PFPC NEWSLETTER #9

PFPC NEWSLETTER #9:

"Fluoride, Gingivitis & Oral Cancer"
© 2002 PFPC http://64.177.90.157/pfpc/html/newsletter_9.html

Summary:

Gingivitis and periodontal disease are the oral diseases requiring most urgent intervention. Over 90% of the U.S. population over 13 is affected. Strong links have been made to heart disease and low birth weight and infant mortality. For heart disease the association with gingivitis is stronger than the one for smoking or high cholesterol. As heart disease is the #1 killer in the US, many efforts are undertaken to reduce this alarming figure. In Canada large pictures of a diseased heart are placed on cigarette packs alerting to the fact that smoking causes heart disease.

It is of great importance that warning labels and pictures of periodontal disease, oral cancer, diseased hearts, pituitary and thyroid glands, as well as Alzheimer’s brains - just to name a few - are placed on all oral care products containing fluoride.

Why?

A patent by the pharmaceutical company Sepracor discloses that concentrations of fluorides from fluoridated toothpastes and mouthwashes activate G proteins in the oral cavity, thereby promoting gingivitis and periodontitis, as well as oral cancer. Incomprehensibly, this vital information is being withheld from the public by all parties involved, including the company, at least two well-known Universities, and numerous oral disease experts. This includes a much-decorated ADA scientist who was involved in setting the CDC recommendations for fluoride intake in children, served as head of a Food and Drug Administration subcommittee that decides which dental products to make available to the public, and who chaired the panel on safe use of fluoride for the Centers for Disease Control (CDC, 2001).

An extensive section of this Newsletter deals with biochemical aspects [Part 4].

Part 1

INTRODUCTION
THE PATENT
GINGIVITIS - Statistics
ORAL CANCER - Statistics

Part 2

FLUORIDATION AND ORAL CANCER

Part 3

BRIEF LITERATURE REVIEW - EVIDENCE

Part 4

BIOCHEMISTRY - G PROTEINS
Background
Oral Cancer - The ras oncogene
G q/11 Diseases

Part 5

ADDITIONAL COMMENTS/UPDATE
Aluminum Fluoride Complexes
Candidiasis
Dentists & Oral Cancer
Richard Gracer, MD

Part 6

THYROID HORMONES & GINGIVITIS

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Part 1

INTRODUCTION

Many of our children have experienced oral diseases which miraculously disappeared when fluoride intake was curtailed. For example, some had consistent “white spots” on their gums which vanished upon elimination of fluoridated toothpaste, but returned as soon as such toothpaste was used again.

Some of these white spots and patches were diagnosed as pre-cursors to oral cancer (squamous cell carcinomas), while others were deemed to be "allergic reactions" by medical professionals. Yet other doctors identified oral yeast infections (Candidiasis).

When we investigated the scientific literature on fluoride toxicity we found that such oral conditions have been related to fluoride intake countless times. There is extensive evidence of such disease in humans from areas with water fluoridation, from toothpaste and mouthrinse use, as well as in workers exposed to fluorides.[See:Part 3]

Studies in workers exposed to fluoride have shown that the severity of periodontal disease is directly correlated to the fluoride levels in systemic fluids (i.e. Domazalska, 1972). The more fluoride in the system - the more severe the periodontal disease. The same findings have been made for Asthma.

THE PATENT

In 1996 three biochemists (Aberg, Jerussi & McCullough, 1998), working for the pharmaceutical company Sepracor, speculated on fluoride implications in periodontal disease. Realizing that fluorides activate G proteins, they reasoned that fluorides would also be involved in the activation of those G proteins which regulate the pathways involved in gingivitis and periodontitis - and they decided to test for the ability of fluoride to activate two integral receptors involved in periodontal disease - the prostaglandin E2 receptor (PGE2) and the thromboxane A2 (TXA2) receptor. Both are coupled to G proteins called G q/11.

