The purpose of personal oral hygiene (usually called home care of the teeth) is (1) maintenance of oral cleanliness, (2) prevention of caries, (3) prevention of periodontoclasia. It is desirable not only to prevent initiation of the lesions of these diseases, but also to prevent, to the maximum extent possible, further advancement of lesions that already exist. An effective method must fulfill all three of these important purposes. A clean tooth does not decay. Periodontoclasia does not occur about a clean tooth. Therefore, a method which satisfies well the first purpose named, at the same time accomplishes the other two. No amount or quality of treatment and restorations by dentists can maintain dental health unless they are followed by effective personal oral hygiene. The success and durability of the dentists' work depend largely upon the subsequent personal oral hygiene of each patient. Of the many methods of personal oral hygiene now generally followed, none is entirely effective. This statement is confirmed by the fact that practically all adults, and many younger persons, have already sustained more or less damage from caries, and that periodontoclasia lesions are present around many or all of the teeth of practically all adults. This means that the methods of personal oral hygiene generally followed, whatever the source of instruction, are inadequate to prevent these diseases. Several years ago I designed and described1 the method of personal oral hygiene which is necessary for prevention of caries and periodontoclasia. It was based upon accurate information, secured mostly through laboratory research, upon the etiological conditions' at the locations where the lesions of these diseases originate and advance. Measures for successful prevention must provide for effective prevention or minimizing of these local etiological conditions. Correct information (not merely opinions) as to what these conditions are is necessary. Measures based upon incorrect information, erroneous beliefs, or misinterpretation of scientific observations, however authoritative they may seem to be, are unlikely to be effective. The causative organisms in these diseases are microscopic, the pathological processes originate and advance microscopically, the tissues involved are composed of microscopic elements and the lesions themselves, at first, are only microscopic in extent. Therefore, correct information about these conditions must be based upon microscopic research. Opinions and ideas not conforming to the basic facts, which can be confirmed only by microscopic work, are confusing, often entirely erroneous. During the past several years there has been opportunity to demonstrate, to their satisfaction, and to teach to a considerable number of dentists, the fundamental facts as to the local etiological conditions in these two diseases. With these facts known and understood, and any previously existing confusion or conflicting ideas cleared up, it is evident to anyone that effective personal oral hygiene is necessary for prevention of these diseases; and to significantly retard or prevent further advancement of existing lesions. It is also evident that methods generally taught and practiced are inadequate and could not be entirely effective. The necessary method, which I have described,1 is quite different from, and in some particulars quite the opposite of, ineffective methods generally advocated and followed. Dentists who have the necessary information have their expectations confirmed and are profoundly impressed by the effect they themselves experience personally, and the beneficial effect upon their patients whom they successfully teach. Hundreds of people (including a good many dentists) can be named who now, by this method, are maintaining a degree of oral cleanliness and dental health far greater than is possible in any other way. The purpose of this paper is again to direct attention to this method, I now have had considerable experience in presenting the fundamental facts upon which it is, based, and in teaching, the method to a considerable number of people (mostly university personnel). But before describing the method it seems desirable to recall briefly or present important information about the local etiological conditions which must be minimized or prevented and to recall or present some of the fundamental facts regarding the disease processes involved. Clear understanding of the cause of a disease is necessary for the adaptation of means for its prevention. If the disease be local, such as caries and periodontoclasia, clear understanding of the essential local conditions which cause the lesions and promote their advancement, is necessary for adaptation of means of preventing these local conditions.
Locations where enamel caries lesions originate. ~ Caries lesions of the enamel first appear in the occlusal pits and fissures and on the proximal surfaces between the teeth, at locations where there is more or less protection from natural cleaning. They do not originate on surfaces from which foreign material is frequently removed by functional friction or otherwise. Nature of the material in protected areas. - In uncleaned areas on the teeth there is continuously present a heavy film (Fig. 1) of bacterial material (usually called plaque) consisting Of long rod and filamentous types of microorganisms, characterized by having one end attached to the tooth (Fig. 2) and the other extending outward to the surface of the film where there are the growing ends and.usually fruiting heads of the fungi making up the 'pad. The thickness of this bacterial film varies greatly at different locations, determined largely by the depth of the space and by the exposure to friction by which the ends of the filaments at the surface are frequently rubbed off. At the surface there are not only the growing ends and fruiting heads of the filaments making up the pad. but also largenumbers of the very many varieties of other bacteria in the mouth. These are accumulated upon the surface and interspersed, more or less, between the outer ends of the filaments. Deeper in, however, the pad at any particular place is made up of the filamentous types only, each filament extending outward, at right angles, from the surface of the tooth to which it is attached. Breaking off the ends of the filaments at the surface of the pad still leaves a film consisting of stumps and stems (Fig. 3) attached to the tooth. Most of these are living and capable of growing in length again under favorable circumstances, thus restoring, in time, the former thickness