Control of gingival inflammation in a teenager population using ultrasonic prophylaxis

Gingival inflammation is clinically characterized by gingival redness, swelling and increased tendency of bleeding of the soft tissue. Bacterial biofilm is the etiological agent. If, at this stage, the bacterial biofilm is removed and appropriate control methods are applied, remission of gingival inflammation occurs. This study evaluated the effectiveness of a single session of ultrasonic prophylaxis for the reduction of gingivitis in an adolescent population using the Plaque Index (PI) and Gingival Index (GI). The study sample consisted of 15 male adolescent students selected at a dentist's office of a public high school. Prior to treatment (baseline), plaque index (PI) and bleeding on probing (BOP) were recorded. The patients then received oral hygiene instructions and ultrasonic prophylaxis. Follow-up exams were made 15 and 30 days after the ultrasonic prophylaxis, again recording PI and BOP. The data were analyzed by the Student's t-test for dependent samples. Correlation analysis between presence of biofilm and bleeding on probing was also made using the Pearson correlation test. There was a statistically significant decrease in the plaque index and bleeding on probing between baseline and examinations at both 15 days and 30 days (p<0.05). However, the difference between the means at 15 and 30 days was statistically similar. The correlation analysis showed correlation between both parameters (p<0.05). The results indicate that a single session of ultrasonic prophylaxis associated to oral hygiene instructions is efficient to reverse gingivitis in adolescents.     

Primary hepatic presentation of Hodgkin's lymphoma: A case report

Hodgkin's lymphoma (HL) is in general a lymph node‐based disease. Hepatic involvement usually occurs in the advanced disease. Primary and prominent manifestation of the disease in the liver is extremely rare. We report magnetic resonance imaging leading to diagnosis in a rare case of liver involvement as the first sign of HL.     

Subepithelial connective tissue graft for root coverage in smokers and non-smokers: a clinical and histologic controlled study in humans

BACKGROUND: The aim of this study was to evaluate root coverage of gingival recessions and to compare graft vascularization in smokers and non-smokers. METHODS: Thirty subjects, 15 smokers and 15 non-smokers, were selected. Each subject had one Miller Class I or II recession in a non-molar tooth. Clinical measurements of probing depth (PD), relative clinical attachment level (CAL), gingival recession (GR), and width of keratinized tissue (KT) were determined at baseline and 3 and 6 months after surgery. The recessions were treated surgically with a coronally positioned flap associated with a subepithelial connective tissue graft. A small portion of this graft was prepared for immunohistochemistry. Blood vessels were identified and counted by expression of factor VIII-related antigen-stained endothelial cells. RESULTS: Intragroup analysis showed that after 6 months there a was gain in CAL, a decrease in GR, and an increase in KT for both groups (P <0.05), whereas changes in PD were not statistically significant. Smokers had less root coverage than non-smokers (58.02% +/- 19.75% versus 83.35% +/- 18.53%; P <0.05). Furthermore, the smokers had more GR (1.48 +/- 0.79 mm versus 0.52 +/- 0.60 mm) than the non-smokers (P <0.05). Histomorphometry of the donor tissue revealed a blood vessel density of 49.01 +/- 11.91 vessels/200x field for non-smokers and 36.53 +/- 10.23 vessels/200x field for smokers (P <0.05). CONCLUSION: Root coverage with subepithelial connective tissue graft was negatively affected by smoking, which limited and jeopardized treatment results.     

Pneumocystis jiroveci pneumonia as a complication of glucocorticoid therapy for interstitial pneumonia]

We evaluated the clinical features of pneumocystis jiroveci pneumonia (PCP) as a complication of glucocorticoid therapy for interstitial pneumonia We analyzed 74 interstitial pneumonia patients receiving glucocorticoid therapy, of whom 7 patients developed PCP. At the time of PCP diagnosis, the average duration of the glucocorticoid therapy was 71 days and the average daily dose of predonisolone was 37 mg. Circulating CD4+ lymphocyte counts were 370/microl on the average and more than 200/microl in three cases. PCP cases showed less circulating lymphocyte counts four weeks after the initiation of the therapy. Any cases receiving sulfamethoxazole-trimethoprim (TMP-SMX) did not develop PCP. In conclusion, interstitial pneumonia patients, who are treated with glucocorticoid, are benefit from TMP-SMX as PCP prophylaxis, but CD4 + lymphocyte counts greater than 200/microl is no reason to denying PCP.     

