Microleakage and shear bond strength of a new sealant containing prereacted glass ionomer particles.

A new fluoride-releasing sealant system is claimed to allow easier and faster placement while providing high bond strengths without the need for phosphoric acid etching. A study was designed to compare the microleakage and shear bond strength of a self-etching, Giomer-based sealant system with those of a traditional resin sealant. Group 1 received traditional sealant applied after use of a 35% phosphoric acid etchant; group 2 received Giomer sealant after use of a self-etching primer; and group 3 received Giomer sealant after the addition of an initial phosphoric acid etching step and placement of the primer. The sealants were placed in the occlusal pits and fissures of extracted human third molars, thermocycled, placed in dye, and sectioned. The extent of microleakage (dye penetration) was expressed as a percentage of the cross-sectional length of the sealed interface. The sealants were also bonded to the facial enamel of bovine incisors. Specimens were thermocycled and tested in shear mode in a universal testing machine. The new self-etching sealant demonstrated significantly greater microleakage (P < 0.017) and lower bond strength (P < 0.05) than both the traditional sealant system and the new system when placed with phosphoric acid etchant. Phosphoric acid etching significantly improved the shear bond strength and reduced the microleakage of the new sealant.

Enhanced endothelial cell senescence by lithium-induced matrix metalloproteinase-1 expression.

Endothelial cell (EC) senescence and dysfunction occurring after chronic injury and inflammation are highly associated with the development and progression of cardiovascular diseases. However, the factors involved in the establishment of EC senescence remain poorly understood. We have previously shown that lithium, an inhibitor of glycogen synthase kinase (GSK)-3beta and activator of the Wnt/beta-catenin signaling pathway, induces an EC senescent-like phenotype. Herein, we show that lithium induces a rapid and pronounced up-regulation of the matrix metalloproteinase (MMP)-1, an inflammation and senescent cell marker, at the mRNA and protein levels, whereas the induction of two other senescent cell markers is either weak (interleukin-8) or delayed (plasminogen activator inhibitor-1). Lithium effect on MMP-1 expression is also specific among other MMPs and not mediated by GSK3beta inhibition. Lithium affects MMP-1 expression mainly at the transcriptional level but neither the AP1/Ets regulatory sites nor the redox sensitive (-1607/2G) site in MMP-1 promoter are involved in lithium-dependent MMP-1 regulation. However, down-regulation of p53, a target of lithium in EC, dampens both basal and lithium-induced MMP-1 expression, which further links MMP-1 up-regulation with the establishment of cell senescence. Although increased MMP-1 levels are usually associated with angiogenesis in enabled proliferative EC, the exogenous addition of activated MMP-1 on lithium- arrested EC increases the number of EC positive for the senescent-associated-beta-galactosidase marker. Conversely, down-regulation of MMP-1 expression by small interfering RNAs blunts the lithium-dependent increase in senescent-associated-beta-galactosidase positive cells. Altogether our data indicate that lithium-induced MMP-1 may participate in the reinforcement of EC senescence and reveal a novel mechanism for lithium-induced tissue remodeling.