The New York State Dental Journal: Vol. 38, No. 3: 285-295: May, 1972
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Chelation and Proteolysis-Chelation
Theories of Dental Caries:
Their Origin, Evolution
Albert Schatz, Ph.D.
Joseph J. Martin,
Vivian Schatz, M.S.
paper was an invited lecture presented by one of us (A.S.)
at the October 20, 1971, Seminar at the School of Dentistry,
explanation of this too-neglected theory by its
Honorary Professor, Faculty of Medical
Sciences, Autonomous University of Santo Domingo; Most Distinguished
Professor, Faculty of Chemistry and Pharmacy, University
of Chile; and Professor of Science Education, Temple
July 22, 1971.
Associate, Radburn Research
Eleventh Street, Fair Lawn, New Jersey.
requests and other correspondence should he sent
to the Radburn Research Institute.
ACID THEORY. ACCEPTANCE
Chelation Theory1 and the Proteolysis-Chelation
Theory2-4 were first
1954 and 1955. To understand how and why
these theories originated,
and how they differ from
one another and from other theories,
it is necessary
to know what dental investigators were doing,
they were thinking, and how little had been accomplished
by 1950. When we began work on caries in 1953, we were surprised
to discover how often acid was unequivocally declared to be
the cause of tooth decay, as if it were a fact. Numerous statements
to that effect are still being made by well-known authorities;
they appear in many textbooks and journals; and they emanate
even from such agencies as the American Dental Association
and the United States Public Health Service.5-8
But no one has ever proved that acid causes
therefore able to quickly understand the unscientific
nature of so much research being done at that time. We realized
that most investigators had accepted the Acid Theory on faith,
and then naively equated tooth decay with simple acid decalcification.
Consequently, the real objective of their research was not
to determine what caused caries. They were convinced that
had already been done by W. D. Miller. Instead, they aimed
in one way or another to provide "more proof for Miller's
Acid Theory," as they put it. Some of these researchers
were literally shocked when we told them they would never
achieve their objective if caries resulted from something
beside acid. They had never considered any other possibility.
Some of them even seemed incapable of understanding what we
PHILOSOPHY OF "PROOF"
We were also dismayed by how many people did not understand
what proof is. They became nonplussed when we informed them
that proof is qualitative, not quantitative. If something
is proved, it is completely proved; no further proof is necessary.
Until it is proved, there is no proof at all. In other words,
unless something has been conclusively established, it has
not been established at all. For until then, there is always
the possibility of error. Proof is therefore absolute. It
is all or nothing. There is no such thing as partial proof,
or degrees or stages of proof. "More proof" would
not be needed to substantiate Miller's Acid Theory if it had
ever been proved in the first place.
MISCONCEPTIONS AND FALLACIES
We were also taken aback by the lack of understanding of acid.
Almost everybody was playing the game called "Follow
the Leader" by equating acid with hydrogen ions, and
disregarding the anions and undissociated molecules of acids.
True, the more sophisticated investigators did distinguish
between hydrogen ion concentration, which they measured as
pH, and titratable acidity. However, it seemed that nobody
was aware of the fact that the anions and undissociated molecules
of certain acids could also decalcify enamel and dentin, just
as hydrogen ions do, but by an entirely different mechanism,
i.e., the formation of chelates and other
numerous reports on the lack of correlation between
decalcifying ability and pH or titratable acidity, researchers
then ignored (as many still do) the demineralization resulting
from the complexing ability of acid anions and Undissociated
we therefore saw in 1953 was not an overemphasis or even
just a plain ordinary emphasis on acid per se, but a psychological
fixation or fetish, so to speak, with the hydrogen ion. Miller's
disciples had in effect converted his original Chemico-Parasitic
Theory into a virtual Acid Theory, without being aware of
how they had restricted and thereby distorted their master's
views. We prefer to use the expression Acid Theory rather
than Hydrogen Ion Theory because acid as such has become indelibly
associated with Miller's concept. The term Acid Theory also
more accurately reflects how Miller's followers have overemphasized
the "chemical" part of his Chemico-Parasitic Theory
and have almost completely disregarded the "parasitic"
aspect. They have therefore created and have been working
within the framework of what we call an Acid Theory, in contrast
to his original Chemico-Parasitic Theory. In other words,
those who declare their allegiance to Miller have really not
been following his precept.
