Effect of plaque ecology

29-03-2010

Owing to differences in local environmental conditions, the microflora of mucosal surfaces differs in composition from that of dental plaque. Similarly, the plaque microflora varies in composition at distinct anatomic sites on the tooth ¾ for example, in fissures, on approximal surfaces, and in the gingival crevice. The resident microflora of a site acts as part of the host defenses by preventing colonization by exogenous (and often pathogenic) microorganisms.

The early colonizers of the tooth surface include members of the genera Streptococcus, Actinomyces, Haemophilus, Neisseria, and Veillonella (Liljemark et al, 1986; Nyvad and Kilian, 1987). These bacteria adhere to the acquired enamel pellicle by specific and nonspecific molecular interactions between adhesions on the cell and receptors on the surface (Busscher et al, 1992; Gibbons, 1989). Once established, the microflora at a site remains relatively stable over time, despite regular minor disturbances in the oral environment (Marsh, 1989). This stability (termed microbial homeostasis) stems not from any metabolic indifference among the components of the microflora but rather from a dynamic balance of microbial interactions, including both synergism and antagonism (Sanders and Sanders, 1984).

It has been proposed that the ability to maintain homeostasis within a microbial community increases with its species diversity (Alexander, 1971). In dental plaque, diversity is enhanced by the development of food chains between bacterial species and their use of complementary metabolic strategies for the catabolism of endogenous nutrients, such as glycoproteins and proteins. Individual species possess different but overlapping patterns of enzyme activity, so that certain mixed cultures of oral bacteria can synergistically degrade complex host molecules (van der Hoeven and Camp, 1991). Antagonism is also a major mechanism in maintaining microbial homeostasis in plaque (James and Tagg, 1988; Marsh, 1989).

Unless removed by diligent oral hygiene, plaque accumulates preferentially at stagnant or retentive sites, such as the posterior approximal surfaces, the fissures of erupting molars, and along the gingival margin. Igarashi et al (1989), studying the effect of rinsing with sucrose solution on 4-day-old plaque, showed that the fall in pH in plaque was significantly greater on the approximal surfaces of the molars than in the fissures.

The ecological plaque hypothesis, introduced by Marsh (1991), proposes that a change in a key environmental factor (or factors) will trigger a shift in the balance of the resident plaque microflora, and this might predispose a site to disease. The occurrence of potentially pathogenic species as minor members of the resident plaque microflora would be consistent with this proposal. Under the conditions that prevail in health, these organisms would be only weakly competitive and might also be suppressed by intermicrobial antagonisms, thus constituting only a small percentage

of the plaque microflora, without clinical effect. Microbial specificity in disease would result from the fact that only certain species are competitive under the new (changed) environmental conditions.

It is a basic tenet of microbial ecology that a major change in an ecosystem produces a corresponding disturbance in the stability of the resident microbial community (Alexander, 1971; Brock, 1966; Fletcher et al, 1987). An increasing mass of plaque impedes penetration by saliva to protect the enamel. Microbial homeostasis can break down, and major shifts in the composition of the microflora can occur.

For example, frequent consumption of fermentable dietary carbohydrates is associated with an increased risk of dental caries (Loesche, 1986). Such diets lead to a rise in the proportions of mutans streptococci (MS) and lactobacilli, with a concomitant fall in levels of other streptococci, especially members of the Streptococcus oralis group, which include S sanguis, S oralis, and S mitis (Dennis et al, 1975; de Stoppelaar et al, 1970; Minah et al, 1985; Staat et al, 1975). The metabolism of plaque also changes from a heterofermentative pattern to one in which sugars are converted primarily to lactic acid.

Studies by Bradshaw et al (1989a) have shown that low pH, rather than the availability of carbohydrates per se, is the factor driving the selection of potentially cariogenic species. This selection is at the expense of acid-sensitive species, some of which are associated more with oral health. The experiment was repeated to determine if there were a “critical pH” at which this breakdown in homeostasis would occur. Plaque microorganisms were pulsed with glucose in three replicate experiments in which the pH was allowed to fall only to fixed values of pH 5.5, 5.0,

or 4.5. The microbial community was disrupted irreversibly only when the pH fell regularly below 5.0 (Bradshaw et al, 1989b).

