RECENT THEORIES OF THE FORMATION OF PUS, CONSIDERED 
WITH REFERENCE TO DENTAL OPERATIONS. 
Read before the Connecticut Valley Dental Society at Montreal, P. Q., 
July 20th, 1887. 
BY G. V. BLACK, M. D., D. D. S. 
The ancient and time-honored theory that the formation of pns 
is an act of the tissues themselves, or is a mechanical effect simply 
following molecular death, has, within the last few years,’ been 
questioned by the strictest experimental inquiry, and apparently 
has been disproven. The surgeon of the past has seen the forma- 
tion of pus occur in open wounds with such promptness and regular- 
ity, that it came to be regarded as a necessary part of the series of the 
phenomena taking place during the processes of repair. That this 
formation of pus was an act of inflamed tissue, was unquestionably 
the opinion of the medical world down to a very recent date, and 
is, perhaps, yet held by the masses of the medical profession. The 
fluid portions of pus were regarded as liquefied portions of tissue and 
escaped serum, in which were commingled large numbers of so- 
called pus corpuscles. These latter were very properly held by 
almost all observers to be nothing more than ameboid cells, which 
had been so unfavorably placed that they had died, and were 
thrown off with the fluids, or had wandered out from the tissues 
and were carried away with the secretions. In this view of the 
case, pus came to be regarded generally as a normal secretion, and 
was looked for as an essential result in any considerable wound 
which involved the integrity of superficial parts. 
While this was looked for as an essential occurrence, surgeons 
had learned to regard the characters of pus with interest in each 
particular case, and Avhen this product was thick, creamy and in- 
odorous, it was regarded as a good omen. This was called laudable 
pus, healthy pus, etc., and so long as this character was maintained 
the wound was regarded as in good condition. If, however, the 
pus departed from these qualities, it was known to portend evil for 
the patient. Therefore, different qualities of pus came to be rec- 
ognized. I 1 y r\ 2 
It had long been observed, however, that wounds in which the 
integrity of the skin was not disturbed, very generally healed with- 
out suppuration. A bone might be broken, and even comminuted, 
and if not complicated by an opening upon the surface, the wound 
would generally heal without the formation of pus. The case 
might present as much inflammatory movement as the open wound, 
the extent of injury might be great, and the case present a grave 
aspect, but yet it would very generally run through the course of 
repair without the formation of pus. These facts gave rise to 
much inquiry as to why this clinical difference, and the conjecture 
that it was in some way brought about by exposure to the air, was 
entertained. 
These theories received the first severe discredit by the brilliant 
experiments of Joseph Lister, of Glasgow, Scotland. This surgeon, 
by what became known later as the Lister method, a method which 
had for its object the exclusions of micro-organisms from wounds, 
demonstrated that open wounds might be so treated that the pro- 
cess of repair would be essentially the same as that of internal in- 
juries. He arrived at the idea that the formation of pus was in 
some way influenced by the life and growth of micro-organisms, but 
how, seems not to have been very clearly made out. However, the 
ancient idea that the formation of pus was a vital act, was not 
questioned by him. He seemed rather to look upon the micro- 
organisms as having the effect of farther depressing the vital ener- 
gies of tissues already inflamed, or of increasing the inflammatory 
movement already present in such a way as to increase the suppura- 
tion, or to produce it in cases in which it would not have occurred 
without their presence. But down to the time of the World’s 
Medical Congress, which met at London, in 1881, he certainly had 
no idea of questioning the general opinion that the formation of 
pus was a vital act of inflamed tissue. At that time Prof. Volk- 
man, of Halle, and some others, held the opinion that without 
micro-organisms there was no pus formation. He says; “ In the 
worst constitutions, and with the most disordered state of health, 
no suppuration takes place if septic infection is prevented.” (Lon- 
don Congress, Yol. II, p. 362.) At that time this was regarded by 
Mr. Lister and others as a very extreme view. 
