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Browne RM, Tobias RS: Microbial microleakage and pulpal inllanimation: A review. Endod Denl Traumatol 1986; 2: 177 183. Abstract - The evidence relating microbial microleakage and pulpal inflammation is reviewed. In vitro experiments show that all current dental materials permit fluid microleakage at the material/eavily wall interface. In vivo, this fluid microleakage is accompanied by bacterial growth, unless the material has lasting antibaclcrial properties. An association does exist bclwecn the presence of bacteria at the material/cavity wall interlace and the presence of pulpal ijiflanimation. The role of the siiirai' layer in minimizing (he harmful eifects of microbial microleakage and o( c'hemical toxic ity o( restoi-ative material is reviewed, l'urthcr research sliould be aimed al rliniinating microleakage by the development of more fully adhesive materials or by inipro\'ing their atitibacterial jjrojjertics. Roger M. Browne and Rosalind S. Tobias
Deparlmenl ot Oral Pathology, Dental School, St Chad's Queeiisway, Birmingham, U. K.
Key words: microbial microieakage, pulpal inflammation, smear layer, review. Professor R. M. Browne, Departmenf of Oral Pathology, Dental School, St Chad's Queensway, Birmingham B4 6NN, U. K. Accepted for publication 20 April 1986.
U n t i l rccciUly, most stutlies have conc-ludcd that pulpal indanimation observed beneath carefully prepared experimental cavities containing filling materials is due to cheniic al irritation from the materials ( 1 4 ) . Fui-lhcr, it i,s widely held tliat, the d e e p e r ihe cavity (thai is, the It'ss tlic thirkness of residual dcnlin beneath the cavity lloor, between t h e material and the pulp cavity), the greater the a m o u n t ol' pul|ial irritation (5). Whereas there is little doubt that such a relationshi]) exists in the eonsideration ol'thermal damage generated during careless cavit)" prcjjaration, it is far less certain with toxic damage from dental materials. In the earliest studies in which the relationship between cavity d e p t h and pulpal inflammation due to different materials was reported (6 8), tlic damaging effects of e a v i t y preparation itself were not fully appreciated. I n d e e d , some subsequent studies (9) have failed to establish any relationship between residual detitin thickness and pulpal inflammation observed in ca\ i\\cs filled l)y a variety of matei'ials. Present e\'idetice suggests that none of the current d e n t a l materials provides a perfect seal witli the e a v i t y wall and there is always a microspace at the interface between the two along whieh fluids and microorganisms (an petietrate from the oral environment (10 15). Microorganisms, introduced d u r i n g cavity preparation, may also remain alt a e h e d to tlie eavity walls, perlia|)s in the smear layer, and proliferate after insertion of the material.
The effect of microbial microleakage at the material cavity/wall interface oti the dental pulp has been a lacuna in the biological testing of dental restorative matei'ials. 1 his paper reviews the evidence relating microbial microleakage and pulpal inllammalion. Microleakage Mieroleakage is the term used for the ]:)enetiation of oral fluids and microorganisms along the material ca\-it.y/wall interface following insertion of a restoration. As mentioned above, there is always a microspace at this interface, caused partly by the contraction of the mass of material during the setting proc'ess and partly because none of the currently available tuaterials adhere coiiipleteh' to the cavity walls. The size of the mierosjjaee (16) \aries from material to material and as a consequenc'e the amount of microleakage is also likely to vary. A measure oi the amount of microleakage in vitro might thus be used to ]irediet the performance of restorative materials in the oral environment, because as a clinical occurrence it remains a jjrimary source of restorative failure (17). A wide variety of methods has been used in vitro to determine the extent of microleakage around, and the marginal adaptation of dental restorations. A discussion of these is beyond the scojie of this paper, but sc\'eral comprehensive
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Browne and Tobias reviews have appeared elsewhere (12, 13, 17, 18). In general terms, microleakage is evaluated by measuring the passage of tracer molecules along the material cavity/wall interface or demonstrating the biological consequences of this trallic by inducing recurrent caries. However, there appears to be considerable variation in the results obtained by the different methods with the same materials, itidicating that there is a need for better understanding and standardization of ihe test methods (18). The results can be briefly summarized by saying that all currently available materials exhibit microleakage in viLro, but to a different degree. As might be expected, those materials which adhere to some degree to the ctivity walls, in particular the glass ionomer cements, demonstrate the ieasl degree of microleakage. However, microleakage to tracer molecules dose not necessarily imply that microbial microleakage will also occur. Although the microspace appears to be sufliciently large to allow microbial spread with all materials, there are other factors which will also determine this, in particular the availability of nutrients, including oxygen, and the antibacterial pro]jerties of the material. These latter factors are of particular importance in vivo and may explain conflicting findings. For exatnple, in vitro tracer studies have shown tliat zinc phosphate cement allows less microleakage than zinc oxide/eugenol cement (15, 19). Yet, in vivo, mieroorganisms are rarely found at the material cavity/wall interface around zinc oxide/eugenol fillings but are usually present around zinc phosphate cement. These in vivo findings probably t-eflect the lastitig antibacterial effect of zine oxide/eugenol (20) which, despite its poor seal, prevents colonization ol' the microspace by Ijacteria. These observations support the view (18) that mo.st investigations of microleakage in vitro are of donbtlul chnical relevance. Bacterial microleakage The evaluation of the possible toxic effects of restorative materials upon the dental pulp was first undertaken in a scientific way in the 1930s. It was not until 1959 that it was first suggested that bacterial microleakage at the material cavity/wall