We were also perplexed, in 1953, by the seemingly endless
number of publications on the pH of saliva, dental plaques,
and fermenting debris in cavities. Tooth decay is not a disease
of saliva, dental plaques, or fermenting debris in cavities.
It is a disease of teeth. Nobody has ever determined the pH
at the site where and at the time when caries first begins.
Until that is done, those who claim that acid causes caries
are expressing only wishful thinking and deluding themselves
along with others. Since they do not know whether the earliest
stage of caries occurs in a microcosmos that is acidic at
that time, they do not really know whether hydrogen ions cause
claim that acids produce apparently typical
in vitro or in vivo have not provided proof that the
action is due to hydrogen ions. Indeed, some of these studies
show that anions and undissociated molecules may be more important
than hydrogen ions. Even when an enamel surface is exposed
to a solution that is acidic, it is not only hydrogen ions
which diffuse into the tooth. Anions and undissociated molecules
likewise do so, and can demineralize by complexing calcium
beneath the surface of the tooth where the first observable
loss of minerals is supposed to take place. No one knows what
the pH is when and where this earliest decalcification begins.
Therefore, no one really knows whether this loss of minerals
is due to hydrogen ions.
The disciples of Miller have also overlooked important implications
of the fact that they are dealing with a two-phase system
where reactions occur at a solidliquid
assume that the pH at the plaque-enamel interface
the same as the pH within the liquid phase of the plaque.
However, numerous studies of clay, soils, and biogeochemical
weathering have shown that this is usually not true for such
systems. The pH within the bulk of a plaque or within fermenting
debris of a cavity may therefore be quite different from the
pH at the plaque-enamel interface of an intact tooth, or the
debrisenamel or debris-dentin interfaces in a cavity. The
pH within intact enamel and within intact dentin may be still
serious criticism may also be directed at the belief, widely
accepted but unproved, that the earliest observable loss of
minerals is the earliest stage in the caries process. Decalcification,
regardless of how early it is detected, can be the resuit
of previous effects (some of which may involve organic components)
that made possible the subsequent loss of mineral matter.
Also open to serious question it the belief that the initial
attack in caries must be on mineral components because the
organic matrix appears to be intact after minerals have been
removed. One cannot justifiably conclude that the organic
matrix has not been altered prior to, during, or as a result
of decalcification merely because it appears normal when viewed
microscopically. The appearance of the organic matrix would
not be altered if only its coordinate covalent linkages to
mineral components were ruptured. Nevertheless, this kind
of change on a molecular level could have most drastic implications
with respect to tooth structure, susceptibility versus resistance
to caries, loss of minerals, etc. In any event, Miller's disciples
have disregarded the considerable and convincing evidence
that proteolysis may well precede the loss of minerals in
the caries process.11, 12
HOW ACIDS AND CHELATING AGENTS
DISSOLVE TOOTH MINERALS
It is necessary to know how Miller's disciples think, because
their thinking reveals why they are inevitably doomed to failure
in their efforts to provide proof (or "more proof")
for their Acid Theory. Tooth minerals normally dissolve to
a small but finite esxtent in aqueous media. To understand
how hydrogen ions and chelating agents dissolve tooth minerals,
let us, for simplicity, consider
in distilled water. This salt normally dissolves to
extent to form a dilute but saturated
calcium ions and phosphate
A fixed amount
of the compound will dissolve under given conditions.
This amount is defined by the solubility product
an acid such as HCI is added, the hydrogen ions from
the acid reduce the concentration of phosphate ions by converting
them to HPO4=,
This in turn lowers the Ksp. More
will then dissolve until the
again equals that
value which is constant for the given conditions.
chelating agent, on the other hand, reduces the
by removing calcium
ions from solution. It does this by tying
them up in
the form of undissociated complexes. More
will then dissolve until the
again reaches its
fixed value. Of course, some substances
by acting both ways; they may chelate calcium and
also provide hydrogen ions. Miller's
disciples have been concerned
only with hydrogen
ions. They can therefore never account
under weakly acidic or non-acid conditions. Nor
they explain the lack of correlation between cariogenicity
and pH or titratable acidity.