In the consideration of this question there are certain facts that 
are so firmly established by direct observation that they must be 3 
regarded as fundamental, and no theory can be entertained that 
will not include them. What may be termed the anatomical or 
physical process of the formation of pus has been so well observed 
in the past, and agreed upon by so large a group of observers, that 
it must be regarded as definitely settled, and beyond the possibility 
of dispute. We may properly look for factors in this process here- 
tofore overlooked, and seek different explanations of the phenom- 
ena observed, but those phenomena that have heretofore been 
prominently apparent are, and will ever remain, prominent phe- 
nomena of this process. Briefly, these are inflammation with its 
usual phenomena of heat, redness, pain, and swelling, as stated 
from the more superficial observation. But from the standpoint of 
histological inquiry, they consist essentially of certain local disturb- 
ances of the circulation, the formation within the tissues, or upon 
the surfaces of membranes, of a certain plastic or coagulable exu- 
date, the gathering of white blood corpuscles, wandering cells, ame- 
boid cells or leucocytes to the spot, and certain disturbances of the 
fixed cells in the focus of the inflammatory movement. These ame- 
boid cells are properly undeveloped connective tissue cells, or cells 
derived from rejuvenated connective tissue, and one of their func- 
tions in the economy of nature is the repair of injuries. In this 
process these cells are developed into the new tissue, or tissue of 
repair. The plastic exudate is essential. All tissue of a primary 
character is first developed in a homogenous matrix. This is true 
of the development of the tissues of the foetus, and is equally true 
of the development of tissues of repair. The plastic exudate thrown 
out in the process of inflammation forms the matrix in which the 
ameboid cells develop. These cells are always found imbedded 
within this exudate, and it is essential to their growth or develop- 
ment into tissue. In the formation of pus, this plastic exudate is 
observed to liquefy. The ameboid cells are found floating in the 
liquid mass, and are then known as pus corpuscles. Indeed, the 
cells under these circumstances are no longer capable of develop- 
ment. The matrix in which they were lodged, and in which, nor- 
mally, their development should proceed, has become liquid, and is 
so changed in its chemical qualities that it fails to support them, 
and they die. 
Furthermore, this plastic exudate, as I have said, is also thrown 
out among the fixed cells, the older elements of the tissue in which 4 
an inflammation occurs. Liquefaction may and does occur in this 
position also. Here we find that the ameboid cells mingle among 
the fixed cells of the part, and all become imbedded in a matrix of 
plastic exudate. In the event of suppuration the plastic exudate 
becomes liquid, and the tissue already divided by its presence dies, 
and is in part rendered fluid and floats away with the liquid mate- 
rial as shreds and cells, together with the ameboid cells. All of 
these combined, form what we know as pus. 
In open wounds this process is observed to begin superficially, or 
upon the exposed surface. In the development of phlegmonous 
abscesses, it may have its beginning in the midst of the tissues. In 
the latter case, after its establishment, the further development of 
pus proceeds from the walls of the abscess, as in the open wound it 
proceeds from the surface.' Ameboid cells that come to the surface 
tend to pile up in the form of living granulations, but more or less 
of them float away in the liquefying exudate that should form their 
matrix. In this way the formation of the matrix filled with \ resli 
ameboid cells, which tend to develop into granulations, is constantly 
proceeding. And the liquefaction of this exudate, carrying with it 
the ameboid cells in the form of pus, is also constantly proceeding. 
If the former exceed the latter, the healing of the wound is being 
accomplished ; but if the latter exceed the former, destruction of 
tissue and the widening of the breach of continuity is the result. 
This much has been observed by histologists and pathologists for 
years past, and may be regarded as so firmly established that our 
views upon these points are not likely to be essentially changed by 
future observations. 
The important questions which present themselves now are two, 
around which all others arrange themselves: 
1st. What visible phenomena are found to be present in suppu- 
ration which had not formerly been observed and considered ? 
2nd. What is the cause of the liquefaction of the plastic exudate 
and the death of the ameboid cells ? 
The answer to the first of these questions must rest purely upon 
direct observation, and can be settled in no other than the experi- 
mental way. For many years past microbes have been observed in 
pus, but the idea that they were in anywise essential to pus forma- 
tion was not seriously entertained until a comparatively recent date, 
and had not been considered. Many phenomena may be presented during the occurrence of such changes as that we are considering, 
that are purely accidental and not necessary to the process. There- 
fore, to establish that a certain accompanying phenomenon is really 
essential, it is necessary to show that it is always present, and that 
the process cannot proceed without it. 
