Preventive Medical Case-Finding Opportunities and Responsibilities of the Dentist

It is the purpose of this article to consider how the dentist can best serve as a member of the health team. More specifically, it is our cardinal concern to analyze the role of the dental practitioner in the detection of systemic disease. The idea that the stomatologist can and should play an integral role in this program is not new. This thought has occurred to many members of both the medical and dental professions. This concept has been tossed about in both the professional and lay literature. However, despite the talk and the writings, little actually has been accomplished to show beyond any question that the dentist is playing his part in the over-all health program.

In order to clarify the role that the dentist should and can take in the health program, this paper will be divided into three parts: (1) a rather basic consideration of the nature of disease in general, (2) the place of the oral cavity in the over-all picture of disease states, and finally, (3) the role of the dentist in the detection of systemic pathoses.

The Nature of Disease

There are two inescapable features about disease processes which are peculiarly pertinent to this discussion. They are (1) that a pathologic process is the result of more than one operating factor, and (2) that health and disease seldom become clinically apparent in pure blacks and whites–in other words, that sickness and health are relative states which are usually demonstrable in a series of shades of gray. Because of the importance of these two aspects of disease, they will now be considered in some detail.

Disease a Product of Multiple Factors

The Layman’s Observations. The point that more than one factor is required to cause disease is abundantly evident to the man on the street. It is a common experience for two persons, simultaneously drenched in a rainstorm, to fare very differently. Mr. A. contracts a severe upper respiratory infection or even pneumonia and may possibly die. Mr. B. remains unscathed. This type of crude observation suggests that the very same insult, in this instance chilling, yields different results because of differences in people. The layman calls this difference by many names–most often resistance. And so it is that we hear in common parlance that ‘he caught a cold because his resistance was low.’

The Experience in Medical Practice. The point that more than one factor operates in the causation of disease is also plentifully evident in everyday medical practice. For example, a seemingly healthy person (at least free of any symptoms and signs) steps out into the bright sun. Shortly thereafter he notes a dermatitis. The examining physician, with almost cursory inspection, recognizes that the character and distribution of the lesions can only mean one thing–pellagra. No one will argue that Mr. X was just as pellagrous the day before the actinic exposure. This illustration emphasizes that a suitable systemic substrate, in this instance a niacin deficiency, can exist unnoticed until some local insult, in this case the sun rays, does something to bring about a net result which is clinically recognized as proof of sickness.

The Experience in Dental Practice. Examples of the interplay of local trauma and an appropriate systemic substrate are not confined to observations by the layman, nor are they restricted to the sphere of medicine. In fact, there is every reason to believe that these same interrelationships are as important, if not more so, in the oral cavity. For example, it is common knowledge that two patients may present themselves in the dental office with abundant and, within limits, equal amounts of calculus. Yet, in one individual there is no alveolar bone loss whereas in the other there is extensive bone destruction. Obviously, the calculus alone cannot be considered to be the cause of the bone picture. Illustrations of this same type are plentiful in dental practice.

It would appear from these few, simple examples that the observable pattern of disease fits into a formula which may be expressed as follows:

Systemic substrate X Exciting factor = Observable evidence of disease

The clinical cases cited and the formula shown above represent attempts to underscore the point that a pathologic process is the result of more than one causative factor. The question which now arises is why clinical (observable) proof of disease should equal the product rather than the sum of a suitable systemic substrate and an appropriate exciting factor as shown on the left side of the above equation. The answer to this question may be found by analyzing the examples already presented.

It should be recalled that the pellagrin was asymptomatic and free of signs of disease until he stepped out into the sun. In other words, as long as there was no exciting factor of critical threshold, in this instance no cutaneous trauma, this variable in the equation was zero. The arithmetic of this example is shown in the following equation:

Systemic substrate X Exciting factor = Observable evidence of disease

Niacin deficiency X 0 = 0

Thus, regardless of the systemic imbalance, the niacin deficiency alone does not produce clinical proof of disease. The right hand side of the equation is zero.