WHAT WE CONCLUDED IN
It thus became
clear to us in 1953 that the concept of pH,
general importance in science cannot be overestimated,
had oversimplified the pathology of caries in the minds of
most researchers. It became so easy and so fashionable to
measure pH that dental researchers became infatuated with
the technique. They made endless pH measurements and discovered
and rediscovered, in terms of pH, that fermenting carbohydrates
give rise to acids. With such experiments repeated ad infinitum,
they convinced themselves that acid causes caries. The pH
concept may therefore be more responsible than anything else
for the lack of progress in our understanding the etiology
of this disease and our efforts to control it. What we therefore
concluded in 1953, when we began working on tooth decay, was
that a century of caries research had been doomed to failure
from the very start because it had in effect built a house
THE "EITHER . . . OR" APPROACH
Although several different theories had been developed to
explain caries,13, 14 philosophically
the over-all or prevailing approach rested essentially on
an "either . . .or" basis. On the one hand, the Proteolysis
Theory explained caries in terms of an enzymatic attack on
enamel protein. On the other hand, the Acid Theory claimed
that tooth decay was due to decalcification. And this, as
we have pointed out, was attributed almost exclusively to
the action of hydrogen ions. There are so many unjustified
assumptions, inadequacies, misconceptions, and fallacies in
this approach that it was difficult for us to understand how
and why so many people took it so seriously for so long.15,
thing, the "either . . .or" approach assumed
that, in enamel, the protein (or organic matter) existed separately
from the minerals; and that the initial attack must therefore
be on one or the other. But if the two are joined; that is,
chemically united to one another, then the initial reaction
might conceivably be a rupture or breaking of the linkage,
as shown in Figure 1. This kind of attack would not be directed
against protein (i.e., organic matter) per se or
minerals as such. Nor would it result in the loss of any tooth
constituents. Everything would
representation of an initial
which ruptures bonds linking
inorganic components of enamel but does
remove any material.
be there, but the
enamel would be structurally altered or
disorganized. Another kind of initial attack might result
in the simultaneous loss of both organic and inorganic matter.
The "either . . .
or" approach did not take such
into account. It considered only a loss of protein
by enzymatic degradation or the loss of minerals by acid dissolution.
And it chose the latter. The "either . . . or" approach
also failed to take into account the ability of acid anions
and undissociated acid molecules to dissolve tooth minerals
by complexing calcium. Demineralization, as we have indicated,
was attributed almost exclusively to hydrogen ions. Moreover,
although all acids have hydrogen ions, only those acids originating
from the fermentation of carbohydrate food in dental plaques
were considered responsible for caries. Thus, the "either
. . . or" approach disregarded the possibility that amino
acids derived from the breakdown of tooth protein might also
decalcify, by chelation.
Despite these and other weaknesses, the "either . . .
or" approach dominated caries research for almost a century.
Most investigators assumed that there were these two and only
these two possible causes of caries; namely, proteolysis and
acid. The problem, as they saw it, had been to decide between
them. Having chosen acid, they deluded themselves into thinking
they had the answer.
What particularly impressed us in 1953 was that hardly anyone
was engaged in research on other possible mechanisms beside
acid. We quickly realized that caries was unique among major
diseases in that so much time, money, and effort continued
to be invested in an approach which had been so unprofitable
for so long.
the Chelation Theory of dental caries in 1954
because our early studies revealed that chelation was widely
operative throughout nature, and was the most important mechanism
for the dissolution, transportation, and utilization of minerals,
both in vitro and in vivo. Our alkaline
blood maintains calcium in solution by means of chelation.
The formation, normal turn-over or replacement, and pathologic
demolition of bone involves chelation. This is also the most
plausible mechanism whereby primary tooth roots are resorbed.
