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acid reflux

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Source
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Post by Source »

halitosisux wrote:Ruch, I have never been h.pylori positive.
What made my BB reduce by about 99% was the extraction of 1 of my wisdom teeth.
I still get slight odour at the back of the tongue when things stagnate for a long time, but I've got that under control too, by brushing my tongue with Oral-B ProEnamel toothpaste which contains zinc lactate, followed by 60 seconds gargling with chlorhexidine gluconate.

The idea for using zinc lactate/chlorhexidine gluconate combination came from the basis of CB12 mouthwash which uses zinc acetate/chlorhexidine diacetate.

That remaining odour I have is either perfectly normal, or it's due to my PND, or it's due to my 1 last remaining impacted wisdom tooth, or it's due to other unknown reasons.
How long have you been using Chlorhexidine mouthwash? I was told by a doctor not to use it for long periods of time because it will darken teeth.

But I guess BB relief is better than slightly discolored teeth.


halitosisux
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Post by halitosisux »

I don't allow it to come into contact with my teeth, so staining isn't a problem. I've used chlorhexidine in the past for long periods of time without any detrimental effects. Used correctly it's action is probably broader than any antibiotic/antifungal rinse.
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compor
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Post by compor »

Take a look at this study:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2359469/
An association between GERD and halitosis is biologically plausible for 3 reasons. First, it has been proposed that odor from the posterior tongue dorsum derives mainly from postnasal drip accumulating there.24 In GERD, acidic contents of the stomach can reach the nasopharynx and cause irritation of its walls, resulting in postnasal drip. Thus, postnasal drip and tongue coating may be mediators of the pathway between GERD and halitosis. Second, impaired lower esophageal sphincter function in subjects with GERD allows intestinal gas and stomach contents to reflux into the esophagus,10 which might produce malodor. Third, halitosis may be produced by direct acid-peptic injury to susceptible supraesophageal tissue.
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