| AN EFFECTIVE METHOD OF PERSONAL ORAL HYGIENE* |
by CHARLES C. BASS, M.D.
NEW ORLEANS
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This is a long slow microscopic and microchemical process resulting from the often repeated slow action of delicate amounts of weak acids produced on or within the bacterial film at the particular location. Time is required for the passage of such weak acid through the bacterial film, (Fig. 9) at the same time interchanging with, and being diluted by fluids of different reaction and composition before it reaches the surface of the tooth which is covered by enamel cuticle. Time is also required for osmotic passage of acid through the cuticle against substances of different reaction and composition resulting from the action of previously introduced acids upon the enamel.
Still more time must be required for passage of the acid into the enamel, especially as the partial decalcification extends deeper and deeper. Not only must the acid pass through the already partially decalcified enamel to the depth of the process but there is a great tendency for this process to follow the course of individual enamel prisms. In suitable preparations under high enough magnification, we usually find the acid action extending along one prism farther than another (Fig. 10) in the immediate vicinity.
This means that acid arriving at already partially decalcified enamel passes along the course of the individual prisms until it reaches the farthest point to which previous acid action has extended. Along this course of the prism the minute acid must interchange with products of previous acid action and finally reach the point of activity in effective quantity and strength. Again this is a very slow process. Thus the chalky enamel caries lesion represents the cumulative effect, over considerable periods of time, of minute amounts of weak acids produced, at various times, by bacterial action upon carbohydrate food material at the particular location.
Pertinent facts relative to the caries process in dentin. If the partial decalcification of enamel (early stage caries lesion) continues to progress, it finally reaches the dentin. Minute quantities of acids produced at the surface now slowly pass through the chalky enamel, especially along the cracks (lamella) and channels that may exist there, thus reaching the dentino-enamel junction and on into the dentin. The caries process in dentin differs substantially from the process in enamel. This results largely from the different composition and structure of dentin. Dentin consists of about 30 per cent organic matter and water, and 70 per cent inorganic material.26 Acids remove the inorganic material leaving the cartilagelike dentinal matrix material which is now softer and can easily be cut or torn apart with suitable instruments.
During the dentinal caries activity decalcification advances deeper and deeper into the dentin, and the decalcified dentin at the surface (bottom and walls) of the cavity slowly disintegrates, thus increasing the depth and size of the cavity. Some of the bacteria of different kinds within the cavity grow and advance into the dentin by way of the open-ended dentinal tubules, towards the pulp chamber.
Near the surface of the cavity wall all the tubules are packed with bacteria. (Fig. 11). The pressure of the growing and enlarging mass of multiplying bacteria within the tubules in the decalcified dentin expands the tubules, compresses the decalcified softened matrix material and tends to split and break it up. Dislodged particles of the decalcified dentin are continuously being shed off from the disintegrating surface, thus increasing the depth and size of the cavity. (Fig. 5). Much deeper in only part of the tubules contain bacteria, many others at the same level do not. (Fig. 12). This means that the forward advance of bacteria into the dentin proceeds down separate tubules independently of other nearby tubules.
The dentinal tubules extend through the dentin from the pulp chamber to the dentino-enamel junction. Their size near the pulp is several times that near the outer surface.26 They contain long protoplasmic projections (Tomes fibers)27 from the odontoblasts. In normal vital dentin a nutritional fluid, dental lymph,28,30 circulates in the dentin, principally through the dentinal tubules and their many anastomosing branches.
Irritation from severe wear, erosion and caries stimulates the formation of secondary dentin (irregular dentin, Orban26 at corresponding areas on the pulpal wall. This new-formed secondary dentin effectively closes off the tubules of the involved regular dentin. This is now spoken of as a dead tract. Dental lymph cannot pass through the now closed tubules of the area and bacteria cannot advance toward the pulp, as they can in open tubules.