of the film pack at any given location. The presence on teeth of filamentous types of microorganisms, usually spoken of as Leptothrix or thread forms, has been long recognized, some authors associating them with caries, others not. More than eighty-five years ago Leber and Rottenstein2 described filamentous forms of Leptothrix as the "microorganisms of caries." Their Figs. 1, 2, 3 in Plate II, illustrate the organisms and a pad of filamentous forms attached to, and radiating from, a decaying tooth surface. Wedl3 in 1870, emphasized the proliferation of Leptothrix in relation to, caries and illustrated this in several of the engravings in his Atlas to the Pathology of the Teeth, showing uniformly disposed, firmly adherent Leptothrix masses on exposed surfaces of teeth, especially those at which caries lesions originate. W. D. Miller4 in 1883, observed filamentous forms of Leptothrix on the teeth and in caries lesions. He describes, on the border of decaying dentin, indistinguishable masses of fungi from which project numerous threads of Leptothrix buccalis (See his Fig. 2). Later, in 1890, in his book5 on The- Microorganisms of the Human Mouth, his Figs. 63, 67, 79, indicate filamentous organisms composing the bacterial film on teeth. He was not able to identify these filamentous forms, or any other forms of bacteria found in the mouth, as the specific cause of caries. He evolved his well known chemicoparasitic theory to the effect that acids are produced by the breakdown of carbohydrates by acidogenic bacteria at the vulnerable locations; which acids decalcify tooth material and thereby cause and promote caries. All firm information to this day confirms and -supports the correctness of this theory formulated more than sixty years ago. In a recent survey of the literature relative to the cause- of caries Boedecker6 came to the general conclusion that "intact enamel surfaces in vitro exhibit widely variable resistance to attack by acids produced by acidogenic bacteria. There is no evidence that acidogenic bacteria and carbohydrates can initiate dental caries". (I do not accept this conclusion. Acidogenic bacteria and carbohydrates are essential for the initiation of caries lesions). "The progress of dental caries, once initiated, is effected by bacteria acting during the acidogenic phase on a carbohydrate substrate." "There is probably no specific microorganism associated with dental caries . . ." The conclusions reached by Bartels7 from a survey of the recent literature on the subject do not conflict with or contradict Miller's5 original theory, but rather support it. The fact that bacterial action on cariogenic food material within the mouth is necessary for production of caries is further substantiated by the work of Kite, Shaw, and Sognnaes 8 who showed that susceptible rats fed a cariogenic diet by stomach tube do not develop caries; and by Orland9 to the effect that rats maintained entirely free from bacteria, reared upon a cariogenic diet, do not develop caries, whereas controls on the same diet have a high percentage of caries. The work of J. Leon Williams, toward the close of the nineteenth century, contributed more than all others had previously, to the cause of caries and the microscopic conditions at the locations where the lesions originate. His paper10 in 1897, not only shed much light upon the microscopic caries process, but it showed clearly the nature of the bacterial film upon the surface of teeth beneath which the caries lesion originates- and advances. In numerous photomicrographs (See his Figs. 61, 62, 63, 64, 66,67, 69, 71, 75) he showed beyond question that the film pack is composed of long filaments radiating outward from the surface of the tooth to which they are attached. His work substantiated the claims of Miller5 and of G. V. Black11, that caries is caused by acids produced by conditions at the location of the lesions, and showed the morphologic characteristics of the principal microorganisms composing the film pack.
Later, Williams12 directed attention to the numerous microorganisms found in material scraped from the surface of the teeth, some of them long rods and filaments, together with many other forms large and small rods, and coccal forms. He directed attention especially to an organism which had been described previously by Vicentini13 and named by him Leptothrix racemosa. This organism consists of a long relatively coarse filament or stem, attached to the tooth, on the outer portion of which numerous spores are produced. This spore-bearing conidiophore, which they called a fruiting head, is found projecting at, and just beyond, the surface of the film pack. The striking, characteristic fruiting head serves as a convenient means of identifying the organism. Although it contributes largely to the bacterial film on many teeth, there is no evidence that it bears any specific relationship to caries. However, it is usually one of the several thread-form and filamentous type organisms making up the film on teeth, beneath which caries lesions originate and advance. In many specimens the deeper part of the film is made up largely of the stems of this fungus. Vicentini13 claimed that it is present in all mouths. Williams, in his first paper describing it12, states that it "is common to all mouths which I have examined." I have found it present in material from most of the hundreds of extracted human tooth specimens, from many different sources, which I have examined. The morphologic characteristics of this organism and the way in which it often makes up a large part of, the film pack are shown by Williams12 by numerous photomicrographs. (See his Figs. 14, 17, 18, 20, 31, 32, 33, 34, 37). I have also shown 1 (See my Figs. 6, 7, 8, 9) how the fruiting heads of this organism tend to project above the surface of the film pack and to accumulate in masses at the surface. Throughout the literature since the historic paper of Williams10 in 1897, there may be found numerous pictures of preparations which confirm the fact that the bacterial film on teeth is composed largely of long filamentous forms, each one extending outward from the surface to which they are attached. Since an effective method of personal oral hygiene must be based upon correct information as to the characteristics of this bacterial film, it may be helpful to refer to a few of such illustrations: 10 (Figs. 6, 8, 9, 11, 24), 11 (Figs. 2, 3), 12 (Figs. 82, 84, 109), 13 (Figs. 3, 4), 14 (Figs. 86, 87), 1 (Figs. 4, 5, 6, 7, 8,), 15 (Fig. 3), 16 (Fig. 3), 17 (Fig. 3, 4), 18 (Figs. 86, 87), 19 (Fig. 2), 20 (Fig. 3).