The two most important pigments in the plant and animal kingdoms
are chelate complexes. Hemoglobin is an iron chelate, and
chlorophyll is a magnesium chelate. Enzymes which require
trace metals such as zinc, copper, iron, cobalt, and manganese
operate as chelate systems. Chelation appears to be the major
mechanism in biogeoa chemical weathering, pedogenesis (i.e.,
soil formation), and soil fertility. The assimilation and
transport of mineral nutrients by plants is accomplished by
chelation. In the alkaline ocean, from which our alkaline
bodies have evolved, the cycle of mineral elements is mediated
and made possible by means of chelation.
From a comparative biochemical point of view, it was inconceivable
to us that a mechanism so important and so widely operative
throughout nature would not
Figure 2. Salt and chelate structures for calcium-amino
acid compounds. Three complexes
amino acid ratios of 1:1, 1:2, and 1:3 are
be involved as a means
of decalcification in the caries process.
So, on the
basis of these considerations and our experimental
results we formulated the Chelation Theory1
in 1954. According to this concept, tooth decay results from
demineralization by chelating agents which dissolve enamel
minerals by forming complexes. Figure 2 illustrates the structures
of some of these complexes and also shows a salt structure
for comparison. An amino acid is used here as an example of
a chelator. The Chelation Theory took into account a wide
variety of sequestering agents which include acidic, neutral,
and alkaline compounds that form calcium chelates under acid
and non-acid conditions. Because dental researchers did not
understand the chemistry of these coordinate covalent compounds,
we discussed this subject in detail9
in a report in 1958. It is interesting to note, in this respect,
that Eggers-Lura's so-called non-acid complexing
is no more than a
special case of our Chelation Theory.1
He attributed decalcification to the ability of sucrose to
chelate calcium. We had previously considered this in our
first report1 published in 1954.
Our original report on the Chelation Theory appeared in
editors in the United States rejected
manuscript and others which we submitted for publication
in their journals. The reasons they gave for refusing to print
our papers were:
had been proved that acid causes tooth decay.
(b) Tooth minerals can be dissolved only by acids, not by
chelating agents, and certainly not under neutral or alkaline
does not occur in vivo and cannot be
interest or importance in tooth decay.
To those editors who refused to publish our papers for these
reasons, we replied: "Never has so much ignorance been
concentrated in so few words!"
Having satisfied ourselves that chelation could be responsible
for the loss of minerals in tooth decay, we next sought answers
to such questions as the following:
(a) Which compounds are the most important chelating agents
(b) Where do
they come from?
How are they formed?
discussed these aspects of the problem among ourselves
and with others, we became aware of a flaw in the Chelation
Theory. We had explained demineralization in terms of complexation
by acid anions and a wide variety of other organic and inorganic
compounds capable of sequestering calcium. But the agents
we considered were essentially of exogenous origin; that is,
they arose from outside the body.
We therefore found ourselves in a dilemma. If caries were
due simply to demineralization by exogenous agents, then tooth
decay would be nothing more than highly localized erosion.
This would be true regardless of whether the decalcify-
Schematic representation of Miller's Chemico-Parasitic
Theory, the Acid Theory, and the Chelation Theory. For
reasons which are discussed in the text,
have distinguished between Miller's
Chemico-Parasitic Theory and the Acid Theory
which his followers have in effect developed.
ing agents were hydrogen ions or chelating agents. We also
encountered another dilemma. If caries resulted from decalcification
by compounds produced by bacteria in dental plaques, then
it could not possibly be an infectious disease. As we have
already pointed out, Miller's disciples overemphasized the
strictly "chemical" action of exogenously produced
acids and disregarded the "parasitic" aspect of
his Chemico-Parasitic Theory. We became concerned when we
realized that our Chelation Theory was open to the same criticism.
We had considered demineralization only and agents of exogenous
origin only. So we too had not viewed caries as an infectious
live in dental plaques or cavities and feed
that we have eaten are not actually invading our bodies.
They are therefore neither parasites nor pathogens. Infectious
diseases are caused by organisms which penetrate our bodies.