It would appear logical, then, that the converse might also be true. In other words, had the patient not had aniacinosis, if this factor were now zero, then regardless of the actinic exposure, the product would once again be zero. There would not be the typical pellagrous dermatosis, as shown in the following equation:

Systemic substrate X Exciting factor = Observable evidence of disease

0 X Actinic exposure = 0

In the final analysis, it is rare, if not impossible, to eliminate (reduce to zero) either of the variables on the left side of the formula. This is so because disease states are not clinically observable in simple blacks and whites but rather in an infinite number of shades of gray–in other words, in degrees.

Degrees of Disease

There is no argument that a person can be seemingly very healthy or undeniably sick. These are the blacks and whites of disease. However, too little attention is directed to the fact that there are degrees of sickness and well-being. In all probability, white (perfect health) is never attainable. Black, at the other pole, represents disease in its classic form. Between these two limits are an infinite number of shades of gray–a limitless gradation of health to sickness.

This concept of degrees is not without clinical support. The clinician is constantly confronted by the patient who is clinically well today and clinically ill ten years hence. Surely, the patient with diabetes mellitus, rheumatoid arthritis, ascorbic acid deficiency, to pick but a few examples, does not develop his illness overnight. But more relevant to this discussion is the person who at age twenty has no alveolar bone loss, who continues to be well but yet at age fifty shows severe alveolar bone loss. Obviously, this picture did not develop in a week, a month, or a year. During the thirty year interval between white (age twenty) and black (age fifty), the patient cannot have been in perfect health. The question now is, “How does this new information fit into the formula?”

For illustrative purposes only, let us assign numbers to the two variables on the left side of the formula. Let us say that there are gradations from zero to ten. Zero for the first variable in this scheme indicates a perfectly healthy systemic substrate. Zero for the second variable signifies the complete absence of any exciting factors. Translated into a practical situation, we are confronted with a subject who has absolutely no systemic disorder. Also, in this hypothetical situation, the patient is free of calculus, there are no overhanging restorations, the occlusion is perfect.

Systemic substrate X Exciting factor = Observable evidence of disease

0 X 0 = 0

On the other hand, we shall assign the value ten to each of the two factors on the left side of the equation. For example, a factor of ten means that the patient is suffering with diabetes mellitus in its classic form with polyuria, polyphagia, polydipsia, weight loss. A value of ten for the second variable signifies abundant calculus, a host of ill-fitting restorations, marked occlusal imbalance, etc.

Systemic substrate X Exciting factor = Observable evidence of disease

10 X 10 = 100

The value on the right of the equation is high, representing the presence of many and marked symptoms and signs of disease. Thus, in the diabetic patient who meets these specifications, there are polyphagia, polyuria, polydipsia, weight loss. In addition, there are marked gingivitis, extensive alveolar bone loss, possibly a history of slow post-extraction healing, perhaps gingival bleeding, etc. The clinical evidence is clear–the patient is indeed systemically ill and there are plenty of oral symptoms and signs to prove it.

The two extremes, the 0 X 0 = 0 and the 10 X 10 = 100–the whites and the blacks–are simple to comprehend. But there are many other possible combinations:

Systemic substrate X Exciting factor = Observable evidence of disease

Equation A

Severe diabetes mellitus 10 X Minor local trauma 1 = 10

Equation B

            Mild diabetes mellitus 1 X Marked local trauma 10 = 10

Equation A represents a severe diabetic patient with only minor local (oral) irritating problems. We note on the right side of the equation the value ten. This means that there are some observable symptoms and/or signs of disease. Translated into clinical terms, the ten on the right side of Equation A may represent minimal alveolar bone loss in a severe diabetic patient with minimal oral trauma. Equation B shows the same end result, a value of ten. In this case, we are faced with a mild diabetic subject with marked local irritation.

