The relevance of microleakage to secondary caries

Microleakage refers to the clinically undetectable leakage between the cavity wall and the filling [Kidd, 1976]. Irie et al. found that a gap of 6-10^m formed immediately even after applying an acid etch and a bonding agent [Irie et al., 2002]. Iwami et al. have confirmed that any restorative material can completely eliminate the microleakage between restoration and the cavity wall [Iwami et al., 2005], supported by other researches [Irie and Suzuki, 1999; Huang et al., 2002; Piwowarczyk et al, 2005]. A study in vitro showed that there was no significant difference in the degree of microleakage between conventional caries removal and chemo-mechanical removal [Mousavinenasab and Jafary, 2004]. Those above all show us that microleakage is inevitable.

The microspace between the restoration wall and tooth can allow salivary pellicle accumulation and bacterial invasion [González-Cabezas et al., 1999; González-Cabezas et al., 2002; Splieth et al., 2003]. In a sense, it provides a favorable environment for the oral bacteria, especially cariogenic bacteria, such as S. mutants and Lacotobacilli, to demineralize the tooth structure along the cavity wall, as long as conditions are adequate and suitable. The histopathological appearance of the wall lesion in the secondary caries is also explained by hydrogen ions due to the diffusion of bacteria into the space between restoration and cavity wall and its acdiogenic activities afterwards [Hals and Nernaes, 1971]. So microleakage has been considered as a potential predictor for secondary caries and has caused serious concern to many researchers. In some article, the wall lesion was described as the consequence of microleakge [Diercke et al., 2009].

Up to now, there has been no conclusive statement about the relationship between microleakage and secondary caries. Several studies in vitro have shown a positive relationship between the two things. J0rgensen and Wakumoto in a 1968 research found that there was an increasing likelihood of secondary caries with the increasing size of the microspace [J0rgensen and Wakumoto, 1968], which is in agreement with that reported by some other researches [Goldbeg et al., 1981; Dérand et al., 1991]. In a recent in vitro study on relationship of gap size and secondary caries, the findings suggested that the gap size between tooth and restoration affected the development of secondary caries along the cavity wall [Totiam et al., 2007], for which the rationale was that bigger gaps would provide necessary space for bacterial colonization and enough nutrients for cariogenic microorganisms leading to the creation of larger wall lesions. On the other hand, within smaller spaces, minerals dissolved from the tooth structure due to the acid attacks would supersaturate the space immediately and create the remineralization of tooth tissue and smaller wall lesions.

In contrast, other studies have not stated any association between gap presence and secondary caries [Kidd and O'Hara, 1990; Pimenta et al., 1995]. Some suggested that there was no caries lesion along the cavity wall, unless large voids or gaps of > 250^m [Ozer and Thylstrup, 1995] or even >400^m [Kidd et al., 1995]. J0rgensen and Wakumoto found poor correlation between the two only when gaps was >50^m [J0rgensen and Wakumoto, 1968]. Thomas et al. found no clear caries along the cavity wall next to composite, but to acrylic resin through an in situ study [Thomas et al., 2007]. Besides, observed cracks in teeth might be the best clinical evidence for microleakage does not lead to dental caries. These cracks and the adjacent areas can be stained over time, however, there is no caries development. The stained component is considered to be the proteinaceous material in the crack or crevice, and similar in composition to that of the biofilm which normally covers all teeth and restorations [Mjor, 2005].

Recently, a few studies have been conducted concerning the relationship between gap size and secondary caries in the presence or absence of fluoride. Cenci et al. in 2008 suggested that microleakage did not seem to influence secondary caries while the presence of fluoride in the plaque like biofilm (PLB) provided either by glass ionomer cement (GIC) or fluoride dentifrice (FD) [Cenci et al., 2008]. In 2009, Cenci et al. demonstrated that carious lesion depth increased with gap size for composite resin (CR) and suggested that the gap width affected secondary caries formation at the cavity wall, but only in the absence of fluoride released from fluoride-containing materials, such as GIC [Cenci et al., 2009]. Thus, these findings give implications for clinical caries treatment choices and further studies in vivo or clinical experiments are needed to investigate the relationship between the gap size, fluoride presence and secondary caries.

In sum, up to the present, there is no specific conclusion on the relationship between microleakage and secondary caries, specially the wall lesion of the cavity. The possible reasons are as follows: 1) Oral cavity is such an extremely complex that it is impossible to simulate completely, so the research results may be not all-inclusive. 2) Secondary caries is caused by various factors, so it might be difficult for researchers to consider fully when designing their experiments. Thus, in consequence, different experiments bring out different results, and sometimes those results are even conflicting. 3) For individual differences, people have varying degrees of susceptibility to caries. Therefore, different clinical studies may lead to different results and conclusions. 4) Some clinical studies may lack reasonable designs, which lead to incomprehensive results. However, there is a consensus that microleakage is indeed associated with secondary caries due to the existence of bacteria. It seems that microleakage is just a necessary but not a sufficient condition for the formation of a wall lesion [Kidd et al., 1995; Thomas et al., 2007], although in 2009, Diercke et al. carried out a pure in vitro experiment, in which the development of the outer lesion in the secondary caries was inhibited to study the relation between the gap size and the wall lesion independently, and confirmed the occurrence of wall lesions without the presence of outer lesion and indicated the extent of wall lesion increased with increasing gap width ranging from 50 to 250^m [Diercke et al., 2009]. Therefore, more in-depth studies are needed to get a thorough understanding about the relationship between microleakage and secondary caries.

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