybridised intermicrobial matrix may not affectbonding, at least in the short term, providing thatthe self-etching primer can effectively etch throughthis layer into the underlying bonding substrate.This is analogous to the hybridised smear layers insound dentine. It remains to be seen whether theeventual degradation of the bacteria in this layerwould lead to decrease in bond strength with time.The large standard deviation in bond strengthresults in natural sclerotic lesions may simplyreflect the large biological variation in the thick-ness of such a layer.

The presence of a hybridised hypermineralisedlayer together with an underlying zone of hybri-dised dentine does not necessarily result in lowbond strength. This is comparable to the infiltrationof a self-etching primer through smear layer-covered sound dentine. Provided that the acidscan penetrate the overlying diffusion barriers toengage the underlying substrate with even a verythin hybrid layer, strong initial bonds may still beachieved. However, erratic bonds may be expectedwhen the hypermineralised layer in sclerotic dentinis too thick for acids to etch through. Resinattachment to the partially demineralised surfaceof this layer is still strong and may be comparablewith bonding to unground, aprismatic enamel.121

However, since a layer of hybridised dentine is notproduced, the strength of the bond will be highlydependent upon the strength of the hyperminer-alised layer to the intact sclerotic dentine.

The fact that higher bond strength was observedalong the gingival site of total-etched naturallesions (Fig. 23) merits further discussion. Thissuggests that the inability of the adhesive to formresin tags in tubule lumina that are blocked bymineral deposits is an important parameter thatleads to the reduction in bond strength. If the abovehypothesis is correct, then grinding of the surfacehypermineralised layer of these cervical wedge-shaped defects prior to bonding122 should not resultin an increase in bond strength, since the underlyingsclerotic dentine still contains dentinal tubules thatare blocked by whitlockite crystallites. Application

Figure 23 Regional microtensile bond strengths in self-etching and total-etching sound (light shade bars) orsclerotic (dark bars) dentine. Groups with the same letterabove the bars were not statistically significant ðp ,

0:05Þ: Number of teeth from which slabs were made ineach group ¼ 10.

Resin bonding to cervical sclerotic dentin: A review 191

of stronger phosphoric acid to these defects couldhave resulted in partial dissolution of the scleroticcasts and/or complete removal of the surroundingperitubular dentine, allowing resin infiltration intothe dentinal tubules. This may result in higher bondstrength along the gingival site of phosphoric acid-etched, sclerotic dentine.

Restoring the class v sclerotic lesion

Maintaining the marginal integrity and retention ofClass V resin composite restorations without the useof additional retention has always been a challengefor clinicians. One major factor, already analysed isthe difficulty in bonding to sclerotic dentine.Removing the hypermineralised surface layers bygrinding or by using stronger acids (Fig. 23) arepossible strategies to improve micromechanicalretention in sclerotic dentine. While it is possibleto produce hybrid layers in sclerotic dentine withthin diffusion barriers, these hybrid layers becomeerratic or even nonexistent in the presence of thickbarriers. As clinicians have no way of discerningthese differences at a clinical level, removal of thesurface layer of sclerotic dentin prior to bondingshould be adopted.42,122 Although such a rec-ommendation may not result in an increase inbond strength to sclerotic dentin, it does removeone potential source of inconsistency that leads tobond failure. Based on the results of a two-yearclinical trial, it has been suggested that micro-mechanical retention by acid etching of the enamelmargin is still indispensable for the clinical successof cervical Class V composite restorations.123 Such aconcept, however, was recently challenged by twoJapanese studies, in which the authors maintainedthat sclerotic dentine, being a part of the body’snatural defence mechanism, should be preserved asmuch as possible and that acid-etching should beavoided to promote the marginal integrity of resincomposites that are bonded to these lesions.45,124

While one may remove bacteria overgrowthsfrom the surface hypermineralised layer, it is notpossible to remove bacteria entirely from dentinaltubules. This is analogous to the application offissure sealants to stained enamel fissures,125,126 orthe bonding of resins to the inner layer of cariousdentine.127,128 The use of bactericidal solutions(i.e. chlorhexidine) or adhesive resins with anti-bacterial activity129,130 would be helpful. However,the longevity of bonds that contain dead, degrad-able bacteria should be further investigated. This isparticularly applicable to adhesives that contain anincreasing amount of hydrophilic resin monomers

that absorb water. Recent studies showed that bothhydrophilic resins131,132 and collagen fibrils withinthe hybrid layer133 –136 degrade upon long termwater storage.137

Conclusions

The structural complexity of noncarious scleroticcervical dentine is remarkable. The common pre-sence of adherent bacteria on such surfaces andtheir incorporation into the bonded restorations isdisconcerting. This raises issues such as whetherthese bacteria are dormant, and whether theirconfinement by adhesives will create any long termliability. These questions have also recently beenraised in reports that bacteria are present in resin-bonded caries-affected dentine.127,128 The pre-sence of bacteria on these surfaces justifies theuse of 2% chlorhexidine disinfectant treatment orthe use of antibacterial adhesives to disinfect thesubstrate prior to bonding.

Microtensile bond strengths of self-etchingprimers to sclerotic dentine were comparablewith those made to phosphoric acid-etchedsclerotic dentine, although they were lowerthan those attained with sound dentine. Thesebond strengths are probably high enough toretain class V restorations even under heavyloads, if is bonding is performed with etching ofthe enamel to create additional micromechanicalretention. Although there are clinical studies thatshowed encouraging results with the use ofdentine adhesives on noncarious cervicallesions,138 –140 the failure rates of some specificadhesives have been reported to be high in otherstudies. For example, the retention rate for One-Step, a total-etch single-bottle adhesive, innoncarious cervical lesions involving scleroticdentine was only half of that of nonscleroticdentine.141 The retention rate of the sameadhesive in noncarious cervical lesions wasreduced from the original 100% at 6 months to75% after three years.142 There are also otherclinical studies that reported more favourableretention rates when glass-ionomer basedrestorative materials were compared with den-tine adhesives/resin composites in restoring theselesions.143 –145 Unfortunately, there are no TEMstudies that examine the bonding of glass-ionomer cements and resin-modified glass-iono-mer cements to sclerotic dentine. Admittedly,TEM work on these types of restorative materialsthat are susceptible to dehydration is difficult toperform. However, this should be done to

F.R. Tay, D.H. Pashley192

complete our understanding of this alternativetype of chemical/micromechanical interaction70

with sclerotic dentine.

Acknowledgements

This work was supported by grant DE014911 fromthe NIDCR, USA, and by grant20003755/90800/08004/400/01, Faculty of Dentis-try, the University of Hong Kong. The authors aregrateful to Michelle Barnes and Zinnia Pang forsecretarial support.

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