No doubt laying down of this wall of secondary dentin which closes the tubules and shuts off the passage of dental lymph into them, is nature's most important protection against advancement of bacteria into the tubules, and ultimately infection of the pulp. Bodecker29 has called these changes "protective metamorphosis."
Cervical Caries. The cervical caries lesion begins at the cemento-enamel junction, and only after the gum has receded enough to expose the area. For unknown reason some people seem to be especially susceptible to this type of lesion. This is probably related to varying relationships in the area where enamel and cementum join.26-81 In some instances their edges do not quite meet, thus leaving an area of dentin covered only by soft tissue. After this is removed there is left an area of exposed dentin with open-ended tubules, which does not have the usual protective covering of either cementum or enamel. They are now open to invasion by bacteria.
In other instances the cemento-enamel junction presents a V-shaped groove of considerable size which, after the soft tissue is removed, offers a favorable situation for accumulation of filamentous type bacteria, as occurs elsewhere in grooves and depressions. Whatever the special conditions may be that initiate the cervical caries lesion, it advances into the dentin in much the same way as do lesions originating in the enamel after they reach dentin.
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Inactive Caries (Arrested Caries) - Caries lesions usually begin at the vulnerable locations during the first two or three years following eruption of the particular tooth. If the local etiological conditions which initiated the lesion continue, the disease process continues to advance. In time a cavity (advanced stage lesion) develops large enough to be recognized by the patient or by the dentist. The preceding early stage chalky enamel lesion has existed and progressed unrecognized for months previously.
If at any time, the local conditions which cause the lesion and promote its advance are prevented or altered sufficiently, the progress of the disease process slows down or stops entirely. This may occur at any stage of the lesion from the earliest (microscopic) chalky enamel stage to the advanced cavity stage. Obviously the earlier this occurs the less damage will have been done.
A large part of all proximal caries lesions stop advancing - become inactive - before cavities are formed. Often small cavities in this region also cease to advance. This slowing down or cessation of proximal caries activity coincides with the incidence and increasing activity of periodontoclasia in the same region. Bibby32 has recently reviewed the literature relative to the apparent antagonism between caries and periodontol disease. The available information cited. tends to support some such antagonism.
Gingivitis is characterized by a continuous flow of minute, quantities of inflammatory exudate which consists of serum containing pus cells and some blood cells. Constant presence of such exudate in the environment of the caries lesion between the teeth tends to neutralize and counteract the effect of minute quantities of weak acids in the area. It is possible also that it may influence the local bacterial flora and promote the growth of proteolytic bacteria in the environment, thereby lessening acid production by acidogenic bacteria. On the other hand, periodontoclasia has little or no influence upon occlusal caries. Inflammatory exudate does not reach the area in effective amounts and concentration.
Early stage caries - chalky enamel - always appears pure white throughout the life of the tooth, as long as the cuticle remains intact. Usual stains of the mouth do not pass through normal cuticle. On the other hand, chalky enamel from which the surface has been destroyed becomes stained-usually varying shades of brown. Stains are also carried into chalky enamel through cracks (lamella) and other channels that may exist there. The staining of such lesions tends to increase, although they may remain inactive, throughout the life of the tooth. Usually chalky enamel lesions which had advanced sufficiently to be stained because of loss of cuticle or penetration of lamella or small cavities remain white around the borders in areas in which the cuticle is still intact.
Occlusal caries lesions start at the entrance and sidewalls of occlusal pits and fissures of molars and bicuspids where the depressions favor accumulation of bacterial film, retention of food material, and production of acids. The partial decalcification - chalky enamel stage - progresses and finally cavities develop. There is a tendency for the decay process to extend down any channels and after it reaches the dentin, to spread and undermine the enamel along the dentino-enamel junction.
Extensively undermined enamel may crack off leaving the decaying dentin widely exposed. Bacterial film and food material in such wide open occlusal cavities may be disturbed or rubbed off several times every day. Occasionally dentinal decay in wide open cavities ceases to advance and the dentin becomes very hard, similarly to the way in which dentin exposed by severe wear becomes almost as hard as enamel. This is an example of what often happens when such a wide open cavity is frequently cleaned out by whatever means.
