Previous studies have reported that oxidative stress increases intracellular Zn

concentrations and induces cytotoxicity. However, no studies have investigated whether oxidative stress induces such changes in periodontal tissue cells. In the present study, we investigated the effect of oxidative stress on intracellular Zn

concentration in periodontium constituent cells and its potential relationship with periodontal disease.

We analyzed changes in intracellular Zn

concentrations in human gingival epithelial (epi4) cells treated with hydrogen peroxide (H

O

). The fluorescent probes FluoZin-3 AM and CellTracker Green CMFDA were used to detect intracellular Zn

and thiol groups, respectively. Western blot analyses, luciferase reporter assays, and real-time polymerase chain reaction (PCR) analyses were performed to examine the effect of intracellular Zn

on epi4 cells.

H

O

treatment increased intracellular concentrations of Zn

in epi4 cells by facilitating the movement of Zn

from cellular nonprotein thiols to the cytoplasm and promoting cell membrane permeability to Zn

. Furthermore, H

O

-induced increases in intracellular Zn

activated the p38 cAMP response element-binding protein/mitogen-activated protein kinase (p38 CREB/MAPK) cascade, upregulated nuclear factor kappa B (NF-κB) DNA binding, and increased the expression of inflammatory cytokines and matrix metallopeptidase-9 (MMP-9).

Increases in intracellular Zn

induced by oxidative stress activate signaling pathways involved in inflammation, potentially contributing to the progression of periodontal disease.

Increases in intracellular Zn2+ induced by oxidative stress activate signaling pathways involved in inflammation, potentially contributing to the progression of periodontal disease.Within the panniculus carnosus-associated skeletal muscles in the human, the palmaris brevis and the platysma showed myotendinous/myofascial junctions with clear distance to the corium and the specific connection collagen type XXII. The orbicularis oris muscle, in contrast, contained bundles of striated muscle fibers reaching the corium at two distinct levels the predominant inner ending was connected to the elastic network of the inner corium and the outer ending was within the more superficial collagen network. At both locations, the striated muscle fibers showed brush-like cytoplasmic protrusions connecting a network which was not oriented toward the muscle fibers. Collagen type XXII was not present.Although the development of the sympathetic trunks was first described >100 years ago, the topographic aspect of their development has received relatively little attention. We visualised the sympathetic trunks in human embryos of 4.5-10 weeks post-fertilisation, using Amira 3D-reconstruction and Cinema 4D-remodelling software. Scattered, intensely staining neural crest-derived ganglionic cells that soon formed longitudinal columns were first seen laterally to the dorsal aorta in the cervical and upper thoracic regions of Carnegie stage (CS)14 embryos. Nerve fibres extending from the communicating branches with the spinal cord reached the trunks at CS15-16 and became incorporated randomly between ganglionic cells. After CS18, ganglionic cells became organised as irregular agglomerates (ganglia) on a craniocaudally continuous cord of nerve fibres, with dorsally more ganglionic cells and ventrally more fibres. Accordingly, the trunks assumed a “pearls-on-a-string” appearance, but size and distribution of the pearls were markedly heterogeneous. PFI-3 datasheet The change in position of the sympathetic trunks from lateral (para-aortic) to dorsolateral (prevertebral or paravertebral) is a criterion to distinguish the “primary” and “secondary” sympathetic trunks. We investigated the position of the trunks at vertebral levels T2, T7, L1 and S1. During CS14, the trunks occupied a para-aortic position, which changed into a prevertebral position in the cervical and upper thoracic regions during CS15, and in the lower thoracic and lumbar regions during CS18 and CS20, respectively. The thoracic sympathetic trunks continued to move further dorsally and attained a paravertebral position at CS23. The sacral trunks retained their para-aortic and prevertebral position, and converged into a single column in front of the coccyx. Based on our present and earlier morphometric measurements and literature data, we argue that differential growth accounts for the regional differences in position of the sympathetic trunks.

The aim of this study was to determine differences in GCF and serum levels of fractalkine/CX3CL1 and its receptor/ CX3CR1 between the patients with stage III/grade B periodontitis and periodontally healthy subjects.

Fractalkine (CX3CL1), the only member of CX3C chemokine family, is involved in the pathogenesis of several systemic inflammatory diseases’ disorders including rheumatoid arthritis, cardiovascular diseases, tonsillitis, and diabetes mellitus. It has critical functions in inflammatory cell migration, adhesion, and proliferation.

20 stage III/grade B periodontitis (P) and 20 healthy individuals (control; C) were included in this clinical study (all never smokers and systemically healthy). Clinical periodontal parameters were measured. Serum and GCF levels of CX3CL1, CX3CR1, and IL-1β were quantified by enzyme-linked immunosorbent assay and reported as total amounts and concentration.

The GCF concentrations and also total amount of CX3CL1, CX3CR1, and IL-1β were statistically significantly higher in the patients with periodontitis compared with control group (P<0.05). CX3CL1, CX3CR1, and IL-1β levels in the GCF were significantly and positively correlated with all the clinical periodontal parameters (PI, PPD, BOP, and CAL; P<0.01, P<0.05). There was a significant correlation between IL-1β, CX3CL1, and CX3CR1 concentrations in the GCF (respectively; r=0.838 and r=0.874, P<0.01).

Fractalkine and its receptor may play role in mechanisms through the regulation of inflammation or on the pathogenesis of periodontal disease.

Fractalkine and its receptor may play role in mechanisms through the regulation of inflammation or on the pathogenesis of periodontal disease.