Posted on 08/26/2011 1:12:38 PM PDT by Swordmaker
Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria.
Judith Miklossy
Correspondence: Judith Miklossy judithmiklossy@bluewin.ch
Journal of Neuroinflammation 2011, 8:90 doi:10.1186/1742-2094-8-90
Published: 4 August 2011
Abstract (provisional)
It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis. Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum, could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (AD). Here, we review all data available in the literature on the detection of spirochetes in AD and critically analyze the association and causal relationship between spirochetes and AD following established criteria of Koch and Hill. The results show a statistically significant association between spirochetes and AD (P = 1.5 x 10-17, OR = 20, 95% CI = 8-60, N = 247). When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of AD cases. Borrelia burgdorferi was detected in the brain in 25.3% of AD cases analyzed and was 13 times more frequent in AD compared to controls. Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi were detected using species specific PCR and antibodies. Importantly, co-infection with several spirochetes occurs in AD. The pathological and biological hallmarks of AD were reproduced in vitro. The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and AD. Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of AD a comprehensive entity. As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Support and attention should be given to this field of AD research. Spirochetal infection occurs years or decades before the manifestation of dementia. As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
That's one of our videos.
"Lyme DiseaseLyme disease is caused by the bacterium Borrelia burgdorferi and is transmitted to humans through the bite of infected blacklegged ticks. Typical symptoms include fever, headache, fatigue, and a characteristic skin rash called erythema migrans. If left untreated, infection can spread to joints, the heart, and the nervous system. Lyme disease is diagnosed based on symptoms, physical findings (e.g., rash), and the possibility of exposure to infected ticks; laboratory testing is helpful if used correctly and performed with validated methods. Most cases of Lyme disease can be treated successfully with a few weeks of antibiotics. Steps to prevent Lyme disease include using insect repellent, removing ticks promptly, applying pesticides, and reducing tick habitat. The ticks that transmit Lyme disease can occasionally transmit other tickborne diseases as well.
They just don’t want it to be true.
Sad, but that what it has all come to.
The idea of preventing and curing disease, rather than treating it fecklessly for decades, is alien to Allopathy.
And now we even have the idea offered up that a “Syndrome” can cause disease.
>> “The other interesting fact that my research on longevity showed that tribes in Peru I believe that were reported to live beyond 100 YO all lost their teeth around age 25” <<
.
My father, who lived 90 years, lost all of his teeth at 30, to pyorrhea.
You picked bad ancestors? It's possible to have weak dentin, bad enamel, poor gums, bad bone that holds the teeth, all due to genetic factors while still having excellent oral hygiene. It's just the luck of the draw of DNA. We've seen some people come in with horrible dental hygiene with NO bugs at all... they don't brush, they don't floss... but beautiful teeth! You want to shoot them! ;^)>
An upper jaw abscess is nothing to fool around with, editor-surveyor. The nasty bugs that are out there that are immune to the ordinary antibiotics can get you into big trouble these days. I had one, I know. I had a tooth that started, out of the blue, hurting and it was loose. My dentist thought it was nothing serious... but when he got into it, discovered a 50¢ diameter abscess above it below my right eye! The abscess did not show up on the x-ray as it was filled with tissue with the same radio-density as bone... but was putrefying. He cleaned me out, sent the tissue for biopsy—not cancerous—thank God!—and let me heal for six months before building me an implant. However, the cyst that had formed went all the way into my sinus cavity and I could literally breath through the hole in my gum for over a month!
Had it gone any longer, I would have lost the sight in my left eye...
My doctor had one patient about 15 years ago who did not come in soon enough. The pain was excruciating, but he was a "man," and he could "take it." When he finally did come it, it was too late. The infection had gone from his tooth, into his right eye, through the optic nerve into his brain. My dentist sent him from our office by ambulance to the emergency room. He was airlifted by helicopter to UC Davis Med Center for brain surgery. He was dead in a week.
We had one this week that thought it was an abscess. It wasn't. Cancer. Bad one. Young guy, too.
I understand that there is the possibility that infection could remain in the tooth root, but I am very confident that the infection in the soft tissue is clear.
The swelling and the pain were relieved within about two hours after treatment with the TENS. The gum is also very tight. I will take your advice to heart though, and watch it carefully. The tooth may yet go for an implant when the zirconium implants become available.