The scientists conducted a test with sodium fluoride based on a well-established in-vitro protocol model involving HL-60 cells. These are Human Leukemia cells often used in biochemistry investigations, as one can observe fundamental and critical signals involved in the activation of the body's immune system - because of the cells’ ability to respond to foreign organisms.

The authors reported:

"We found that fluoride, in the concentration range in which it is used for the prevention of dental caries, stimulates production of prostaglandins and thereby excaberates the inflammatory response in gingivitis and periodontitis.... Thus, the inclusion of fluoride in toothpastes and mouthwashes for the purpose of inhibiting the development of caries may, at the same time, accelerate the process of chronic, destructive periodontitis."

A very important finding as it relates to public health!

In the 1986 National Institute of Health (NIH) survey, 93% of adults indicated that their children used toothpaste with fluoride, obviously putting all at risk. Gingivitis and periodontal disease constitute THE major public oral health problems in the US.

The patent findings supply the biochemical explanation for earlier reports by many researchers who had found increased gingivitis and gum inflammation due to fluoridated water, or other sources of fluoride.

Even T. Dean himself - the so-called "Father of Fluoridation", made such observations.[see: Part 3]

However, instead of alerting the public health officials to their findings, those men apparently decided to take another avenue.

They went looking for an agent which would counteract the adverse effects of fluoride and therefore could be used together WITH fluoride. After all, fluoride was/is the "proven caries fighter"!

They chose a non-steroidal anti-inflammatory agent (NSAID) called ketoprofin, conducted more studies to see if ketoprofin was efficient in off-setting the damaging fluoride effects, and then filed a patent on their new concoction now containing both fluoride and ketoprofin (Aberg et al, 1998).

Subsequently, a study was instigated at the Harvard School of Dental Medicine (funded by Sepracor), documenting the ‘wonderful’ effects of ketoprofin upon gingivitis. The first study on beagles included one of the three co-inventors (McCullough) together with two Assistant Professors from two separate well-respected Universities, and was subsequently published in the Journal of Clinical Periodontology in 1997 (Paquette et al, 1997).

In the study not one word is mentioned about fluoride being a causative/promoting agent of gingivitis, as stated in the patent claims.

Another study - this time on rats, and again as a direct result of the patent research - was conducted involving yet another of the three co-inventors from Sepracor (Jerussi).

This time the study was done with two professionals from the University of Rochester, one being Prof. Bowen, the much-adorned and decorated ADA scientist involved in setting the 2001 CDC recommendations on fluoride intake.

Results of this study were published recently in the Journal of Oral Diseases (Bowen et al, 2000) Full Text

Again, not one single word about fluoride promoting and causing gingivitis appears in the entire text.

GINGIVITIS - Statistics

According to the National Institute of Dental and Craniofacial Research (NIDCR; Brown et al, 1996), over 90% of persons 13 years or older experience some form of periodontal disease.

74.9 % of all people between 35 and 44 years suffer from periodontal disease (Fig.4.7, Oral Health Report, 2000). 29% of males and 15 % of females between 35 and 44 years old have destructive periodontal disease (Healthy People 2010-Conference Edition).

60% of all people between 18 and 44 suffer from periodontal disease (Figure 4.8, OHR).

Compared to these figures - up to 46% of adults over 18 years old have untreated caries (Figure 4.5, OHR).

Not surprisingly, periodontal disease has recently become the primary focus for dental researchers because of the very strong links which have been made to other conditions such as heart disease (Loesche 1994, 1998; Herzberg and Meyer 1996), as well as infants with low birth weight and premature births. For heart disease the association is stronger than for smoking (Loesche et al, 1998).

The NID(C)R, in their 1999 appeal to the Appropriation Committee for $276,518,000 in funding, stated that gum disease is now also known as a high risk factor for low birth weight babies. Said Crawford in his plea for the big money:

"Care of low birth weight babies costs the nation approximately $5 billion dollars each year. If we can lower the incidence of low birth weight babies by treating gum disease it will mean that 1:10 babies born in the US have a better chance of a healthy start in life."

