A study of oral health condition in individuals with no oral hygiene and its association with plaque acidogenesis.

OBJECTIVE: To study the association of long-term deposited plaque, due to lack of oral hygiene, with acidogenesis of the plaque bacteria. METHODS: Seventy-seven subjects with poor oral hygiene were selected. Debris index (DI) and calculus index (CI) were recorded. Among them, 16 were DMFS > 8, and comprised the caries active (CA) group; 27 were caries free, and comprised the caries free (CF) group. Plaque fluids in both groups were analyzed for organic acids, phosphate, and inorganic cations by use of capillary electrophoresis, while pH was measured by microelectrodes. RESULTS: No differences were found on debris index (CF group measured 2.07-0.47, CA group measured 2.01-0.53) or calculus index (CF group measured 2.47-0.50, CA group measured 2.48-0.53) relative to carious status, although there was a positive relationship between DI and CI (r = 0.52, P < 0.001). The main finding in this study was that the quantity of lactic acid produced by sucrose exposure in these individuals with poor oral hygiene was much less (increased no more than 2 times, compared with content at rest) than in a previous report (increased 3 to 5 times, compared with content at rest) on subjects with good oral hygiene habits. CONCLUSIONS: Long-term deposited plaque due to lack of oral hygiene may have less cariogenic capability, although patients' susceptibility to periodontal disease would increase.

[Pathways of signal transduction of intracellular Ca2+ increase mediated by three subtypes of alpha 1-adrenoceptor in HEK293 cells].

In HEK293 cell lines in which alpha 1a-, alpha 1b- or alpha 1d-adrenoceptor subtypes were stably expressed, fluorescence intensities due to traces of Ca2+ were investigated using fura-2/AM with the aim of exploring signal transduction pathways of intracellular Ca2+ increase mediated by these receptor subtypes. Pertussis toxin had no effect on [Ca2+]i increase mediated by all three subtypes of alpha 1-adrenoceptors. However, U-73122 and PMA could inhibited the [Ca2+]i increase induced by NE, which was not affected by Foskolin and Rp-cAMPs. Pretreatment with calphostin C abolished the [Ca2+]i response to PMA. Quercetin and tyrphostin inhibited maximal [Ca2+]i increase but had no effect on the plateau phase in all the three transfected cells. In the HEK293 cells, the phosphatide-Ca2+ signalling system mediated by the 3 subtypes of alpha 1-AR was brought into play by activation of phospholiphase C via coupling with PTX-insensitive G proteins. PKC system inhibited both mobilization of internal Ca2+ stores and the Ca2+ influx across the plasma membrane. Tyrosine kinase, but not cAMP system, might participate in such Ca2+ signalling.

[Phospholipid components in BALFS from bleomycin induced pulmonary fibrosis in rats].

Qualitative and quantitative analysis was performed on 5 components of phospholipids (PL) isolated from bronchoalveolar lavage fluid (BALF) during the development of bleomycin induced pulmonary fibrosis in rats with high-performance liquid chromatography (HPLC). The measurement of cells and protein in BALF, the pathologic and morphometric observation with light and electronic microscope were also done. Results indicated that the changes both in BALF cells and in lung histopathology were similar, the amount of protein in BALF increased, the total amount of PL in BALF increased more than 1.8-fold over control animals at days 28 after administration of Bleomycin, phosphatidylglycerol (PG) decreased with time, phosphatidylinositol (PI) and phosphatidylethanolamine (PE) increased, PG/PI ratio decreased, the PG/PI ratio could be used as a marker for pulmonary fibrosis.