The crowns that go on the implant are already available. The implant is what goes into the bone of the jaw. You want that to be made out of Vitalium: an alloy made of Cobalt Chromium and Molybdenum—not Titanium. The zirconium tooth is mounted on the implant. Where are you located?
Thanks, Swordmaker, for an interesting post!
The cobalt is not a problem?
Nor the Molybdenum?
What’s wrong with Titanium?
How long for the implant post process?
Have also long wondered . . . wouldn’t the implant posts have a more solid foundation if the bone were drilled maybe 3 smaller or 4 smaller holes around the eventual site but very close . . . allowed to heal etc.
Because I understand that healed bone as where a break occurs is a lot stronger than the normal bone. Seems to me that causing such a healed/scared bone before drilling the final implant hole into it would be stronger than just a hole in normal bone.
Then there’s the noise about implants loosening from lateral pressures.
No money to even fantasize really but would sure like to be able to have 4 posts for my lower dentures.
THANKS TONS FOR THIS.
HEALTH PING TO MY PING LISTS.
Am 63.
Have had all my teeth out for about a year to year and a half.
Would the protocol below be wise, for me? Do I need to get any test to check for such critters first or just go ahead with the protocol?
Thanks tons for your caring and redemptive post.
God’s best to you and yours for such helpful, life saving info. My mother died of Alzheimer’s.
Yes, because it is averaged into the studies to bring down the negative correlation, even though it SHOULD NOT be included, Miklossy continues to include it. Why? Because...
Oral spirochetosis is present in 30+% of patients with no AD. In order to make the correlation appear to be a causation, she averages studies with "all spirochetes" and with "all studies." Why? Because the actual causal inference for oral spirochetes is quite poor when 30+% of non-AD patients have them.
And it turns out it is just as I thought! They used an old technique called "dark field" microscopy, using old style, standard microscopes. It turns out, in fact, that you are mistaken. Reread your own citation. They used dark field microscopy and electron microscopy.
they did mention in their paper they had observed other spirochetes that "could correspond to oral Treponema," but weren't interested in them.
Again, wrong. Reread the citation. What is said is that in the ONE case observed, they may have observed Treponema. Miklossy attempts to cover her tracks by claiming they weren't looking for the "right" spirochetes, by mumbling some weasel words about it "not being clear..." that does not justify what you've written here, AND the original authors SAY NO SUCH THING.
Any re-infection data from an Alzheimer's patient to his family would be just noise amongst the over all data. The secondary factor to the problem is poor dental health at some point for an extended period.
You don't understand epidemiology very well if you think an epidemiologist can't find a very small signal amongst an enormous background of noise. It's what they do. In a population of 60 million, epidemiologists were the first to sound the alarm that BSE was being transmitted to humans on the basis of just nine additional cases of of what appeared to be CJD (now known to be vCJD) in humans. Epidemiologists CAN connect transmissible diseases, even when the mechanism is unknown and the transmissibility is very weak or masked by other factors -- like "poor dental hygiene over an extended period." Your claim that they cannot is simply false.
We have now had 18 years since Miklossy's original "finding." She has lots of excuses for the fact that effectively no one has reproduced her results; what she does NOT have is reproducibility from other researchers.
My dentist is one of the top implantologists in the world... he was the keynote speaker at the Indian Society of Oral Implantolgists in Pune, India in January where he gave a talk on the Custom Osseous Integrated Implant (COII) system that he was instrumental in helping develop. He also presented a class on them and gave a presentation on the spirochetes.
These COII implants heal in bone, not in scar tissue like the older sub-periosteal implants that are now considered to be failures at placement and should be removed. Sub-periosteal implants have a survival rate of 50% at ten years. The COIIs our office place (now over 120) have shown a 100% survival rate at 10 years because they heal in bone. . . unfortunately, these Custom Osseous Integrated Implants are virtually indistinguishable on an x-ray from a subperiosteal implant so an uninformed dentist on seeing one in a radiograph is likely to advise its immediate removal thinking it's a subperiosteal implant!
Most dentists who call themselves implant dentists, know only one or two screw implant systems. This system is far beyond that.
The head dentist at our office has an alphabet of letters behind his name... he's a:
His most recent scientific research was published in The Journal of Biomedical Materials Research—"Bone properties surrounding hydroxyapatite-coated custom osseous integrated dental implants" where they reported the findings that the bone did indeed integrate to the implants in the COIIs in three jaws recovered from three of my dentist's patients (one of which was my ex-wife's mother), contrary to the claims of all other dentists that it could not and would not happen!
