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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was conducted to study chemically and serologically the characteristics of the Ureaplasmas isolated from the human oral cavity. Two hundred and fifty-one healthy and 12 periodontitis subjects were examined for the incidence of the isolation of Ureaplasmas from their oral cavity. A total of twenty-six strains was isolated from the healthy human saliva. But no strains could be isolated from a variety of clinical specimens obtained from the patients. The serological properties of the isolates were tested by the method of metabolism inhibition test (MI test). Seven out of 26 isolates were serologically identical with either one of the ATCC standard strains. However, the serological types of the other strains could not be demonstrated by the MI test. The biological characteristics of 4 isolates and ATCC strains were tested by the usual method. The isolates did not metabolize glucose and arginine, while all strains hydrolyzed urea. On the other hand, none of the isolates lysed skimmed milk and gelatin. The proteolytic activity of the isolates could be demonstrated by using casein and horse serum proteins as substrates. Zymogram patterns from one of the isolates and Streptococcus salivarius were obtained by polyacrylamide gel electrophoresis of the cells lysed with digitonin or cell protein extracts. On the basis of the gel electrophoresis patterns, it is clear that the urease of the Ureaplasma is different from that of the Streptococcus salivarius.
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PMID:Biochemical and serological studies on oral ureaplasma. 659 16

The polymerase chain reaction was used for the detection of Helicobacter pylori from subgingival plaque in 336 periodontitis patients. A pair of primers derived from the H. pylori urease gene A served to amplify a targeted 411-bp fragment of genomic DNA. This technique permitted the detection of as few as 60 H. pylori cells. Paper point samples from 3 deep periodontal pockets per patient were immersed in 1 ml of phosphate-buffered saline or distilled water, DNA was solubilized by detergent/protease method, 3.7 microliters or 37 microliters of lysate supernatant was used as template, and the amplification product was analyzed in 1% agarose gel containing ethidium bromide. Each experiment included purified DNA and cell lysate of H. pylori as positive controls. The presence of bacteria in the sample was verified by a primer pair common to prokaryote 16S rRNA. The present study did not reveal the specific polymerase chain reaction amplification product characteristic of H. pylori. We conclude that periodontal pockets do not constitute a natural reservoir for H. pylori.
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PMID:Absence of Helicobacter pylori in subgingival samples determined by polymerase chain reaction. 780 77

The aim of study was the evaluation of periodontal pockets microflora in patients with advanced periodontitis. From each subject 16-20 samples were taken using paper points. Pooled sample after 60 s. mixing was serially diluted in reduced BHI. For total cell counts and for the isolation of black pigmented anaerobes Brucella agar supplemented with 5% sheep blood, hemin, menadione, with and without Kanamycin-Vancomycin mixture and BM agar plates were used. For isolation of A. actinomycetemcomitans TSBV agar plates were used. Cultures were incubated in anaerobic chamber at 37 degrees C for 7 days and TSBV agar plates in an atmosphere of 95% air-5% CO2 at 37 degrees C for 5 days. Microorganisms were identified by Gram staining, colony morphology, fluorescence in UV-light, haemagglutination of 3% sheep erythrocytes, fermentation of sugars, production of indole, urease (API 20A), specific enzymes (Rapid ID 32A). Twenty seven subjects with clinically recognized periodontitis were examined. Microorganisms important in periodontitis were isolated from periodontal pockets of almost all examined subjects. The number of bacteria obtained from the sample of one patient ranged from 1 x 10(4) CFU/ml to 3,6 x 10(6) CFU/ml. Porphyromonas gingivalis was identified in the samples taken from 17 patients, Prevotella intermedia-19, Actinobacillus actinomycetemcomitans -11, Fusobacterium nucleatum-9, Peptostreptococcus spp.-22.
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PMID:[Microflora of periodontal pockets in advanced periodontitis]. 941 Oct 79

