Oral Lichen Planus and other oral lesions including squamous cell
cancer: The Primary Cause is Immune Reactivity to Amalgam Fillings B Windham (Ed)
I. Introduction
Dental amalgam has been
documented by medical lab tests and Government agencies to be the largest
source of mercury in most who have amalgam fillings (42).
Mercury is one of the most
toxic substances in existence and is known to bioaccumulate in the body of
people and animals that have chronic exposure (35,41). Mercury
from occupational exposure and dental fillings is primarily from elemental
mercury vapor. Mercury vapor is highly absorbed by the lungs and in
saliva or blood is rapidly converted to ionic or methyl mercury. Mouth
bacteria and yeast as well as other methyl donors convert other forms of
mercury to methyl mercury, so that most mercury in the
blood is methyl mercury, irregardless of source(9,15a,42).
Mercury in amalgam
fillings, because of its high volatility and galvanic action due to
presence of dissimilar metals in the mouth, has been found to be continuously
vaporized and also released into the body through galvanic
currents(29,43,etc.), and has been found to be the largest source of
mercury in the majority of people (WHO(27), 9,30,32,42,1,14). The
level of daily exposure commonly exceeds the U.S. EPA health guideline for
daily mercury exposure (35,42). Mercury vapor given off by amalgam
fillings accumulates in the teeth, tooth roots, gums, jawbone, and oral
tissue. The number of amalgam surfaces has a statistically
significant correlation to the level of mercury in oral mucosa
and saliva (1,12,13,26,30,33,36,42).
II. Oral Effects of Dental Amalgam
High levels of mercury have
been documented to accumulate in the gums, jawbone, and oral mucosa of those
with amalgam fillings and to be transferred to the blood stream and other parts
of the body(43). Concentrations of mercury in
oral mucosa for a population of patients with 6 or more amalgam fillings taken
during oral surgery were 20 times the level of controls(25). Studies
have shown mercury travels from amalgam into dentin, root tips, and the gums,
with levels in roots tips as high as 41 parts per million(ppm)(25). Studies have shown that mercury in the gums such as
from root caps for root canalled teeth or amalgam tattoos result in chronic
inflammation and proliferation of inflammatory cytokines, in addition to
migration to other parts of the body (31,7,6,43,54,51).
Mercury, silver, and
other metals from fillings can be seen in the tissues as amalgam “tattoos”,
which have been found to accumulate in the oral mucosa as granules along
collagen bundles, blood vessels, nerve sheaths, elastic fibers, membranes,
striated muscle fibers, and acini of minor salivary glands. Dark
granules are also present intracellularly within macrophages, multinucleated
giant cells, endothelial cells, and fibroblasts, and metals also accumulate in
tooth roots and the jaw bone(7,6). There
is in most cases chronic inflammatory response or macrophagic reaction to the metals(7,18), usually in the form of a foreign body
granuloma with multinucleated giant cells of the foreign body and Langhans types(29). In a group of patients with amalgam
tattoos that were tested, 74% of the
patients revealed high lymphocyte reactivity (positive MELISA test) to one or
more metal components of dental restorations(7k). The majority of MELISA
positive patients suffered from serious health problems (various allergies,
autoimmune diseases, Parkinson's syndrome etc.). Nickel and inorganic mercury
were the most common sensitizers in vitro. The cytokine assay revealed that
mercury chloride activated predominantly TH2 lymphocytes, while nickel chloride
activated mainly TH1 lymphocytes.
Many dentists are not aware
that the main source of amalgam tattoos is “oral galvanism”, where electric
currents caused by mixed metals in the mouth take the metals into the gums and
oral mucosa, accumulating at the base of teeth with large fillings or metal
crowns over amalgam base(29,43). Such mercury
including that in the commonly formed amalgam tattoos moves to other parts of
the body over time in significant amounts and more rapidly than the other
metals. Macrophages remove mercury by phagocytosis and the mercury moves to
other parts of the body through the blood and along nerves(7).