All of the combinations thus far analyzed are clinically demonstrable. However, even more often the clinician is faced with a mild to moderate diabetic patient with mild to moderate local oral trauma. In clinical parlance, the examiner is confronted with a patient with minimal alveolar bone loss who appears, for all practical purposes, to be perfectly well.

Systemic substrate X Exciting factor = Observable evidence of disease

(Mild diabetes mellitus) 3 X (Minor trauma) 3 = 9

We have now established a formula for health and disease. The question which now arises is, “How does the oral cavity fit into this equation?” In order to answer this very important question, one must analyze the structure and function of the mouth.

The Oral Cavity

The mouth is a most unusual area of the body. This is so because (1) it is, in many respects, exactly like other regions, and at the same time, (2) it is unlike any other part of the body. This is true from both a structural and a functional standpoint.

The Structure of the Oral Cavity

Generally speaking, the mouth is very much like other mucosa-bounded cavities. It is lined by an epithelium much like that of the vagina, the anus, and the nose. Beneath the mucosa are various types of connective tissue histologically similar to their homologues in other parts of the body. Thus, with such structural similarities, it is understandable why changes in the oral tissues parallel alterations in like tissues elsewhere in both health and disease. Herein lies the explanation for the simultaneous cyclic epithelial changes in the oral and vaginal mucosae during physiologic menstruation and the climacteric. This is the basis for the similarity of cutaneous and mucosal lesions (e.g., intestinal polyposis and angioneurotic edema).

At the same time, there are cells and tissues in the mouth which are truly unique in that they are not found elsewhere. The teeth and the associated periodontal structures are the most striking examples. The presence of the odontogenic apparatus makes the oral cavity special in two different ways: (1) problems arise in the mouth, notably dental caries and periodontal disease, not encountered anywhere else in the human body, and (2) the oral symptoms and signs of systemic disease states are modified by the presence of the special cytoarchitecture of the teeth and the periodontium. Thus, simply by way of example, the oral findings of plumbism and pityriasis are far different from the evidence of these same diseases in the leg, or abdomen, or chest.

The discussion of the anatomy of the mouth can be simply summarized. First, the oral tissues are like their counterparts elsewhere. In other words, epithelium is still epithelium and fibrous tissue basically remains fibrous tissue. Consequently, a so-called collagen or bone disease implicates the collagenous or osseous elements wherever they may be. And so, understandably, systemic diseases do have their oral reflections. But secondly, the oral tissues are in some anatomic respects quite unique. Hence, problems arise in the mouth which are not encountered elsewhere. Thus it is that the filiform papillae of the tongue atrophy in various nutritional disorders. So it is that the teeth become subclinically more mobile during the pregnancy state.

The Function of the Oral Cavity

Not only is the mouth structurally like and unlike similar cavities, but it is also functionally like and unlike other mucosal orifices. The similarities require little elaboration. What are more important are the differences–the unusual functional demands placed upon the oral tissues.

The mouth, it should be recalled, is expected to participate in a host of vital functions, notably speech and mastication. Within the very same breath, the oral mucosa is expected to tolerate high temperatures (boiling coffee) and low temperatures (freezing ice cream). No other tissue of the body is asked to withstand such insult. It is of parenthetic interest that when one conducts a similar experiment on the supposedly tougher skin, an erythema results. Yet the mouth is expected to, and does, handle such constant microtraumata. The oral tissues, it must be emphasized, can only weather such persistent local irritation as long as the systemic substrate is in good health.

This last point bears directly on the present discussion of a formula for disease. This, as we shall learn, is directly pertinent to the analysis of the dentist’s role in the detection of systemic disease.

We have already observed that the product of a systemic substrate and an exciting factor yields observable evidence of disease. Now we add that, under so-called physiologic conditions, oral irritation is high. Thus, in our formula, we might say that local trauma is to be assigned a value of 3, or 4, or 5 or more. It then becomes clear that the higher the value on the left side of the equation, the greater will be the product of the two variables on that side. Or, to put it another way, observable evidence of a systemic disease in the oral cavity is very apt to be present even when the systemic substrate is minimally pathologic.

