| The Necessary Personal Oral Hygiene For Prevention of Caries and Periodontoclasia* |
by
Charles C. Bass, M.D.
New Orleans, La.
August 1948
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Almost all loss of teeth results from either caries or periodontoclasia. These two diseases can be prevented by the necessary personal oral hygiene. They cannot be prevented in any other way now known. The purpose of this paper is to present the oral hygiene procedure every person must follow in order to entirely prevent these diseases and their consequences, and in order to maintain the state of oral cleanliness most people would like to maintain. The personal oral hygiene procedure here presented as essential has evolved from practical application of already well known fundamental information and more recent additional pertinent information that has been published or is in process of publication.1~4 By intensive microscopic study of extracted teeth, employing technical procedures1,2,5 not usually employed for this purpose, it has been possible to secure more accurate information regarding the conditions at the locations and in the environment where caries and periodontoclasia begin. To prevent the occurrence and progress of the lesions of these diseases their early stage must be prevented. The oral hygiene necessary to prevent these diseases, therefore, must effectively meet and counteract the etiological conditions at the locations where the lesions originate.
WHERE CARlES BEGINS
Enamel caries begins principally at or about occlusal pits and fissures and at or about the contact area between teeth. The earliest lesion consists of a "white spot" of "chalky", partially decalcified enamel. If the conditions are prolonged the lesion extends in area and depth and finally this fragile, partially decalcified enamel breaks down producing a cavity - the advanced stage of caries. The cavity, if large enough, usually can be diagnosed by the dentist but most of the earlier stage lesions cannot be recognized, except upon extracted teeth.
Some idea of the frequency and extent of these early stage lesions can be gained by very simple procedure, even without any microscopic laboratory equipment or experience. All that is necessary is to place extracted teeth (preferably from persons under 20 years of age) in 10 per cent hydrochloric acid (water 85, formalin 5, HCl 10) for one minute, then wash and brush with an ordinary toothbrush to remove the loosened cuticle, bacterial film and debris. Any "white spot," early stage caries lesions present can be seen satisfactorily (Figure 1) with the unaided eye.
*Studies promoted by facilities to which the author has had access at the School of Medicine, Tulane University of Louisiana, and by aid for equipment and supplies provided by the University. The substance of this paper was presented before a special meeting of the New Orleans Dental Association March 11, 1948.
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| Figure 1 |
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They contrast well with the more transparent normal enamel. The contrast is even sharper after the specimen has been allowed to dry. Under magnification, the lesions may be observed and studied better. Ordinary hand lenses are quite helpful. The dissecting microscope is still more helpful in studying such preparations.
It will be observed that some of these partially decalcified areas have more or less brown stain. In most instances these are old lesions which have been inactive for some time, due to changes in the environmental conditions which formerly initiated the lesion and promoted activity. A good example is proximal lesions on a tooth where the contacting tooth was lost some time previously. Such inactive lesions are more often found on teeth from people past 25 years of age.
Sometimes a small broken down area (cavity) may be observed in a larger area of partially decalcified enamel which still holds its form. It will be observed that most small to medium size cavities have more or less unbroken chalky enamel about them. (Figures 2, 3).
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| Fig. 2 |
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| Fig. 3 |
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No cavity ever forms except as a result of breaking down of this earlier stage decalcified enamel. The early stage, partial decalcification, therefore always precedes cavity formation. Prevention of cavity formation and its consequences can be accomplished only by recognition of the etiological conditions at the location where the earlier partial decalcification occurs and by application there of effective measures for preventing or minimizing those conditions.
THE ENAMEL CUTICLE IN RELATION TO THE EARLY STAGE OF CARIES
It has been shown2 that the enamel cuticle bears an important relationship to the early stage of caries. The enamel cuticle is an extremely thin keratin-like, transparent membrane covering the entire enamel surface at all times. It is thinner over areas where it is repeatedly worn by functional or other friction than in other areas where it is not exposed to such friction, however it is extremely thin in such areas also. In view of some confusion and conflicting opinion as to the continued presence throughout life of an enamel cuticle, it may be worthwhile to give here a simple procedure whereby anyone who is interested can clarify the matter for himself. Again this can be done without the aid of microscopic laboratory equipment or experience.
