Of metalicized mouths, mycotoxicosis, and oxygen

Townsend Letter for Doctors and Patients,  June, 2005  by Philip Mollica,  Robert Harris

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At the energetic-molecular level, the boundary between health and the state of absence of health is marked by oxidosis, acidosis, and dysoxygenosis (dysox). (1-4) Microbial toxins and mercury are the most potent and common inciters of those three furies in the oral cavity. Regrettably, there is little, if any, appreciation of those crucial important causes of systemic disease among physicians. I have yet to meet a neurologist who seriously considers the role of mercury in the causation of multiple sclerosis, or a rheumatologist who searches for etiologic factors in oral microabscess of a patient presenting with lupus erythematosus. Nor have I met a cardiologist who suspects oral mycotoxicosis as the cause of cardiac arrhythmia. Later, I present data about one such case to underscore the importance of this relationship.

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The general community of dentists has not fared much better in the past. Except for some enlightened biologic dentists, the crucial importance of oral toxicity in triggering, amplifying, and perpetuating systemic inflammatory and infectious disorders has largely been ignored by dentists. That is not so because the relationship between oral pathologies and systemic disease has not been recognized. Indeed, it has been described since antiquity, including some texts devoted to this subject written by an Arab physician. (5) Fortunately, that is changing. An ever-enlarging community of dentists is becoming increasingly aware of issues of oral dysoxygenosis and how to effectively address it.

In this column, one of the authors (MA) explores some aspects of the man-microbe conflict in the context of oral dysox. The other two authors follow that with their clinical observations on the use of oxystatic therapies for insidious and indolent infectious processes in the oral cavity, with focus on ozone therapeutics

Oxygen and Biofilms

Below is reproduced some text from "Heavy Metal Load and Toxicity," the seventh volume of The Principles and Practice of Integrative Medicine, (6) to provide a framework of reference for presenting ozone therapeutics.

Biofilms are microbial tribes abiding by Darwinian imperatives--adapting to dynamic changes in the oxygen order and availability of their growth requirements in their microecologic conditions. Oral dysoxygenosis is the state in which oxygen homeostasis is regionally disrupted by local conditions in the mouth. Mercury from dental amalgams appears to be one of the most, if not the most, potent disrupters of oxygen metabolism in the oral cavity. Other such disrupters are thioethers and other microbial toxins. Those factors also alter the local conditions that either inhibit or foster microbial growth, so facilitating biofilm formation. Such dynamics seem to play crucial roles in the pathogenesis of systemic disorders rooted in the oral cavity.

In the classical sense, Costerton described biofilms as complex, heterogeneous bacterial colonies embedded in a protective slimy, polymeric polysaccharide matrix that they themselves produce. (7-9) Such microbial communities are well known for their resistance to various antibiotics and are increasingly recognized as the roots of many chronic and indolent infections. (10,11) Disruptions of local tissue architecture--fibroproliferative or occlusive lesions, for instance--facilitate biofilm formations and so impede healing with resolution. Antibiotic resistance of biofilms has been attributed to differentiated, structured groups of cells with communal characteristics that are distinct from those of the parent cells. Some Candida albicans biofilms examined were composed primarily of yeast and hyphal forms, with some pseudohyphae. Upper regions of such biofilms were made up of tangled masses of hyphae with openings between germ tubes about 10 to 50 mM across. Such biofilm architecture markedly alters effective diffusion coefficients of various substances, such as chlorhexidine digluconate. Such changes in diffusion rates are of considerable consequence in terms of diminished fungicidal activities of various agents employed to eradicate infections caused by Candida and other mycotic species.

Biofilms also appear to play central roles in initiating, amplifying, and perpetuating anomalous and unremitting inflammatory responses--locally in the oral cavity and other locations as well as systemically in tissues far removed from the sites of biofilm formation. Such phenomena also set the stage for chronic and indolent lesions--infectious as well as noninfectious--again, not only locally in the dental, periodontal, and sinusoidal tissues, but also systemically in tissues distant from the oral and sinusoidal cavities.

The biofilm studies of direct relevance to the subject of oral dysoxygenosis, of course, are those that directly examine the oxygen dynamics and effects of reactive oxygen species on the biofilm formation and how the characteristics of biofilms, in turn, affect oxygen metabolism. In essence, we are interested in how dysfunctional oxygen metabolism may lead to biofilm formation and how biofilms increase the degree of local dysoxygenosis. In the context of dental amalgams, such considerations lead to the larger question of the impact of the "mercury-dysoxygenosis-biofilm dynamics" on the health/disease/disease continuum in the oral cavity as well as in systemic tissues.