The interleukin-1 genotype as a severity factor in adult periodontal disease.

Although specific bacteria, dental plaque, and age are associated with periodontal disease, there are currently no reliable predictors of periodontitis severity. Studies in twins have suggested a genetic contribution to the pathogenesis of periodontitis, but previous attempts to identify genetic markers have been unsuccessful. The pro-inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF alpha) are key regulators of the host responses to microbial infection. IL-1 is also a major modulator of extracellular matrix catabolism and bone resorption. We report a specific genotype of the polymorphic IL-1 gene cluster that was associated with severity of periodontitis in non-smokers, and distinguished individuals with severe periodontitis from those with mild disease (odds ratio 18.9 for ages 40-60 years). Functionally, the specific periodontitis-associated IL-1 genotype comprises a variant in the IL-1B gene that is associated with high levels of IL-1 production. In smokers severe disease was not correlated with genotype. In this study, 86.0% of the severe periodontitis patients were accounted for by either smoking or the IL-1 genotype. This study demonstrates that specific genetic markers, that have been associated with increased IL-1 production, are a strong indicator of susceptibility to severe periodontitis in adults.

[Varices of the colon in the roentgenologic picture]. / Varixy tracníku v rentgenovém obraze.

The authors describe a double contrast X-ray picture of varicosities of the large intestine. In the literature so far irrigoscopic changes specific for varicosities were not described. The authors observed that the defect of the filling increased after Valsalva's manoeuvre. The authors consider this symptom specific for varicosities.

Primary sclerosing cholangitis. Light and electron microscopy of hepatic tissue in two cases.

In an 18 year-old woman presenting with an intra- and extrahepatic form of sclerosing cholangitis needle biopsy of the liver revealed, in addition to a conspicuous proliferation of biliary ductules and mild inflammatory infiltrations of the portal tract, piece-meal necroses and focal intralobular inflammatory changes. In the second case - a 49-year-old man - presenting with an extrahepatic location of stenoses there were infrequent proliferating biliary ductules in the enlarged fibrotic portal tracts. Ultrastructural investigations revealed in both patients adverse regressive changes in the epithelium of proliferating biliary ductules, seen as microvillous damage on the luminal surface, dilation of the endoplasmic reticulum and mitochondrial swelling; in the second patient there was, moreover, electrondense material in epithelial cytoplasm, probably corresponding to bile components. In the first patient predominated among ultrastructural changes increase of cytoskeletal filaments in some epithelia and pronounced reduplication of the basement membranes of small biliary ducts. These "cholestatic" modifications, expressed in different form in the two patients, were accompanied by dilatation and damage, sometimes total disappearance of microvilli of biliary canaliculi.