Friday, August 29, 2008
One thing surprised me in that OLP was referred to as a common condition. I had no idea. I guess everyone else who has it is close mouthed about it. (Pun intended.) I have a tendency to tell everyone, and anyone who will listen whatever the heck is going on with me, whether it is big old rotten gashes on the sides of my tongue, underneath and on top, or even the latest on my 19 year old cat. I have a very open Johari window Sometimes I wish it would close a bit. I'm sure some people don't want too much information!
Found another excellent article published in 2000, called The Bullous Desquamative Lesions of Oral Mucosa.
Monday, August 18, 2008
Patients with oral lichen planus (OLP) often relate the onset and aggravation of oral symptoms to increased levels of stress.
Under normal conditions, stress induces increased cortisol secretion that counteracts inflammatory reactions. The objective of the present study was to assess whether patients with OLP have an impaired capacity to elevate their cortisol concentrations as a response to stress. .....
......The OLP patients did not present with different stress scores when a psychometric test (MACL) was used. No statistically significant correlation between cortisol concentration and stress level was observed. Thus, no support for an impaired capacity of OLP patients to suppress an immune response through cortisol induction in conjunction with experimental stress was revealed.
Accepted for publication July 25, 2000
Friday, August 15, 2008
The other day while talking with the doctor about the return of symptoms after titering down to 40 mg of Prednisone, she asked if it could be candida or thrush. I didn't think so, because I had already had a ten day dosing of Diflucan along with the days I was taking 60 mg of Prednisone. When people are taking steroids it can lower a person's resistance to whatever fungoids that our bodies carry naturally. They don't ususally present problems if we are healthy, but if we are immune compromised then the fungal conditions can proliferate.
So, on the thought of fungal infections, I did a little visited Pubmed today. In the search engine I put, oropharyngeal AND candidiasis. Which brought up 739 returns. Um... Maybe if I have time... like a day when I am really, really sick in bed with my laptop and my brain still works, I will peruse them all.
One abstract in particular caught my eye, and there was a free article on it. The concept of it was how well does one rinse out their mouth after using an asthma spray/inhaler. This is important because those inhalers contain steroids, which as I mentioned above can cause fungoids to proliferate.
The article is entitled: Kinetic Analysis of Effects of Mouth Washing on Removal of Residues Following Inhalagion of Fluticasone Propionate Dry Powder
Since I also have asthma, I found this very interesting. I really probably am not one of those who rinse well after using my asthma medicine, and so have caused some of my own miseries sometimes. From now on I am going to be more careful!
For information on Mouth Thrush there is a much more layman friendly reading located here.
Saturday, August 9, 2008
Oh No! awakened her, without the memory of why the foreboding and despondency was coming through her in waves like nausea.
The mirror told it all. The dark circles. The sleep tangled hair. The frown frozen on her face. The dried salt rimming her eyes. Telltale signs. Had it been a long dream. It had been bad.
What was it? Seeming to be her mother? Looking back against time? Regretting and understanding the missed opportunities for cherishing the joy? Instead dying into the darkness? Perhaps.
The awakening to the sense of the glass is half full. Half full with a cesspool of dark liquid threatening to suck her into the burning acid of heartache. It tortures her soul. She clings to the side of the glass. The fragile glass, like herself, ready to crack under the weight of pressure.
The cup of tea, the piece of toast, the swallowing of pills. Nothing to detract from the sensations of the dream still enveloping her.
Hang on! Hang on! It will go away!
Wash a dish. Feed the cat. Pacing back and forth. Clean a cupboard. Keep distracted. It is like a persistent oily, ugly debt collector his foot well placed in the door. Hold him back! But, he has gained and now inside at the shoulder, leaning his face too close, breathing stale air.
No escape! A banana. Turn on the TV. Make some pudding. Clean off the counter. Put a banana in the pudding. Add some walnuts. Yes. Food will put it off. It used to do that so well. Like an alcoholic with the relief of a drink. But, no. Food doesn't do it anymore.
Throat squeezing. The eyes burn, forehead crinkled in pain. The cheeks begging for release of tears. The prayers ask for comfort. But, it does not work. So, it is another bad ride. Especially bad ride this time.
ScienceDaily (Aug. 8, 2008) — B cells, the source of damaging autoantibodies, have long been thought to depend upon T cells for their activation and were not considered important in the initiation of autoimmune diseases like lupus or rheumatoid arthritis.
In the Aug. 7 online issue of the journal of Immunity, Yale University researchers turn this paradigm on its head by showing that in systemic autoimmune diseases B cells can be activated the absence of T cells.
The study suggests new ways to intervene in the immune system's chronic attacks on the body's own tissue.
The findings were surprising because many scientists believed that B cells remain quiet in autoimmune diseases unless they are stimulated first by T cells, said Mark Shlomchik, MD, professor of laboratory medicine and immunobiology at the Yale School of Medicine and senior author of the study.
"It became a chicken or egg problem. If cooperation between T and B cells is needed to create an autoimmune disease, who falls off the fence first, and why?'' Shlomchik said.
Recently this same Yale group along with collaborators at Boston University discovered an unexpected role in autoimmunity of Toll-like receptors, previously thought to be stimulated by molecules expressed on microbial pathogens. Shlomchik and his colleagues showed that they can also recognize and react to "self" molecules, in particular mammalian DNA and RNA. When this occurs, these receptors help activate B cells that make the classical autoantibodies of lupus.
The new Yale study now shows that these signals substitute for T cells in starting the autoimmune process in B cells. The researchers propose that once B cells are activated via Toll-like receptors, they can subsequently recruit T cells and that this can lead to a "vicious cycle" of chronic autoimmune disease in which the two types of cell activate each other.
The findings might explain why treatments that target T cells in autoimmune diseases have fared relatively poorly, while newer treatments aimed at B cells have shown great promise, he said.
The current study is a direct outgrowth of groundbreaking work conducted at Yale over the last 15 years that showed that elements of the innate, or non-specific immune system such as Toll-like receptors, needed to be triggered before more sophisticated adaptive immune system of humans and other animals could hone in on specific pathogens.
Other authors on the paper are Robin A. Herlands, Sean R. Christensen, Rebecca A. Sweet and Uri Hershberg.
The research was funded by the NIH Institutes of Arthritis and Musculoskeletal and Skin Diseases and of Allergy and Infectious Diseases.
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