The bacteriology of the supragingival plaque of child dental patients in Kuwait.

OBJECTIVE: To investigate the bacterial flora of the gingival plaques of pediatric dental patients in order to establish baseline data for future studies on the complex microbiota of the oral cavity of this group of child dental patients. SUBJECTS AND METHODS: Forty subjects, aged 3-12 years, were enrolled and investigated after informed consent was obtained. During the patients' first visit to the dental clinic supragingival plaque samples were collected from the gingival area of buccal and lingual tooth surfaces of all primary and permanent molar teeth using sterile curettes. Serially diluted samples were inoculated onto a set of selective and nonselective media and then incubated at the appropriate atmospheric conditions and temperatures. Representative colonies of isolates were identified by standard methods, including hemolytic characteristics on blood agar and profiling on API 20S and API 20A as appropriate. RESULTS: A total of 183 isolates (123 aerobes and 60 anaerobes) were recovered from the 40 patients with a mean count of 3 per sample of aerobes compared to 1.5 per sample for the anaerobes. Streptococcus sanguis was the predominant aerobic species (23.6%) isolated from 29 (72.5%) of the 40 patients, followed by Streptococcus mitis, 19.5 and 60%, Streptococcus salivarius, 17.1 and 52.5% and Streptococcus mutans, 17.1 and 52.5%. The frequency of isolation of anaerobic bacteria was Prevotella spp. 50% from 30 (75%) of the 40 patients, Fusobacterium spp., 18.3 and 27.5%, Bacteroides spp., Porphyromonas spp. and Peptostreptococcus spp., 6.7 and 10%, 6.7 and 10%, and 5 and 7.5%, respectively. Prevotella intermedia was the single most common species. CONCLUSION: The results show that there were more aerobic/facultative anaerobic bacteria than the obligate anaerobes in the dental plaque of the pediatric dental patients in Kuwait. The high prevalence of the pioneering streptococci as well as black-pigmented Prevotella spp. and Fusobacterium spp. indicates that the dental plaques of the children were in the developing stage, a precursor to the development of periodontal diseases.

Variation in mitogenic response of cardiac and pulmonary fibroblasts to cerium.

Fibroproliferative response of rat heart and lung fibroblasts to the lanthanide cerium was examined, as the element has been implicated in the causation of cardiac and pulmonary fibrosis. Fibroblasts from both of the organs were morphologically identical, and the response to fetal bovine serum, a nonspecific mitogen, was also comparable. The oxygen radical generator (hypoxanthine + xanthine oxidase [Hyp. + XO]) induced a proliferative response that was neutralized in both cardiac and lung fibroblasts by free-radical scavengers. Superoxide dismutase was more effective than catalase in reducing the mitogenic effect of Hyp. + XO. The free-radical scavenger N-acetyl-L-cysteine neutralized the free-radical-mediated changes in pulmonary fibroblasts but had a negative effect in cardiac fibroblasts, indicating a tissue-dependent variation. Reactive oxygen species are known to act as biological mediators of tissue fibrosis induced by metallic compounds. Exposure to low levels of cerium (0.5 microM) stimulated a mitogenic response in cardiac fibroblasts, but the pulmonary fibroblasts were not sensitized by the element. Tissue-dependent variation in proliferative response to cerium shows a positive association with intracellular generation of reactive oxygen species. Fibrotic changes in cerium pneumoconiosis may either be replacement fibrosis following tissue damage or mediated by nonfibroblastic cells. The study confirms that cardiac and pulmonary fibroblasts are dissimilar cellular subtypes.

Superoxide anions mediate proliferative response in cardiac fibroblasts.

The study was undertaken to examine whether superoxide anions mediate a proliferative response in cardiac fibroblasts. Cardiac fibroblasts isolated from newborn Wistar rats were exposed to superoxide anion generating system (hypoxanthine + xanthine oxidase) and its effect on cell growth was assessed. A stimulatory response on fibroblast proliferation was observed. The proportion of proliferating cells increased within 3 h of treatment compared to the control and the cell density after 96 h of exposure remained significantly high (P < 0.0005). Inclusion of antioxidants neutralised the stimulatory response, fortifying the role of superoxide anions in cell proliferation. This observation indicates that superoxide anions can mediate a fibrotic reaction in the cardiac tissue.

Stimulation of cardiac fibroblast proliferation by cerium: a superoxide anion-mediated response.

UNLABELLED: Cardiac fibroblasts play a multifarious role in the maintenance of the functional and structural integrity of the heart. Therefore inadvertent proliferation of these fibroblasts can affect the normal functioning of the heart. The proliferation of fibroblasts could be due to various factors. We have worked on the hypothesis that low levels of cerium may stimulate cardiac fibroblasts to undergo proliferation and that free radicals act as the mediators of the stimulatory response. Cardiac fibroblasts isolated from neonatal Wistar rats were cultured. Proliferation of the cells was measured by cell count and immunohistochemical visualization for proliferating cell nuclear antigen. The response to cerium was assessed by comparison with control. A stimulatory response at low levels of cerium was observed with a peak at 0.5 micrometer concentration of cerium. A concomitant increase in the generation of free radicals was also seen. The cerium-stimulated cell proliferation and free radical generation was neutralized by the inclusion of superoxide dismutase in the culture medium. CONCLUSION: Low doses of cerium, at levels comparable to those found in the serum of patients with EMF, has a stimulatory effect on cardiac fibroblasts and the abrogation of proliferation by antioxidant superoxide dismutase indicates that superoxide anion acts as a biological intermediate in cerium-induced cardiac fibroblast proliferation.