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Journal of Dental Research
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GUEST EDITORIAL

Toxicology of Dental Materials and ‘Clinical Experience’

Werner Geurtsen

Department of Restorative Dentistry, School of Dentistry, University of Washington, Box 357456, Seattle, WA 98195-7456, USA; wgert{at}u.washington.edu

Key Words: dental materials • toxicology • clinical experience • systemic effects

Dentistry has always been a discipline with strong emphasis on manual skills and clinical experience. Therefore, it is not surprising that these two aspects still characterize or at least severely influence dental education worldwide. Consequently, ‘clinical experience’ or, in aggravation, ‘vast clinical experience’ is frequently used, in private practice and academia as well, as a strong argument in favor of or against a hypothesis, an experimental finding, a new technique, or a dental material.

But what does the expression ‘clinical experience’ really stand for? It means that no reproducible scientific data exist, either from clinical investigations or from in vitro studies. This widespread approach in dentistry is clearly inconsistent with modern ‘evidence-based’ medicine, which is indicative of a widening gap between dentistry and medicine. Although it is not too amazing that ‘clinical experience’ still plays a major role in private practice, it is all the more unacceptable and unscientific to accept or reject hypotheses or experimental findings based on ‘clinical experience’ in the dental scientific community. Just recently, it has been stated in this Journal that the transfer of the ‘best available research evidence’ into daily practice rather than ‘clinical experience’ is critical for the future of our discipline (Chiappelli et al., 2003).

As a researcher who has investigated the toxicology of dental materials for more than 25 years, I am very familiar with the aforementioned discussion. Several months ago, my co-workers and I submitted a manuscript to one of our major dental journals about the effect of a resin compound on an important cell-biological parameter. Both referees unanimously stated that the investigated problem is of importance. But one reviewer also argued that the ‘vast clinical experience’ does not confirm our experimental data.

This objection is (at best) naïve. It is simply wrong that there is no clinical proof that resins, such as TEGDMA, or other materials, like alloys, may have systemic side-effects. In reality, no systematic effort has been made, so far, to identify such consequences, mainly because it is almost impossible to do retrospectively (Geurtsen, 2000, 2002; Geurtsen and Leyhausen, 2001). Systemic side-effects (except for an acute inflammation due to very high concentrations) may take many years or even decades before they are clinically manifest.

How can we solve this problem? The scientific approach is to investigate in vitro whether a substance has the potency to damage cells and tissues in a specific manner. Interactions with DNA are of particular interest (Schweikl et al., 1998; Schweikl and Schmalz, 1999). Thereafter, it makes sense to look selectively to see if these effects can be found in animals and humans. For example, it takes about 20 years for a tumor to become clinically ‘visible’ (Loeb, 2001). It would be very naïve to try to correlate such a neoplasm retrospectively to a certain cause—for instance, a resin filling which has been in place for 20 years or more (except for specific occupational risks, like long-term exposure to asbestos, or unhealthy lifestyle habits, such as smoking or excessive alcohol consumption).

In contrast, cancer researchers usually try to discover, in vitro and in animals, what may cause mutations in DNA or trigger uncontrolled and malignant cell proliferation. Subsequently, correlations are made between various types of tumors and specific causes (Reid et al., 1994; Loeb, 2001).

With the perspective of this scientific approach, the view that (dental) ‘clinical experience’ does not indicate systemic side-effects due to oral biomaterials reveals a deficit in our understanding of the complex events and the time frame characteristic of the generation of systemic side-effects. It is not justified to draw such conclusions from uncontrolled ‘involuntary field experiments’ without having more than fragmentary data about the biological long-term behavior of dental materials and their components.

It is our responsibility, and duty, to investigate in vitro and in vivo whether current restorative materials do or do not have the potency to generate systemic diseases and/or chronic local adverse effects over time. It is obvious that these important ‘evidence-based’ data are of great significance for the development of new biocompatible dental materials, and thus for the future of restorative dentistry.

Received for publication March 17, 2002. Accepted for publication March 21, 2003.

REFERENCES

  • Chiappelli F, Prolo P, Newman M, Cruz M, Sunga E, Concepcion E, et al. (2003). Evidence-based practice in dentistry: benefit or hindrance. J Dent Res 82:6–7.
  • Geurtsen W (2000). Biocompatibility of resin-modified filling materials. Crit Rev Oral Biol Med 11:333–355.[Abstract/Free Full Text]
  • Geurtsen W (2002). Biocompatibility of dental casting alloys. Crit Rev Oral Biol Med 13:71–84.[Abstract/Free Full Text]
  • Geurtsen W, Leyhausen G (2001). Chemical-biological interactions of the resin monomer triethyleneglycol dimethacrylate (TEGDMA). J Dent Res 80:2046–2050.
  • Loeb LA (2001). A mutator phenotype in cancer. Cancer Res 61:3230–3239.[Abstract/Free Full Text]
  • Reid TM, Feig DI, Loeb LA (1994). Mutagenesis by metal-induced oxygen radicals. Environ Health Perspect 102:57–61.
  • Schweikl H, Schmalz G (1999). Triethylene glycol dimethacrylate induces large deletions in the hprt gene of V79 cells. Mutat Res 438:71–78.[Medline] [Order article via Infotrieve]
  • Schweikl H, Schmalz G, Rackebrandt K (1998). The mutagenic activity of unpolymerized resin monomers in Salmonella typhimurium and V79 cells. Mutat Res 415:119–130.[Medline] [Order article via Infotrieve]

Journal of Dental Research, Vol. 82, No. 7, 500 (2003)
DOI: 10.1177/154405910308200701


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This Article
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