Interfacial sealing between normal dentin and caries-affected dentin with glass-ceramic and three types of bonding systems.

PURPOSE: To compare the bonding effect of normal dentin (ND) and caries-affected dentin (CAD) on the surface of glass-ceramics using three types of bonding systems. METHODS: 39 teeth with caries involving the superficial layer of dentin were randomly divided into three groups and two subgroups: nanoleakage group (n=5) and shear bond strength group (n=8). The infected dentin was removed, and the CAD was retained. The surface of the tooth was polished, and one 2 mm × 2 mm × 4 mm CAD block and one 2 mm × 2 mm × 4 mm ND block were made. The total-etch adhesive A, self-etch adhesive B, or self-adhesive resin adhesive C were used to bond the glass ceramics. The bonding specimens of the nanoleakage group were stained with ammoniated silver nitrate and observed. In the shear bond strength group, the maximum load of the loading head F (N) was recorded, and the shear bond strength of the specimen was calculated. RESULTS: The nanoleakage values were significantly lower than those in the CAD group. The nanoleakage value of group B was significantly higher than that of group C, and that of group C was significantly higher than that of group A. Both dentin type and adhesive type had an effect on shear bond strength; under the same adhesive system, normal dentin demonstrated higher shear bond strength than CAD. However, the shear bond strength of adhesive A was higher than the bond strengths of adhesives B and C, but there was no significant difference in shear bond strength between adhesives B and C. CLINICAL SIGNIFICANCE: This study showed that dentin type and bonding system influenced shear bond strength and nanoleakage. The total-etch adhesive system showed the best interfacial sealing and bonding effect.

Dectin-1-induced RIPK1 and RIPK3 activation protects host against Candida albicans infection.

Necroptosis is a recently defined type of programmed cell death with the specific signaling cascade of receptor-interacting protein 1 (RIPK1) and RIPK3 complex to activate the executor MLKL. However, the pathophysiological roles of necroptosis are largely unexplored. Here, we report that fungus triggers myeloid cell necroptosis and this type of cell death contributes to host defense against the pathogen infection. Candida albicans as well as its sensor Dectin-1 activation strongly induced necroptosis in myeloid cells through the RIPK1-RIPK3-MLKL cascade. CARD9, a key adaptor in Dectin-1 signaling, was identified to bridge the RIPK1 and RIPK3 complex-mediated necroptosis pathway. RIPK1 and RIPK3 also potentiated Dectin-1-induced MLKL-independent inflammatory response. Both the MLKL-dependent and MLKL-independent pathways were required for host defense against C. albicans infection. Thus, our study demonstrates a new type of host defense system against fungal infection.

Listeria hijacks host mitophagy through a novel mitophagy receptor to evade killing.

Cells use mitophagy to remove damaged or unwanted mitochondria to maintain homeostasis. Here we report that the intracellular bacterial pathogen Listeria monocytogenes exploits host mitophagy to evade killing. We found that L. monocytogenes induced mitophagy in macrophages through the virulence factor listeriolysin O (LLO). We discovered that NLRX1, the only Nod-like receptor (NLR) family member with a mitochondrial targeting sequence, contains an LC3-interacting region (LIR) and directly associated with LC3 through the LIR. NLRX1 and its LIR motif were essential for L. monocytogenes-induced mitophagy. NLRX1 deficiency and use of a mitophagy inhibitor both increased mitochondrial production of reactive oxygen species and thereby suppressed the survival of L. monocytogenes. Mechanistically, L. monocytogenes and LLO induced oligomerization of NLRX1 to promote binding of its LIR motif to LC3 for induction of mitophagy. Our study identifies NLRX1 as a novel mitophagy receptor and discovers a previously unappreciated strategy used by pathogens to hijack a host cell homeostasis system for their survival.

Effect of two aging methods on the bonding interface between glass ceramics and dentin / 口腔疾病防治

Objective@#To study the effects of bacterial invasion and artificial saliva immersion on the bond strength and nanoleakage between healthy dentin and glass ceramics-bonded specimens using three types of resin cements and provide a reference for the selection of clinical bonding materials.@*Methods @#One hundred eight dentin blocks were selected to prepare bonded specimens with Variolink N, Multilink N, RelyX Unicem and glass ceramics blocks. The adhesive specimens of each type of resin cements were divided into three groups according to the aging method: bacterial invasiveness group (the specimens were cultured under anaerobic conditions for 14 days after inoculation with Streptococcus mutans), artificial saliva immersion group (the specimens were immersed in artificial saliva for 6 months), and control group (the immediate test group). Each group comprised 12 specimens: 6 were selected to test the bonding strength, and 6 were observed by scanning field emission scanning electron microscopy (FESEM). @*Results @#The bond strength of Variolink N in the immediate test group was significantly higher than that of Multilink N and RelyX Unicem, and the difference was statistically significant (P < 0.05). However, no significant difference was found in the bacterial invasiveness group and artificial saliva immersion group (P > 0.05). In the bacterial invasion group, the difference in the nanoleakage of the three adhesives was statistically significant (P < 0.05), with a trend of Variolink N > Multilink N > RelyX Unicem, and pairwise comparison was statistically significant (P < 0.05). The nanoleakage of the three resin adhesives showed an increasing trend in the bacterial invasion group and artificial saliva group compared with that of the immediate test group. @* Conclusion@#Both artificial saliva soaking and bacterial invasion can reduce the sealing property of the adhesive interface of 3 types of resin cements to different degrees. The presence of Streptococcus mutans in the oral cavity may reduce the sealing performance of the resin dentine adhesive interface.

FGF2 cooperates with IL-17 to promote autoimmune inflammation.

IL-17 is a pro-inflammatory cytokine implicated a variety of autoimmune diseases. We have recently reported that FGF2 cooperates with IL-17 to protect intestinal epithelium during dextran sodium sulfate (DSS)-induced colitis. Here, we report a pathogenic role of the FGF2-IL-17 cooperation in the pathogenesis of autoimmune arthritis. Combined treatment with FGF2 and IL-17 synergistically induced ERK activation as well as the production of cytokines and chemokines in human synovial intimal resident fibroblast-like synoviocytes (FLS). Furthermore, ectopic expression of FGF2 in mouse joints potentiated IL-17-induced inflammatory cytokine and chemokine production in the tissue. In the collagen-induced arthritis (CIA) model, while ectopic expression of FGF2 in vivo exacerbated tissue inflammation and disease symptom in the wild-type controls, the effect was largely blunted in Il17a -/- mice. Taken together, our study suggests that FGF2 cooperates with IL-17 to promote the pathogenesis of autoimmune arthritis by cooperating with IL-17 to induce inflammatory response.