• Journal of Dental Anesthesia and Pain Medicine
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• v.16 no.1
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• pp.17-24
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• 2016

Background: To evaluate the antimicrobial activity of lidocaine (LD) topical anesthetic spray against oral microflora. Methods: Antimicrobial effects of 10% LD spray were assessed against six bacterial cultures obtained from volunteers: Escherichia coli, Enterococcus faecalis, Staphylococcus aureus, Streptococcus salivarius, Streptococcus pyogenes, and Streptococcus sanguinis. The filter papers contained $50-{\mu}l$ LD, brain heart infusion (BHI) broth, or 0.2% chlorhexidine. Papers were placed on the cultured blood plates for 1-3 min. After the papers were removed, plates were incubated for 24 h. Bacterial growth on the contact areas was recorded as the antimicrobial score. The split mouth technique was use in for sample collection in clinical study. Filter papers soaked with either BHI broth or LD were placed on the right or left buccal mucosa for 1 min, and replaced with other papers to imprint biofilms onto the contact areas. Papers were placed on blood plates, incubated for 24 h, and antimicrobial scores were determined. Experiments were conducted for 2- and 3-min exposure times with a 1-day washout period. Results: LD exhibited bactericidal effects against E. coli, S. sanguinis, and S. salivarius within 1 min but displayed no effect against S. aureus, E. faecalis, and S. pyogenes. The antimicrobial effect of LD on oral microflora depended upon exposure time, similar to the results obtained from the clinical study (P < 0.05). LD showed 60-95% biofilm reduction on buccal mucosa. Conclusions: Antimicrobial activity of 10% LD topical anesthetic spray was increased by exposure time. The 3 min application reduced oral microflora in the buccal mucosa.

• Journal of Oral Medicine and Pain
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• v.37 no.2
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• pp.75-79
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• 2012

Helicobacter pylori(H. pylori) associated with gastritis and gastric cancer is mainly detected dental plaque and saliva in the oral cavity. Most infection is probably acquired in childhood, but the route of transmission is not clear. The oral cavity has been indicated as secondary reservoir of H. pylori, and may therefore be argued in the route of transmission and reinfection of the stomach which follows treatment of H. pylori infection. So this review aimed to discuss about H. pylori in the oral cavity. H. pylori in stomach can appear in the oral cavity by gastroesophageal reflex or vomiting, but infection of stomach and oral cavity is different. Diagnostic methods are serological method, urea breath test, PCR method, urease test, histologic method and so on. Nested PCR recommend for detection of H. pylori in saliva and dental plaque. H. pylori infection in the oral cavity appear variously and is no relation with dental diseases. The antimicrobial mouthrinse recommend in patients with periodontal diseases because of high detection rate fo H. pylori. Thus H. pylori may be considered as the normal oral microflora.

• Microbiology and Biotechnology Letters
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• v.32 no.2
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• pp.195-198
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• 2004

Molec-ular analysis was performed on the microflora found In the necrotic pulpal tissue collected from 5 infected root canals that were diagnosed as a periapical abscess. 16S rRNA coding gene (rDNA) library construction and sequencing were performed in order to identify the microflora, The 16S rDNA sequences from 278 clones were identified by a comparison with the database sequence in GenBank. Three phylum and 31 species, which were related to the oral microflora, were identified from the 3 samples (No. 87, 105, and 115). Dialister invisus (5.6％), Peptostreptococcus micron (18.3％), and Veillonella sp. (3.3％) were the organism present in all tee samples. Lac-tobacillusfementum (2.8％),Eubacterumsp./E. infirmum (6.7％), Shuttleworthiasatelles (3.9％), Psudorarnihacfer alactoiyticus (13.3％), Bulleidia moorei (2.8％), and Prevotella denticola (1.1％) were found in two samples. Two phylum and low species of environmental microflora were identified from 2 samples (No.95 and 101). The reason for this might be contamination of the samples with dental water. These results showed that molecular analysis could reveal more diverse microflora that are associated with endodontic infections than that revealed by conventional cultural methods. In addition, these results may of for the basic data to epidemiological studies related with endodontic infection.