The predominant species in these experiments always became Streptococcus mutans, Lactobacillus casei, and Veillonella dispar (Bradshaw et al, 1989b). These three species have been associated with nursing caries (Milnes and Bowden, 1985) and progressing caries (Boyar et al, 1989) in humans. Pure culture studies have also shown that the growth of these three species is less sensitive to low pH than is that of other oral bacteria (Bradshaw et al, 1989a; Harper and Loesche, 1986). Furthermore, mouthrinsing with acidic buffers (pH 3.9) was found to increase the proportions of mutans streptococci in human fissure plaque (Svanberg, 1980). Studies by van Houte et al (1991) have shown that streptococci other than mutans streptococci will increase the acidogenic potential of plaque at low pH. Collectively, these findings show that

the selection of cariogenic species following regular sugar consumption is likely to be a consequence of their aciduric physiology, which enables them to compete successfully at low pH.

On the other hand, in subjects with a conventional low-sugar diet, the composition of plaque microflora would be stable, only small amounts of acid would be produced at main meals, and the processes of demineralization and remineralization would be in equilibrium. If the frequency of fermentable dietary carbohydrate intake were to increase, however, there would be longer periods of low plaque pH (Loesche, 1986a).

Such conditions would favor the proliferation of mutans streptococci and lactobacilli at the expense of less acid-tolerant species, tipping the equilibrium toward demineralization.

Factors reducing the flow of saliva (eg, xerostomia) would lead to similar shifts in the microflora. Greater numbers of mutans streptococci and lactobacilli would lead to even faster rates of acid production from sugars, enhancing demineralization still further, while the elevated levels of lactic acid in plaque would also select for Veillonella spp. Acid-sensitive species, such as members of the S oralis group (eg, S sanguis, S oralis, and S mitis), would decline in proportion, thereby accounting for the widely reported inverse relationship between S sanguis and mutans streptococci seen in plaque. Other bacteria could also produce significant amounts of acid under similar conditions, at slower rates (van Houte, 1993), but nevertheless providing an explanation for demineralization in the absence of mutans streptococci.

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Comments

Р“РѕСЃС‚СЊ:
Hi Subramaniam: Junk food does no good for our teeth, but it is incorrect to say that tootaphstes can handle their cleaning better than toothpowders. Toothpastes (as would be evident from my post) and modern dentistry methods are harmful to teeth in the long run as is evident from the fact that once you go to a dentist you end up going repeatedly, and using tootaphstes does not give you complete relief from most dental problems.I would also always ask you to believe empirical evidence and not what anyone (including us) say. Switch over to a natural toothpowder without any change in your diet, and try out the oral care routine I’ve suggested, and see if you can see any visible results in a month’s time. If it does work well (and I think it will), then do try slowly switching over to a more holistic way of living as well (including a good diet by cutting out junk / processed food).Do let me know how your experiments proceed.

Р“РѕСЃС‚СЊ:
Hi,We haven’t tried Himalaya dental cream, so can’t rlealy comment Does it foam? If yes, I would not use it. I’ve found oil swishing to be the best mouthwash and as it acts internally makes for a great daily detox. Would not recommend any toothbrush finger brushing isn’t hard and if you follow the whole system I’ve outlined (oil swishing + brushing with your finger and a toothpowder) the mouth feels rlealy rlealy clean.Oil swishing is the same as using a mouthwash shoudn’t pull out any fillings unless they are ready to come out.Yes, gum massage with the finger and the toothpowder. Soapnut / Soapberry is the powdered fruit of the pericarp of Sapindus trifoliatus / mukorossi Quite easil available in Bangalore / Bombay.We don’t sell our tohpowder yet we started Krya with the Krya detergent which is a completely soapberry based detergent powder. I’m still not sure if we will ever commercial make and sell toothpowder.