Place a tooth specimen in the 10 per cent HCl for one minute; remove gently and dip in water for a moment to reduce the acid; place in 0,5 per cent crystal violet solution (crystal violet 0,5 gm in water 100 cc) for one minute or less; again dip in water to remove excess of stain. Now observe the loosened cuticle with the tooth immersed in a shallow dish of water in which the membrane may be teased off with some suitable delicate instrument (No.2 or No.7 Clevdent or S. S. White Explorer) and manipulated in the water. The cuticle itself is slightly stained and the bacterial film upon it is heavily stained. When floating in the water the membranous nature of this material from the surface of the enamel is readily recognized. One who examines a few specimens in this simple way knows, of his own knowledge, that an enamel cuticle is continuously present on teeth. This enamel cuticle is of interest in relation to caries because the bacterial film over the early stage lesion is firmly attached to the cuticle (Figure 4) and because the acid or acids which cause the first partial decalcification there must pass through the intact membrane to reach the enamel.
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| Fig. 4 |
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NATURE OF THE BACTERIAL FILM OVER THE EARLY STAGE LESIONS
A film or pad of soft bacterial material of variable thickness is present on the surface of the tooth at all areas where it is protected from removal by functional or other friction. It is thickest where it is best protected. Microscopic examination of appropriate preparations of this material ("soft tartar") shows it to be composed entirely of bacteria, usually of many different kinds. (Figure 5).
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| Fig. 5 |
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One characteristic of such bacterial material over early stage caries lesions (and elsewhere in most cases) is that it consists mostly of long rod and filamentous forms, one end of which is attached to the cuticle on the tooth. The rods and filaments extend outward, more or less parallel to each other, toward the surface of the pile or pad. At the surface there are the growing ends and fruiting heads of the long forms of which the deeper part of the film is composed (Figures 7, 8, 9); and among these, large numbers of other bacteria of many different kinds.
PRODUCTION OF ACIDS AT CARIES LOCATIONS
Food, as it is masticated, is thoroughly and heavily inoculated with many different kinds of bacteria in the saliva, derived from all the different locations within the mouth. The bacteria in such heavily inoculated food material lodged and retained upon the constantly present bacterial film pad at favorable locations about teeth, multiply and, through the action of their enzymes, break down the material which serves as their culture media. Many bacteria, when growing in the presence of favorable carbohydrates, produce acids. Such acids produced by bacteria at the surface of the bacterial film or within it, are carried, as if by a sponge or wick, through the film to the cuticle through which they pass to the enamel beneath. If such acids are produced at the particular location in sufficient strength and over sufficient length of time, decalcification of the enamel occurs. This decalcification is only partial, giving rise to the softened "white spot" caries lesion. The enamel is not completely dissolved by such weak acids in the same way as it may be, experimentally, by stronger acids. For instance, the enamel is completely dissolved and disappears (except for some remaining enamel matrix material) from a tooth immersed in 10 per cent HCl for an hour or two. On the other hand the enamel on a similar tooth immersed in 0.15 per cent HCl, even for much longer time, is not dissolved in the same way. Only partial decalcification occurs, similar to the partial decalcification of the "white spot" caries. The enamel on the tooth becomes softer and may be broken up or crushed like a piece of chalk in much the same way as that of the early stage lesion may be. Anyone interested can confirm this observation by the simple procedure of immersing (suspending) tooth specimens in solutions of acid of the suggested strengths, for several hours (several days for weak acids).
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| Fig. 6. |
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What seems to be the same kind of partial decalcification may be produced experimentally by solutions of organic acids, such, for instance, as lactic acid - the one generally supposed to be the most important in caries production. However, weak solutions of organic acids, such as can be assumed to be formed at caries disposed locations, act very slowly. It is only after long continued exposure to such weak acids experimentally that demonstrable partial decalcification occurs. Likewise it is only after long continued and repeated production of acids by bacterial action, that a caries lesion results. It is very apparent that to prevent early stage caries at any vulnerable place on a tooth, it is necessary to prevent the formation of acids by bacteria growing there*.