• Journal of Oral Medicine and Pain
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• v.18 no.1
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• pp.73-82
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• 1993

To investigate the changes in aerobic and facultative anaerobic oral microflora during remission-induction chemotherapy in patients with acute myeloid leukemia, 10 consecutive patients were studied during a period of 28 days. One day before, during and after the induction therapy, patients were given 10% Betadine solution for mouthrinses after breakfast and kept from eating and drinking. After 3 hours, paraffin-stimulated whole saliva was obtained for 2 minutes and transported to the laboratory. The samples were dispersed and homogenized by use of vortex mixer for 20 seconds. From these samples 10-fold serial dilutions (from 10-1 through 10-3) were prepared. Each dilution of 0.1 ml was plated on duplicate set of one nonselective medium (Blood agar) and four selective media (Sabourauds dextrose agar, Mannitol salt agar, Mac-Conkey agar, SF medium ) using applicator woods. All agar plate were incubated at 37$^{\circ}C$ for 48 hours. The total number of microorganisms was calculated and the percentage distribution of the various microorganisms from each specimen was drawn. 1. The salivary flow rate decreased by 66%, going from 5.38 ml/2min to 1.81 ml/2min over two days during the chemotherapy. 2. The total number of microorganisms in saliva increased by 22%, going from 4.88$\times$105/ml to 6.00$\times$105/ml over two days during the chemotherapy. 3. The salivary flow rate and the total number of microorganisms in saliva were recovered within 28 days after the chemotherapy. 4. The quantitative alteration in oral Enterobacteria, Enterococci, Staphylococci, Cndida during the chemotherapy had no statistical significance. 5. In saliva of the patients with acute myeloid leukemia who ahd intraoral ulcer, Enterobacteria was quantitatively predominent. Our study suggests that chemotherapy-induced transient xerostomia may induce acute oral infection. Consequently, the use of saliva substitute, the removal of intraoral infection source and the consistent oral hygiene care seem to be required to avoid the transmission of potential pathogenes in this group of patients.

• Journal of Oral Medicine and Pain
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• v.25 no.4
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• pp.365-369
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• 2000

Oral mucositis or stomatitis produced by stomatotoxic chemotherapy and/or radiation therapy are painful, restrict oral intake and, importantly, act as sites of secondary infection and potals of entry for the endogenous oral microflora often leading to bacteremias or sepsis. A number of clinical observations and studies of animal model suggests a pathophysiological complexity in the development of mucositis. The condition appears to represent a sequential interaction of the oral mucosal cells and tissues, pro-inflammatory cytokines, and local environmental factors in the mouth. This article discussed and reviewed biological process of the mucositis and, the role of cytokines as initiators and amplifiers of the process. The recognition that the pathophysiology of mucositis is a multifactorial process has presented opportunities for intervention based upon biological attenuation.

• Journal of Oral Medicine and Pain
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• v.25 no.2
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• pp.153-158
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• 2000

This experiment was performed to investigate effects of boiled-water extract of artemisia on the important oral microflora, Staphylococcus aureus, Streptococcus mutans, and Candida albicans, and to examine the difference of antimicrobial effects according to concentration of extract. The bacteria was cultured in broth media containing 0.1%, 0.5%, 1.0% of artemisia extract, and sterile distilled water respectively. After harvesting the culture, the genomic DNA of each aliquot was extracted and DNA concentration was relatively compared by means of agarose gel electrophoresis. As a result, we found out that the boiled-water extract of artemisia had significant antimicrobial effects on Staphylococcus aureus, Streptococcus mutans, and Candida albicans and its antimicrobial effects was increased in proportion to its concentration.

• The Journal of the Korean dental association
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• v.22 no.9 s.184
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• pp.793-801
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• 1984

Though oral microgranisms were among the first to be observed by humans, the interest in oral microbiology lagged. When it became apparent that the oral microflora did influence systemic disease of the body, interest was aroused in the nature and kinds of the microgranisms. The risk of infection in dental procedures is due to the abundant flora of the mouth. This hazard can be reduced to some extent by the use of a local disinfectant. The present studies were undertaken to evaluate and compare the various disinfectants which are commonly used in clinics and hospitals. The results were as follows. 1. The bactericidal activity of the disinfectants mainly depends upon the kinds of the agents, not upon the kinds of the microorganisms. 2. In H₂O₂(3%), the bactericidal activity was greatly related to the contact time. So, at least 4 minitues of contract time was required to use it as an oral antiseptic. 3. In ethyl alcohol (70%), Pseudomonas aeruginosa and Streptococcus salivarius surived a little after 15 seconds of contact time, but, no other colony was discovered after more than 15 seconds of contact time in any kins of microorganisms. 4. Merthiolate (0.1%) showed low antibacterial activity, more in Gram-positive organisms and less in Gram-negative organisms. 5. Benzalkonium chloride (0.1%) and povidone-iodine (10%) showed the most excellent results, revealing no surviving organisms only after 14 seconds of contact time.

