ABSTRACT
In this study,the colonization and distribution of Helicobacter pylori (Hp) in patients with chronic gastric diseases were investigated and the relationship between the periodontal initial treatment and presence of Hp in oral cavity was examined to better understand the connection between Hp infection and chronic diseases.Primers for PCR amplification were designed according to ureC gene and cagA genes of Hp.Specimens were harvested from different sites of 96 patients with chronic gastric diseases and the specimens of dental plaques,gargles and dorsal mucosa were tested for Hp.The 96 patients were treated by bismuth triple therapy and among them,52 subjects were additionally given periodontal initial therapy.The eradication rate of gastric Hp and oral Hp detection rate were determined 4 weeks and 1 year after the treatment.The results showed that the detection rates of oral specimens were in the order of dental plaques (82.3％),gargles (51.1％) and scrapings of dorsal mucosa of tongue (37.5％).One year after bismuth triple therapy or the triple therapy in com bination with periodontal initial treatment,the eradication rate of gastric Hp was significantly higher in the combination treatment group than in group treated by the triple therapy alone (62.8％ vs.32.4％,P＜0.05).Moreover,the Hp detection rate was significantly lower in the combination group than in the group treated only with the triple therapy.We are led to conclude that Hp is present at various parts of oral cavity,oral Hp might be an important source of gastric Hp and the triple therapy plus periodontal initial treatment can enhance the long-term eradication rate of gastric Hp in patient with both chronic gastric diseases and chronic periodontitis.
ABSTRACT
The estimation of chronologic age based on the stages of third-molar development was evaluated by using the eight stages (A-H) method of Demirjian and the third-molar development was compared, in terms of sex and age, with results of previous studies. The samples consisted of 291orthopantomograms from young Chinese subjects of known chronologic age and sex (including 139males with a mean age of 14.67±3.62 y and 152 females with a mean age of 14.85±3.70 y). Statistical analysis was performed by employing the Mann-Whitney U-test and the t-test. Regression analysis was conducted to obtain regression formulas for calculating dental age from the chronologic age. Our results showed statistically significant differences (P＜0.05) in third-molar development between males and females, at the calcification stages D, E and H. And a strong correlation was found between age and third-molar development in both males (r2=0.65) and females (r2=0.61). New equations (Age=8.76+1.32 Development stage) for estimating chronologic age were derived. It is concluded that third-molar genesis took place earlier in males than in females. The use of third molars as a developmental marker is appropriate in young adults of Central China. The formula obtained in the present study can be used as a guide for estimation of dental maturity and a standard for age estimation for young adults of Central China.
ABSTRACT
To observe the effects of basic fibroblast growth factor (bFGF) on human adenoid cystic carcinoma ACC-2 cell line proliferation and ERK, cyclin D1/p21waf/ciplsignaling pathways, human adenoid cystic carcinoma cells (ACC-2) were cultured and the influence of bFGF of different concentrations on cell proliferation was determined by MTT. Protein was detected by im muno-precipitation and ERK activity by using ERK agent kit. P-ERK1/2 and down-stream cyclin D1, p21waf/ciplexpression were detected by Western blotting and the interfering role of mitogen pro- tein-activated kinase (MEK) suppressor U0126 in the afore-mentioned indicators was examined. MTr demonstrated ACC-2 cell proliferation was substantially enhanced by bFGF, immuo-precipitation displayed ERK activity was up-regulated by bFGF, and immuno-imprinting also showed p-ERK1/2, cyclin D1 expression was greatly enhanced and p21waf/ciplexpression was inhibited by bFGE U0126 suppressed the effect of bFGE It is concluded that bFGF can promote the proliferation of human adenoid cystic carcinoma ACC-2 cells, and its pathways are associated with the up-regulated activity and expression of p-ERK1/2, inhibited p21waf/cipl expression and enhanced cyclin DI expression.