Р“РѕСЃС‚СЊ:
Excellent article, Preethi! While I’ve been told that the haerdr you brush with toothbrushes having equally hard bristles, the worse it will be for the teeth, I somehow couldn’t accept that; I sort-of concluded that a good hard dirty-vessel-cleaning-scrub (to quote your words) especially before bed at night is the best possible thing for the teeth. Doing away with toothbrushes is a paradigm shift, I can see. And eventually accepting that the index finger will do a better job is going to be even more difficult but I’m going to try!Also, I notice in your reply to Sarika on April 26, Vicco tooth powder doesn’t get a mention. I’ve now been using Vicco toothpaste since turning vegan but you haven’t mentioned this company who are the only one to say it boldly on their toothpaste box cover that they don’t test their products on animals. I’m curious to know why!

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Articles for theme “caries”:

Colonization of microenvironments

29-03-2010

Colonization of microenvironmentsThe oral cavity consists of several major and minor compartments, each constituting a separate microenvironment not easily affected by major events in the oral cavity. Examples of major compartments are the tongue, the oral mucosa, and the tonsils. The different approximal tooth surfaces, occlusal fissures, and gingival sulci are regarded as minor compartments. A specific area that supports a bacterial flora is termed a habitat. The flora of a habitat develops through a series of stages, collectively called colonization.

Role of the Oral Environment – Introduction

29-03-2010

Role of the Oral EnvironmentIntroductionIn certain aspects, the oral cavity may be regarded as a single microbial ecosystem. A major regulatory factor is the flow rate of saliva, which decreases to almost 0.0 mL/min during sleep, is approximately 0.4 mL/min at rest, and increases to 2.0 mL/min after stimulation. Although saliva is not a good medium for supporting the growth of many bacteria, 1.0 mL of whole saliva may contain more than 200 million microorganisms, representing more than 300 different species.

Rate of accumulation (Plaque Formation Rate Index)

29-03-2010

Rate of accumulation (Plaque Formation Rate Index)The quantity of plaque that forms on clean tooth surfaces during a given time represents the net result of interactions among etiologic factors, many internal and external risk indicators and risk factors, and protective factors:· The total oral bacterial population· The quality of the oral bacterial flora· The anatomy and surface morphology of the dentition· The wettability and surface tension of the tooth surfaces· The salivary secretion rate and other properties of saliva· The intake of fermentable carbohydrates· The mobility of the tongue and lips· The exposure to chewing forces and abrasion from foods· The eruption stage of the teeth· The degree of gingival inflammation and volume of gingival exudate· The individual oral hygiene habits· The use of fluorides and other preventive products, such as chemical plaque control agents This observation has been the rationale for the development of the Plaque Formation Rate Index (PFRI) by Axelsson (1989, 1991).

Measurement of plaque – Amount of accumulation

29-03-2010

Measurement of plaqueAmount of accumulationSeveral indices for recording supragingival plaque have been developed. The two most frequently used are the Plaque Index (PI), developed by Silness and Loe (1964), and O’Leary’s Plaque Index (O’Leary et al, 1972).The Silness and Loe Plaque Index has a four-point scale:· Score 0 = The tooth surface is clean.· Score 1 = The tooth surface appears clean, but dental plaque can be removed from the gingival third with a sharp explorer.

Role of Plaque – Development of plaque

29-03-2010

According to Dawes et al (1963), dental plaque is “the soft tenacious material found on tooth surfaces which is not readily removed by rinsing with water.” It is estimated that 1 mm3 of dental plaque, weighing about 1 mg, will contain more than 200 million bacteria. Other microorganisms, such as mycoplasma, “yeasts,” and protozoa, also occur in mature plaque; sticky polysaccharides and other products form the so-called plaque matrix, which constitutes 10% to 40% by volume of the supragingival plaque.