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yep..gets more interesting when your pandas kid has episodes of picking at gums and you can't figure out if it is OCD related or infection related...and then you start to study gum disease and the immune system. The immune response to trauma to the mouth produces a much higher rate of cytokines, which cause inflamation, than anywhere else in the body. Of course your mouth is in your head, near your brain, which I don't think helps. We still don't know if DS picks his gums because of pandas, and that infected them, or if they were infected and he therefore picked at them. There are also studies of gum infection - where stress will trigger an episode of inflamation...so who knows.


I think between the autoimmune reaction that gum trauma causes, the fact that strep is present (and probably spurring the autoimune reaction), and that escessive cykotines are released all in proximity to your brain and BBB you;ve got a triple threat with pandas kids- oh and did I over look that neutrophils are critical have to fight it off? If your child is low on neutrophils, is much, much harder to get rid of the bacterial infection in the mouth. (or even balance the bacteria that is always present).


When I looked back as DS's neutrophil counts - he was at 40 (I think that was the number) and the normal range was 40-100 (or something like that - point is once it was on the line, and the other time is was 42, only 2 points into the normal range).


It makes perfect sense to me that gum disease is related to heart health.


Here is and excerpt from one of a number of papers on this - http://www.bio.davidson.edu/courses/immunology/students/spring2000/wright/restricted/paper.html


The Immune Response


Although periodontal disease is caused by bacterial infection, the resulting tissue damage is due to the immune response (Yamazaki).


The first response triggered by bacterial infection is the innate immune response. Bacteria are taken up by macrophages, causing the macrophage to release cytokines. The cytokines cause the inflammation associated with periodontal disease. Cytokines cause the blood vessels to dilate and become permeable, leading to increased local blood flow, thus causing inflammation. The inflammation attracts neutrophils and more macrophages (Janeway). Studies have shown that polymorphonuclear neutrophils (PMN) are the most abundant immune cells found in areas of periodontal disease. Interleukin-8 (IL-8) is a chemoattractant for neutrophils, therefore it is logical that increased levels of IL-8 are found in gingival cells. PMN acts as an autoamplifier by secreting IL-8 and it also releases an oxidative burst of H2O2. The increase PMN and IL-8 are likely contributors to the inflammatory response (Gainet).


The adaptive immune response is initiated by dendritic cells which act as antigen presenting cells (APC) to stimulate naive T cells. Porphyromonas gingivalis, one of the many bacteria involved in periodontal disease, is able to sensitize and activate dendritic cells (Cutler). Once dendritic cells are activated and presenting bacterial peptide, they travel to the nearest lymph node in order to activate T cells. A major source of bone loss has been attributed to the presence of CD4(+) T cells and the cytokines they secrete (Baker). Th2 cells are the predominant form of T cell in cases of adult periodontitis (Sigusch). Th2 cells are known to activate B cells to secrete antibodies. The epithelial cells of patients with periodontitis contain high levels of IgA and IgG, while IgM is found in deeper tissues (Kinane). The antibodies are able to aid in the fight of infection through neutralization, opsonization, and/or complement activation (Janeway). The latter two scenarios utilize the abundance of neutrophils and macrophages in order to phagocytize the bacteria.


The bacteria that cause periodontal disease have adapted in a couple of different ways to increase their effectiveness. The first adaptation is displayed by Porphyromonas gingivalis; they cause apoptosis of lymphocytes, thereby increasing the spread of infection and leading to greater pathogenesis (Geatch). The second adaptation by periodontal causing bacteria is the production of superantigens (Zadeh). Superantigens are able to activate a large subset of T cells by binding to MHC class II molecules and V beta domains on the T cell receptor (Janeway).


Research has been conducted that associates periodontal disease with cardiovascular disease, premature births, and other problems. One possibility for this association is an inflammatory response trait which would make an individual susceptible to developing both periodontal disease and atherosclerosis (Beck). Another possibility is that the cytokines (especially TxA2, IL-1 beta, PGE2, and TNF-alpha) and other inflammatory mediators produced during periodontal disease could reach levels where they begin affecting the cardiovascular system and/or placental tissues. Finally, the mouth may serve as a "bacterial reservoir" for the lungs, possibly resulting in bacterial pneumonia (DeBowes). Research is currently being done to further substantiate the afformentioned associations.

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