Helicobacter pylori is an important gastrointestinal pathogen associated with gastritis, peptic ulcers, and an increased risk of gastric carcinoma. The oral cavity has been indicated as a possible H. pylori reservoir, and may therefore be involved in the reinfection of the stomach which sometimes follows treatment of H. pylori infection. The objective of the present study was to evaluate the prevalence of H. pylori as detected by polymerase chain reaction (PCR) in the oral cavity of periodontitis patients testing positive for this bacterium in the stomach. Thirty adult patients with alterations of the superior digestive tract, testing urease positive after endoscopy and biopsy, were selected. A full-mouth periodontal examination was performed in every patient and the subjects were allocated to two groups: gingivitis (15 patients) and chronic periodontitis (15 patients). Plaque and saliva samples collected from each patient were stored in 0.5 ml of TE buffer. DNA was extracted from the samples by the boiling method and was evaluated for the presence of H. pylori using the PCR method. JW 22/23 primers were used. The DNA of ATCC H. pylori 43629 (positive control) and water (negative control) were used for controlling the reactions. Of the 30 evaluated patients, 13 (43.3%) harbored H. pylori in the mouth. The bacterium was not found on the dorsum of the tongue of any patient, but was found in saliva in three patients (10%), in the supragingival plaque in six patients (20%), and in the subgingival plaque in eight patients (26.6%). The presence of H. pylori was similar in the gingivitis and chronic periodontitis groups. In conclusion, a high percentage of patients harbored H. pylori in their mouth. The bacterium was detected in saliva, supragingival and subgingival plaque, suggesting that these sites may be considered reservoirs for H. pylori in urease-positive patients.
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PMID:Prevalence of Helicobacter pylori detected by polymerase chain reaction in the oral cavity of periodontitis patients. 1521

As introduced by different studies, dental plaque is known as a reservoir of Helicobacter Pylori (HP) and a potential source for gastric re-infection. Also, it has been demonstrated that individuals with gastric HP infection manifest a greater plaque index and a higher incidence rate for gingivitis. The goal of the present research was survey of severity and prevalence of periodontal diseases associated with gastric HP infection among patients having referred to the endoscopy wards of Imam Khomeini and Milad hospitals. In this research, 122 patients with gastric HP infection were investigated for determining 4 indices: plaque index (PI), gingival index (GI), clinical attachment loss (CAL) and pocket depth (PD), for all existing teeth, using RUT (rapid urease test). The results indicated that about 86.9% of patients had developed gingivitis of various degrees and 100% of them were afflicted with periodontitis of different degrees, and about 64.8% of patients showed a weak PI, and 61.5% had a low level of education. This low-level education seen in majority of the studied subjects, addresses a high degree of importance and influence of the oral hygiene in gastric HP infections. Hence, gastroentrologists are required to refer patients to dentists in line of preserving oral and dental health.
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PMID:Correlation between oral hygiene and Helicobacter pylori infection. 2113 68

Recent advances in molecular biology have facilitated analyses of the oral microbiome ("Who are they?"); however, its functions (e.g., metabolic activities) are poorly understood ("What are they doing?"). This review aims to summarize our current understanding of the metabolism of the oral microbiome. Saccharolytic bacteria-including Streptococcus, Actinomyces, and Lactobacillus species-degrade carbohydrates into organic acids via the Embden-Meyerhof-Parnas pathway and several of its branch pathways, resulting in dental caries, while alkalization and acid neutralization via the arginine deiminase system, urease, and so on, counteract acidification. Proteolytic/amino acid-degrading bacteria, including Prevotella and Porphyromonas species, break down proteins and peptides into amino acids and degrade them further via specific pathways to produce short-chain fatty acids, ammonia, sulfur compounds, and indole/skatole, which act as virulent and modifying factors in periodontitis and oral malodor. Furthermore, it is suggested that ethanol-derived acetaldehyde can cause oral cancer, while nitrate-derived nitrite can aid caries prevention and systemic health. Microbial metabolic activity is influenced by the oral environment; however, it can also modify the oral environment, enhance the pathogenicity of bacteria, and induce microbial selection to create more pathogenic microbiome. Taking a metabolomic approach to analyzing the oral microbiome is crucial to improving our understanding of the functions of the oral microbiome.
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PMID:Oral Microbiome Metabolism: From "Who Are They?" to "What Are They Doing?". 2637 70