Background and Objective
Occlusal trauma is an important factor that influences the progression of periodontitis, but it is unclear whether occlusal trauma influences periodontal destruction at the ...onset of periodontitis. We established an experimental periodontitis model with both site‐specific loss of attachment and alveolar bone resorption. The purpose of the present study was to investigate the effects of occlusal trauma on periodontal destruction, particularly loss of attachment, at the onset of experimental periodontitis.
Material and Methods
Sixty rats were used in the present study. Forty‐eight rats immunized with lipopolysaccharide (LPS) intraperitoneally were divided into four groups. In the trauma (T) group, occlusal trauma was induced by placing an excessively high metal wire in the occlusal surface of the mandibular right first molar. In the inflammation (I) group, periodontal inflammation was induced by topical application of LPS into the palatal gingival sulcus of maxillary right first molars. In the trauma + inflammation (T+I) group, both trauma and periodontal inflammation were simultaneously induced. The PBS group was administered phosphate‐buffered saline only. Another 12 nonimmunized rats (the n−(T+I) group) were treated as described for the T+I group. All rats were killed after 5 or 10 d, and their maxillary first molars with surrounding tissues were observed histopathologically. Loss of attachment and osteoclasts on the alveolar bone crest were investigated histopathologically. To detect immune complexes, immunohistological staining for C1qB was performed. Collagen fibers were also observed using the picrosirius red‐polarization method.
Results
There were significant increases in loss of attachment and in the number of osteoclasts in the T+I group compared with the other groups. Moreover, widespread distribution of immune complexes was observed in the T + I group, and collagen fibers oriented from the root surface to the alveolar bone crest had partially disappeared in the T, T+I and n−(T+I) groups.
Conclusion
When inflammation was combined with occlusal trauma, immune complexes were confirmed in more expanding areas than in the area of the I group without occlusal trauma, and loss of attachment at the onset of experimental periodontitis was increased. Damage of collagen fibers by occlusal trauma may elevate the permeability of the antigen through the tissue and result in expansion of the area of immune‐complex formation and accelerating inflammatory reaction. The periodontal tissue destruction was thus greater in the T+I group than in the I group.
Background and Objective
The barrier function of long junctional epithelium is thought to be important after periodontal initial therapy and periodontal surgery. Although the difference between long ...junctional epithelium and normal junctional epithelium regarding their resistance to destruction of periodontal tissue has been investigated, the mechanism still remains unclear. Using our rat experimental periodontitis model in which loss of attachment and resorption of alveolar bone is induced by the formation of immune complexes, we investigated the resistance of periodontal tissue containing long junctional epithelium and normal junctional epithelium to destruction.
Material and Methods
Rats were divided into four groups. In the immunized long junctional epithelium (I‐LJE) group, rats were immunized with lipopolysaccharide (LPS), and curettage and root planing procedures were performed on the palatal gingiva of the maxillary first molars to obtain reattachment by long junctional epithelium. In the immunized normal junctional epithelium (I‐JE) group, rats were immunized without curettage and root planing procedures. In the nonimmunized long junctional epithelium (nI‐LJE) group, rats were not immunized but curettage and root‐planing procedures were performed. In the control group, neither immunization nor curettage and root‐planing was performed. In all rats, periodontal inflammation was induced by topical application of LPS into the palatal gingival sulcus of maxillary first molars. The rats were killed at baseline and after the third and fifth applications of LPS. Attachment loss and the number of inflammatory cells and osteoclasts in the four groups were compared histopathologically and histometrically.
Results
After the third application of LPS in the I‐LJE group, attachment loss showed a greater increase than in control and nI‐LJE groups, and inflammatory cell infiltration and osteoclasts were increased more than in the other groups. After the fifth application of LPS, attachment loss was greater and there was a higher degree of inflammatory cell infiltration in nI‐LJE and I‐LJE groups than in control and I‐JE groups.
Conclusion
Our findings suggest that the destruction of periodontal tissue is increased in tissue containing long junctional epithelium compared with normal junctional epithelium and that the immunized condition accelerates the destruction by forming immune complexes.
We present a microstructural study of a surveillance test specimen from a reactor pressure vessel steel of a Russian-type nuclear reactor after neutron irradiation, post-irradiation annealing and ...re-irradiation, using atom probe tomography (APT) and positron annihilation spectroscopy (PAS). The APT results showed the formation of Cu-rich solute nano-clusters (CRCs) during the initial irradiation and their subsequent coarsening during annealing. After re-irradiation, new CRCs have been observed. The irradiation-hardening almost recovered during annealing. However, by re-irradiation, hardening comparable to that by the initial irradiation was observed. The hardening due to the CRCs formed during the initial irradiation, estimated using the Russell–Brown model, was almost the same as that observed. However, the estimated hardening after the re-irradiation was about half of the measured one. The other hardening is attributed to the newly formed MDs by the re-irradiation, which was evidenced by PAS.
The correlation of microstructure evolution and hardening was studied in two kinds of A533B-1 steel with high and low levels of Cu irradiated in a range of dose from 0.32 to 9.9
×
10
19
n
cm
−2 (
E
>
...1
MeV) under a high flux of about 1.7
×
10
13
n
cm
−2
s
−1 using three-dimensional local electrode atom probe (3DAP), positron annihilation (PA) techniques, and Vickers microhardness. The early rapid hardening was found to be caused by mainly matrix defects such as mono- or di-vacancies (
V
1
−
V
2) and/or dislocations indicated by the PA analysis. The 3DAP analysis showed that dense dispersion of dilute Cu rich clusters and lean distribution of Mn–Ni–Si rich clusters, which
were
identified to possess the same dislocation-pinning effect
by applying a Russell and Brown model,
were responsible for large and small hardening in high- and low-Cu steels irradiated above 0.59
×
10
19
n
cm
2, respectively.
