Some Newer Light on the Acid

Some Newer Light on the Acid Base Aspect of Paradentosis
By M. Francis Wielage, D.D.S.
Our previous studies leading up to a new theory of dental caries, will help us to understand the systemic conditions which underly the other great dental problem, paradentosis. We will refer to them often in bringing forward the sequence of conditions which lead to this oral phenomenon.
It is well to state here the classification and nomenclature accepted at the International Dental Congress in Paris in 1931.
1. Gingivitis Marginalis Suppurativa.
Superficial inflammation with pus at the gingival margin. Local findings: tartar, pus, no definite pocket.
2. Paradentosis.
(a) Paradentitis profunda (supp) simplex. Local findings: deepening of pockets and pus, no loosening.
(b) Dystrophia diffuse. Local findings: irregular atrophy, migration or loosening, no pus.
(c) Paradentitis dystrophican complicata. Local findings: deepening of pockets, pus, eventually loosening, eventually migration or both.
In the latest stage a, b, and c, all tend to merge into the same picture; severe loosening, deepening of pockets, pus.
3. Alveolar atrophy.
(a) Atrophia preacox. Local findings : early retraction of the gingival margins and regular horizontal atrophy of bone.
(b) Atrophia senilis. The same findings at more advanced age.
The first important observation we can make is, that we can have a flow of pus without having paradentosis, and then again, we can have paradentosis without a flow of pus (2 b. Dystrophia diffusa).
The term pyorrhea alveolaris, meaning flow of pus, therefore is obsolete, and though the laymen will still use that terminology they will gradually adopt the other nomenclature if dentists will educate them. This has been successfully accomplished in some European countries.
Many investigators have observed that the supporting structures can break down without a single cavity being present in the teeth. In fact the tooth seems to be extremely solid and dense, presenting a color which has a definite yellow hue.
The opposition to the theory that caries and paradentosis are antagonistic is caused by the occasional findings of cavities when paradentosis lesions are present.
The acid-base theory accounts for this condition in a simple manner.
We must differentiate between active caries and passive caries, active paradentosis and passive paradentosis. When the two conditions, caries and paradentosis are present in the same individual’s oral cavity, one of them is passive or inactive.
It pictures clearly that the body mechanism is subject to shifting changes. For instance, a shift to the acid side, in time, thru whatever cause, would remove the condition of alkalosis. The existing active paradentosis becomes inactive when the body again is in normal acid-base equilibrium.
The pockets are purulent granulation tissue are still present.
So again, when a shift to the alkaline side, in time, takes place, thru whatever cause, the condition of acidosis would be removed. The existing active caries become inactive when the body is in normal acid-base balance. The cavities produced by the acid condition are still present.
The Jarvis study group became aware of this shift, and in the systemic treatment of the related conditions, hayfever, asthma, acne, etc. an effort was made to shift the patient in the acid direction, out of the too alkaline state. They produced thereby a reduction of parasympathetic dominance with relief of symptoms.
They recognized this too alkaline a condition as a state in which the allergic phenomena became manifest, and referred to this state as the allergic zone. The colloid equilibrium seemed to be easily disturbed with flocculation and hydration as dominant factors.
This great instability of the colloid mechanism in certain individuals has been noticed by a great many investigators. The complicated pathologic results are often not correlated, or escape our observation. The flocculation produced has been linked to the “great arthritic state,” and is now easier understood since we understand some aspects of colloid chemistry and the colloid state of the matter.

Pyorrhea Systemic Origin
It was Hulin, who, from a dental angle, discarded temporarily the general pathologic complications of paradentosis and focused the attention of dentistry on the unstable systemic state, or pyorrhetic state, which was to coincide with the flocculation phenomenon of colloid chemistry.
True, different authors surmised an underlying systemic condition, the majorit, however, and, I believe, many dentists today, consider paradentosis to be due to local factors only.
