Oral Lichen Planus and other oral lesions including squamous cell cancer: The Primary Cause is Immune Reactivity to Amalgam Fillings B Windham (Ed)
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
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
In a recent study of patients with
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 (
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 (
People with oral lichen planus often
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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).