*Note: I am aware of the suggestion, belief or claim by recent authors (6, 7, 8, 9, 10, 11, 12, 13, 14) that caries is, to some extent, a proteolytic process by which the organic material of the enamel is invaded and broken down by the enzymes of proteolytic bacteria and that this is followed or accompanied by disintegration or decalcification of the inorganic material. The personal oral hygiene for prevention herein specified would be equally applicable to such order of events in the caries process.
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TIME FACTOR IN PRODUCTION OF ACIDS BY BACTERIA
Some bacteria grow and produce acids much more rapidly than others. However any of them require considerable growing time, under the most favorable conditions, for production of appreciable amounts (or strengths). Perhaps the most familiar example for those who have been medical or dental students is the testing of acid production by pure cultures of different bacteria inoculated into litmus milk. Litmus milk is blue, a tube of such culture media inoculated with a loopful of a pure culture of an acid producing organism and placed in the incubator still remains blue for several hours, usually twelve or fifteen or more. After the necessary incubation time it will be noted that the color is changing to a faint pink and finally, within twenty four hours or a longer period, to red, indicating production of considerable lactic acid from the sugar in the milk. Stephan and Miller15 showed that brushing the teeth thoroughly before rinsing with 10 per cent glucose solution eliminated the fall in pH which otherwise would have occurred. They found that in testing plaque material in situ for pH drop following the glucose rinse, subjects who refrained from brushing their teeth for three or four days, thereby insuring a sufficient amount of bacterial material on accessible surfaces, gave most satisfactory results. Therefore a considerable period of time is required for sufficient growth and accumulation of bacteria to occur before much acids can be produced in the presence of carbohydrates.
However another factor plays an important role in the production of acid, i. e., the amount of inoculum or number of bacteria with which the culture medium is inoculated. If, for instance, a tube of litmus milk is inoculated with say 2 or 3 cc. of rich culture, containing enormous numbers of viable bacteria, instead of the loopful as suggested above, containing relatively only a fraction as many, then we find acidity developing and the color changing within a shorter time, sometimes only a few hours.
Applying the above elementary information to our problem of preventing acid formation and thereby preventing caries, it is evident that removing from about a tooth all food material which may serve as culture media for acid producing bacteria and removing from the same location most of the bacteria, there will be little growth of bacteria (for lack of culture media) and no production of acid (for lack of fermentable carbohydrates) until food is again lodged at the particular place and sufficient time elapses for bacteria to multiply and produce acid.
Decomposing food material that has been retained and has accumulated about the teeth during the daytime gives the bacteria growing there a good start towards acid production by bedtime. If these conditions are allowed to continue through the night during sleep the most favorable conditions exist for more rapid bacterial growth and production of acids, and their action upon the teeth. As a matter of fact, the caries process progresses principally at night and during sleep. Therefore to prevent the initiation and further progress of caries the teeth must be effectively cleaned of food and accumulated bacterial material at night before retiring. Nothing else will suffice.
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EARLY STAGE PERIODONTOCLASIA
Periodontoclasia begins and progresses as a local microscopic disease process. The earliest stage lesions are too small and inaccessible to be recognized except by microscopic examination of suitable sections or other preparations of the tissues involved. What is ordinarily diagnosed clinically as periodontoclasia (pyorrhaea) on the basis of flow of visible amounts of pus, receded periodontal soft tissue, alveolar resorption, pocket formation, loosened drifting teeth, etc., represents, in fact, the far advanced stage and results of a disease that usually has existed and progressed at the particular location for many years. Long previously, there was an earlier stage, actually a beginning, of the same disease about the same tooth. It is this earlier stage against which effective prevention must be directed. Measures for this purpose must be based upon clear understanding of the etiological conditions at the locations where the disease starts and from which the lesions about each tooth advance.