Sometimes radical changes in diet habits or in oral hygiene habits and methods at any time, may slow down or stop the activity of early stage occlusal caries lesions. However, in most instances, no such circumstance arises, especially during the age period (up to 12 or 15 years of age) of greatest activity of such lesions.
Periodontoclasia - Definition. - Various terms have been used to indicate the disease process encompassed by periodontoclasia. Such terms as periodontal disease, periodontosis, periodontitis, pyorrhea, pyorrhea alveolaris, alveolodental pyorrhoea, Riggs disease, gingivitis have been applied to the disease in general or to some particular phase or prominent clinical condition. The disease is characterized by inflammation and suppuration of the epithelial tissue within the gingival crevice, and by long continued, progressive chronic inflammation in the parodontal tissues resulting in destruction and resorption of periodontal fibers and alveolar bone.
Periodontoclasia is caused by foreign material, consisting of bacterial film and or concretions (mostly calculus) upon the surface of the tooth at the entrance to, and within, the gingival crevice. Prevention of the disease and prevention of further progress of existing lesions can be accomplished only by preventing or minimizing these local etiological conditions - conditions without which lesions do not originate or advance.
Early stage of the disease - All periodontoclasia lesions begin at the gingival margin and are, at first, only microscopic in extent, therefore not recognized.
It has been pointed out1,10,12,14 and emphasized above, that bacterial film (plaque) on protected areas on the surface of the tooth consists of a pad of filamentous types of micro-organism, one end attached to the tooth and the other extending outward towards the surface of the pad. At the surface of the pad there may be found more or less of any and all of the many other kinds of bacteria in the mouth.
At the entrance to the gingival crevice this bacterial material tends to grow or advance into the crevice and to impinge upon the epithelial surface there. The deeper part of the bacterial material continuously present upon the tooth tends to harden, calcify, and form rough concretions there. (Fig. 13). Normally, the marginal gingival tissue rests upon the soft smooth non-irritating enamel cuticle. Hard, rough material superimposed upon the cuticle acts as a mechanical irritant like a foreign body.
Soon the gingival margin is irritated by this foreign (and perhaps toxic) material against which it rests. Inflammation of the epithelial tissue ensues, characterized by migration of polymorphonuclear cells through the affected tissue (Fig. 14) to the point of irritation, where they tend to accumulate as pus cells.
At first the amount of inflammatory exudate, which consists of pus cells and serous fluid, is not sufficient to be recognized by the unaided eye. However, material properly collected from the location always contains pus cells, upon microscopic examination; and, sections always show polymorphonuclear cells passing through the epithelial tissue opposite the irritating foreign material on the tooth against which it rested.
As the inflammation continues the bacterial film on the tooth tends to extend deeper and deeper into the gIngival crevice, (Figs. 15, 16) the amount of the associated calculus on the tooth within the crevice increases, and there is increase in the amount of pus produced. The inflamed slightly congested and edematous condition of the marginal gingiva may now be recognized upon careful examination. It bleeds easily upon slight pressure or manipulation. The condition may now be noticed by the individual and by the dentist. Usually the importance and significance of gingivitis, as the early stage of the periodontoclasia lesion is not recognized.
However it is, in fact, the beginning of a progressive pathological process which never ends spontaneously, until the tooth is finally lost. The origination, activity, and rate of advancement of early stage lesions, and also, of the more advanced stage lesions, are determined largely by the effectiveness of the personal oral hygiene habits of the individual. These vary greatly with different individuals, at different times, and as applied to different tooth areas.
Nature of the subgingival bacterial film and calculus. Once the foreign material (bacterial film and calculus) has advanced into the crevice and inflammation is set up there, more or less inflammatory exudate is continuously present in the crevice thereafter. This exudate consists of diluted serum (lymph) containing pus and blood cells. It provides a favorable environment for the establishment and growth of types of micro-organisms which are favored by partial anaerobiosis and by the serum-rich substrate. Such filamentous type organisms as actinomycetes and certain leptotrichia are encouraged.
