A current Med-line search from 1966 to present cited over 344 juried publications employing the term microleakage. Dentistry recognizes microleakage as a multifaceted biological phenomenon. Brännström et al. (1967), Trowbridge (1982), Närhi (1983), and others have reported the sensory component of microleakage as a consequence of hydrodynamic fluid movement within the dentinal tubule complex. This movement of dentinal fluid has been demonstrated to displace nociceptive receptors which stimulate the nerves of the Group A fibers which run and terminate within the odontoblastic layer (see Matthews 1992). Penetration of oral fluids, bacteria and their toxic products within the preparation-material interface following material insertion accounts for the pathological component of microleakage (Browne and Tobias 1986). Continued microleakage of bacterial infiltrates eventually present as an inflammatory process which may initially signal the dentin complex to respond by deposition of a hypermineralized or sclerotic dentin. The pulp-dentin interface will repair with a specialized zone of reparative dentin. An overwhelming carious lesion often results in pulp infection and eventual necrosis. Vital dentin is an extension of the pulp, presenting the first line of defense to the consequences of microleakage. Recent publications have demonstrated that microleakage of dental materials in non-exposed and exposed pulps is a function of controlling bacterial infection. In an exposed mature dental pulp, the mesenchymal tissue permits the reorganization of pulp tissue and regeneration of a new dentin bridge in the presence of a biological seal. New odontoblastoid cells appear to regenerate from deeper pulpoblasts in the presence of various dental materials, apparently without an epithelial stimulating factor (Yamamura 1985). This inherent healing of the dental pulp and regeneration of a new dentin bridge is expressed in the presence of various dental materials, but only in the absence of bacterial infection. Data which evaluates the biological deposition of reparative and dentin bridges as either repair or regeneration are presented as a basis for considering the clinical selections of dental materials. Recent data demonstrate that dentin and pulp healing are ensured when a proper biological seal is provided to control and prevent microleakage.