The Mouth as a Barometer of Systemic Disease

And so it is that systemic disease often makes its clinical debut by way of oral symptoms and/or signs. This is so because, though both the systemic disease and the local irritation are often of a relatively low magnitude, their product is great enough to produce complaints or visible findings in the oral tissues.

The Formula of Disease

The equation which has just been developed suffers from one great fault–its simplification. It implies that there are but two variables, systemic substrate and exciting factor. It suggests or implies, to pursue our example, that a patient must be diabetic and must, in addition, have calculus. Actually, each of these factors in the equation may indeed be a host of variables. Is it not conceivable that a patient may be a very mild diabetic, suffering with early rheumatoid arthritis, complicated by a marginal ascorbic acid deficiency? Is it not further possible that there may be a slight collection of calculus, imperceptible overhanging restoration(s), minimal occlusal imbalance, in a person who smokes just a little too much, who grinds his teeth while asleep, and who brushes his teeth a bit too enthusiastically? Thus, in the formula below, a might represent mild diabetes mellitus, b early rheumatoid arthritis, and c marginal ascorbic acid deficiency, with possibly other pathologic problems up to n. At the same time, p signifies calculus deposition, q overhanging filling materials, r occlusal imbalance, s tobacco irritation, t vigorous toothbrushing, and other local irritants up to x.

Systemic substrate (a + b + c…. n) X Exciting factor (p + q + r + s + t… x) = Observable evidence of disease

The Role of the Dentist in the Detection of Systemic Disease

We now see that the dentist is in an admirable position to detect early systemic disease. As a matter of fact, the dental practitioner has, in some respects, the advantage over his medical confrere for two reasons. In the first place, oral trauma is high. Therefore, systemic disease will often show up in the mouth before it can be recognized elsewhere. Secondly, it is of some interest that approximately only one-twentieth (5 per cent) of the physician’s time is spent in the routine examination of so-called healthy folks. In other words, more often than not, people visit the physician only when they are ill. In contrast, more and more apparently well persons are visiting the dentist regularly for periodic examinations. This is the time, the optimal time, to detect early systemic disease.

Systemic Diseases with Oral Manifestations

Actually, there are over 200 systemic diseases which, at some point in their clinical course, show oral symptoms and/or signs. In some cases, the oral findings precede the clues elsewhere. This is classically illustrated by the Koplik’s spots which precede, by 24 or more hours, the cutaneous eruption of measles. In other disorders, the oral findings parallel those in other areas. The enanthem of chickenpox falls into this category. Finally, there are situations where the oral changes follow the symptoms and signs in other parts. This sequence may occur, for example, in lupus erythematosus.

Needless to say, it is impossible in these few pages to list, let alone discuss, all of the oral manifestations of all of the systemic diseases. Nor is this necessary since such accounts are readily available in the literature. Rather, an attempt will be made to show, by example, how the oral cavity fits into the general picture of systemic disease and how the dental practitioner can serve in the detection of such disorders.

Case Report No. 1. Among the varied causes for systemic diseases, some are due to chemical agents. Sometimes, the cause for the chemical intoxication is occupational–the agent is ingested, inhaled, or is absorbed from the body surface. Occasionally, the drug is taken for suicidal purposes. Finally, chemical intoxication may be a sequela following the ingestion of an agent for medicinal purposes. The case to be described falls into the latter category.

Findings. This middle-aged white woman was admitted to the hospital with a chief complaint of excessive salivation and sore mouth. Examination of the oral cavity revealed full upper dentures and only the lower anterior teeth remaining (Fig. 1). There was an end-to-end bite with obvious traumatic occlusion. There was also considerable gingival recession and blue-black subepidermal pigmentation in the marginal gingiva.