Further, he reasoned:

"As we come to the end of this, century, 50% of heart attacks (the number one cause of death in the Western World) and 25% of low birth weight babies have no aditional risk factors associated with them. We now have strong evidence that gum disease is a risk factor for both these conditions - in fact - as strong a risk factor for heart disease as elevated cholesterol or smoking!"(Crawford, 1999)

This clearly means that fluorides - by promoting gingivitis - also contribute to heart disease and low birth weight. Heart disease has long been known to be higher in workers exposed to fluorides, or caused by fluorides in medications (PFPC, 2001). Biochemical investigations have identified the pathways.

The patent findings implicating the fluoride "topical" activation of G proteins in the oral cavity have many far-reaching and serious implications - not only for periodontal disease, but also for oral cancers - which involve "mutated" G proteins, and which are activated by fluoride, often even "preferring" fluoride activation.[see Part 4: Biochemistry]

ORAL CANCER - Statistics

Oral cancer is the sixth most frequent cancer in the world (Buffalo Sisters Hospital, 2000).

Oral cancer claims the life of one American every hour. Over thirty thousand Americans are diagnosed with oral or pharyngeal (throat) cancer every year and 8,000 people die annually from these cancers. Only half survive more than five years. This overall 5-year survival rate (52 percent) has not changed in the past five decades - coincident with the appearance of fluoride as a ‘preventive treatment’ for caries.

Black people have higher incidence and mortality rates than other subgroups (OHR, 2000; Caplan et al. 1993; NIH Press Release, 1996), as they do with most thyroid hormone-related disorders, including, of course, "dental fluorosis" (PFPC, 2000).

“White Patches” - Cancer

As was mentioned in the INTRO, many of our kids have had these "white patches" in the mouth, often diagnosed as "precursors" for an ‘oral squamous carcinoma’.

A benign squamous papilloma is the obligate precursor of squamous cell carcinoma, and again, numerous laboratory investigations have shown that these are brought about by fluoride. Mere ras oncogene activation is sufficient to produce the papilloma phenotype in skin cancers, and fluoride is known to act additively with the ras oncogene in producing this papilloma (Camp & Hoffman, 1993). (-> Cancer promotion).

[see Part 4: Biochemistry]

Part 2

FLUORIDATION AND ORAL CANCER

In 1981 Dr. John Yiamouyiannis and Dean Burk, chief chemist emeritus of the National Cancer Institute (NCI), first showed very convincingly that there was an increase in oral cancer in fluoridated areas.

An investigation done by the Battelle Institute on behalf of the National Toxicology Program (NTP) (NTP, 1991; also see: Yiamouyiannis, 1993) showed a clear dose-response relationship between oral cancers and fluoride intake in the animals tested.

According to the late Yiamouyiannis, the National Cancer Institute (NCI) - in response to the NTP findings - decided to examine the incidence of oral cancer in fluoridated and non-fluoridated areas. The resulting data showed at least a 33% to 50% increase in the incidence of oral cancers in fluoridated areas, indicating at least an additional 5000 - 7500 or more cases or oral and pharyngeal cancer per year as a result of fluoridation alone (Yiamouyiannis, 1993).

Table

An increase in oral carcinomas and their precursors has also been observed in workers exposed to fluorides.[see next section]

Part 3

BRIEF LITERATURE REVIEW - EVIDENCE
(Compiled by Wendy Small)

Gingivitis and oral diseases due to fluoride excess have been reported many times in the world literature.

In 1936 Dean - the "father of fluoridation" himself - wrote in the Journal of the American Medical Association:

"From observations that I made in areas of relatively high fluoride concentration (more than 4 parts per million of fluorine) there is sufficient evidence to suggest that there is an apparent tendency toward a higher incidence of gingivitis."

Remember, at that time water with fluoride at 4ppm was thought to produce a total intake of 4 mg/day. In 1991 the US PHS estimated that TOTAL intake exceeded 6.5 mg/day in U.S. cities having one part per million (1ppm) of fluoride in their water supply!

