Structural aspects of degenerative disease of the temporomandibular articulation

The authors, after having considered some structural aspects of the temporomandibular joint, examine the histologic features of the degenerative disease (arthrosis, remodelling, deviation in form)

Gastric atrophy and intestinal metaplasia changes 8 years after Helicobacter pylori eradication. A blind, randomised study.

BACKGROUND: Chronic atrophic gastritis and intestinal metaplasia are regarded as predisposing factors for gastric cancer associated with Helicobacter pylori infection, and their severity appears to influence gastric cancer risk. Our purpose was to determine the outcome of chronic gastritis after H. pylori eradication in a long-term follow-up. METHODS: Fifty-four consecutive patients with duodenal ulcer and H. pylori infection were enrolled in the study. Endoscopic examination with antral and corporal biopsy was done at baseline and yearly after conventional eradication therapy (omeprazole 40 mg b.i.d., amoxocyllin 1 g b.i.d and clarithromycin 500 mg b.i.d.). Gastritis, atrophy, and metaplasia were graded according to the updated Sydney System. RESULTS: Twenty-four patients were successfully treated; infection persisted in 14 and 16 dropped out (during the first 5 years of follow-up). Inflammation and mean neutrophil activity significantly decreased in patients in whom H. pylori was eradicated. Glandular atrophy improved in 2 and disappeared in 5/17 patients, whereas intestinal metaplasia improved in 3 and disappeared in 2/12. In the patients in whom H. pylori persisted, inflammatory infiltrate, atrophy and intestinal metaplasia had not significantly decreased during follow-up. In contrast, glandular atrophy worsened in 2 and developed in 5/7 patients. Similarly, intestinal metaplasia did not improve when present and developed in 5/13 cases. CONCLUSIONS: In a long-term follow-up, H. pylori eradication does not affect glandular atrophy, but it seems to prevent the development of precancerous lesions such as intestinal metaplasia

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