Fig. 1. A middle-aged white woman with a chief complaint of excessive salivation and sore mouth. Examination reveals full upper dentures, only natural teeth are lower anterior ones, end-to-end bite, gingival recession and blue-black subepidermal pigmentation in the marginal gingiva.

 

The patient reported that she had no oral complaints until four months previously. Interestingly enough, it was at that time that she was first given mercurial diuretics because of refractory cardiac decompensation. Shortly thereafter her cardiac status improved and the diuretics were discontinued. She reported that her oral complaints improved. However, because the cardiac failure could not be satisfactorily controlled with digitalization, the mercurial diuretic was resumed. Once again her mouth became sore and salivation increased to the point that her hospitalization became necessary, not because of her cardiac status but because of the oral picture.

Comments. Here is a patient who is subjected suddenly to relatively small amounts of mercury. This is a common practice, since mercury paralyzes the renal tubules and so decreases tubular reabsorption of water. Thus, there is greater fluid loss and a reduction in cardiac edema. The important point to emphasize is that this patient developed a mild case of mercurialism.

In our formula, then, we now have a systemic substrate of some magnitude. Let us assign the value of 5:

Systemic substrate X Exciting factor = Observable evidence of disease

(Mild mercurialism) 5 X 0 = 0

If the oral cavity were in perfect health, then the other variable would be zero and the product (no observable evidence of disease) would be zero. However, this patient, with full upper dentures, only a few lower teeth and an end-to-end bite, was obviously suffering with occlusal stress. Parenthetically, the point should be made that diseased tissue liberates hydrogen sulfide. Also, the evidence is clear that circulating heavy metals unite in diseased tissue with hydrogen sulfide and become deposited as, in this case, mercuric sulfide. Finally, the few remaining teeth were expected to carry the impossible load for all of the lower teeth. Thus, the other variable in the equation (local trauma) is certainly not zero. Let us, arbitrarily, assign to it a value of 5 as shown in the following equation:

Systemic substrate X Exciting factor = Observable evidence of disease

(Mild mercurialism) 5 X (Traumatic occlusion) 5 = 25

The evidence in this case suggests that, had there been no oral irritation, there would have been no oral complaints. The evidence also suggests that, had there been no mercurialism, there would not have been oral findings.

Case Report No. 2. Frequent reference has been made in this paper to diabetes mellitus. It might, therefore, be well to analyze one such case as it presented itself in the dental office.

Findings. This 31 year old woman was referred to the dental clinic for full mouth extraction because of extensive, generalized alveolar bone loss and considerable tooth mobility, most obvious in the lower central incisor. There was occasional gingival bleeding. Oral examination revealed reasonably normal gingiva but moderate tooth mobility (Figs. 2 and 3). As part of the routine diagnostic workup on all patients with tooth mobility, a glucose tolerance is done. The patient’s glucose tolerance curve is shown in Figure 4. It is clear that the patient is suffering with diabetes mellitus despite the absence of the classic symptoms and signs of this disease. She was referred to the diabetic clinic where the diagnosis was confirmed and an appropriate diet prescribed. When next observed three months later, the patient stated that she had been resting better, did not fatigue as easily, and that her teeth, and particularly the lower central incisor, were not as loose.

  

Fig. 2. A 31 year old woman with a chief complaint of moderate mobility of all of teeth and especially the lower central incisor. The gingivae appear normal in color, position, shape, contour and consistency.

Fig. 3. Representative periapical roentgenograms showing the generalized alveolar bone loss.

Fig. 4. The glucose tolerance curve of the patient compared to that of a nondiabetic patient. The small zeros and the ** indicate the absence and presence of sugar in the urine. It is of interest that the fasting urine was sugar free and the fasting glucose level was within normal limits.