Genetic background markedly influences vulnerability of the hippocampal neuronal organization in the "twitcher" mouse model of globoid cell leukodystrophy

The twitcher mouse is well known as a naturally occurring authentic mouse model of human globoid cell leukodystrophy (GLD; Krabbe disease) due to genetic deficiency of lysosomal galactosylceramidase. The twitcher mice used most commonly are on the C57BL/6J background. We generated twitcher mice that were on the mixed background of C57BL/6J and 129SvEv, the standard strain for production of targeted mutations. Twitcher mice on the mixed background were smaller and had a shorter lifespan than were those on the C57BL/6J background. Many twitcher mice on the mixed background developed generalized seizures around 30 days that were never seen in twitcher mice on the C57BL/6J background. Neuropathologically, although the degree of the typical demyelination with infiltration of macrophages was similar in the central and peripheral nervous systems, in both strains, marked neuronal cell death was observed only in twitcher mice on the mixed background. In the hippocampus, the neuronal cell death occurred prominently in the CA3 region in contrast to the relatively well-preserved CA1 and CA2 areas. This neuropathology has never been seen in twitcher mice on the C57BL/6J background. Biochemically, the brain of twitcher mice on the mixed background showed much greater accumulation of lactosylceramide. Genetic background must be carefully taken into consideration when phenotype of mutant mice is evaluated, particularly because most targeted mutants are initially on a mixed genetic background and gradually moved to a pure background. These findings also suggest an intriguing possibility of important function of some sphingolipids in the hippocampal neuronal organization and maintenance.     

Distinct mechanism of cell death is responsible for tunicamycin-induced ER stress in SK-N-SH and SH-SY5Y cells

In order to elucidate underlying mechanism of cell death pathways in neuronal cells in humans, we studied responsible pathways involved in the endoplasmic reticulum (ER) stress-induced cell death in neuroblastoma cells, SK-N-SH and its neuroblast-type subclone SH-SY5Y cells. A time-dependent induction of ER chaperons, glucose regulated protein (GRP)78 and GRP94, was observed after treatment with tunicamycin (TM), and cell death was also induced concomitantly in both cells. Although the pro-caspase-12-like protein was defined in both cells, a decrease in the protein was observed in only SH-SY5Y cells after exposure to TM. In contrast, pro-caspase-4 was detected in only SK-N-SH cells, and the cleaved-form was induced by the treatment with TM. A caspase-4 inhibitor, Z-LEVD-FMK attenuated TM-induced cell death in SK-N-SH cells. Calpain- and caspase-3-mediated proteolysis of alpha II-spectrin was also increased after the treatment with TM in both cells. A calpain inhibitor, calpeptin, repressed TM-induced cell death in only SK-N-SH cells. GADD153/C/EBP homologous protein (CHOP) was significantly induced after exposure to TM in only SH-SY5Y cells and RNA interference to GADD153/CHOP repressed TM-induced cell death. These results demonstrate that induction of GADD153/CHOP plays a pivotal role in mechanism of ER stress-induced cell death in SH-SY5Y cells, on the other hand, cleavage of pro-caspase-4 by activation of calpain play a crucial role in SK-N-SH cells. It is also suggested that the relevance of caspase-4 to ER stress is cell-specific even between human-origin cell lines.     

