PFPC NEWSLETTER #9:
Gingivitis & Oral Cancer"
© 2002 PFPC
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
A patent by the pharmaceutical company
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].
ORAL CANCER -
FLUORIDATION AND ORAL CANCER
BRIEF LITERATURE REVIEW - EVIDENCE
BIOCHEMISTRY - G PROTEINS
Cancer - The ras oncogene
G q/11 Diseases
Dentists & Oral Cancer
THYROID HORMONES & GINGIVITIS
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
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
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
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
A very important finding as it relates to
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
However, instead of alerting the public health
officials to their findings, those men apparently decided to take
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
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
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
Again, not one single word about fluoride
promoting and causing gingivitis appears in the entire
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
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,
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
- "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
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
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:
ORAL CANCER -
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"
“White Patches” -
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). (->
[see Part 4: Biochemistry]
FLUORIDATION AND ORAL
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
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
An increase in oral carcinomas and their
precursors has also been observed in workers exposed to
fluorides.[see next section]
BRIEF LITERATURE REVIEW -
(Compiled by Wendy Small)
Gingivitis and oral diseases due to fluoride
excess have been reported many times in the world
In 1936 Dean - the "father of fluoridation"
himself - wrote in the Journal of the American Medical
- "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
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.
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)
"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)
"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)
"....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
Rishi, Shella - "We are more prone to caries"
Bathinda/India; India Express - Thursday, July 20 (2000)
"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
"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
Olsson B - "Dental findings in high-fluoride areas in
Ethiopia" Community Dent Oral Epidemiol 7(1):51-6 (1979)
"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
"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)
“...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)
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."
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)
"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."
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
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
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
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
(MAPK). MAPKs are
regarded as "switch" kinases in the phosphorylation
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
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
- 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,
As fluoride mimics TSH, we usually check on
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
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,
One such well-known mutated G protein is the
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
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,
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).
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
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
“White Spots” -
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,
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).
How much do
Dentists know about Oral Cancer?
article by Richard Gracer, MD
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
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
In women with general periodontitis all
hormonal systems were shown to be excessively shifted (Puzin et
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."
Bob J, Vishal R, Andreas S, Wendy S,
Trent H, Marshall G
Thanks to: Jack S, Peter M,
Jane J, Bob G, and Randy T
Editor: Andreas Schuld
© 2002 PFPC
(Parents of Fluoride Poisoned