 

Comments. Here is a young lady who presents herself in the dental clinic with complaints almost exclusively confined to the oral cavity. It should be emphasized that the patient did not show any of the classic evidence of diabetes mellitus. Hence, in our equation, we shall assign some intermediate value to the systemic substrate. As we have seen, local trauma was minimal (possibly of a magnitude of 2 or 3). And so, the formula now is:

Systemic substrate X Exciting factor = Observable evidence of disease

(Mild diabetes mellitus) 5 X (Minimal oclusal trauma) 2 = (Insidious bone loss) 10

Case Report No. 3. This last case is included because it provides the rare opportunity to observe the interplay of local and systemic factors and also allows the chance to show the effects of modifying these two variables independently.

Findings. This 15 year old girl was first observed in the dental clinic because of a history of bleeding with toothbrushing from the embrasure between the left maxillary second premolar and first molar. Oral examination proved negative except for an ill-fitting MOD amalgam restoration in the first molar with an overhang into the embrasure. The only other findings of importance were seemingly spontaneous ecchymoses in the skin and a very poor history of citrus intake. Her fasting plasma ascorbic acid level proved to be marginal (0.62 mg. per cent).

She was started on a regime of 1 gm. of ascorbic acid by mouth daily in divided doses (250 mg. four times a day), as shown in Figure 5. When seen four days later, the patient reported that both the ecchymoses and the toothbrush bleeding had subsided. However, the ascorbic acid regime was continued. On the twenty-second day (Fig. 5), because of no ecchymoses and decreased gingival bleeding, the ascorbic acid dosage was halved. The plasma ascorbic acid level was then 1.4 mg. per cent (roughly more than twice that on admission). When observed about three weeks later, on the forty-eighth day, the gingival bleeding had reappeared while the plasma level was 1.07 mg. per cent. The 1 gm. per day ascorbic acid regime was re-instituted. Two weeks later, on the sixty-second day, the plasma level was 1.33 mg. per cent. Most interestingly, the gingival bleeding had again subsided. This time, the dosage was again halved and the ill-fitting restoration replaced with a more acceptable filling. The fasting plasma ascorbic acid level at the next visit, three weeks later on the eighty-third day, was 1.16 mg. per cent. The patient reported that the gingival bleeding had vanished completely.

Fig. 5. A pictorial representation of the fasting plasma ascorbic acid level of a 15 year old girl. The patient had a marginal ascorbic acid deficiency and local irritation due to an ill-fitting restoration, with resultant gingival bleeding associated only with toothbrushing.

 

Comments. This case emphasizes very well the delicate interplay of systemic and local factors. Here is a child who was obviously suffering with a mild ascorbic acid deficiency, as evidenced by the spontaneous cutaneous ecchymoses, even if one wishes to explain away the gingival bleeding on purely local irritation. However, the same increased capillary fragility and permeability which produced ecchymoses might well have contributed to the gingival bleeding with toothbrushing. This seems a likely explanation, since decreasing capillary fragility (without local treatment) by means of ascorbic acid caused the disappearance of the ecchymoses and a reduction in gingival bleeding. However, when the ascorbic acid dosage was halved, the product of the local irritation and the capillary fragility was sufficient to once again cause gingival bleeding. This is borne out by the fact that the dose of ascorbic acid was again increased and gingival bleeding once again decreased. But when the local trauma was reduced (by the replacement of a satisfactory restoration) and capillary fragility diminished (by ascorbic acid), then the product was reduced to the point at which there was no observable evidence of disease.

Summary

An attempt has been made to show that observable evidence of disease, in general, is the product of more than one operating factor. Since oral trauma, even under physiologic conditions, is quite high, the product of it and even a marginal systemic imbalance may be great enough to produce oral symptoms and/or signs. This concept has been underscored by three examples: (1) a disorder due to a chemical agent, mercurialism; (2) a hormonal imbalance, diabetes mellitus; and (3) a nutritional problem, ascorbic acid deficiency.

The analysis of disease in general and the oral cavity in particular described in these pages underscores the fact that the dentist is in an excellent position to detect early systemic disease.