Broderick, in 1928, considered pyorrhea alveolaris to be the manifestation of a disturbed acid-base balance in the alkaline direction, in other words, considered the underlying systemic condition to be one of chronic alkalosis. He tried to explain at length and in detail the disturbances that lead up to this condition, and used the CO2 combining power of the blood (van Slyke) and the pH determination of blood, saliva and urine to prove his point.
We inferred previously, that these arguments we successfully opposed at times by laboratory investigations with the result that the theory was not readily accepted. In his second edition, Broderick readily accepted. In his second edition, Broderick showed that his earlier approach apparently lacked something, and at length went into McDonagh’s theories of disease to prove his point.
Gottlieb referred to this systemic condition as the “Factor X.”
We ourselves held to the acid-base disturbance as the underlying systemic condition of caries and paradentosis. It was appreciated that the methods for the measurement of the acid-base balance were not complete, and, as shown in a previous article, we searched for a more complete theory and measurements which would give us the acid-base balance of the tissues. (True Alkalosis.)
Hulin seems to have brought forward an explanation which is more readily understood and acceptable, and, though we can agree readily with his explanation and theory, we will try to show that the acid-base balance disturbance is still the fundamental systemic factor in paradentosis, as it is in caries.
In a previous article, we tried to clarify the apparent cloudiness in the accepted theories of acid-base balance. We will now attempt to show, that no matter how close Hulin came to the real underlying condition, it was still depending upon the distrubanc eof the acid-base balance. The latter being the fundamental factor, no matter if Broderick’s approach and the pH determination failed to carry the point.
As our explanation of the phenomenon of dental caries made use of the distrubance of the Ambard equation in time, namely, that it was >0.50, and that there existed a systemic condition of a surcharge of HCl on the protein network, therefore a true acidosis (of the tissues), so we will bring forth that the condition which leads to the phenomenon of paradentosis starts with a disturbance of the Ambard equation, namely, that it is <0.50 and that there exists a systemic condition of sub-charge of HCl on the protein network in time, therefore a true alkalosis (of the tissues). This, of course, would be related to a chlorine shift from the red blood corpuscles to the plasma, and the factors which will tend to produce same over a long period of time would be responsible for the alkalosis. These factors are many. This shift of the body to a chronic alkalosis corresponds to a decreased dispersion in the colloid state, thereby manifesting the flocculation phenomenon linking it to the “great arthritic state,” and, at the same time, producing a shift from colloid equilibrium into the allergic zone. (Jarvis). It is now desirable to take up the subjects of Immunity and Anaphylaxix, for the scientific explanation of paradentosis by Hulin will fit nicely into the picture. IMMUNITY: If a small quantity of a toxic substance is introduced into the living organism (a substance generally chosen from the crystalloids), and if we see to it that the dose is not a fatal one, it is noticed that the living body is not disturbed when progressively larger quantities of this toxic substance are introduced. Finally a quantity can be injected that certainly would have been fatal if it had been administered at the start. (Arsenic eaters in Switzerland.) The capacity of an organism to tolerate larger and larger quantities of toxic material is spoken of as immunity. We notice that the toxic ingredients used belong to the crystalloids; in any event, they are not produced by a living organism, or are not introduced in a state in which they exist in a living organism. ANAPHYLAXIS : Let us now remember that the living body when out of normal acid-base equilibrium towards the alkaline side in time, which would be a true alkalosis (of the tissues) enters what is called the allergic zone. If an organism, when in the allergic state, is now subjected to the above experiment, and there is introduced into the blood stream a substance which is colloid in nature, for instance, an animal or vegetable albuminoid, which in themselves are deprived of toxic properties, it is possible at the first injection to introduce a large quantity of substance without producing a disagreeable reaction. If, however, later on a small quantity (as small as a fraction of a drop) is again introduced into this same living organism, there will be a manifestation in the nature of a cataclysm which