Conditions within cavities.-If the conditions on the tooth which initiate and promote the first stage, chalky enamel, caries lesions continue long enough, sooner or later a cavity develops and advances, usually at an accelerated rate. Active cavities in enamel finally reach, and advance into the dentin; thus progressively increasing in depth and in width. Cavities, and to a less extent normal pits and fissures, present favorable receptacles for lodgment and retention of food material. The larger and deeper the cavity, the more food material it will hold. Many cavities are never free of remnants of food, and this material is continuously in various stages of decomposition. Before lodgment in the cavity food is heavily inoculated (or contaminated) with the many different kinds of bacteria5.12, 20-23 of the oral flora. In the cavity it is exposed to the abundant transient bacterial flora there, arising from decomposition that is going on of previously introduced food material, and also to the more or less permanent or continuous bacterial film lining the base and walls, (Figs. 4, 5) of the cavity. Such a conglomerate bacterial environment always contains many species which produce acids when growing in the presence of fermentable carbohydrates, and others which do not. Food material (particles) retained within a cavity may, and usually does, contain variable amounts of such carbohydrates. In addition to that present in the particular material when it was introduced into the cavity, the carbohydrates may be replenished, more or less, from carbohydrate containing fluids (drinks) taken into the mouth subsequently. The production of acids, upon which caries activity and enlargement of the cavity depend, is determined largely by the retention and break-down of fermentable carbohydrates within the cavity. The nature of the more or less continuous bacterial film lining the walls of the cavity is of great importance, from the standpoint of oral hygiene for prevention of further advancement of the lesion. This film is made up of countless millions of filamentous type organisms (Fig. 6) similar to those making up the film on the surface of teeth beneath which caries lesions originate. One end of the filament (Fig. 7) is attached to the decaying walls of the cavity, from which it extends outward to the surface of the film, where there are the growing ends and fruiting heads.
The thickness of this bacterial film within the cavity varies greatly, depending largely upon the dimensions of the cavity and how frequently and completely its contents are disturbed or removed. Many of the films within cavities in extracted tooth specimens which I have measured range from about 100 to 400 microns (Fig. 8); some considerably thicker.
Most of the filaments of the different kinds of organisms composing such films are less than 0.5 micron in thickness. Therefore, the attached film within the cavity is made up of millions of separate elements, each of which is many times - usually several hundred times as long as it is thick. Every specimen of decaying teeth shows precisely the same thing. Covering the surface or lining the cavity where decay had commenced there is always to be found a thick, felt-like mass of filamentous types of organisms, each radiating outward from the surface to which it is attached. Pertinent facts relative to the caries process in enamel.-If a tooth specimen is suspended in a strong solution (5 to 10 per cent) of HCl, the enamel is rapidly dissolved. The enamel cuticle is set free within a minute or two, by the dissolving of the enamel immediately beneath it, and this loosened keratin-like membrane now may be removed or brushed off. If the acid is greatly weakened by sufficient dilution, or by less dilution plus the addition of tribasic calcium phosphate, then decalcification proceeds very slowly; and in the latter case only the carbonates are removed at first24,25. Only partial decalcification occurs. The enamel becomes porous and softened like chalk and it may be dug into easily with suitable sharp instruments. If the quantity of diluted, weakened or buffered acid is frequently renewed, this partial decalcification may extend deep into, or in time all the way through, the enamel. In this way I have partially decalcified the entire enamel cap, which could then be shelled off in large pieces from the underlying dentin. If, on the other hand, all the enamel is covered with wax, except for a limited area, then only the uncovered area which is exposed to the acid is partially decalcified. This corresponds to the natural early stage caries process. If we use organic acids such as lactic (which is supposed to be the principal one involved in the natural caries process) the same phenomena occur except that, in general, the action is much slower. When such weak acid solutions are used the enamel cuticle remains intact and in place. Thus weak acids pass through the cuticle and the products of their action on enamel pass back out through this very delicate osmotic membrane without destroying or impairing it. In this way the early stage* lesion in natural enamel caries is produced. Acids produced at the surface of the bacterial film, and perhaps also deeper within it, pass along through this sponge or wicklike material, which we have seen is composed of countless millions of long filamentous type organisms, down to the cuticle and thence through it into the enamel.
* (For convenience the term early stage may be applied to caries lesions before there is any break of the surface or cavity, and advanced stage where a cavity, of whatever size, has developed.)