Search

Background. To explore whether salivary inflammatory mediators and periodontal indices at different gestational stages can be taken as indicators of preterm birth (PTB). Methods. This nested case-control study enrolled systemically healthy pregnant women at 9 to 36 weeks of gestation. Periodontal indices were measured at the enrollment date, and interleukin-1β (IL-1β), IL-6, tumor necrosis factor (TNF-α), prostaglandin E2 (PGE2), and 8-hydroxy-deoxyguanosine (8-OHdG) in the saliva were determined by enzyme-linked immunosorbent assay (ELISA). The birth outcome was recorded. Results. PTB occurred in 26 women. A total of 104 matched women with full-term birth (FTB) were used as controls. The PTB women enrolled at 24-28 gestational weeks displayed a significantly greater bleeding index (BI), probing pocket depth (PD), PD ≥ 4 mm sites (%), saliva-TNF-α, and saliva-PGE2 ( P < 0.05 ). BI and PGE2 in the saliva were found to be positively associated with PTB ( OR = 4.79 , P = 0.048 , 95 % CI = 1.014 to 22.628 ; OR = 1.07 , P = 0.04 , 95 % CI = 1.004 to 1.135 , respectively). The areas under the receiver operating characteristic curve (ROC) of BI and saliva-PGE2 were 0.82 and 0.78, respectively, and that of the combined detection was 0.91, which was larger than either marker alone, although the differences were not significant ( P > 0.05 ). Conclusions. The combination of BI and PGE2 in saliva at 24-28 gestational weeks could be a predictor of PTB in asymptomatic women. However, the results should be further explored with larger sample size.

The purpose of this study was to prepare carboxymethyl chitosan (CMC) and lysozyme nanogels that could encapsulate amorphous calcium phosphate (ACP) for achieving its controlled delivery, thus forming an aprismatic enamel-like layer on the demineralized enamel surface.CMC/LYZ-ACP nanogels were developed, and the controlled delivery of ACP from the nanogels was induced by the presence of NaCl. The nanogel morphologies at various NaCl concentrations was measured by transmission electron microscopy (TEM). The particle sizes and zeta potentials (ζ-potential) of the samples were determined using a combined dynamic light scattering/particle electrophoresis instrument. Comparing the remineralization effect of the CMC/LYZ-ACP nanogels on the demineralized enamel surface with that of a fluoride treatment, the remineralization effect was examined by nanoindentation tests, X-ray diffraction (XRD), confocal laser scanning microscopy (CLSM), and scanning electron microscopy (SEM).CMC/LYZ-ACP nanogels were negatively charged spherical structures with a particle size of approximately 300 nm. At high concentrations of NaCl (0.15 M), ACP was dissociated from the disassembled nanogels and transformed into hydroxyapatite (HAP). Groups treated with the CMC/LYZ-ACP nanogels showed the regeneration of an aprismatic enamel-like layer on an acid-etched enamel surface, which provided increased mechanical properties (P0.05) and a high impermeability (P0.01) compared to those of the fluoride-treated group.This research provides a new idea for the stable and controllable delivery of ACP from CMC/LYZ-ACP nanogels, which can form an aprismatic enamel-like layer in situ on the surface of demineralized enamel. In regard to further clinical development, this material and method may be promising for treating early enamel caries.

Age-related macular degeneration (AMD) is the most common eye disease in elderly patients, which could lead to irreversible vision loss and blindness. Increasing evidence indicates that amyloid β-peptide (Aβ) might be associated with the pathogenesis of AMD. In this review, we would like to summarise the current findings in this field. The literature search was done from 1995 to Feb, 2021 with following keywords, ‘Amyloid β-peptide and age-related macular degeneration’, ‘Inflammation and age-related macular degeneration’, ‘Angiogenesis and age-related macular degeneration’, ‘Actin cytoskeleton and amyloid β-peptide’, ‘Mitochondrial dysfunction and amyloid β-peptide’, ‘Ribosomal dysregulation and amyloid β-peptide’ using search engines Pubmed, Google Scholar and Web of Science. Aβ congregates in subretinal drusen of patients with AMD and participates in the pathogenesis of AMD through enhancing inflammatory activity, inducing mitochondrial dysfunction, altering ribosomal function, regulating the lysosomal pathway, affecting RNA splicing, modulating angiogenesis and modifying cell structure in AMD. The methods targeting Aβ are shown to inhibit inflammatory signalling pathway and restore the function of retinal pigment epithelium cells and photoreceptor cells in the subretinal region. Targeting Aβ may provide a novel therapeutic strategy for AMD.

Small RNA (microRNA or miRNA) is a kind of small noncoding single-stranded RNA that regulates complementary mRNA at the posttranscriptional level in eukaryotic organisms. As important regulatory factors, miRNAs play an important role in the occurrence and development of glaucoma and widely participate in regulating biological processes of glaucoma-related genes. This article reviews the connection between the aqueous humor, trabecular meshwork, the apoptosis of retinal ganglion cells, and miRNA.

It has been suggested that microRNAs (miRs) are involved in the immune regulation of periodontitis. However, it is unclear whether and how miRs regulate the function of B cells in the context of periodontitis. This study is to explore the role of miR-146a on the inflammatory cytokine production of B cells challenged by Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS). Primary B cells were harvested from mouse spleen. Quantitative real-time polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA) were used to detect the expression of inflammatory cytokines in B cells in the presence or absence of P. gingivalis LPS and/or miR-146a. Bioinformatics, luciferase reporter assay and overexpression assay were used to explore the binding target of miR-146a. Our results showed that miR-146a level in B cells was elevated by P. gingivalis LPS stimulation, and the mRNA expressions of interleukin (IL)-1β, 6 and 10, and IL-1 receptor associated kinase-1 (IRAK1), but not TNF receptor associated factor 6 (TRAF6), were also upregulated. The expression levels of IL-1β, 6, 10 and IRAK1 were reduced in the presence of miR-146a mimic, but were elevated by the addition of miR-146a inhibitor. MiR-146a could bind with IRAK1 3' untranslated region (UTR) but not TRAF6 3'-UTR. Overexpression of IRAK1 reversed the inhibitory effects of miR-146a on IL-1β, 6 and 10. In summary, miR-146a inhibits inflammatory cytokine production in B cells through directly targeting IRAK1, suggesting a regulatory role of miR-146a in B cell-mediated periodontal inflammation.

