|Some Important Developments Presently Influencing Dental Health In America -|
2-Placing Undue Emphasis Upon Brushing The Teeth Immediately After Each Meal
In 1938 Stephan26 designed a microcolorimetric technic for determining the pH of plaque material removed from the surfaces of teeth, and of debris from cavities. In 1940,27 employing a delicate antimony electrode, he measured the pH of plaques and cavities in situ. He found that the lowering of the pH of the plaque reaches its greatest intensity during the first thirty minutes after a glucose rinse and that little or none of the effect remains after two or three hours. Fosdick and associates,28,29 testing plaque material from teeth for pH with a microglass electrode, found similar rapid reduction after ingestion of carbohydrates.
Stephan30 also found that there is a quantitative difference in the intensity and duration of the acidity produced by carbohydrates on the teeth of caries-free and caries-active individuals, the pH drop being greatest in cases with extensive caries activity.
With the idea of making practical application of the above information, dentists and dental authorities have advocated brushing the teeth immediately after each ingestion of sugar-containing food.31 The American Dental Association got out a pamphlet32 advocating the procedure.
Commercial interests, taking advantage of this information and especially the later clinical report of Fosdick,33 have extensively and continuously advertised the idea that the teeth must be brushed immediately after each meal. This is done in connection with appealing, extravagant and misleading advertising for the purpose of promoting the sale of their "superior dentifrices". For several years anyone who reads current periodical literature, listens to the radio or watches T.V. programs has been repeatedly advised to brush his teeth promptly after each meal.
In 1950, Fosdick published33 the results of an extensive study carried out over a two year period by a group of 10 dentists on a total of 946 (423 controls, 523 test subjects) college students in 7 institutions. The test subjects were required to brush their teeth after each meal. The controls were allowed to follow their usual procedure. Both clinical and x-ray examinations were employed. Statistical methods were employed in analyzing the data. The results varied considerably when different methods of estimating them were used but a reduction in the neighborhood of 50 to 60 per cent in the average number of new carious surfaces over the two year period was indicated.
The test subjects were instructed to rinse the dentifrice from the mouth after each brushing and when brushing was impossible to rinse the mouth thoroughly with water. The author33 recognized that the rinsing and not the brushing may play a large part in the results. "It is obvious that the toothbrush or the abrasive cannot physically reach the inner portions of the proximal areas. Hence it is to be expected that the forcible dilution of the material in these areas might account for the results. There is considerable evidence to substantiate this possibility". Thorough rinsing of the mouth soon after each meal not only dilutes but it washes away much of the soluble material, in addition to particles of food material on the teeth.
Brushing the teeth immediately after meals, if properly done with the right kind of toothbrush, probably does no direct harm, but emphasizing and promoting it tends to encourage placing undue reliance upon it and to detract from the essential and entirely effective cleaning of the teeth at night before retiring. It only promises some preventive effect against caries. Rinsing vigorously without the brushing or dentifrice does about as much good.
Brushing alone, in the usual way, could have little or no preventive effect upon the other more important disease, periodontoclasia, for the reason that it does not clean the proximal surfaces within the gingival crevice where the etiological material (bacterial film and calculus) accumulates.
Since the teeth must be cleaned effectively (by the proper use of the right kind of both toothbrush and dental floss) every night before retiring, and they should also be brushed upon arising in the morning, brushing also after each meal, making a total of 5 times a day, would increase any harm that may result from overvigorous use of current harsh inappropriate brushes. "Nothing has been so destructive of tooth structure or has caused so much recession of the investing tissue as the use of stiff, ill-shaped brushes." Most people who have habitually brushed their teeth for several years with the usually employed brushes have worn back the edges of their gums over the high places to some extent.
Brushing the teeth immediately after each meal is not convenient or practical and will not be carried out by many people. Since, it is not necessary, and of itself, is not of any considerable benefit, placing undue emphasis upon it tends to mislead and confuse the public and thereby to unfavorably influence dental health.
|3- Artificial Fluoridation Of Communal Water Supplies|
Previous observations relative to "mottled enamel"34,38 led to the discovery by Churchill,39 in 1931, that this condition was caused by the fluoride ion in the water supply. Dean and Evolve40 concluded that 1 ppm fluoride in drinking water was not harmful and therefore "has no public health significance". Dean41 in 1942, announced that caries incidence in children was about 60 per cent less in areas where the fluoride was at or above 1 ppm, as compared with nonfluoride areas.
This and much other confirmatory evidence of substantial reduction in caries damage from naturally fluoridated water provided a logical and supposedly sound basis for artificially adding fluorides to communal water supplies, up to what was considered to be the optimum level of 1 ppm. The catch was, and still is, the unwarranted assumption that this powerful chemical, in such small doses, has no harmful effect upon other organs and tissues of the body; while at the same time it is capable of profoundly affecting the teeth, and in some unknown but supposedly harmless way, of significantly reducing the incidence and retarding the pathological process of caries. Just why fluoride selects only the teeth to thus favorably affect or how this beneficial action by it is brought about have remained confused or unrecognized. The general belief is that such teeth, which contain somewhat more fluorine are therefore more resistant to caries activity.
