Correlation between gingival phenotype and Schneiderian membrane thickness.

PURPOSE: The most common complication during sinus graft surgery is tearing or perforation of the Schneiderian membrane. Perforations are most likely to occur if the sinus membrane is thin. Preoperative prediction of the antral membrane thickness may be of practical importance during maxillary sinus augmentation procedures. The purpose of this investigation was to analyze a possible association between gingival phenotypes and thickness of the healthy sinus mucosa. MATERIALS AND METHODS: Twenty consecutive patients without preoperative anamnestic, clinical, or radiologic signs of maxillary sinus pathologies were enrolled in the study. During otorhinolaringologic surgical interventions, maxillary mucosal biopsy specimens were endoscopically obtained from the sinus floor, and gingival thickness was measured at the maxillary anterior teeth. RESULTS: Eleven out of 20 individuals had thick gingival tissues, and the remaining 9 presented with thin gingival phenotype. The average thickness of the Schneiderian membrane was 0.97 +/- 0.36 mm with a wide inter-individual variability. Thickness of the sinus mucosa amounted to 1.26 +/- 0.14 mm in individuals with thick gingival architecture and 0.61 +/- 0.15 mm in subjects with thin gingival tissues. The association between thickness of the antral mucosa and periodontal phenotypes was statistically significant (P < .0001). CONCLUSIONS: Gingival thickness seems to represent a reliable parameter to predict sinus membrane thickness. Further investigations are needed to support these preliminary data.

Effect of Helicobacter pylori eradication on bulbitis and duodenal gastric metaplasia.

BACKGROUND/AIMS: Duodenal gastric metaplasia seems to be linked to infection by Helicobacter pylori, to the extent of acid secretion and to bulbitis. An investigation was made of the relationship between bulbitis and duodenal gastric metaplasia, or whether bulbitis can arise along with duodenal gastric metaplasia after Helicobacter pylori eradication in an average of six years. METHODOLOGY: We compared 22 patients with duodenal ulcers [male/female 16/6; (mean age+/-SD) 55+/-12 years] Helicobacter pylori-negative after eradication, with 23 Helicobacter pylori-positive patients free from active duodenal ulcers [male/female 17/6; (mean age+/-SD) 59+/-12 years]. RESULTS: The bulbitis score was found to be lower in the Helicobacter pylori-negative than in the Helicobacter pylori-positive group (p=0.02). The duodenal gastric metaplasia score in the Helicobacter pylori-negative was higher than in the Helicobacter pylori-positive group (p=0.001). We failed to find any relationship between the presence of bulbitis and duodenal gastric metaplasia. We found a non-significant inverse correlation between the presence of duodenal gastric metaplasia and chronic body gastritis (p=0.07). CONCLUSIONS: Bulbitis and duodenal gastric metaplasia may depend on different causal factors not related to Helicobacter pylori infection. The extension of duodenal gastric metaplasia with time following recovery from peptic ulcer disease may represent a mucosal protection factor against acid.