Almost half of dental restorations have failed in less than 10 years, and approximately 60% of practice time has been consumed to replace these dental restorations. As such, contemporary dentin adhesives should be modified to treat secondary caries and prevent the degradation of adhesive–dentin interfaces. To achieve this goal, we developed a versatile therapeutic adhesive in the present study by incorporating quercetin, which is a naturally derived plant extract, into a commercial adhesive at three concentrations (100, 500 and 1000 µg/mL). An unmodified adhesive served as a control. The antibacterial ability on Streptococcus mutans biofilm, conversion degree, microtensile bond strength, failure modes, in situ zymography, nanoleakage expression and cytotoxicity of quercetin-doped adhesive were comprehensively evaluated. Results showed that the quercetin-doped adhesive (500 µg/mL) preserved its bonding properties against collagenase ageing and inhibited the growth of S. mutans biofilm. Efficient bonding interface sealing ability, matrix metalloproteinase inhibition and acceptable biocompatibility were also achieved. Thus, a simple, safe and workable strategy was successfully developed to produce therapeutic adhesives for the extension of the service life of adhesive restorations.

Epidemiological and experimental animal studies show that suboptimal environments in fetal and neonatal life exert a profound influence on physiological function and risk of diseases in adult life. The concepts of the 'developmental programming' and Developmental Origins of Health and Diseases (DOHaD) have become well accepted and have been applied across almost all fields of medicine. Adverse intrauterine environments may have programming effects on the crucial functions of the immune system during critical periods of fetal development, which can permanently alter the immune function of offspring. Immune dysfunction may in turn lead offspring to be susceptible to inflammatory and immune diseases in adulthood. These facts suggest that inflammatory and immune disorders might have developmental origins. In recent years, inflammatory and immune disorders have become a growing health problem worldwide. However, there is no systematic report in the literature on the developmental origins of inflammatory and immune diseases and the potential mechanisms involved. Here, we review the impacts of adverse intrauterine environments on the immune function in offspring. This review shows the results from human and different animal species and highlights the underlying mechanisms, including damaged development of cells in the thymus, helper T cell 1/helper T cell 2 balance disturbance, abnormal epigenetic modification, effects of maternal glucocorticoid overexposure on fetal lymphocytes and effects of the fetal hypothalamic-pituitary-adrenal axis on the immune system. Although the phenomena have already been clearly implicated in epidemiologic and experimental studies, new studies investigating the mechanisms of these effects may provide new avenues for exploiting these pathways for disease prevention.

One of the primary causes for the failure of glass ionomer cement (GIC) is secondary caries. To enhance the anti-microbial performance of GIC without affecting its mechanical properties, chlorhexidine (CHX) was encapsulated in expanded-pore mesoporous silica nanoparticles (pMSN) to synthesize CHX@pMSN. CHX@pMSN was added at three mass fractions (1%, 5%, and 10% (w/w)) to GIC powder as the experimental groups. Pure GIC was set as the control group. The mechanical and anti-biofilm properties of GIC from each group were tested. The results demonstrated that CHX was successfully encapsulated on/into pMSN, and the encapsulating efficiency of CHX was 44.62% in CHX@pMSN. The anti-biofilm ability was significantly enhanced in all experimental groups (p < 0.001) compared with that in the control group. CHX was continuously released, and anti-biofilm ability was maintained up to 30 days. In addition, the mechanical properties (compressive strength, surface hardness, elastic modulus, water sorption, and solubility) of 1% (w/w) group were maintained compared with those in the control group (p > 0.05). In conclusion, adding 1% (w/w) CHX@pMSN to GIC led to conspicuous anti-biofilm ability and had no adverse effect on the mechanical properties of this restorative material. This study proposes a new strategy for preventing secondary caries by using CHX@pMSN-modified GIC.

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Poor bonding stability remains the "Achilles' heel" of dentin bonding, a simple and effective approach to inhibit the activities of both exogenous collagenases and endogenous MMPs, and prevention of the growth of bacterial biofilm is therefore highly demanded. In the present study, a quercetin/ethanol solution was developed as a multifunctional primer to pretreat the dentin surface during adhesive restoration. The results showed that pretreatment with quercetin/ethanol solutions (0.5 and 1.0 wt%) on the dentin surface effectively preserved the bonding strength after one-month of collagenase aging (p < 0.05). Irrespective of aging, lower nanoleakage expression and less cohesive failure in dentin were observed in the quercetin-treated groups (p < 0.05). Compared with the control group, the in situ zymography test revealed that the 0.5 and 1.0 wt% quercetin-treated dentin effectively inhibited MMP activity, while their contact angles significantly increased. Live/dead bacterial staining and the MTT assay demonstrated that the 0.5 and 1.0 wt% quercetin groups exerted significant bactericidal effects while inhibiting biofilm growth of Streptococcus mutans (p < 0.05). We believe that a quercetin/ethanol solution might serve as a simple but versatile primer to provide dentists with a promising approach to obtain desirable bonding stability and to prevent secondary caries, thereby preventing the frequent replacement of resin-based restorations.

This study aimed to evaluate the effects of two calcium-containing desensitizing pastes on the bonding stability of an etch-and-rinse (E&R) adhesive to dentine. After dentine hypersensitivity model established, dentine surfaces were assigned one of the following pretreatment: Group 1, no desensitizer; Group 2, CPP-ACP; and Group 3, Novamin. Specimens were then bonded with an E&R adhesive. Beams from each tooth were randomly divided into three subgroups and then subjected to microtensile bond strength (MTBS) test after 24 h; 12 months of water storage; or 15 runs of pH cycling. Failure modes, nanoleakage, and tubule-occluding effectiveness were analyzed. Results showed that CPP-ACP-or Novamin-pretreated specimens mainly preserved the bonding strength after 12 months of water storage, while effective tubule occlusion could be observed. The results suggested that the calciumcontaining desensitizers were compatible pretreatment for bonding with E&R adhesives to obtain reliable long-term bonding strength and prevention of post-operative sensitivity.

No abstract

This study aimed to investigate the effects of prenatal nicotine exposure (PNE) on thymocyte apoptosis and postnatal immune impairments in vivo and further explore the epigenetic mechanisms of the pro-apoptotic effect of nicotine in vitro. The results showed that PNE caused immune impairments in offspring on postnatal day 49, manifested as increased IL-4 production and an increased IgG1/IgG2a ratio in serum. Enhanced apoptosis of total and CD4+SP thymocytes was observed both in fetus and in offspring. Further, by exposing thymocytes to 0–100 μM of nicotine in vitro for 48 h, we found that nicotine increased α7 nicotinic acetylcholine receptor (nAChR) expression, activated the Fas apoptotic pathway, and promoted thymocyte apoptosis in concentration-dependent manners. In addition, nicotine could induce Tet methylcytosine dioxygenase (TET) 2 expression and Fas promoter demethylation, which can be abolished by TET2 siRNA transfection. Moreover, the α7 nAChR specific antagonist α-bungarotoxin can abrogate nicotine-induced TET2 increase, and the following Fas demethylation and Fas-mediated apoptosis. In conclusion, our findings showed, for the first time, that α7 nAChR activation could induce TET2-mediated Fas demethylation in thymocytes and results in the upregulation of Fas apoptotic pathway, which provide evidence for elucidating the PNE-induced programmed thymocyte apoptosis.