RELATION OF THE ENAMEL CUTICLE TO EARLY STAGE LESIONS
It has been shown2 that the enamel cuticle bears an important relationship to the early stage of the periodontoclasia lesion. The marginal gingiva normally rests upon the smooth, non-irritating enamel cuticle. Bacteria allowed to grow and accumulate for a long time on the tooth at the gingival margin, tend, in time, to produce microscopic roughness and hardened concretion upon the cuticle. The tendency is for this to increase, not only encroaching upon the gingival margin but extending into the gingival crevices (Figure 10). In time a narrow portion of the free gingiva (the free gingiva is that portion extending occlusalward from the level of the bottom of the crevice) rests against a surface covered with hard concretion and a pack of soft bacterial material. The irritation caused by the presence of this foreign material upon the tooth, where normally smooth, non-irritating cuticle exists, soon causes inflammation; at first only microscopic in extent. Minute and microscopic quantities of inflammatory exudate and pus cells are poured out through the inflamed tissue into the gingival crevice, and these tend to promote the growth of microorganisms and increase of the concretion. As the foreign material on the tooth increases and advances further into the gingival crevice, the soft tissues attached to the tooth are forced back by the accompanying inflammation and ulceration. Gradually and almost imperceptibly a larger and larger portion of the tooth is exposed as the gingival margin moves further away from the occlusal level. The gum "recedes."
Many factors influence the progress of the lesions at different locations about a given tooth, about different teeth in the same individual and in different individuals. For our present purpose of prevention of the disease (lesions) and prevention of further progress of lesions that already exist, it is only necessary to adopt and direct effective measures against the conditions at and within the gingival crevice. The disease process involving the more remote tissues - periodontal membrane, alveolar bone - rapidly subsides as soon as the local lesions consisting of inflamed, suppurating and broken surface of the epithelial tissue of the gum within the crevice, subside and disappear.
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| Fig. 10. |
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From the earliest stage and continuously as the lesion progresses, the tooth surrounded by this concretion and bacterial material adhering to it within the gingival crevice is, in effect, a foreign body infected with many different kinds of bacteria. It is a suppurating lesion constantly exposed to invasion by any and all of the many different kinds of bacteria within the mouth which are capable of growing in such an environment.
This foreign body effect was recognized and emphasized as the cause of periodontoclasia more than seventy years ago by Dr. John W. Riggs.16 He supported his claims by the marked benefit and control of the disease he secured by removing this foreign material from the surface of the tooth and polishing it so it no longer caused the constant irritation and suppuration characteristic of the disease. The treatment had to be repeated frequently as the material soon reformed. How different it would have been if he and those who followed him could have had their patients carry out the personal oral hygiene procedure we now know to be possible and essential, thereby preventing the recurrence of the local conditions which originally caused and promoted the disease!
MATERIAL UPON THE TOOTH AND WITHIN THE CREVICE
In order to devise and adapt personal oral hygiene measures for prevention of the formation of the material upon the tooth which causes and promotes progress of the disease, correct conception of the nature of this material is necessary. We have already seen that the bacterial film (tartar) on the surface of a tooth above the gingival margin at the more protected places where it can accumulate and where it is not dislodged by functional friction (Figures 10, 11), consists largely of a thick pad or pile of long rod and filamentous bacteria, one end of which is attached to the enamel cuticle. The other end extends outward to the smice of the film pack where there are usually an abundance of other bacteria of many different kinds.
The gingival margin must rest against this bacterial mass of foreign material which causes irritation, inflammation and suppuration. As the foreign material on the tooth builds up and advances into the gingival crevice (Figure 12) the inflammatory exudate there offers favorable environmental conditions and nutritive material for the growth of other types of microorganisms that do not grow outside of the crevice. They are organisms, such as certain leptotrichia, actinomyces, spirochetes, ameba, etc., which prefer or require the more or less anaerobic conditions, inflammatory tissue exudate, blood and pus present in such diseased gingival crevices. After a lesion, although small, is well established at any particular location and any time thereafter during the advancement of the lesion, the surface of the tooth within the crevice against which the inflamed gingival surface rests, has more or less hard calculus on it at most areas. The inner border of such calculus approaches but usually does not quite reach the zone of disintegrating epithelial attachment cuticle1, a landmark that can be seen on extracted teeth and indicates the exact location of the outer border of the epithelial attachment. Superimposed upon and attached to the calculus and any part of the tooth on which there is none, within the gingival crevice, there is a pad or pile of soft bacterial material. This bacterial film consists largely of closely packed parallel long rod and filamentous forms, one end of which is attached to the calculus or the tooth from which the rod or filament extends outward toward the surface of the pad against which the inner inflamed surface of the gum rests. At the surface of the bacterial film within the crevice there are growing ends and fruiting heads of the rods and filaments composing the pad, and among these more or less other bacteria that invade the lesion from the mouth. Among elements making up the film pad on the tooth within the gingival crevice perhaps the stems and fruiting heads of Leptothrix falciformis are the most noticeable and the most constant. This organism was first described in material from around teeth by Beust17 in 1906 and 1908. I5 have called attention to the fact that the habitat of Endameba buccalis is among the stems, branches and fruiting heads composing this film pack.