Protective effect of S-allyl-L-cysteine,a garlic compound,on amyloid beta-protein-induced cell death in nerve growth factor-differentiated PC12 cells

Aged garlic extract (AGE) contains several neuroactive compounds, including S-allyl-L-cysteine (SAC) and allixin. We characterized cell death induced by amyloid beta-protein (Abeta), 4-hydroxynonenal (HNE), tunicamycin, an endoplasmic reticulum (ER) stressor, or trophic factor deprivation, and investigated whether and how SAC could prevent this in nerve growth factor (NGF)-differentiated PC12 cells, a model of neuronal cells. Exposure of the cells to amyloid beta-protein(1-40) (Abeta(1-40)) decreased the extent of [3-(4,5)-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium (MTT) reduction activity and loss of neuronal integrity, but these effects were not prevented by Ac-DEVD-CHO, a caspase-3 inhibitor. Simultaneously applied SAC protected the cells against Abeta-induced cell death in a concentration-dependent manner. It also protected them against tunicamycin-induced neuronal death. In contrast, it afforded no protection against cell death induced by HNE and trophic factor deprivation, which is mediated by a caspase-3-dependent pathway. These results suggest that SAC may selectively protect cell death induced by Abeta and tunicamycin, which may be triggered by ER dysfunction in NGF-differentiated PC12 cells.     

Case of chromosome 6p25 terminal deletion associated with Axenfeld-Rieger syndrome and persistent hyperplastic primary vitreous

Axenfeld-Rieger syndrome is inherited in an autosomal dominant pattern and is characterized by anomalies of the anterior segment of the eye and systemic signs including craniofacial dysmorphic features and cardiac defects. The disorder is genetically heterogeneous and one causative gene, FOXC1, is located on chromosome 6p25. Persistent hyperplastic primary vitreous (PHPV) is a congenital ocular disorder in which there is a failure of the normal regression of the primary vitreous and a proliferation of fibrous tissue from the remnants of the primary vitreous. Deletions of chromosome 6p25 have been reported in a small number of patients with Axenfeld-Rieger syndrome; however, no case of chromosome 6p25 deletion has been reported with PHPV. We report a newborn girl who had both Axenfeld-Rieger syndrome and the combined type of PHPV, in whom the G-banding and spectral karyotyping revealed a 6p monosomy of terminal deletion with a breakpoint at chromosome 6p25.1. The karyotype was 46,XX,del(6)(p25.1). We conclude that PHPV in the context of Axenfeld-Rieger syndrome can be caused by 6p25 terminal deletion.     

Implications for induction of autoimmunity via activation of B-1 cells by Helicobacter pylori urease

Besides various gastroduodenal diseases, Helicobacter pylori infection may be involved in autoimmune disorders like rheumatoid arthritis (RA) or idiopathic thrombocytopenic purpura. Such autoimmune disorders are often associated with autoreactive antibodies produced by B-1 cells, a subpopulation of B lymphocytes. These B-1 cells are mainly located in the pleural cavity or mucosal compartment. The existence of H. pylori urease-specific immunoglobulin A (IgA)-producing B cells in the mucosal compartment and of their specific IgM in the sera of acutely infected volunteers suggests the possibility that urease stimulates mucosal innate immune responses. Here, we show for the first time that purified H. pylori urease predominantly stimulates the B-1-cell population rather than B-2 cells, which produce antigen-specific conventional antibodies among splenic B220(+) B cells. The fact that such stimulation of B-1 cells was not affected by the addition of polymyxin B indicates that the effect of purified H. pylori urease was not due to the contamination with bacterial lipopolysaccharide. Furthermore, the production of various B-1-cell-related autoreactive antibodies such as IgM-type rheumatoid factor, anti-single-stranded DNA antibody, and anti-phosphatidyl choline antibody was observed when the splenic B cells were stimulated with purified H. pylori urease in vitro. These findings suggest that H. pylori components, urease in particular, may be among the environmental triggers that initiate various autoimmune diseases via producing autoreactive antibodies through the activation of B-1 cells. The findings shown here offer important new insights into the pathogenesis of autoimmune disorders related to H. pylori infection.