In any case, my ex-wife's mother had a jaw that had only 1/16" left at the time of the placement of a raymus frame titanium full lower jaw implant system. This was a pre-Vitalium custom made implant that was built on a CADCAMed jaw model made from a CAT scan of her jaw. She had reached the point that relines of her dentures would no longer work at all. There literally was no jaw under the gums to support anything because the forces of chewing were not being transferred from the denture and the body had reclaimed the calcium of the jaw. As mentioned, there was only 1/16" of her jaw left. She came in for the surgery after the implant was engineered and manufactured by the dentist. It was a single surgery that opened her gums, the implant mounted on her jaw with some screws, and then closed. Her existing denture was modified to fit the titanium bar that went around her gum line above the gums... and clamped on to it. Where before, her denture would fall out of her mouth, it now literally had to be pried out of her mouth with a spoon. At that time, she was allowed to go home and eat a steak that night! We no longer allow that because we now know better for best results.
Eleven years later, she died at age 95, having lived far longer than she would have done if she had to live eating pablum. She was able to eat apples, steak, anything she liked. She had given permission to have her jaw taken for research purposes. The dentist went to the mortuary and removed her lower jaw and it was sent to the University of Alabama for histology study.
There it was found that not only had the implant survived, but her jaw had regrown to full size and function in the eleven years... and not only that, the bone had grown to and into the implant at the microscopic level... down to the electron microscopic level... basically molecular level! The implant had integrated with the bone! The implant had transferred the stresses of chewing back to the jaw and the body had responded by regrowing the bone and put the calcium it had reclaimed back!
We now have, I believe 11 cases, including several from other doctors doing the same type of implants, showing the same thing... and zero cases where this has not happened! We have to wait for more patients who no longer need their implants to check more. . . however, there is a statistical model that says when we reached seven, we had enough data to conclude that every case would show the same results, and each additional would extend the degree of confidence toward certainty.
Now, we heal implants like broken bones... we don't load them for six weeks. We still do the single surgery and we can do bone grafting with HydroxyApatite (a manmade material that bones are made of) at the same time... in a method that sort of works like aggregate and cement where the HA works like the aggregate, the patient's own blood acts like the cement, and the body heals the mix into natural bone! We can pack this mixture around the implant, use no screws into the bone, unless absolutely necessary, and keep the load off the implant, and allow the implant/bone to heal naturally like a broken bone. After six weeks, we progressively load the implant with soft to harder foods until totally healed and the patient can then eat anything they want to.
The more screws or holes you put in the bone, the more failure points you add to the case, the more opportunities you add for infection. Not a good idea. We try to avoid screws for these types of implants.
Single tooth implants can be done with a screw post.
The cobalt is not a problem?
Nor the Molybdenum?
What’s wrong with Titanium?
The CoCrMo Alloy is far stronger than Titanium and that means you don't have to use as much metal to get the same strength as a much larger amount of Titanium. The CoCrMo can be 1/2 the thickness of the Ti part for equal strength. Like Ti, CoCrMo is medically inert... and the body will accept it as part of itself if it is properly prepared and super-cleaned. We used to use a device called a "picotron" which bathed the implant in electrons and cleaned it of any contaminants. It was then coated with HA... and then a drop of the patient's own blood was touched to it. It was fascinating to watch. Touch a drop of blood anywhere on the implant and it instantly covered the implant! The implant was immediately placed... and granular HA packed around it, blood added, gums carefully and tightly closed. The patients existing modified or a temporary denture made to fit the implant... and the patient sent home. Total time of surgery, an hour to two hours.
Now, we find we no longer need the picotron... the same results can be gotten with super clean distilled water very high temperature steam. Lots of research went into finding out that water could do what an expensive piece of equipment could do. ;^)>
Then there’s the noise about implants loosening from lateral pressures.
That's why the implants healed in scar tissue fail... they aren't supported well. But if they are healed in BONE... the bone surrounds them and they are well supported. Bone is hard, scar tissue is, well, soft. and movement causes irritation, and eventually space develops, and inflammation and infection.