Subgingival calculus consists of calcified bacterial material.33,34. The inorganic portion is derived from the inflammatory exudate (serum). The bacterial portion consists largely of filamentous types of microorganisms, especially actinomyces.35
A pad or film of filamentous type organisms is always present on the surface of the tooth, and on the surface of any calculus, within the periodontoclasia pocket. (Fig. 17). This constantly present bacterial film is composed of long filaments with one end attached to the tooth or to the calculus, (Fig~ 18) and extending outward in palisade form to the surface of the pad which is in contact with the inflamed crevicular epithelial surface. At the surface of the pad there are the growing ends and fruiting heads of the particular organisms composing the film pack.
One of the important thread form organisms usually found in the pyorrhea pocket was first described by Beust36 and named by him Leptothrix falciformis. He later 37 called attention to this organism in material from about the teeth, and pointed to the association of it with spirochetes.
I38 have observed that the habitat of Endameba buccalis is the outer surface of the filamentous bacterial film on the tooth within the periodontoclasia lesion. "There they are protected and live, grow and multiply among the strands and fruiting heads of leptotrichia, principally L. falciformis." This observation conforms with the observations of others39-42 as to the distribution of this parasite in the periodontoclasia lesion. Kofoid39 confirmed especially the observation43 that ameba are most numerous at the very bottom of the pyorrhea pocket. This ameba cannot be the specific cause of periodontoclasia, as sometimes has been erroneously supposed, for the reason that it is found in the lesions of not more than about 50 per cent of adults under 30 years of age. This does not necessarily mean that the parasite may not be harmful whenever it is present.
The fact has been shown44 that the film pack is composed of filamentous types of micro-organisms, largely leptotrichia, attached to the surface of the tooth or to the calculus within the periodontoclasia lesion and that there is a tendency of the fruiting heads of L. falciformis to extend into the deepest part of the lesion. This conforms with observations of Box45 in this regard.
It has been observed44 also that the film pad of L. falciformis in the deeper part of the periodontoclasia lesion, and the conditions there, are especially favorable for the growth of spirochetes. These are found in greatest abundance upon and among the fruiting. heads of the leptotrichia at the very bottom of the pocket, and therefore overlying the zone of disintegrating epithelial attachment cuticle (zdeac).46 This zdeac serves as a useful landmark which accurately indicates, on extracted tooth specimens, the location of the outer border of the epithelial attachment and the bottom of the periodontoclasia lesion 47 at any place around the tooth when it was in situ. The great abundance' and constant presence of spirochetes' at this location, which is where the lesion is advancing on the surface of the tooth-the location where the outer border of the epithelial attachment is receding apexward - suggests the possibility that spirochetes have some etiological significance in the advancement of the lesion.
While the flora and fauna tend to be limited to fewer varieties in the deeper part of the pocket, the entrance to the crevice and the part just within, are constantly exposed to infection and reinfection by any and all of the many species in the mouth. Material collected from this location always contains more or less of such mouth organisms. It is interesting to mention also that this location is where fusiform organisms are most abundant in mouths in which they and associated spirochetal organisms predominate.
Apexward advancement of the subgingival bacterial film and calculus. - The subgingival bacterial film and/or calculus tend to continuously advance apexward at various rates at different locations on a given tooth and on different teeth in the same mouth. As a result of the inflammation, suppuration, and destruction of the parodontal tissues which this foreign material on the tooth within the crevice causes, the location of the epithelial attachment moves apexward,47,61,60 thus deepening the pocket and leaving more and more of the tooth without its normal soft tissue covering. Such bared tooth surface is always entirely covered with bacterial film right down to the outer border of the epithelial attachment. Calculus formation follows along not far behind.48 However, there is always a narrow band or space, of variable width, between the inner (or deeper) border of the calculus and the outer border of the epithelial attachment.