Similar observations of the link between fluoride and periodontal disease have been made many times since (Dean & Arnold, 1943; Day, 1940; Spira, 1953; Ramseyer et al, 1957; de Toledo, 1970; Grimbergen et al, 1974; Poulsen & Moller,1974; Waldbott et al, 1978; Olsson, 1979; Reddy et al, 1985; Wei et al, 1986; Yiamouyiannis, 1993).

In 1953 Leo Spira had identified gingivitis and bleeding gums as signs of chronic fluoride poisoning. In 1957 Ramseyer observed gingivitis in older rats drinking water fluoridated at 1 ppm. By 1982 Domazalska observed a direct correlation between the severity of periodontal disease and fluoride levels in systemic fluids.

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From around the world...

"Most children in both urban and rural areas had gingivitis...Children who brush their teeth every day were 88.5% in urban and 72.8% in rural areas and most of them used fluoride tooth paste."

Suksu-art N, Arkasuwan N - "Survey on the oral health status of primary school children in urban and rural areas, Hat Yai, Songkhla" Research/Government Report, Thailand (2000)

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"A significant relationship between the concentration of F- in dental plaque...and the condition of periodontal tissues was established."

Borysewicz-Lewicka M, Kobylanska M - "Periodontal Disease, Oral Hygiene And Fluoride Content Of Dental Deposits In Aluminum Workers" Fluoride 16(1):5-10 (1983)

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"Fluorosis was endemic...Periodontal disease was moderate at 15 yr of age, but seemed to be a predisposing factor in caries from the late teens onward. ... More than half of persons in the 55-64 yr age group required full maxillary and mandibular dentures while 10% already possessed them."

Speake JD, Malaki T - "Oral health in Tuvalu" Community Dent Oral Epidemiol 10(4):173-177 (1982)

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"....We are more prone to caries...The incidence of dental fluorosis is on the rise in Bathinda. Experts reveal that the disease is commonplace due to fluoride contamination in the ground water of the region. Studies indicate that nearly 90 per cent of the population ...is suffering from dental caries and chronic gingivitis, which often leads to pyorrhoea [periodontitis]..."

Rishi, Shella - "We are more prone to caries" Bathinda/India; India Express - Thursday, July 20 (2000)

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"There were some controversies in the results of fluoridation studies with one study reporting as high as 47.2% of the children to be afflicted with enamel fluorosis.... 93% of the 12-yr-olds had bleeding, 98% had calculus and 15% had shallow pockets, with 100% of the children needing prophylaxis."

Wei SH, Shi Y, Barmes DE - "Needs and implementation of preventive dentistry in China" Community Dent Oral Epidemiol 4(1):19-23 (1986)

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"Teeth with moderate and severe fluorosis more frequently had dental caries than teeth with no or very mild and mild fluorosis.... Gingivitis was seen in 97% of the children..."

Olsson B - "Dental findings in high-fluoride areas in Ethiopia" Community Dent Oral Epidemiol 7(1):51-6 (1979)

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"The article deals with the problem of relation of the incidence and prevalence of various parodontal diseases in subjects with various degrees of fluoride intake to the content of this element in various systemic fluids. ...A correlation was observed between the parodontopathy index of Kotzschke and F levels in the systemic fluids calculated by means of the correlation coefficient of Pearson."

Domazalska W - "Incidence of periodontal diseases in subjects with various degree of exposure to fluorides" Czas Stomatol 25(10):1005-1011 (1972)

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"Stomatological and mycological examinations of the workers [exposed to fluorides]at the fusion department of the RZWM "Silesia" showed a considerable intensification of paradontium diseases (about 80% of cases). Leukoplakia [pre-cancerous growth] and candidiasis were the most common changes found on the mucous membrane in the oral cavity. Mycological investigations carried out on the Sabourand culture showed Candida albicans in 73.7% of cases."