While the COIIs heal, we have our patients avoid lateral pressure to make sure no scar tissue develops. Once healed, there's no possibility of that happening. We do have some problems develop, but with proper engineering design, it may only require the removal of one infected post out of several... and the implant survives, still functional. Placing up/down minor thrust is not too bad, but the lateral can leverage the partially healed bone and prevent proper healing. We usually recommend removing the dentures at night for people who might be "thrusters" until the healing is done.
Before, when the implants were made out of massive titanium metal, and were mounted on scar tissue, the whole thing had to be removed because the struts were connected below the gum line for support (not necessary with the vitalium) and the infection followed the connected metal, the scar tissue, being soft, infectable meat, rapidly deteriorated, and the entire implant could be lost in a matter of days.
With the COII implant, when made out of strong CoCrMO, each strut is independent, not connected below the gum line so no connection to the next and therefore no pathway for infection to follow to the next strut, revision surgery is simple and straight forward, leaving the implant structure in place and functional when only one infected strut has to be removed. Safer, easier, and less healing time. No money to even fantasize really but would sure like to be able to have 4 posts for my lower dentures.
Strange that you should mention that. The Arthur A. Dugoni School of Dentistry at the University of the Pacific (a Stockton educational institution) at their San Francisco campus is offering to place four mini-implant screws to secure a lower denture for $7000. They claim they have a 92% survival rate of their mini-implants at ten years which is pretty good. Our office has been running a special for the last four months. Two full size screw implants to secure your lower denture, 2 year guarantee or free replacement, with our doctor's 100% at 10 year track record and his world renowned reputation, for only $1600. You don't need four... two full size screw implants with O ring attachments to your denture is more than enough to secure your lowers. I'm not trying to sell dentistry here on FR, I've carefully avoided even saying my office name or the dentist's name... but it's a great bargain. If you are close to Stockton, you might want to check us out. We don't really like taking patients from more than an hour away. It's too much of a problem if something happens to the implant and revision surgery becomes necessary. If you are interested in implants, tell me where you are and perhaps we can refer you to a good implant dentist in your area... one who knows more than just a screw.
Well, if you don’t have holes in your gums, you don’t have much to worry about any more. There’s no bleeding gums to allow the spirochetes entry to your blood vessels from your mouth! We found that edentulous people don’t have the problems IF they lost their teeth early. Not too sure how early is best.
My father’s mother had all her teeth pulled at 15... The quack who ordered it said she had “guitar of the bowels” so the treatment was to pull her perfectly healthy teeth. She was perfectly healthy... even if mean and nasty and very self centered... until she died at 92. Neither one of my Grandmothers was nice... and neither one had any teeth from an early age. Both lived beyond 90. Neither one had heart disease, diabetes, or alzheimers... just an even disposition... angry and mean all the time.
Thanks for the ping Quix.
Excellent information, I am spreading it around.
You may very well have saved a few people a fate worse than just death.
:)
You know, Fred, you impute an awful lot of venality and almost criminality to Miklossy's work... when I do not see any and the other scientists who have talked to us about this report do not see any either. WHAT IS YOUR MOTIVE HERE? "...covering her tracks"? What are you saying? Are you implying that she has falsified her data? That she has somehow LIED??? Does she have a motive to LIE???? Does she have an axe to grind to present false evidence... to obfuscate and present something that is not TRUE in her search for a prevention to Alzheimer's disease. What, exactly, is the dark and sinister motive that you are imputing to her?
And it turns out it is just as I thought! They used an old technique called "dark field" microscopy, using old style, standard microscopes. It turns out, in fact, that you are mistaken. Reread your own citation. They used dark field microscopy and electron microscopy.
I'm mistaken? I don't need to reread it. I know what I said and I addressed it. Did you even bother to read what I wrote? I suspect not. I discussed the electron Microscopy. These guys apparently can't afford a phase-contrast microscope and you think they can afford to do the thorough job an electron microscopy survey would require??? Hell no. They were Looking for one specific species of spirochetes, not anything else.
You are all over the board on this. Do you know what it costs to run an electron microscope? To prepare the samples? You just don't do it on everything you find. A research isolates what they are looking for and THEN prepares the sample for that... not a shotgun approach of everything. I don't think you have even bothered to read Miklossy's paper yet, have you?