Objectives The formation of biofilm around implants, which is induced by immediate bacterial colonization after installation, is the primary cause of post-operation infection. Initial surface modification is usually required to incorporate antibacterial agents on titanium (Ti) surfaces to inhibit biofilm formation. However, simple and effective priming methods are still lacking for the development of an initial functional layer as a base for subsequent coatings on titanium surfaces. The purpose of our work was to establish a novel initial layer on Ti surfaces using phase-transited lysozyme (PTL), on which multilayer coatings can incorporate silver nanoparticles (AgNP) using chitosan (CS) and hyaluronic acid (HA) via a layer-by-layer (LbL) self-assembly technique. Methods In this study, the surfaces of Ti substrates were primed by dipping into a mixture of lysozyme and tris(2-carboxyethyl)phosphine (TCEP) to obtain PTL-functionalized Ti substrates. The subsequent alternating coatings of HA and chitosan loaded with AgNP onto the precursor layer of PTL were carried out via LbL self-assembly to construct multilayer coatings on Ti substrates. Results The results of SEM and XPS indicated that the necklace-like PTL and self-assembled multilayer were successfully immobilized on the Ti substrates. The multilayer coatings loaded with AgNP can kill planktonic and adherent bacteria to 100% during the first 4 days. The antibacterial efficacy of the samples against planktonic and adherent bacteria achieved 65%-90% after 14 days. The sustained release of Ag over 14 days can prevent bacterial invasion until mucosa healing. Although the AgNP-containing structure showed some cytotoxicity, the toxicity can be reduced by controlling the Ag release rate and concentration. Conclusions The PTL priming method provides a promising strategy for fabricating long-term antibacterial multilayer coatings on titanium surfaces via the LbL self-assembly technique, which is effective in preventing implant-associated infections in the early stage.

To investigate the influence of high glucose on Porphyromonasgingivalis (Pg) lipopolysaccharide (LPS) stimulating human gingival fibroblasts (HGF) to secret the cytokines.HGF were obtained from the primary culture of the tissue explants. Cells were divided into four groups, low glucose (5.5 mmol/L) + 1 mg/L Pg LPS (group A);low glucose + 10 mg/L Pg LPS (group B); high glucose (25 mmol/L) +1 mg/L Pg LPS(group C); high glucose+10 mg/L Pg LPS (group D). The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in cell supernatants were detected by enzyme- linked immunosorbent assay at 6 h and 12 h. The expressions of toll-like receptor 2, 4 (TLR-2, 4) were examined by real-time polymerase chain reaction. After pretreatment with anti-TLR2 and anti-TLR4 monoclonal antibody in HGF, TNF-α and L-1β levels were detected.TNF-α concentration increased obviously in high glucose 6 h and 12 h after Pg LPS stimulation (P0.01). IL-1β secretion increased (P0.01). Meanwhile, TLR2, 4 mRNA expression increased, especially in high glucose+10 mg/L Pg LPS (P0.01). After inhibition of the TLR2, 4 in high glucose + 10 mg/L Pg LPS respectively, TNF-α level [(297.16±11.49), (390.01±12.81) ng/L] decreased (F = 166.02, P0.01), and IL-1β level [(49.90±4.08), (99.35±5.01) ng/L] also decreased (F = 153.51, P0.01).High glucose may promote Pg LPS to stimulate the secretion of TNF-α and IL-1β through regulating TLR2, 4 expression, which suggests that the elevating blood glucose precipitate in aggravating the process of periodontal disease.

We previously demonstrated that endogenous interleukin-6 (IL-6) is upregulated and may be neuroprotective after retinal ischemia. The purpose of this study is to investigate the role of nuclear factor kappa-B (NF-kappaB) in regulating IL-6 expression after ischemia. NF-kappaB p65 mRNA levels were significantly elevated between 2 and 12 h after the insult. A high number of NF-kappaB p65 positive cells were detected in the inner retina at 12 h after ischemia. Activated nuclear NF-kappaB p65 and IL-6 were colocalized in cells, which were also marked by a microglial/phagocytic cell marker (ED1) in the inner retina. Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132, a proteasome inhibitor, which inhibits IkappaB degradation and hence prevents the activation and translocation of NF-kappaB into the nucleus) abolished the increase in NF-kappaB p65 mRNA levels after the insult, while there was no effect by helenalin (an inhibitor which inhibits NF-kappaB activity by alkylation of the p65 subunit, thereby blocking its binding to the target DNA). However, MG-132 and/or helenalin significantly diminished the increase in IL-6 mRNA levels after the insult. Small interfering RNAs (siRNAs, inhibit target gene expression through the sequence-specific destruction of the target messenger RNA) against NF-kappaB p65 significantly reduced the increase in NF-kappaB p65 mRNA levels as well as IL-6 mRNA levels after ischemia. The number of retinal ganglion cells (RGCs) was also significantly decreased using the inhibitors of NF-kappaB compared with those of the controls after ischemia. These findings support the hypothesis that upregulation of endogenous retinal IL-6 in retinal I/R injury in microglial/phagocytic cells is controlled predominantly by NF-kappaB p65.