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| Fig. 11. |
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| Fig. 12. |
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| Fig. 13. |
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We do not know exactly what role any of the different microorganisms found in the gingival crevice play relative to disease there. Probably it is a very complex process. However it is clear that for the purpose of preventing initiation of the lesions of this disease and preventing further progress of lesions that have already been established, effective measures must be applied to prevent or minimize the growth and accumulation of bacterial material on the tooth at the entrance to, and within, the gingival crevice, which cause the disease (Figures 10, 11, 12),
Food material retained at the entrance to the gingival crevices and between the teeth, and packed into the crevices, promotes growth of bacteria there and increases inflammation of the tissues against which it rests. If food and bacterial material that has accumulated at and within the gingival crevices during the day is effectively removed at night before retiring, there follows a period of many hours during which there is greatly lessened bacterial growth. Rapid subsidence of inflammation occurs. Therefore to effectively prevent the initiation and further progress of periodontoclasia lesions the teeth must be cleaned at and within the gingival crevices every night before retiring. Nothing else will suffice.
DIAGNOSIS OF EARLY STAGE PERIODONTOCLASIA
The periodontoclasia lesion begins at the entrance to and just within the gingival crevice, principally the interproximal crevices, the distal and mesial crevices about teeth where there is no approximating tooth and the crevices at the buccal, labial and lingual embrasures. At first the lesion is only microscopic in extent. Even then there are a few (often only microscopic quantities) pus cells passing through the inflamed inner surface of the free gingiva. These tend to accumulate just within the crevice and at the entrance to it. Material removed from within the crevice by proper technic, stained and examined shows some to many pus cells. There are no pus cells within uninflamed healthy gingival crevices. Therefore, the presence of pus in material from the gingival crevice is diagnostic of inflammation there. Likewise the absence of pus cells means absence of inflammation and absence of periodontoclasia.
Microscopic examination for pus is a very simple procedure. Material must be properly taken from the gingival crevice, spread upon a microscope slide and stained with some one of the many appropriate stains for such specimens. The material must be delicately scraped from within the crevice with an appropriate small instrument, although some of the instruments usually used by dentists for other purposes may be used, the best results can be obtained with an explorer and scraper which the author first made from a D. C., R & L, Premierlite explorer (Figure 13). The blade is ground to a width of .55 mm and suitably shaped for entrance and manipulation within the gingival crevices-especially the interproximal crevices. A cross section of the blade is half disc shaped. With it one can obtain small amounts of material from the inflamed surface of the gum within the crevice and from the very bottom of the space, where the disease is progressing. Success depends upon correct technic in collecting and preparing material for examination rather than upon collecting large amounts improperly.
The material is spread in a small area (2 to 5 mm. in diameter is enough) upon a microscope slide. Removal of the small amount of material from the blade of the explorer and spreading it upon the slide can be facilitated by the use of some kind of teasing needle or other small pointed instrument. Several such specimens from different crevices can be placed at different locations on one slide, and all stained and examined at the same time. The author usually mounts on one slide for examination all the specimens taken at a sitting from a given subject.
The slide is ready for staining and examination. Anyone of many staining methods may be used satisfactorily, A good one for general purposes is as follows: (1) Fix with heat; (2) Carbolfuchsin one-half minute; (3) Rinse; (4) Crystal violet one-half to one minute; (5) Wash, dry and mount in oil for examination.
Pus and other cells are satisfactorily seen with the low power (16 mm) objective. Higher powers and the oil immersion objective are needed for study of the bacteria, spirochetes and ameba Endameba buccalis) that may be present.
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