Oral spirochetosis is present in 30+% of patients with no AD. In order to make the correlation appear to be a causation, she averages studies with "all spirochetes" and with "all studies." Why? Because the actual causal inference for oral spirochetes is quite poor when 30+% of non-AD patients have them.
I see. Again, you are all over the place. You seem to think that only people with diagnosed, and symptomatic AD have spirochetes... and that they have to be required therefore to be symptomatic? Your logic is completely flawed. What about PRE-symptomatic AD? Or do the spirochetes just instantly appear when the Symptoms become overt? That would be a stupid assumption, Fred. Remember, this is apparently a LONG exposure disease that is observably endemic in mouths of 85-90% of the population. It would be logical to accept that there are asymptomatic people with spirochetes in their systems because we KNOW it takes a LONG time for these diseases to evince. It does not happen over night, Fred. Ergo your argument that the existence of 30+% of patients (sic) with no AD but with oral spirochetes is completely without merit. It's remarkable that with the observed oral infections in the mouths, that the rate is not higher! In addition, these studies did not include histories that determined the condition of their hearts, arteries, or whether these people might be type 2 diabetics or pre-diabetics.
You don't understand epidemiology very well if you think an epidemiologist can't find a very small signal amongst an enormous background of noise. It's what they do. In a population of 60 million, epidemiologists were the first to sound the alarm that BSE was being transmitted to humans on the basis of just nine additional cases of of what appeared to be CJD (now known to be vCJD) in humans. Epidemiologists CAN connect transmissible diseases, even when the mechanism is unknown and the transmissibility is very weak or masked by other factors -- like "poor dental hygiene over an extended period." Your claim that they cannot is simply false.
You seem to have an agenda here and I certainly don't know what it is... but it is strange. I think YOUR claim is the false one. There is NO WAY that an epidemiologist can find that kind of thing you claim. NO WAY. When 85-90% of the population has these bugs in their mouths and you say epidemiologists would see that an Alzheimer's patient, in the later years of their lives would somehow GIVE their family what they ALREADY have. It simply is NOT possible. BULL SHIT! The relatives ALREADY have had it for years when the Alzheimer's patient first evinces symptoms of Alzheimers. What is there for the epidemiologist to find that is any different? An epidemiologist would SEE NOTHING different in the family of the AD patient than they would seen in the families of non-AD patients! You are just blowing smoke! This is a transmissible disease that everyone already has in their mouths... You are making stuff up when you say different. We in the dental offices are the one's seeing an epidemic of oral spirochetes and YOU say that epidemiologists will see something different? BAH!
This is NOT based on her original finding. Her original finding was an indicator to start looking at several things, she lists them and spirochetes were just one among several... and you are extrapolating a lot out of that. This paper is about other research that DID duplicate her findings and is a compendium and review of those findings. There is a list of those researchers at the end of the 2011 paper. . . and their findings.
Exactly what is your interest in this, what is your background that you are so upset at this research? You are the one I've found representing things I find not to be the case when I've looked. You've claimed things on this forum that were demonstrably NOT true when I've checked them. Now you are claiming their ONE case of B. Burgdorferi is somehow the other cases of seeing spirochetes. You are the one using weasel words. You are the one who started by making your claims using only the abstract. . . and apparently not even bothering to read the actual paper. You are the one using completely OUTDATED refutations that are 18 and 13 years old, when protocols usually used suggest using only papers within the last 5 years be used for refutations. You stretch credibility. You impugn the credibility of the researcher without proof... using ad hominem arguments such as "covering her tracks" from an article in a "peer-reviewed" journal. I don't know you or YOUR reputation from Adam. On the other hand, I DO know the scientists I have been working with... and they have reputations beyond reproach. WHAT ARE YOU AFRAID OF, Fred?
It is.
GREAT INFO. THANKS TONS.
I can’t even come up with that amount or the travel expenses . . . unless by God’s Grace in the not distant future my Kindle book becomes popular.
I will share your info with my dentist. He’s just taken implant training. I don’t know if it’s of the type you speak, or not.
Imho, orientals are hard to beat when it comes to fine motor surgery stuff. I’d feel most comfortable with the better ones for eyes, brain or teeth.
Great info. Much appreciated. God’s best to you.
My authentically Christian Dentist here is a saint of a man. Does mission work in Thailand and has a wonderful personality. And, does great work. Incredibly patient.
Thanks tons for your input.
Printing it off to share with my Dentist.
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