These are parasitic because they utilize parts of our living
bodies as their food supply. They are pathogenic because their
metabolic activities within our body tissues produce an abnormal
or pathologic condition. This is what we call "disease."
representation showing the Proteolysis Theory
and the Chelation Theory, and how the idea of a proteolysis-chelation
was developed into the
It was in an effort to resolve these and other dilemmas that
we formulated the Proteolysis-Chelation Theory of dental caries
in 1955. What originally suggested proteolysis-chelation as
a mechanism for tooth decay was our realization that the Proteolysis
Theory provided for the formation by parasitic organisms of
those compounds in vivo or in situ which,
according to the Chelation Theory, demineralized by sequestering
calcium. We therefore named our new theory Proteolysis-Chelation
to indicate its origin. In developing this theory, we demonstrated
the susceptibility of organic matter in normally calcified
enamel to direct microbial attack. We even showed that keratinous
proteins were subject to attack by oral
did not restrict our theory to protein or limit it
only to keratinous proteins as some of our critics mistakenly
assume. Nor did we confine the Proteolysis-Chelation Theory
to chelation per se. The concept is applicable to
and takes into account all organic constituents in the tooth
and all complexation reactions, of which chelation is a special
case. The term Proteolysis-Chelation was therefore used in
a very broad sense.
5. Schematic representation of the Proteolysis-Chelation
Theory showing different possible pathways of attack on
enamel. The reactions would be essentially the same for
We also showed that the proteolysis-chelation mechanism was
operative over a broad range of acid, neutral, and alkaline
conditions. We pointed out that our theory could explain those
cases of caries that occurred under non-acid conditions, which
the Acid Theory could not. But we never restricted the Proteolysis-Chelation
Theory to non-acid conditions, as some of our critics mistakenly
assume. We also did not attempt quantitative calculations
in terms of the stability constants, as other critics pointed
out, because stability constants are not applicable to in
vivo systems which are chemically heterogeneous and continuously
changing in chemical composition. These constants are derived
from and can be applied only to welldefined, homogeneous systems
under equilibrium conditions.
The theories of dental caries with which we are concerned
in this report are schematically represented in Figures 3,
4, and 5. The Acid Theory and our original Chelation Theory
both view caries as a disease resulting from decalcification.
In the former, this is brought about by hydrogen ions; in
the latter, by complexing agents. The Proteolysis Theory,
on the other hand, is concerned exclusively with enamel protein,
the enzymatic breakdown of which is believed to result in
caries. The Proteolysis-Chelation Theory differs fundamentally
from Miller's original Chemico-Parasitic Theory. According
to the latter, caries results from two separate and sequential
actions. The first attack on the tooth is a decalcification
by fermentation acids of exogenous origin. Then there is a
subsequent attack on tooth protein by proteolytic bacteria.
The Proteolysis-Chelation Theory, on the other hand, postulates
two interrelated actions: an enzymatic attack on organic constituents
and a more or less simultaneous demineralization initiated
by substances, able to complex calcium, which arise endogenously
from the degradation of the organic constituents.
The Proteolysis-Chelation Theory considers the possibility,
already mentioned, that the earliest change in tooth decay
could be a rupture or breaking of bonds linking organic and
mineral components of enamel. This may take place without
the loss of anything from either phase. In one sense, such
an attack cannot be said to affect either the minerals alone
or the organic matter alone, because they do not exist independently
of one another at the tme the attack occurs. From another
point of view, however, such an attack does affect both components
simultaneously since it makes them separate entities, whereas
they were previously joined together. Incidentally, this kind
of change may be initially responsible for the formation of
chalky enamel. Most caries researchers mistakenly assume that
the least detectable loss of enamel mineral is the earliest
lesion in caries. They do not realize that many changes may
have taken place before then. The Proteolysis-Chelation Theory
is concerned, among other things, with those biochemical changes
or biochemical lesions, so to speak, that have occurred on
a molecular level before there is any loss of enamel mineral
From the point of view of what is first removed in the decay
process (organic matter or minerals?) the Proteolysis-Chelation
Theory considers an initial attack on organic constituents,
but with a more or less simultaneous loss of both organic
and mineral matter. This can happen because amino acids, peptides,
and many other breakdown products of enamel organic matter
are capable, as soon as they are formed, of dissolving calcium
phosphates by chelation.22-23 The
ProteolysisChelation Theory is not therefore particularly
concerned with the question: "What is removed first,
organic matter or minerals?" Instead, it challenges the
assumption on which that question rests. For such a question
may just not be applicable to the earliest stage of caries
if neither component is removed, or if both mineral matter
and organic material are lost simultaneously.
