Determination of pH turning point with pH mapping of the gastroesophageal junction: an alternative technique to orientate esophageal pH monitoring.

Manometric location of the lower esophageal sphincter (LES) has been mandatory before esophageal pH monitoring, despite costs and discomfort related with esophageal manometry. The aims of the study were: (i) to map the pH of the gastroesophageal junction (GEJ) to determine a pH turning point (PTP) and its relation with LES; and (ii) to test the feasibility of this technique to orientate esophageal pH monitoring. We studied 310 adult patients who underwent esophageal manometry and pH monitoring off acid-suppressive therapy. GEJ pH mapping was carried out by step-pulling the pH sensor from 5 cm below to 5 cm above LES, and a PTP was determined when pH changed from below to above 4, in centimeters from the nostril. Thirty-six patients referred only for pH monitoring were studied with pH sensor placed at 5 cm above the PTP. Out of 310 patients, a PTP was found in 293 (94.5%): inside LES in 86.3%, into the stomach in 8.2% and in the esophageal body in 5.5% of patients. The median distance between PTP and place where pH sensor monitored reflux was 8 cm. Among 36 patients who performed pH monitoring without LES manometry, there was no gastric monitoring during reflux testing. In adult patients investigated off acid suppressive therapy, GEJ pH mapping with reflux monitoring 5 cm above the PTP can be an alternative technique to perform esophageal pH monitoring when LES manometry is not available. Additional studies are needed before the widespread use of GEJ pH mapping in the clinical practice.

A single dose of zoledronic acid reverses the deleterious effects of glucocorticoids on titanium implant osseointegration.

UNLABELLED: This study evaluates the effect of zoledronic acid (ZOL) on the osseointegration of titanium implants in rabbits with glucocorticoid (GC)-induced bone loss, and our findings demonstrated that a single dose of ZOL is able to reverse the detrimental effects of GCs on the osseointegration of titanium implants. INTRODUCTION: The purpose of this study is to evaluate the effect of ZOL on the osseointegration of titanium implants in rabbits with GC-induced bone loss. METHODS: Three groups of six NZW rabbits were treated for 18 weeks with saline (SALINE), GC (methylprednisolone, 0.35 mg/kg three times a week), or GC + ZOL (methylprednisolone + single dose of ZOL, 0.1 mg/kg). The animals received a titanium implant in the left tibia after 6 weeks and were killed at the 18th week. Bone mineral density (BMD) was measured with dual-energy X-ray absorptiometry at baseline, eighth week (W8), and 18th week (W18) after treatment to determine the change upon treatment (BMD). Histomorphometric and serum bone alkaline phosphatase analysis (BAP) were also performed. RESULTS: At W8, GC group had a significant reduction in lumbar spine and tibia BMD compared with SALINE (p = 0.003 and p = 0.000), as also observed for GC + ZOL group (p = 0.014 and p = 0.003) just 2 weeks after ZOL treatment. In contrast, at W18, the GC + ZOL had an evident BMD rescue with similar lumbar spine and tibia BMD compared with SALINE (0.043 +/- 0.006 vs. 0.055 +/- 0.009 g/cm(2), p = 0.457 and 0.027 +/- 0.003 vs. 0.041 +/- 0.011 g/cm(2), p = 0.232) and a significantly higher BMD compared with the GC (p = 0.024 and p = 0.001). Histomorphometry revealed that osseointegration was significantly reduced in GC (tibia cortical thickness and diameter, bone-implant contact, total and peri-implant bone area) whereas GC + ZOL had these parameters similar to SALINE (p > 0.05). Likewise, ZOL reversed the BAP alteration induced by GC. CONCLUSIONS: Our findings demonstrated that a single dose of ZOL is able to reverse the detrimental effects of glucocorticoids on the osseointegration of titanium implants, suggesting that ZOL therapy may improve the outcome of bone implants in patients with glucocorticoid-induced osteoporosis.

Persistence of Helicobacter pylori in the oral cavity after systemic eradication therapy.

AIM: The present study aimed to evaluate if the oral cavity of chronic periodontitis patients can harbor Helicobacter pylori after systemic eradication therapy. MATERIALS AND METHODS: Samples of 30 patients (15 with gingivitis and 15 with chronic periodontitis) positive for H. pylori in the stomach were evaluated. Samples were collected 3 months after triple systemic antibiotic therapy from saliva, microbiota from the dorsum of the tongue, supra- and sub-gingival plaque as well as gastric biopsies. DNA of each sample was extracted by the boiling method and used as a template in polymerase chain reaction with the primers JW22/23. RESULTS: Eighteen patients (60%) harboured H. pylori in their mouths. Five patients (16.6%) were positive in saliva, two (6.6%) on the dorsum of the tongue, nine (30%) in supra-gingival plaque, 14 (46.6%) in sub-gingival plaque and three (10%) in the stomach. There was no statistically significant difference between study groups. CONCLUSION: Eradication of H. pylori after therapy was more effective for the stomach than for the mouth (p<0.001). Mouths of patients with gingivitis or with chronic periodontitis, who are positive for H. pylori in their stomachs, may be considered as reservoirs of these bacteria.

Prevalence of Helicobacter pylori detected by polymerase chain reaction in the oral cavity of periodontitis patients.

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.