In a standard periodontal treatment strategy with consecutive root planings (per quadrant at a one- to two-week interval), re-infection of a disinfected area might occur before completion of the treatment. This study examines, both clinically and microbiologically, whether a full-mouth disinfection within 24 hours significantly improves the outcome of periodontal treatment. Ten patients with advanced chronic periodontitis were randomly allocated to a test and a control group. The patients from the control group received scalings and root planings as well as oral hygiene instructions per quadrant at two-week intervals. Full-mouth disinfection in the test group was sought by the removal of all plaque and calculus (in two visits within 24 hours). In addition, at each of these visits, the tongue was brushed with a 1% chlorhexidine gel for one min and the mouth rinsed with a 0.2% chlorhexidine solution for two min. Furthermore, subgingival chlorhexidine (1%) irrigation was performed in all pockets. The recolonization of the pockets was retarded by oral hygiene and 0.2% chlorhexidine rinses during two weeks. The clinical parameters were recorded, and plaque samples were taken from the right upper quadrant at baseline and after one and two months. The test group patients showed a significantly higher reduction in probing depth for deep pockets at both follow-up visits (p < 0.05). At the one-month visit, differential phase-contrast microscopy revealed significantly lower proportions of spirochetes and motile rods in the test group (p = 0.01). Culturing showed that the test group harbored significantly fewer pathogenic organisms at one month (p = 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
This study examined in vitro the existence of microbial leakage along the components of the Brånemark implant system. Thirty-two implant/abutment assemblies were installed in a liquid blood medium previously inoculated with oral micro-organisms. To examine the leakage at the implant-abutment interface, 16 assemblies were partially immersed. The remaining 16 were completely immersed to observe the leakage at both the implant-abutment and abutment-prosthesis interface. After 7 days of anaerobic incubation, the micro-organisms in the internal part of the implants were collected and incubated on blood agar plates in anaerobic conditions. Micro-organisms were found in the completely immersed assemblies and at lower numbers in the partially immersed implants, indicating that bacterial leakage at both levels seems to exist. Several penetrating bacteria have been associated with peri-implantitis. The clinical importance of this bacterial leakage is not yet well understood. Although the longevity of the Brånemark implants is well documented, this bacterial leakage might play a role in peri-implantitis, both in the etiology as well as in the treatment.
SUMMARY Samples of serum, bile, and urine were collected simultaneously from patients with cholestasis of varying aetiology and from patients with cirrhosis; their bile acid composition was determined by gas/liquid chromatography and mass spectrometry In cholestasis, the patterns in all three body fluids differed consistently and strikingly. In serum, cholic acid was the major bile acid and most bile acids (> 93 %) were unsulphated, whereas, in urine, chenodeoxycholic was the major bile acid, and the majority of bile acids (> 60 %) were sulphated. Secondary bile acids were virtually absent in bile, serum, and urine. The total amount of bile acids excreted for 24 hours correlated highly with the concentration of serum bile acids; in patients with complete obstruction, urinary excretion averaged 71 6 mg/24 h. In cirrhotic patients, serum bile acids were less raised, and chenodeoxycholic acid was the predominant acid. In healthy controls, serum bile acids were consistently richer in chenodeoxycholic acid than biliary bile acids, and no bile acids were present in urine. No unusual monohydroxy bile acids were present in patients with primary biliary cirrhosis, but, in several patients, there was a considerable amount of hyocholic acid present in the urinary bile acids. The analyses of individual bile acids in serum and urine did not appear to provide helpful information in the differential diagnosis of cholestasis. Thus, in cholestasis, conjugation of chenodeoxycholic acid with sulphate becomes a major biochemical pathway, urine becomes a major route of bile acid excretion, and abnormal bile acids are formed.
In adult germfree C3H mice immunized with horse spleen ferritin, either subcutaneously or intraperitoneally, plasma cells containing specific antibodies were found in lymph nodes and spleen and, in smaller numbers, also in the lamina propria of the intestine. In extraintestinal sites, these antiferritin-containing plasma cells were mainly of the IgM class after a single stimulation, and of the IgG1 class after repeated stimulation. In the intestine, all the anti-ferritin-containing cells appeared to be of the IgA class. Circulating antibodies, after repeated stimulation, were for the major part IgG1 and IgG2.
In germfree mice given ferritin in their drinking water, antiferritin-containing cells were abundant in the intestinal mucosa, much less numerous in the mesenteric lymph nodes, and extremely scarce in other lymphoid tissues. All these cells, whatever their location, appeared to belong exclusively to the IgA class. Similarly, all the circulating antibody in these animals was found to be IgA.
These findings illustrate the role of the gut as a site of antibody synthesis, as well as its selective commitment to the production of antibodies of the IgA class.
The oxidation of pristanic and phytanic acids by human skin fibroblasts was compared to that of their synthetic analogues, 2-methylpalmitic and 3-methylmargaric acids. The synthetic compounds and natural substrates were degraded at comparable rates in control and X-linked adrenoleukodystrophy fibroblasts. The alpha-decarboxylation of 3-methylmargaric acid, similarly to that of phytanic acid, was affected in Refsum disease and Zellweger syndrome, but not in X-linked adrenoleukodystrophy. The beta-oxidation of 2-methylpalmitic acid, similarly to that of pristanic acid, was deficient in fibroblasts derived from patients suffering from Zellweger syndrome, confirming the importance of peroxisomes in the breakdown of 2-methyl-branched fatty acids. No deficiency was observed in fibroblasts from X-linked adrenoleukodystrophy patients. The 1-14C-labelled 2- and 3-methyl-branched fatty acids, which are easier to synthesize that the natural analogues, are therefore valuable tools for the diagnosis of human peroxisomal disorders.
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