Although the Proteolysis-Chelation Theory is primarily concerned
with how teeth decay, and especially with the initial stages
of this disease, it has also tried to explain such aspects
as why caries occurs, the biochemical nature of enamel susceptibility
versus resistance, the post-eruptive maturation of enamel,
the role of nutrition, the influence of systemic factors,
unilateral interproximal caries, fluoride action, the effects
of trace elements, and preventive measures.23-28
IS ENAMEL? WHAT IS CARIES?
What we did in developing the Proteolysis-Chelation Theory
was to reorient our thinking about enamel and about the etiology
and prevention of caries. Most researchers look upon enamel
as a mineral structure. They know, of course, that a small
amount of organic matter is present, but this is residual
material left over from amelogenesis. For them, it is only
of incidental interest and has little or no importance in
the disease process. Since they view enamel as essentially
mineral in nature. they believe that caries results from a
loss of minerals, and that the initial attack is a demineralization.
But we look upon enamel quite differently. To us, it is essentially
organic, just as all other parts of our bodies, including
bone, dentin, and cementum, are fundamentally organic. Ectodermal
structures such as nails, hooves, claws, horns, feathers,
hair, wool, porcupine quills, scales, etc., are all mechanically
modified and adapted for the functions they are required to
perform. Teeth have to be very hard, especially their outermost
layer. The high degree of mineralization of enamel, which
is another ectodermal structure, is the way it has been mechanically
modified and adapted for its particular functions. Nature
has used the same means to strengthen bone, dentin, and cementurn.
Nevertheless, enamel is still essentially organic
in nature. We therefore consider caries to be an infection
or invasion of this organic ectodermal structure by microorganisms
capable of feeding on some of its protein, carbohydrate, fat,
and other organic components. Because so much inorganic material
is present, it is not at all surprising that the disease affects
a large amount of minerals in one way or another. Indeed it
would be surprising if this were not so.
Since we differ philosophically from Miller's disciples in
how we define enamel and caries, our whole approach is fundamentally
different from theirs. They concentrated on physical-chemical
studies of calcium hydroxyapatites, especially structure and
solubility. We, on the other hand, applied information about
the biochemistry, physiology, and pathology of skin and other
ectodermal structures to enamel in an effort to understand
its structure, maturation, and susceptibility to caries; and
the role of such factors as age, diet, trace elements, hormonal
balance, saliva, etc., in this disease. We paid particular
attention to keratinous proteins because ectodermal structures
consist largely of these proteins.
CAN WE LEARN FROM HISTORY
There was a time, not long ago, when the great majority of
dental researchers unquestioningly accepted lactobacilli as
the organisms which cause tooth decay. Those few individuals
who expressed doubts were considered to be uninformed or naive,
and were not infrequently persecuted for what was considered
heresy. Now, no one seriously believes that lactobacilli cause
caries. But no one points out that:
(a) All those authorities who built reputations and achieved
positions of power based on that mistaken notion were completely
(b) The great majority of dental researchers who allowed those
authorities to think for them were also wrong in accepting
without question, what they were told to believe. But there
is a more serious charge against them. They were intolerant
of others who had different ideas.
(c) The few so-called heretics who questioned the role of
lactobacilli and challenged the authorities were the true
scientists. They insisted on thinking for themselves. History
has justified and vindicated them.
