Ecology, Pathogenesis, and Control

In fact, the partnerships can sometimes even be site detail.

The interactions, however, also may be either intra, inter, or multigeneric. Kolenbrander and London, for instance, found that 90% of their A. naeslundii, S. gordonii, strep mitis, Streptococcus oralis, and Streptococcus sanguis cultures coaggregated (2:3247). These they identified as primeval tooth colonizers. wholly were found to additionally coaggregate with F. nucleatum (2:3249). F. nucleatum can associate with all genera. Thus, it acts as a kind of microbial bridge between early colonizers and late colonizers (i.e. Selenomonas flueggei).

Among the oral bacteria, several incompatible adhesins have been identified. The intercellular effects of these structures can often be reversed by simple sugars. Galactosidespecific adhesins seem to be the most common.

Overall, adhesins and cellular coaggregation act to create a microbial support system. This enhances their efficacy to colonize the tooth's surface and, ultimately, promotes the accretion of dental consonant boldness.

The bacteria which pee-pee organisation may act as a commensural phytology (5:533). As Newman (1990) mentions, such flora have the potential for resisting transmission by more harmful microorganisms. Indeed, already this has been demo under a variety of different circumstances in several animal models (5:534).

Newman notes, however, that plaque has also been associated with a matter of widespread

The paper past goes on to detect agents which have been feature successfully into dentifrices. These have-to doe with plant extracts, phenolic compounds, and metal salts. In addition, the phenol, Triclosan, has also been used. When combined with zinc citrate, the agent reduced plaque accumulation and gingivitis without sorry the ecology of patients' natural plaque (4:462).

The subject matter by which these species' pathological effects can be avoided is also described. Marsh assumes that dental diseases are caused by shifts in microflora populations. This means that chemical agents must control rather than eliminate plaque accumulation.

Different therapeutic approaches include reducing the rate of plaque accumulation, removing existing plaque, suppressing the growth of species associated with disease, and inhibiting the production of bacterial virulence factors.

In contrast, diets which tend to be soft in texture have-to doe with reduced chewing, reduced tooth wear, and may lead to disease. Ultimately this slows tooth eruption, cause prolonged contact between the contiguous surfaces of adjacent teeth. The resultant role stagnation then may result in an supernumerary of interdental plaque.

Thus, according to Newman, it seems that the commensal plaque species which occur in health may also have a pathogenic capacity. Whether or not a species of bacteria realizes this potential though could involve any number of complex factors including bacterial antagonisms, virulence, growth factors, and the server response.

Yet another paper dealing with plaque and disease is that written by Christersson and his colleagues. Christersson et al. (1991) summarizes the historical events leading up to the "specific plaque hypothesis." This hypothesis suggests that the dental plaques of diseased tooth areas are different from those in healthy areas (1:441).

The paper then goes on to describe strategies for dealing with periodontal diseases
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