Ilewicz L, Chrusciel H, Korycinska-Wronska W, Maniak B, Szlachta R, Mniszkowa M, Waszkiewicz-Golos H, Wrobel J - "Condition of the periodontium and mouth mucosa in workers exposed to fluorides" Med Pr 33(1-3):153-6 (1982)

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“...cancers of the oral cavity and pharynx, colon and rectum, hepato-biliary and urinary organs were positively associated with FD” [fluoridated drinking water]

Takahashi K, Akiniwa K, Narita K - “Regression analysis of cancer incidence rates and water fluoride in the U.S.A. based on IACR/IARC (WHO) data (1978-1992). International Agency for Research on Cancer” J Epidemiol 11(4):170-9 (2000)

Animals

Krook L, Maylin GA, Lillie JH, Wallace RS - "Dental fluorosis in cattle" Cornell Vet 73(4):340-62 (1983)

"Five expressions of dental fluorosis are described in cattle exposed to industrial fluoride pollution: 1. Hypercementosis with tooth ankylosis, cementum necrosis and cyst formation; 2. Delayed eruption of permanent incisor teeth; 3 Necrosis of alveolar bone with recession of bone and gingiva; 4. Oblique eruption of permanent teeth, hypoplasia of teeth with diastemata; and 5. Rapid progression of dental lesions. The five entities are not recognized in the "standard for the classification of dental fluorosis" by the National Academy of Sciences. Since this classification it too limited and superficial, adherence to this standard has left severe cases of fluoride intoxication in cattle undetected in field surveys."

In-Vitro

Chang YC, Chou MY - "Cytotoxicity of fluoride on human pulp cell cultures in vitro" Oral Surg Oral Med Oral Pathol Oral Radiol Endod 91(2):230-4 (2001)
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11 174602&form=6&db=m&Dopt=r

"OBJECTIVES: Numerous studies have revealed that conventional glass-ionomer cements might release fluoride into an aqueous environment. The objective of this study was to examine the effects of fluoride on human pulp cells in vitro. STUDY DESIGN: H33258 fluorescence, cell proliferation, protein synthesis, and mitochondrial activity assay were used to investigate the pathobiological effects of fluoride on cultured human pulp cells. RESULTS: Fluoride was found to be a cytotoxic agent to cultured human pulp cells by inhibiting cell growth, proliferation, mitochondrial activity, and protein synthesis. CONCLUSIONS: Fluoride release has significant potential for pulpal toxicity."

more papers...

Part 4

BIOCHEMISTRY

Background

As we have stated many times in the past, fluoride is known as the “universal G protein activator” in biochemistry, meaning it can activate all G protein families. The only known receptor which is capable of doing the same, in the human organism, is the receptor for the thyroid-stimulating-hormone (TSH) (Gudermann et al, 1997).

This complex and multifunctional actvity of TSH is the reason why so many different diseases are associated with thyroid hormone dysfunction. It is also the reason why the same associations have been made in fluoride poisoning - fluoride being a TSH clone.

While for many years it was presumed that the TSH receptor was only expressed in the thyroid gland itself, TSH receptors have now been detected in liver, gastrointestinal tract (Duntas et al, 1998), orbital tissue and dermal fibroblasts (Paschke et al, 1994), peripheral lymphocytes, fat, cardiac muscle (Drvota et al, 1995), thymus, peripheral blood mononuclear cells, osteoblasts and osteosarcoma cells (Inoue et al, 1998), or the brain - where it is overexpressed in patients with Down Syndrome or Alzheimer's Disease (Labudova et al, 1999).

In order for us to understand fluoride poisoning better, we have concentrated on the matter of Gq/11, as this is what TSH does - at elevated levels it activates the Gq/11-mediated pathways.

What are G q/11 proteins?

G q/11 proteins are membrane-associated proteins involved in signal transduction - the way cells communicate with each other.

Gq/11 are coupled to receptors which cross the cell membrane seven times ("transmembrane receptors"). Gq/11 proteins are located in the membrane of a cell.