• Archives of Pharmacal Research
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• v.28 no.3
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• pp.325-329
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• 2005

The hepatoprotective activity of lactic acid bacteria (Lactobacillus brevis HY7401, Lactobacillus acidophilus CSG and Bifidobacterium longum HY8001), which inhibited $\beta$-glucuronidase productivity of intestinal microflora, on t-BHP- or CCl$_4$-induced hepatotoxicity of mice were evaluated. These oral administration of lactic acid bacteria lowered $\beta$-glucuronidase production of intestinal microflora as well as Escherichia coli HGU-3. When lactic acid bacteria at a dose of 0.5 or 2 g (wet weight)/kg was orally administered on CCl$_4$-induced liver injury in mice, these bacteria significantly inhibited the increase of plasma alanine transferase and aspartate transferase activities by $17-57\%$ and $57-66\%$ of the $CCI_4$ control group, respectively. These lactic acid bacteria also showed the potent hepatoprotective effect against t-BHP-induced liver injury in mice. The inhibitory effects of these lactic acid bacteria were more potent than that of dimethyl diphenyl bicarboxylate (DDB), which have been used as a commercial hepatoprotective agent. Among these lactic acid bacteria, L. acidophilus CSG exhibited the most potent hepatoprotective effect. Based on these findings, we insist that an inhibitor of $\beta$-glucuronidase production in intestine, such as lactic acid bacteria, may be hepatoprotective.

• Journal of Oral Medicine and Pain
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• v.34 no.1
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• pp.23-37
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• 2009

The antibacterial effect of phytoncide on Porphyromonas gingivalis, which is the main causative agent of periodontal disease and halitosis, has been reported. However, little is known about its effect on normal oral microflora. The present study was performed to observe the effect of phytoncide on oral normal microflora and the inhibitory effect of surviving resident oral bacteria on P. gingivalis. In this study, saliva from each of 20 healthy subjects was treated with 1% phytoncide from Japanese Hinoki (Chamaecyparis obtusa Sieb. et Zucc.). Surviving salivary bacteria were isolated on blood agar plates and identified by 16S rDNA sequencing. In order to select inhibitory isolates against P. gingivalis, the isolates from the phytoncide-treated saliva were cultured with P. gingivalis. The results were as follows: 1. In general, the number of bacteria in saliva from periodontally healthy subjects was decreased when the saliva was treated with 1% phytoncide. 2. The majority of the salivary bacteria surviving the treatment of phytoncide were S. thermophilus (53%). 3. Most of the surviving salivary bacteria (72.5%) inhibit the growth of P. gingivalis A7A1-28 and P. gingivalis W83 on blood agar plates. 4. Among the surviving S. thermophilus, 85.8% of them were observed to inhibit P. gingivalis strains and 75.8% of the surviving S. sanguinis were inhibitory. Taken together, oral resident bacteria surviving phytoncide, which has been shown to inhibit P. gingivalis, may exert an additional inhibitory activity against the periodontopathic bacterium. Therefore, phytoncide can be used for preventing and ceasing the progress of periodontal disease and halitosis, and thus is expect to promote oral health.

• International Journal of Oral Biology
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• v.39 no.1
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• pp.9-13
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• 2014

Streptococci are among the normal human microflora that populate the oral cavity. However, oral streptococci are known as a major causative agent for dental caries and bacterial endocarditis. Tetracycline is a broad-spectrum antibiotic that is used for oral infections but two mechanisms of tetracycline resistance in streptococci have been reported. The tet(K) and tet(L) genes in these bacteria are related to the active efflux of tetracycline, whereas tet(M) and tet(O) confer ribosomal protection from this antibiotic. It has been reported that the tetracycline resistance of streptococci is related mainly to the activity of tet(M) and tet(O). In our present study, we examined the prevalence of tet(M) and tet(O) in oral streptococci isolated from Korean dental plaques using PCR. One hundred and forty eight of 635 isolates (23.3%) were tetracycline resistant; 68 of these strains (46%) harbored tet(M) and 3 strains (2%) were positive for tet(O). However, tet(M) and tet(O) did not co-exist in any of the resistant strains. Seventy seven of the 148 tetracycline resistant strains (52%) were negative for both the tet(M) and tet(O) genes.