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Bisphenol-A in Dental Composites

There is considerable concern among scientists and the public about the hormone-mimicking properties of many chemical components of plastics, including those found in dental composites. The commonly used Bis-GMA resin uses one of the most controversial of these, Bisphenol-A (BPA). Responsible composite manufacturers claim that there is no unreacted BPA in dental resins, and that it takes high temperatures – several hundred degrees – to liberate free BPA. Other critics say that, in fact, the ester bonds in resins are subject to hydrolysis, and BPA can be liberated in measurable quantities. We know that dental sealants can vary in the amount of BPA they leak (reference), but at present there is no good in vitro survey of how much BPA is liberated by the major brands of composite resins. Also, we know that the world is full of plastic chemicals, and every living thing on earth has a measurable tissue level of BPA. We don’t really know if the amount of BPA released from dental composite is enough to raise a person’s exposure above the environmental background level, or if it is truly insignificant. The attached articles spell out the range of issues under investigation.

In 2008, the IAOMT undertook a laboratory study of BPA release from a range of commercially available dental composites under physiological conditions: 37º C, pH 7.0 and pH 5.5. Unfortunately, due to changes in administration at the university laboratory where the experiment was conducted, we had to terminate sooner than planned, and the information we gathered can only be regarded as preliminary. Measurable quantities of BPA were found leaching from composites. They were in the low parts-per-billion range after 24 hours, on the order of one one-thousandth of the known average daily exposure for adults in the industrialized world. These results were presented at the IAOMT conference at San Antonio in March 2009, and the complete lecture is available on the DVD of that meeting. The power point slides are attached, titled “San Antonio BPA.” Results for individual composite samples are on slide 22 of that presentation.

In 2011, the IAOMT conducted a small scale project with the Plastipure, Inc. lab in Austin, Texas, to see if there was any indication of estrogen activity from dental composites under physiological conditions. We looked for estrogen activity not specifically from BPA, but from any of the many chemical species that might be mimicking estrogens. Again, for reasons beyond our control, that lab closed too, before we could expand the study to the level of a publication. But at the level of the pilot study we completed,  no estrogenic activity was found, under physiological conditions of body temperature and pH.

The “BPA Review” article represents the view derived from standard toxicology, that we’ve relied upon in the past. This article reviews the literature on exposure versus toxic threshold data for bishpenol-A (BPA) from dental composites and sealants, and confirms that the known exposure is far below the known toxic dose.

However, the issue of possible hormonal activity of extremely small doses of BPA and other known hormone mimics, in the parts per billion range and lower, presents problems not discussed in standard toxicology. In the standard model, low dose effects are not measured, but are predicted by extrapolation from high dose experiments. Advocates of the low dose view say that extremely low exposures have another mode of activity entirely – “endocrine disruption.” By subtly augmenting normal, hormonally dependent, developmental stages in fetal animals, permanent adverse changes can be induced. These include prostate enlargement and increased susceptibility to cancers later in life.

The “BPA-Forum” article is an easy to follow introduction to this complex subject, with some very interesting comments on the nature of a toxic threshold in this world of endocrine disruption at extremely low doses. The “BPA-Endocrinology” article is a highly technical look at the subject, that contains an extensive tabulation of documented human tissue concentrations of BPA.

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