Upon receptor activation, they may send information directly from the membrane to the cell's nucleus. Consider them an essential "relay station" for cell information, the initiators of other cascades of events. One such cascade involves the mitogen-activated-protein-kinase (MAPK). MAPKs are regarded as "switch" kinases in the phosphorylation cascade.

Gq/11 may be released directly from the plasma membrane to an intracellular location in response to activation by aluminofluoride complexes [AlF(x)], directly translocating immunoreactivity (i.e. Arthur et al, 1999).

Fluoride not only directly augments the already existing hormonal (TSH) activation of Gq/11, it may activate such proteins even in the absence of TSH. [Without TSH, G proteins involved in thyroid hormone regulation are thought to be inactive (Utiger, 1995).]

G q/11 Diseases

Gq/11-regulated pathways have profound effects not only on the pathology of gum disease, but of chronic inflammation overall, as well as cancer, heart disease, stroke, diabetes, Alzheimer's Disease, Autism, etc. - in short - all those conditions which represent the most significant health care problems in the developed world today. We have come to describe this as the “G q/11 disease”.

For example, in heart disease - which kills 725,192 people a year in the U.S. alone, making it the #1 cause of death (CDC, 2002) - it is G q/11 over-expression which leads to enlargement of the heart, in turn leading to congestive heart failure. Therefore recent pharmacological research has focused on creating so-called "decoys" for G q/11 - non-working versions of Gq to prevent the activation and reception of molecular signals that normally would produce such enlargement of the heart (Akhter et al, 1998; Adams et al, 2001).

It has been shown that on-going ("constitutive") G q/11 activation in heart muscle results in downsignalling of thyroid hormone T3 and inhibition of T3-dependent intra-cellular activities (i.e. Wu et al, 1997).

Needless to say, G q/11 are also involved in dental pulp and enamel formation and are also involved in the condition known as "dental fluorosis" (enamel hypoplasia) (Pozo et al, 2000; Bawden et al, 1996). Gq/11 have been unequivocally established to be the transducing G proteins for all Ca(2+)-mobilizing receptors (i.e. Exton,1993).

In Alzheimer's and Down Syndrome patients Gq/11 is elevated in the brain regions. Virtually all Down Syndrome patients suffer from Alzheimer’s in their 40’s.

[NOTE: It is no coincidence that up to 90% of villagers around the NALCO aluminum smelter in Angul, India are experiencing "senility" before the age of 50 (Hindustan Times, Aug. 15, 1999). In fact, Indian parliamentary discussions disclose that, out of 14,000+ fluoride-poisoned villagers in the area, 5,000 are suffering from Alzheimer’s Disease (Lok Sabha Debates, 1999).]

Fluorides are most-established Gq/11 activators, ensuring a firm and most-important rogue role for fluorides in all of the above diseases. Both inorganic and organic fluoride compounds may activate G q/11. It is a matter of degree in the amplification of the F- signal.

Diseases linked to the pathways mediated by Gq/11:

Adenocarcinoma, leukemia, lymphoma, melanoma, myeloma, sarcoma, teratocarcinoma, and cancers of the adrenal gland, bladder, bone, brain, breast, cervix, gall bladder, ganglia, gastrointestinal tract, heart, kidney, liver, lung, bone marrow, muscle, ovary, pancreas, parathyroid, penis, prostate, salivary glands, skin, spleen, testis, thymus, thyroid, and uterus; and immune disorders such as AIDS, Addison's disease, adult respiratory distress syndrome, allergies, Alzheimer’s Disease, anemia, ASD, asthma, atherosclerosis, bronchitis, cholecystitus, Crohn's disease, ulcerative colitis, atopic dermatitis, dermatomyositis, diabetes mellitus, emphysema, atrophic gastritis, glomerulonephritis, gout, Graves' disease, hypereosinophilia, irritable bowel syndrome, lupus erythematosus, multiple sclerosis, myasthenia gravis, myocardial or pericardial inflammation, osteoarthritis, osteoporosis, pancreatitis, polymyositis, rheumatoid arthritis, scleroderma, Sjogren's syndrome, thyroiditis, etc..