Another study (7l) demonstrated a dense mononuclear inflammatory infiltrate
associated with large and powdered debris and positivity for HLA-DR and MT in
inflammatory cells. While blood vessel walls and connective fibers impregnated
with powdered particles were negative for HLA-DR, they were positive for MT. In
addition, wherever epithelial basement membrane impregnation by powdered
amalgam particles was observed, a strong positivity for MT was detected. These
findings demonstrate that residual elements of AT still have noxious local
effects over tissues. Such metals are documented to commonly cause
local and systemic lesions along with other health effects, which usually
recover after removal of the amalgam tattoo by surgery (7fghim). The
high levels of accumulated mercury also are dispersed to other parts of the body(43).
The amount of mercury in
saliva averaged between 1.5 to 1.9 micrograms per Liter for each amalgam filling(30ab),
enough to cause daily exposure of 10 to 100 micrograms of
mercury. The amount of mercury released by a gold
alloy bridge over amalgam over a 10 year period was measured to be approx. 101
milligrams(mg)(60% of total) or 30 micrograms(ug) per day(1), and other studies have found similar
results(26,42). The average
mercury levels in gum tissue near amalgam fillings are often over 100 ppm(29),
and levels in oral mucosa removed during oral surgery averaged over 2 ppm(over
20 times controls ) and levels in root tips of 41
ppm(25,29,7). Having dissimilar metals in the teeth
(e.g.‑gold and mercury) causes galvanic action, electrical currents, and much
higher mercury vapor levels and mercury levels in tissues.
(26,28,29,1,2,4,5,7,8,25). The level of mercury in the gums or
jaw bone is often 1000 ppm near a gold cap on an amalgam filling (5,3,6,8,10),
and similar levels as high as 5600 ppm have been found in the jaw bone under
large amalgam fillings or gold crowns over amalgam by German oral surgeons(44). These levels are among the highest
levels ever measured in tissues of living organisms, exceeding the highest
levels found in chronically exposed chloral kali workers, those who died from mercury in Minamata, or animals that died
from mercury poisoning. The FDA action level for warnings of
dangerous levels in fish or food is 1
ppm and the EPA health criterion level is 0.3 ppm.
Amalgam also releases
significant amounts of silver, tin, and copper which also have toxic effects,
with organic tin compounds formed in the body being even more neurotoxic than
inorganic mercury.
Toxic/allergic
reactions to toxic metals such as mercury often result in autoimmune conditions
such as lichen planus lesions in oral mucosa or gums and play a roll in pathogenesis of periodontal disease. Oral lichen
planus has been found to be an autoimmune process in which the Immune Th1
T-cells mediate the reactivity, including Lymphotoxin-alpha(LTa), Tumor Necrosis Factor-alpha(TNFa),
and Interferon-gamma(IFNa)(18,37,40b). A
high percentage of patients with oral mucosal problems(37,18),
along with other autoimmune conditions such as chronic fatigue(23,39), MS or
lupus(40) have significant immune reactions to mercury, palladium, gold, and
nickel(37,23). Removal of amalgam fillings usually led to cure or
significant improvement for oral lichen
planus (15-17,20-22, 24,37,etc.], as well as for oral
keratosis(pre cancer) (16b,45) and most of other
oral health problems including metallic taste, tender teeth, mouth
sores, bad breath , bleeding gums and throat irritation(43). A
connection between mercury immune reactivity from amalgam and oral cancers has
also been demonstrated(18,19). Most
cases of CFS, MS, or lupus patients also had significant immune reactions
to inorganic mercury(MELISA test) and removal
of amalgam fillings usually results in cure or significant improvement of such
conditions (23,39,40,11). In one clinic(21) that
replaced amalgams for a large number of such patients, there was cure or
significant improvement in over 90% of cases. A Jerome meter was
used to measure mercury vapor level in the mouth, and many had over 50
micrograms mercury per cubic meter of air, far above the Government health
guideline for mercury(35).