The epithelial attachment consists of a thin band or cuff of epithelial cells surrounding the tooth. The width of this cuff varies at different locations. It is widest when it is located on the enamel and becomes narrower as, it moves apexward40,47. Waerhaug49 has presented strong evidence that what has been called the epithelial attachment is, in fact, not organically attached to the surface of the tooth and that a delicate instrument can be passed, with little resistance, into the gingival crevice all the way to the cementoenamel junction. Baume,50 through phase contrast microscopy, finds evidence that enamel epithelial cells are very delicately attached to the tooth surface by tonofibrils, and that similar fibrils hold together the cells of enamel epithelium, and also those of the adjacent oral epithelium.
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The inner border of the epithelial attachment grows apexward to cover over cementum from which periodontal fibers have been destroyed and removed (Fig. 19). As more fibers are destroyed, the epithelial attachment advances farther. Destruction and resorption of the. periodontal fibers which make possible the advancement apexward of the epithelial attachment, and which gives to the disease its name - periodontoclasia - results from chronic inflammation extending into the periodontal tissue among and between the periodontal fibers for considerable distances from the bottom of the pocket. (Fig. 20). This inflammatory process is characterized by round cell and plasma cell infiltration, and by accumulation of these inflammatory cells between the bundles of periodontal fibers. (Figs. 21, 22, 23, 24). As the process continues the involved fibers are broken down and finally resorbed.
The important fact that foreign material (calculus and bacterial film) is always present on the tooth within the inflamed gingival crevice (the periodontoclasia lesion) is well shown in numerous illustrations to be found throughout the literature relative to this disease, or in some instances presented for other purposes. Most pictures show what is usually labeled calculus on the tooth within the pocket. The fact that the calculus and the part of the tooth between the inner border of the calculus and the outer border of the epithelial attachment are covered by heavy bacterial film,44,48 is usually overlooked. Following are listed a few of such publications and the particular illustrations which show this important feature of the disease, upon which effective personal oral hygiene must be based:
51 (Figs. 1 2, 3, 4),
52 (Fig. 6), 53 (Fig. 8)
54 (Figs. 20,23,29),
55(Figs. 2, 7,8),
56(Figs. 1,5, 6),
57 (Figs. 3, 12, 14, 20, 25, 26, 27, 29, 30),
49 (Figs. 17, 18,20,39),
58 (Fig. 10),
119 (Figs. 24, 26, 31),
60 (Figs. 16 (2),
13 (3),24 (7)),
16 (Figs. 278, 287, 288, 289, 293,305),
62 (Figs. 3,4),
63 (Figs. 3, 5),
64 (Fig. 190),
26 (Figs. 138, 218, 222),
65(Figs. 59,64),
18(Fig. 104), 67 (Figs. 491, 713, 733, 734, 735, 738, 767B),
68 (Figs. 261, 264,268),
69 (Fig. 15), 70 (Figs. 6, 8).
The lesion, at first microscopic and later macroscopic, extends around the tooth, but is usually deeper and more active in the interproximal crevices which are deeper and where accumulations of foreign material are less subject to removal by functional friction or customary methods of oral hygiene. The tooth surrounded by concretion and bacterial material adhering to it within the gingival crevice (lesion) is, in effect, a foreign body, constantly subject to infection and reinfection with the many different kinds of bacteria in the mouth.
This foreign body effect was recognized and its importance emphasized more than seventy-five years ago by John W. Riggs.71 More than sixty-five years ago J. N. Farrar 52 urged the necessity of removing this subgingival foreign material and laid special emphasis upon keeping the area clean. He said "the disease vanishes when the pockets are carefully and thoroughly cleaned, and kept clean." To this day, removal of this material from the tooth, which these pioneers advocated at that time, is still essential for successful treatment of the disease. Not only is it essential, but it is perfectly logical, that the local cause of the disease should be removed and its reformation prevented. Prevention of its reformation is accomplished by the method of personal oral hygiene' herein presented.
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