Several separate study projects were set up for testing artificial fluoridation as compared with little or no fluoride in the water. Progress reports42-52 from time to time, and now some final reports after ten years53-56 all confirm the earlier observations that caries damage is significantly reduced in areas of naturally fluoridated water and about as much where water is artificially fluoridated to 1 ppm or more. A liberal over-all estimate from such of these reports as I have seen would be an average of about 50 per cent reduction in the caries rate in children. Some of the more favorable age groups show somewhat greater effect.
These results would be well worthwhile if they were secured without harmful effect, either to children who receive the most caries retarding benefit or to older people who benefit less or not at all. They are not. The reduction in the incidence of cavities in teeth (the advanced stage of caries) from fluoridated water results entirely from the contemporary increase in periodontoclasia (gingivitis) activity. This has not been recognized by the originators, promoters, and advocators of artificial fluoridation. However, it is a fact, nevertheless. The incidence and progress of caries lesions are reduced in the same way by increased gingivitis activity from any other cause, such for instance as Vincent's disease, numerous systemic diseases and conditions, certain vitamin deficiencies and certain other chemical poisons.
In order to understand the relationship between caries and periodontoclasia and the influence of ingestion of fluorides, it is necessary to be clear on certain fundamental facts relative to the nature of the pathological process, the prevalence of the early stage lesions of these diseases and how they advance.
Enamel caries lesions originate at certain locations where fermentable carbohydrates are retained and minute quantities of acids are produced by bacterial action. Caries does not occur without carbohydrates or without bacteria. Traces of acids produced at frequent intervals, or continuously, partially decalcify the enamel giving rise to a chalky white condition in which the enamel at the particular location is softer ("chalky enamel") and can be dug into with a sharp instrument. If the etiological conditions continue, the partial decalcification advances into the enamel and sooner or later may reach the dentin. Disintegration of chalky enamel may result in a break in the surface producing a depression or cavity, small and shallow at first, which continues to enlarge or advance. After cavity formation, and sometimes before, the caries lesion at accessible locations usually may be recognized and diagnosed. This should be considered the advanced stage caries lesion. There was a considerable period of time however, from the normal unaffected condition at the particular location, to this clinically diagnosable caries lesion. During this entire period the early unrecognized caries lesion at first is microscopic, but it usually progressively increases in size and in depth. The rate at which the process in each lesion progresses is determined by several variable factors, some of which may accelerate, others may retard it.
The most important factor in retarding proximal lesions is interproximal gingivitis (early stage periodontoclasia). This is always present to variable extent and in variable degrees of activity, from microscopic lesions only to active visibly inflamed lesions which bleed easily on pressure. Inflammatory exudate, which contains more or less blood serum and therefore has approximately the same pH as blood,57 tends to neutralize or counteract acids produced in the environment and thereby retard the caries process. If gingivitis is sufficiently active the caries process is slowed down or may be prevented from reaching the stage for clinical diagnosis. Many such retarded early stage lesions remain inactive indefinitely, others may progress slowly and break down in later life, leading to the impression that new caries lesions have developed. Actually practically all enamel caries lesions originate within the first year or two after the eruption of any given tooth.
The prevalence of early stage proximal caries lesions, either active, retarded, or inactive, in any given population can be learned only by examination by proper technic of a considerable number of extracted tooth specimens. Good technic for this purpose is to dip the specimen in 5 to 10 per cent HCI for less than thirty seconds to release the enamel cuticle, dip in water followed by 0.25 per cent acid fuchsin to improve contrasts and differentiate other tissues from enamel, and then examine under the dissecting microscope. The depth to which such early stage lesions extend can be satisfactorily observed if the specimen is split through the lesion with a double side flat separating disc or other suitable instrument.
I have examined many hundreds of specimens in this way. Lower incisors seldom decay. If these are omitted I have found proximal caries lesions in from 75 to more than 90 per cent of the specimens in the different collections examined. Many of them, even in those from older people, are still in the chalky enamel stage and have not reached the cavity stage. Their advancement has been retarded or prevented for many years. It is not unusual to find some such lesions with more or less calculus over them, indicating that there was no acid action at the particular location, at the time it was deposited, or since that time.
Reports have shown that the caries preventive effect of fluoride ingestion is remarkably selective58-63 relative to location of lesions. The greatest benefit applies to proximal lesions, much less to occlusal or other lesions. Now the Newburgh-Kingston reports56,64 confirm this pronounced selective effect, even where there is only about 1 ppm fluoride in the water. The antacid effect of inflammatory exudate applies especially to the interproximal region and thereby retards proximal caries. Any increase in gingivitis activity, however slight, increases the amount of exudate and correspondingly retards caries activity. The increase from as little as 1 ppm. of fluoride in the water is sufficient to substantially retard proximal caries but it has much less effect upon caries at other locations.
During the past fifteen years I have examined more than a thousand persons, mostly university personnel, more than half of them medical students. These people have been from different parts of the country, mostly from the gulf and other southern states, a good many of them from areas having naturally fluoridated water. On an average, those from known fluoridated areas have sustained less damage from caries than the others. On the other hand, they have sustained more damage from periodontoclasia and often still have more gingivitis. Several of them stated that although their relatives and acquaintances in their communities did not have much trouble from caries, some of them had more trouble from "gum disease" and sometimes already were wearing dentures at relatively early ages.
People who have naturally fluoridated or artificially fluoridated water will continue to experience less caries and more periodontoclasia damage. Their total dental health, therefore, will be unfavorably influenced as long as these harmful conditions continue.
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