generally produces death. This phenomenon is contrary to the one of immunity, and has been called the anaphylactic phenomenon, (Richer.) These anaphylactic phenomena are again divided into those that give a general reaction, and into those that give a local reaction. If the meeting of the antagonistic colloids takes place in the circulation, one observes a sudden drop in blood pressure, leukopenia, collapse and death by asphyxia. If the meeting of the antagonistic colloids takes place in the tissues or at the surface of the tissues, when bathed in sensitized fluid media (accidentally by sickness or intentionally in experiments), one observes redness, congestion, erythema, with the result of degeneration of cells and progressive atrophy and decay which is called necrosis. Foreign Protein Sensitization According to Hulin’s views then, the body, which shows a manifestation of paradentosis, must at one time (previous) have been subject to sensitization of a foreign protein by whatever procedure, and the gingiva then became foreign, producing the local anaphylactic phenomenon at the gingivo-coronary margin. It shall now be our course to point out, that the requisite for this systemic alteration rests upon an instability of the colloid mechanism of the body, produced by a disturbed acid-base balance in the alkaline direction, in time. (Alkalosis.) This altered condition corresponds to the allergic state. The body now becomes invaded by a foreign protein which places it in a state of sensitization. The oral symptoms of paradentosis then are the result of subsequent attack by the similar protein, producing a local anaphylactice shock with the accompanying symptoms. Latest investigations show that HCl is not secreted in the stomach, but is formed there from a chloride salt. The amount of HCl formed depends upon the sympathetic-parasympathetic balance of the organism, inasmuch as the organs of digestion are controlled by, and are under the influence of the parasympathetic nervous system, and the amount of chlorides present in the bloodstream. A tendency to chronic pyloric spasm not only interferes with the circulation of that part of the digestive tract, but also with the secretion of the glands in the stomach lining. The final result is a change from a hyperchlorhydria to a hypochlorhydria. The diminished activation of pepsinogen into pepsin, and, therefore, a reduced pepsin content. The introduction then, of proteins into a stomach not suited for protein digestion, causes undigested food to enter the intestinal canal. They form chemical reactions in the small intestines which give as end-result incomplete digested proteins )split proteins), which are absorbed as foreign proteins. Here, then, we have a condition, the introduction of foreign proteins into the body which, in itself, as yet produces no ill results, providing the body is not already sensitized to the protein previously. Many of the intestinal phenomena, as colitis, etc., may well be the result of local anaphylactic shock at the surface of the intestinal lining. The diminished HCl in the stomach also reduces the barrier, placed in the path of oral bacteria to the intestinal tract. They are continually swallowed with the saliva. These micro-organisms produce their secretions which are toxins, and the bacteria themselves are foreign proteins composed of albuminous material. The combination of these toxins and albumins form toxalbumins, are now subject to absorption, and foreign protein sensitization takes place. This condition was splendidly portrayed in an article entitle, “A Mechanism of Infection.” Dental Digest, February, 1932, by Carroll W. Stuart. In the path of continued over stimulation and a tendency to pyloric spasm there naturally follow other digestive disturbances. Alkalosis of the Body With the continued alkalosis of the body producing a diminished amount of chlorine salts secretion, the resultant lack of HCl fails to activate the pepsinogen into pepsin. Lack of mucin secretion fails to supply the protective covering of the stomach, and the field is set for the gastric and duodenal ulcer. In sequence there may follow in time the so-called “chronic appendix,” cecal and colic stagnation, diseases of the male and female generative organs, and finally the symptoms appear of diseases of the central nervous system, neurasthemia. This sequence, therefore, gives as the underlying cause of neurasthenia a disturbed acid-base balance towards the alkaline side, in time. A true alkalosis (of the tissues) with an Ambard equation registering 0.50. The diminished HCl also fails to ionize the ingested minerals, the lack of Ca ion assimilation and the lack of the right blood pH to dissolve the insoluble calcium carbonate produces a lack of ionic calcium with consequential disturbed cell permeability and increased nervous irritability.