As fluoride mimics TSH, we usually check on Down Syndrome first - as all DS patients have shown to have higher TSH levels, they will often show us what fluoride poisoning does. As TSH activates G q/11 - to which PGE2 and TXA 2 are coupled - similar oral conditions should be observable in DS. Needless to say, DS patients also have a high degree of periodontal disease (Decoq, 1995;Wilkins, 1994; Ulseth et al, 1991; Barnett et al, 1986).

Gq/11 and the ras oncogene share in mediation of pathways, including MAPK (i.e. LaMorte et al, 1994; Seo et al, 2000).

Oral Cancer - The ras oncogene

Biochemical research in the “search for cancer” conducted during the last few decades has firmly established the involvement of mutated G proteins in the pathogenesis of cancer, including oral cancer (Das et al, 2000; Yoo et al, 2000).

One such well-known mutated G protein is the "ras" oncogene.

These ras oncogenes were first found in human bladder cancer cells, and have now been identified further in pancreas, breast, prostate, thyroid, lung, and uterine cancers, myeloid leukeamias, etc. as well as skin and oral cancers.

Among the cancers which most often include mutated ras genes are adenocarcinomas of the pancreas (90%) (Almoguera et al., 1988), adenocarcinomas of the colon and cancers of the thyroid (50%), as well as carcinomas of the lung and myeloid leukeamias (Bos,1989).

During the last 10 years frantic research has been conducted by the pharmaceutical companies directed at finding agents to counteract ras activity.

In efforts to define the very pathways of ras in cancers - so that treatments can be developed - biochemists have used sodium fluoride or aluminum fluoride extensively in the past, at many different levels, and under various conditions.

This is because fluoride can substitute directly for the ras oncogene, and at levels even below those seen in the Sepracor patent investigations, especially when combined with aluminum.

ras oncogene pathways are readily activated by aluminum-fluoride complexes [(AlF(x)] (i.e. Warner et al, 1999; Kleuss et al, 1994; Camp et al, 1993; Matyas et al, 1989; O'Shea etal, 1987; Spina et al, 1987; Haliotis et al, 1988;Lee et al, 1992), as well as beryllium fluoride compounds (Diaz et al, 2000, 1997; Kuppens et al, 1999).

The activation of some mutations is more pronounced or "amplified" by aluminum fluorides (Warner et al, 1999a,b) while others simply prefer the "false" AlF(x) activation (Natochin et al, 1999; Warner et al, 1999; Clabecq et al, 2000).

For some, the AlF4--induced activation defect is more pronounced at low magnesium (Mg2+) concentrations (Warner et al, 1999).

Part 5

Additional Comments

Aluminum Fluoride

Although the "patent" scientists cite a paper by Kawase et al (1991) which documents the potentiating power of the mere trace amounts of aluminum upon sodium fluoride activation on prostaglandin receptors - in their own calculation with sodium fluoride they fail to account for this important fact. Potentiating effects of aluminum might well exceed 500%, making the fluoride concentrations required for prostaglandin activation much lower than those observed in the patent (see: Imai et al., 1996; Turinsky et al, 1992; Kawase et al, 1989).

Already in 1989 Kawase et al had shown in HL-60 cells - the cells used in the patent investigation - that in the presence of mere trace amounts of aluminum, NaF concentrations ranging from 0.01 to 1 mM increased PGE2 synthesis in a dose-dependent manner, whereas NaF alone at lower concentrations (below 0.1 mM) did not show such a significant effect.

Further, when Kawase investigated HL-60 cells treated with sodium fluoride only, he had many more additional findings to report: not only did sodium fluoride increase prostaglandin E2 production, but NaF- produced marked changes in cellular morphology, increased cellular adhesion to plastic, reduced the nuclear/cytoplasmic ratio, increased cellular expression of chloroacetate esterase, and stimulated production of interleukin 1 alpha (IL-1 alpha), IL-6, and the tumor necrosis factors (Kawase, 1989).