In a recent study
of patients with OLP, 60 % showed sensitization
to 1 or more allergens using a patch test(17a). The greatest frequency of
positive reactions was to dental metals. The order of tested metals
according to frequency of positive reactions was mercury, amalgam nickel
, palladium , cobalt, gold , chrome , and indium. However, patch tests have
been found to not be a reliable indicator of mercury immune reactivity or
allergy. In large number of clinical trials by doctors treating OLP,
between 39 and 53% of patients tested by patch tests were indicated to be
reactive to mercury (16abc,17,24a). However
when patients had amalgams replaced, the majority recovered or significantly
improved in a relatively short time period irregardless
of patch test results (15,16abc,17,24,37). Thus the
authors recommend replacement of amalgam in all cases of OLP and
similar conditions. The MELISA blood lymphocyte immune reactivity
test appears to be a more accurate indicator of immune reactivity than the
patch test(37,39,40). When patch tests
are to be used it should be noted that the clinical trials found that mercury
immune reactivity is often a delayed reaction, with positive patch test
observed only later on the 10th or 17th day of the
test(17,24a). Patients with OLP also commonly have been
found to be immune reactive to gold or nickel(17,16d,37,40) so that
replacement of gold or nickel crowns may be beneficial in such patients when
amalgam replacement is not sufficient to
resolve the problem.
Oral
lichen planus and oral lesions, caused most commonly by reactivity to mercury,
are inflammatory pre-cancerous conditions that have
been well documented in the literature to often develop into oral squamous cell
carcinoma(OSCC)(46,90a). Infection and chronic inflammation have been found to contribute
to carcinogenesis through inflammation-related mechanisms(47,48). Inflammatory
bowel diseases are associated with colon carcinogenesis and inflammatory
oral conditions such as oral lichen planus (OLP) and leukoplakia are associated
with OSCC.
Previous studies have shown significant increases of NF-kappaB dependent cytokines, Tumor Necrosis Factor-alpha(TNF-a), IL-1alpha, IL-6, and IL-8 in different oral
fluids from oral lichen planus (OLP) patients(48,15a,etc.). In
samples of whole unstimulated saliva in this study, for moderate and severe OLP dysplasia,
the level of each cytokine was significantly higher than in control. In
moderate dysplasia, TNF-alpha and IL-1alpha were significantly increased at a
level without difference from OSCC, but IL-6 and IL-8 was detected at a
concentration significantly lower than OSCC. In severe OLP dysplasia,
the level of TNF-alpha was not significantly different from that of Oral
Squamous Cell Carcinoma. The study confirmed preclinical data that NF-kappaB dependent cytokines are upregulated in pre-malignant OLP and
oral carcinogenesis. Cytologic and DNA-cytometric examination of oral lesions and
oral lichen planus have also been found to be reliable indicators of OLP cases
becoming malignant(49). Immunolabeled
oncoproteins were found to b modified in the
premalignant leukoplakia, oral lichen planus and in squamous cell cancer(49,46a). The evidence
supports that dental amalgam is the most common cause of oral squamous cell
carcinoma, similar to the fact it is the most common cause of OLP. The
available pretreatment dental records of 133 patients with carcinoma of the
tongue seen at the British Columbia Cancer Agency between 1958 and 1992 were
reviewed. The majority had amalgam fillings on the side of the
tongue involved in the carcinoma. Of the 7 patients with amalgams on
only one side of the mouth, 6 cases of oral cancer had amalgams on the side of
the cancer and only 1 on the side without amalgams(50).
People
with oral lichen planus often develop OLP at multiple sites(51) and also can have lichen planus in
other locations such as the esophagus(52) or genitals(53). In one study 41
women diagnosed with OLP underwent gynecological exam and 75.6% were
found to have evidence of genital involvement, vulvar lichen planus or vulvar
lichen sclerosis(53b). Such inflammatory conditions can also
become cancerous(52,54). Two siblings
with long standing cutaneous lichen planus of the esophagus both developed
squamous cell carcinoma(52). Since
immune reactivity to mercury is the most common cause of OLP and OSCC
and since immune reactivity to mercury is a systemic condition (37,etc.), systemic immune reactivity to mercury might be the
most likely cause of lichen planus and resulting squamous cell cancers of other
organs such as the esophagus and genitals.
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***************
note: etc. in a list denotes that author is aware of more
references on this subject, generally available in (41 or 43).