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This study examined the surface staining mechanism of a photopolymerized composite by coffee, oolong tea, and red wine.Dental composite was subjected to an experimental 24-hour staining cycle: 17-hour immersion in artificial saliva solution containing 0.3％ mucin followed by 7-hour immersion in coffee, tea, or wine. After one, two, and four weeks, digital images of the composite surface were analyzed in grayscale mode with an imaging analyzer. Specimens polished but not immersed were used as a baseline measurement for color change. Additionally, the effects of mechanical brushing and chlorhexidine on drink-induced staining were examined.Wine caused the most severe staining, followed by tea and coffee. After four weeks of immersion, brushing reduced surface staining by wine. On the contrary, chlorhexidine increased the staining effect of tea and coffee（p＜0.05）when compared to the control specimens. In conclusion, we showed that common drinks stained the dental composite, but each by a specific mechanism that depended on external conditions such as the presence of chlorhexidine.

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S U M M A R Y We have previously reported the TLR4 expression in human intestinal lymphatic vessels. In the study here, microarray analysis showed the expression of the TLR4, MD-2, CD14, MyD88, TIRAP, TRAM, IRAK1, and TRAF6 genes in cultured human neonatal dermal lymphatic microvascular endothelial cells (LEC). The microarray analysis also showed that LEC expressed genes of IL-6, IL-8, VCAM-1, and ICAM-1, and the real-time quantitative PCR analysis showed that mRNA production was increased by lipopolysaccharide (LPS). The LPS-induced IL-6, IL-8, VCAM-1, and ICAM-1 production in LEC was suppressed by the introduction of TLR4-specific small interfering RNA, and also by anti-TLR4, nobiletin, and CAPE pretreatment. These findings suggest that LEC has TLR4-mediated LPS recognition mechanisms that involve at least activation of NF-kB, resulting in increased expression of IL-6, IL-8, VCAM-1, and ICAM-1. Both the LPS effect on the gene expression and also the suppression by nobiletin and CAPE pretreatment on the protein production were larger in IL-6 and in VCAM-1 than in IL-8 and in ICAM-1 in LEC. The signal transduction of NF-kB and AP-1-dependent pathway may be more critical for the expression of IL-6 and VCAM-1 than that of IL-8 and ICAM-1 in LEC. LYMPHATIC VESSELS express not only platelet-endothelial adhesion molecule-1 (PECAM-1) but also the intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in inflamed and uninflamed human small intestine and tongue, and lymphatic endothelium enhances VCAM-1 and ICAM-1 production with tumor necrosis factor-a (TNF-a) (Sawa et al. 1999(Sawa et al. ,2007Ebata et al. 2001). It is well established that VCAM-1 and ICAM-1 induction needs a signaling pathway that involves protein kinase C and p38 mitogenactivated protein kinases (MAPKs)-mediated activation of transcription factors nuclear factor-kappaB (NF-kB) and activator protein 1 (AP-1) (Voraberger et al. 1991;Ahmad et al. 1998;Ishizuka et al. 1998;Oertli et al. 1998;Kobuchi et al. 1999;Lawson et al. 1999;Roebuck 1999). It is thought that lymphatic endothelium has signal transduction pathways to induce leukocyte adhesion molecule expression through receptors for inflammatory cytokines. However, it has not been established whether lymphatic endothelium has the expression mechanisms of immunological functional molecules independent of the inflammatory cytokines.The toll-like receptor (TLR) initiates a series of innate immune mechanisms against various microorganism infections by sensing the presence of pathogen-associated molecular patterns (PAMPs) like lipopolysaccharide (LPS), which is the major component of the outer surface of Gram-negative bacteria. The LPS stimulates leukocyte and blood endothelium through the LPS recognition systems, binding with CD14 and transferring to TLR4 and MD-2 complex, followed by a myleoid differentiation primary response protein (MyD88)-dependent or -independent pathway that culminates in the early-or late-phase activation of the IkB kinase (IKK) complex and MAPK...