The diffusion coefficient and the solubility limit of copper in ferromagnetic iron were directly measured using atom probe tomography at lower temperatures than in previous studies. Cu–Fe diffusion ...couples were annealed at temperatures from 550 to 750°C. The diffusion coefficient was determined to be D=0.48exp(−Q/kBT)ms−1 (Q=3.22eV), which, below 650°C, is about 1.3 times higher than the extrapolation from a previous study considering the magnetic effect. The measured Cu solubility limit is in good agreement with literature.
Background and Objective
Green tea extract exerts a variety of biological effects, including anti‐inflammatory activities. However, there has been no report on the effect of green tea extract on loss ...of attachment, which is an important characteristic of periodontitis. Here, we examined the inhibitory effects of green tea extract on the onset of periodontitis in a rat model.
Material and Methods
Rats were immunized intraperitoneally with Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 12) received a topical application of LPS onto the palatal gingival sulcus every 24 h. The green tea extract group (n = 12) received a topical application of LPS mixed with green tea extract, sunphenon BG, every 24 h. The phosphate‐buffered saline (PBS) group (n = 6) received a topical application of PBS every 24 h. The levels of anti‐LPS immunoglobulin G (IgG) in serum were determined using ELISA. Rats in the LPS and green tea extract groups were killed after the 10th and 20th applications. Rats in the PBS group were killed after the 20th application. Loss of attachment, level of alveolar bone and inflammatory cell infiltration were investigated histopathologically and histometrically. RANKL‐positive cells and the formation of immune complexes were evaluated immunohistologically.
Results
There was no significant difference in the serum levels of anti‐LPS IgG between the LPS group and the green tea extract group. In contrast, loss of attachment, level of alveolar bone, inflammatory cell infiltration and RANKL expression in the green tea extract group were significantly decreased compared with those in the LPS group.
Conclusion
These findings demonstrate that green tea extract suppresses the onset of loss of attachment and alveolar bone resorption in a rat model of experimental periodontitis.
This paper presents a microstructural study of a surveillance test specimen from the Loviisa-1 reactor in Finland, which is a Russian-type pressurized water reactor (VVER-440), after initial ...irradiation to a neutron fluence of 2.5×1019n/cm2 (E>1MeV), post-irradiation annealing at 475°C for 100h and re-irradiation to three different fluences up to 2.7×1019n/cm2. Atom probe tomography (APT) and positron annihilation spectroscopy (PAS) were used to characterize the test specimens. APT results showed the formation of Cu-rich solute clusters (SCs) during the initial irradiation and their subsequent coarsening during annealing. After re-irradiation, a small number of SCs formed once again. The hardening due to the SCs was estimated using the Russell-Brown model based on the APT results, and was in good agreement with the measured hardening after the initial irradiation and post-irradiation annealing. In contrast, during the first-step of re-irradiation, the estimated hardening due to the SCs was smaller than the measured hardening. This suggested that the hardening after re-irradiation was due to some microstructure other than the observed SCs. This difference was attributed to newly-formed matrix defects during re-irradiation, which was supported by the PAS results. However in subsequent steps of re-irradiation, the hardening was almost constant.
Post-irradiation annealing (PIA) behavior of irradiation-induced microstructural changes and hardening of an A533B (0.16wt.% Cu) steel after neutron-irradiation of 3.9×1019n cm−2 (0.061 displacement ...per atom (dpa)) at 290°C was studied by positron annihilation spectroscopy (PAS), atom probe tomography (APT) and Vickers microhardness measurements. Coincidence Doppler broadening and positron lifetime measurements clearly reveal two recovery stages; (i) as-irradiated state to annealing at 450°C and (ii) annealing from 450 to 600°C. The first stage is due to annealing out of the most of irradiation-induced vacancy-related defects, while the second stage corresponds to dissolving of irradiation-induced solute nanoclusters (SCs). APT observations reveal that the SCs are enriched with Cu, Mn, Ni and Si and that their number densities decrease with increasing annealing temperature without coarsening to give almost complete recovery at 550°C. The experimental hardening is almost twice the SC hardening estimated by the Russell–Brown model below 350°C, whereas it is almost the same as that estimated in the range 400–550°C.
A dentin primer containing the antibacterial monomer 12-methacryloyloxydodecylpyridinium bromide (MDPB) has been shown to penetrate and kill the bacteria in artificially demineralized dentin. We ...hypothesized that an experimental adhesive system, which incorporates the MDPB-containing primer, would be effective in inhibiting the progression of root caries in vitro. Artificial caries lesions were prepared by either an acid-gel or a Streptococcus mutans culture technique on the roots of extracted human teeth. The progression of these lesions after the application of the experimental or proprietary adhesive system was examined. Further demineralization was completely prevented by the experimental adhesive system, while lesions managed with the proprietary materials showed limited ability to inhibit further demineralization. We conclude that the experimental adhesive system can inhibit the progression of root-surface caries in vitro, through a combination of its antimicrobial activity and sealing of the demineralized dentin.