At that time, not long ago, the great majority of dental researchers
looked upon the authorities who had established the "lactobacillus
cult" as their leaders. Those men were honored and acclaimed
for their supposedly important contribution to understanding
and controlling caries. But we now know that those authorities
and leaders were completely wrong about lactobacilli. And
because they were wrong, and because they were intolerant
of others who were right, those acclaimed authorities and
honored leaders are directly and personally responsible for
having retarded progress in understanding and controlling
Now streptococci instead of lactobacilli cause caries. Now
some of the acid that decalcifies comes from the fermentation
of streptococcal polysaccharide, originally formed from dietary
sugar. But it is still acid, acid, acid, acid with the great
majority of dental researchers who continue to use their pH
meters more than their heads. They still concentrate on hydrogen
ions and ignore the fact that the anions and undissociated
molecules of fermentation acids can dissolve tooth minerals
by complexing calcium. This is true regardless of whether
these acids derive from sucrose or from polysaccharides. For
them to admit this would open a Pandora's Box that would wreak
havoc with the status quo and lead them inexorably
first to the Chelation Theory and then to the Proteolysis-Chelation
WILL HISTORY REPEAT ITSELF?
We have now reached a stage where history may soon judge those
authorities who have built their reputations on the Acid Theory,
and have achieved positions of power in an "acid cult."
Like their predecessors who established the "lactobacillus
cult," these leaders have been intolerant of others who
insist on thinking for themselves and who question the role
of acid. Like their predecessors, the acid authorities have
also been honored and acclaimed for their supposedly great
contribution to the etiology and prevention of caries. But
they have never proved that acid causes caries. Nor have they
prevented this disease by counteracting acid and nothing else.
Indeed, there is increasing evidence that acid does not cause
caries. More and more people now see the proverbial handwriting
on the wall of the temple of acid which the authorities have
erected, and they know that it says: "You have been weighed
and found wanting."29-34
History may decide that those who conjured up acid as a cause
of caries may be just as wrong as those who invoked lactobacilli
in the etiology of this disease. History may justify and vindicate
the few free and indomitable spirits who have insisted on
thinking for themselves and have questioned acid as a cariogenic
agent. It will then be recognized that those great authorities
and renowned leaders who perpetrated and perpetuated the "acid
cult" are directly and personally responsible for having
retarded progress in understanding and controlling this disease.
1. Martin, J. J, et al.: Chelation, or metalbinding, as a
new approach to the problem of dental caries, Euclides, Revista
Mensual de Ciencias Exactas (Madrid, Spain) 14: 311-317, 1954.
2. Martin, J. J., et al.: Proteolysis-chelation: a new theory
of dental caries. N.J. State D. Soc. 27: 7-10, 1955.
3. Schatz, A., and Martin, I. J.: The proteol. ysis-chelation
theory of dental caries. J.A.D.A. 65: 368-375, 1962.
4. Schatz, A., and Martin, J. J.: What is proteolysischelation?
Stomatologia (Greece) 18: 5-8, 1961. (In English)
5. Schatz, A., and Martin, J. J.: A critique of Miller's acid
theory. (Part 2 in Symposium on Dental Caries: Miller's Chemico-Parasitic
Theory and the Proteolysis-Chelation Theory), Pakistan Dent.
Rev. 14:11-25, 1964. (In English)
6. Schatz, A., and Martin, J. J.: Some historical aspects
of caries research, (Part S in Symposium on Dental Caries
Miller's Chemico. Parasitic Theory and the Proteolysis-Chelation
Theory). Pakistan Dent. Rev. 14:43-53, 1964. (In English)
7. Schatz, A.. and Martin, J. J.: Perspectives in caries research.
(Part 4 in Symposium on Dental Caries: Miller's Chemico-Parasitic
Theory and the Proteolysls-Chelatlon Theory), Pakistan Dent.
Rev. 14 :81-93. 1964. (In English)
8. Schatz, A.. et al. : The implications of Soviet research
on caries. An introduction to the work of Sharpenak, N. Y.
State D. J. 33: 587-591, 1967.
9. Schatz, A., et al.: Quelques considérations sur
la carle dentaire en fonction de la thˇorie de protéolyse-chélation.
Revue Beige Science Dentaire 13: 538-557, 1958.