interface may infiuence the pulpal responses observed beneath experitncntal cavities filled with different materials (21). Since 1969, a grouj) of research workers in Sweden has carried out numerous investigations into the causes of pulpal inflammation a,ssociated wilh dental restorative materials and their results suggest that bacterial irritation is the main cause of pulpal damage beneath silicate, acrylic and composite resin fillings and beneath inlays cemented with zinc phos178 phate or polycarboxylate cements (22 28). Other workers have also demonstrated large numbers of microorganisms at the material/cavity wall interface in cavities filled with silicates (29-34) and composites (34-37). The possibility that bacterial microleakage may complicate the interpretation of puljial responses observed beneath cavities filled with a variety of experimental materials is now widely recognized (5, 33, 34, 38-43). Some investigators have beeti unable lo find any direet correlation between the presence of bacteria withiti the cavity on histolfjgical sections and pulpal inflammalion (4, 44, 45) and consider that growth of bacteria on the cavity floor may be favored by, and thus a consequence of, pulpal inllanimation (44) rather than its cause. Many studies, while recognizing an association between bacterial mieroleakage and ]3ulpal inflammation, have reported cavities in which moderate to severe inflammation is present in ihe apparent absence of bacteria (42, 46, 47). Sueh observations lead to the conclusion that, whereas bacteria are an important cause of pulpal inflammation beneath cavities filled with different experimental materials, chemical toxicity also Inlays some, although probably a mueh smaller, role. One of the major probletns in evaluating any correlation between bacterial microleakage and pulpal inflammation lies in the techniques used for demonstrating bacteria. For practical experimental reasons the presence or absence of bacteria is determined from tissue sections stained by various modifications of Gram's method. It is notoriously diflicult to identify bacteria using such methods, particulary if the bacteria are Gram-negative (48, 49). Further, the incidence of baeteria at the material/cavity wall interface will be influenced not only by the number of sections examined but also by baeterial displacement during the processing of the teeth for histological assessment. Culturing samples from the cavily wall provides more reliable evidence for the presence of baeteria, but this usually precludes microscopical examination of the .same specimen (34, 50). As a consequence the variable data on any correlation between pulpal inflamuiatioii and bacterial microleakage is not unexpected. Reeently, in our laboratory using histological and cultural techniques on the same specimens, we have demonstrated a good correlation between the results obtained by both methods (51, 52). This has allowed us to evaluate the relationship between pulpal inflammalion and bacterial microleakage with greater confidence. A recent study (52) has demonstrated a clo.se correlation between the extent of pulpal inflammation and degree of bacterial mi( roleakage using a wide range of tnaterials. This ecjrrelation
Smear layer
Ifljacterial cause pulpal inflamniation during the first few weeks after insertion of a rnaterial in a test cavity, then their toxins must be able to reach the pulp cells in order to damage them. However, the surface of freshly cut denlin is covered by a smear layer. The smear layer is a mic rothin gelatinous layer which covers the dentinal walls after cavity preparation, .so obstructing the dentinal tubules. It is present regardless of instruments used (75) but the quality and quantity of the smear layer is influenced by the o]x'rating conditions (76). Smear layers are composed of organic and inorganic jjartides 0.5 15 |a,m in size (77). The organic component is thought to consist of heat-coagulated dentin proteins, saliva, blood and microorganisms, whereas the inorganic component is derived from tootli minerals and, possibly, inorganic contaminants (78). The presence of the smear layer provides a physical barrier to baeterial penetration as well as the diffusion of a wide range of substances in vitro (79, 80) and, in vivo, prevents the out-fiow of dentinal fluid onto the cut surface of vital dentin by the hydrostatic pressure of the pulp (80, 81). How ell'ective it is in vivo is not clear, so that although baeteria may l)e present at the material cavily/wall interlace, they may not be able to efl'eetively damage the jjulp. As indicated previously, bacterial products are able to cause |3ul]) damage when applied to freshly cut dentine in vivo, so that it ajjpears that the smear layer is not completely impermeable, and this is supported by in vitro studies (80, 82). It is likely that it is the penetration of toxins through the denlin which is the mechanism by which bacteria cause damage, at. least dtjring th(; first lew weeks after insertion of the material. It follows, therefore, that any procedure designed
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Conclusion
T h i s review has attenij^ted to bring together the evidence that microleakage is an important factor in determining pulpal inflammation beneath recently p r e p a r e d cavities. Largely IVoni /// vitro experiments, it is apparent that all currently available materials p e r m i t fluid microleakage at the inaterial/ca\ ity w^all interface. Frotii in vivo exjiierimeuts, it appears t h a t this fluid mici-oleakage is ac-eonipanied by baeterial growth, unless the niaterial placed in the cavi t y has pc~rsisting antibactei ial properties. There is accummulating evidence that au association exists between the presetice of bacteria at the material/ c a v i t y wall interface and tlie prc\senee of pulpal inflatnmation and that this association is one ol c a u s e and effect. However, the association is not absolute and it is probable that some materials exert chemical toxicity, but that this is of much less imp o r t a n c e than has bccti traditionally thought. It is prcjbable that the sueeessful clinical usage of zinc cjxiclc/eugenol- atid calcittm liydroxide-based materials as liners is a cousec|uence of their antibacterial propetties rather than providing an imperm e a b l e barrier to the chemical toxieity of the overl y i n g filling, further researcli should be aimed at
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