“White Spots” - Candidiasis

As mentioned above, the “white spots” in the mouths of our kids were also frequently attributed to candidiasis (yeast infection) by medical professionals.

Candidiasis is an infection of the moist cutaneous areas of the body, and is generally caused by the fungus Candida albicans. It involves the skin, oral mucous membranes, respiratory tract and vagina.

In workers exposed to fluorides, Candida albicans was seen in 73.7% of cases. 80% of the cases showed a considerable intensification of periodonatal diseases. Leukoplakia [pre-cancerous growth] and candidiasis were the most common changes found (Ilewicz et al, 1982).

Other studies on workers have since confirmed those findings (Borysewicz-Lewicka, 1983; Sroczynski et al, 1991). Case reports on candidiasis caused by fluoride mouthrinse are also known (i.e. Axell & Edwarsson, 1978). [see:Part 3]

How much do Dentists know about Oral Cancer?
Excerpts from article by Richard Gracer, MD

REFERENCES

Part 6

THYROID - GINGIVITIS

Of course many of us who suffer from hypothyroidism and are on replacement thyroid hormone know about gingivitis and periodontal disease, a quite common concern.

During the last 40 years the strong association between periodontal disease and thyroid disorders, especially hypothyroidism has been documented many times over in the world literature (i.e. Riedel & Ordelheide, 1966; Abate, 1968; Baba et al, 1972; Pencea et al, 1978; Saburova & Isaeva, 1971; Schneider, 1969; Shkoliar et al,1967; Pashaev, 1982; Danilevskii et al, 1988; Kerimov, 1989; Puzin et al, 1996, etc).

Yet it has received little or no attention in the US.

In women with general periodontitis all hormonal systems were shown to be excessively shifted (Puzin et al, 1996).

Wendy Small compiled the following “anecdotal evidence” from past newsgroup/e-mail postings:

1) "The pockets around my gums started getting deeper & the dentist had me coming in every 3 months, instead of the usual 6 months. The pockets got so bad I had to have scaling of one area. On my last visit there was a huge difference. I noticed at this time my TSH was 1.3, so I really think our thyroid level effect this. I go back in May & my TSH has increased slightly, hopefully not enough to increase the pocket size again."

#2) "My own periodontal issues did not begin to resolve until after probably six months of thyroid treatment ...My own periodontist had no clue about the connection between hypothyroid and beginning- or worsening- gum disease, until he saw my own problems stabilize and then begin to heal after a few months of thyroid meds. Prior to my dx of hypo I had been receiving treatment for periodontal disease for a couple of years, and it was just getting worse, little by little - never improved one bit until thyroid supplementation began..."

3) "Monday I went to the dentist for a routine cleaning. I had noticed for about a week or two that my gums were sensitive and bleed some when I brush, but nothing really bad. Or so I thought. The first thing the hygienist did was a periodontal measuring (don't know the official name for what she did) but it consisted of taking a very thin pick with measurement marks on it and inserting between my gums and teeth. She did this at a couple of different places on each tooth and noted the numbers. This is supposed to tell them if I have signs of gingivitis or periodontal disease. Anyway, the point of all of this is that by the time she had done all my teeth my mouth was bleeding so bad she wouldn't finish the cleaning. All she did was a treatment with some sort of antibacterial solution (felt like she used a water-pik) and sent me home with some medicine to rinse with. I go back in a few weeks for a recheck and a cleaning. I asked my doctor if it was related and he said he didn't think so, but I was just wondering if anyone else has had similar problems."

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CONTRIBUTORS
Bob J, Vishal R, Andreas S, Wendy S, Danielle F,
Trent H, Marshall G
Thanks to: Jack S, Peter M, Jane J, Bob G, and Randy T
Editor: Andreas Schuld