10. Schalacha. E. B., et al.: Chelation as a weathering mechanism.
I. Effect of complexing agents on the solubilization of Iron
from minerals and granodiorite, Geochimica et Cosmochimica
Acta 31:587-596. 1967. (In English)
11. Bodecker, C. F.: Enamel proteolysis: an important factor
in dental caries, N. Y. 1. Dent. 18: 254-268, 1948.
12. Sharpenak. A. E.: The etiology and prevention of dental
caries, N. Y. State D. J. 33:
13. Schatz, A.: Concerning different theories of dental caries,
N. Y. State D. 1. 27: 95-96, 1961.
14. Schatz, A., and Martin, J. J.: Some historical reflections
on dental research. A comparison of the septic and proteolysis-chelation
theories of caries, J. Dent. Med. 15 :127-133, 1960.
15. Schatz, A.. and Martin. J. J.: Opportunities for creative
research in dental caries, N. Y. J. Dent. 29 :5-10 and 47-53.
16. Schatz, A.. and Martin. J. J.: What caries research offers
the graduating dentist: the challenge of proteolysis-chelation,
N. J. State D. J. 27 127-132. 1961.
17. Eggers-Lura. H.: The Non-Acid Complexing Theory of Dental
Caries. Holbaek, Denmark. 1967.
18. Schatz. A.. et al. : Destruction of tooth organic matter
by oral keratinolytic mciroorganisms, N. Y. State D. J. 21
19. Schatz A.. et al. : Abban von organiscben Schmelzbestandteiien
und keratinfisem Eiweiss (lurch proteolytische Bakterien der
Mundhöhle, Zahniirztliche Rundschau 15: 349-352, 1956.
20. Schatz, A., et al.: Trace element stimulation of keratin
(hair) degradation by oral keratinolytic microfiora. Erperientia
12 : 308. 1956.
21. Schatz, A.. et al.: Some philosophical considerations
on the proteolysis-chelation theory of dental caries. Pakistan
Dent. Rev. 9 : 23-37 (January) and 9:69-17 (April), 1959.
22. Schatz, A.. and Martin. J. J.: Die Proteolyse-Chelatioa-Theorie
der Zahnkaries: Reaktionen der Aminosituren und ihre Derivate
mit Kaizium, Blättsr für Zahnheilkunde 26 :191-203,
23. Schatz, A., and Martin, J. J.: Controversy and scientific
progress : some disagreements about the proteolysis-chelation
theory, Pakistan Dent. Rev. 16 :103-111, 1966. (In English)
24. Schatz. A., and Martin, J. J.: Speculations on lactobacilli
and acid as possible anti-caries factors. N. Y. State D. J.
21: 367-379, 1955.
25. Schatz. A., et al.: A new approach to dentifrices, N.
Y. State D. J. 22 :161-173, 1956.
26. Scbatz, A., and Martin. J. J.: Destruction of bone and
tooth by proteolysis-chelation, its inhibition of fluoride
and application to dental caries, N. F. J. Dent. 30: 124-134,
27. Schatz, A., and Martin, J. J.: Soil, water, food, and
teeth, Environmental Health 5: 55-65, 1962.
28. Schatz, A.: Trace elements, nutrition, fluorine, and dental
health, Pakistan Dent. Rev. 15 :83-94, 1965. (In English)
29. Schatz, A. : The need for objectivity with respect to
Miller's theory and fluoridation. (A philosophical book review).
Pakistan Dent. Rev. 16 : 57-68, 1966. (In English)
30. Schatz. A., and Martin, J. J.: "Fear of change is
the embalmer of progress," N. Y. State D. J. 27: 392-395,
31. Schatz, A., and Martin, J. J: Concerning criticism of
the proteolysis-chelatlon theory of dental caries, N. Y. State
D. 5. 25: 285-292, 1959.
32. Schatz, A.: Caries as a unique disease, Stomatologia (Greece)
20: 56-64, 1963. (In English)
33.Schatz, A., and Martin, J. J.: Changing concepts in dental
caries, N. F. State D. J. 29: 449454, 1963.
34. Schatz, A., and Martin, J. J.: Ode to acid lords of yore,
Pakistan Dent. Rev. 13: 123-125, 1965. (In English)