Observations in regard to the connection of microbes with the 
formation of pus have now been in progress for several years, and 
by the most astute observers of the world. These observations may 
be divided into two classes. First, examinations of pus with a view 
of determining whether or not microbes are uniformly present. 
Second, experimental production of pus under conditions intended 
to illustrate the possible connection of microbes with the process. 
The finding of microbes in pus dates back many years. For a 
long time nothing was thought of the matter, for it was considered 
to be purely accidental and of no consequence. Until comparatively 
recent times, it was supposed that only the pus of open wounds was 
contaminated with these organisms, but as the means of search for 
these approached their present stage of perfection, many individuals 
asserted that microbes were present in all pus, whether it was from 
internal and previously unopened abscesses or not. 
Formerly, before the methods of examination had reached the 
perfection they have acquired within the last few years, observers 
had often failed to find micro-organisms in pus from previously un- 
opened abscesses, but recently this search has been more successful. 
I have myself examined the pus from a large number of abscesses, 
especially alveolar abscesses, and for several years past have found 
cocci in the pus in all cases. Not only this, but I have cultivated 
these organisms from abscesses, in broth, on gelatine, and upon agar- 
agar, and notgd their characters. Dr. Ernst, of Boston, has also 
made a large number of cultivations from various classes of abscesses, 
with similar results. This class of experiments is but a repetition 
of observations by various observers in different parts of the world, 
separated by thousands of miles, and all give substantially the same 
testimony. All pus, no matter where formed, whether in closed 
abscesses deep within the tissues, or upon the surface, contains liv- 
ing micro-organisms, that will grow when placed in suitable culti- 
vating media. 
But the more decidedly practical plan of study, and one that ap- 
peals more strongly to the mind, consists in the effort to produce suppuration in experimental wounds from which micro-organisms 
are rigorously excluded. . This class of experiment has been under- 
taken by a considerable number of persons. In the first of these 
the precautions were not successful, and micro-organisms gained 
entrance, vitiating the results and giving the impression that pus 
was produced under aseptic conditions. A very severe training was 
found necessary to the successful performance of this class of ex- 
periment. But as the plans were improved, success in the exclusion 
of microbes was attained. The results seem to have proven, that 
without the presence of microbes no amount of injury or irritation 
of the tissues will result in suppuration. These experiments have 
now been repeated by so many persons and varied in so many ways, 
and so many irritants have been employed, that the question seems 
no longer doubtful. 
It seems unnecessary that I should now recite all, or any consider- 
able portion, of the experimental evidence that has accumulated in 
the last few years. This may be found in our literature, and the 
more important portions have been collected in convenient form 
for reference by Dr. II. Knapp, of Xew York, in an article in the 
Archives for Ophthalmology, Vol. 15 (1886), page 24, and another 
in the New York Medical Record of Dec. 25, 1886. I have also 
cited some of these in an article in the Dental Review of March 15, 
1887. In addition to these, the work of Dr. Ernst, of Boston, pub- 
lished in the transactions of the American Surgical Association for 
1886, page 53, should not be overlooked. 
As illustrating the character of this work for the benefit of those 
who may not have followed the literature, I may recite the plans of 
a few of these experiments. E. Scheuerlin placed irritants, such 
as croton oil, and turpentine, in very thin glass or tubes, 
which were sealed hermetically and sterilized. These were placed 
under the skin of healthy animals with aseptic precautions, and al- 
lowed to remain until the wound by which they were introduced 
had perfectly healed. The tubes or capsules were then broken, to 
bring the irritant in contact with the tissues. By this plan of ex- 
periment a hard swelling was produced, but no pus was formed, ex- 
cept in one case, and in this the experimenter concludes that the 
wound had not perfectly healed. Cocci were found in its track, 
and in the pus that formed in the focus of the inflammation. This 
form of experimentation has been varied by a number of individuals, with similar results. Dr. Ruys and Dr. Knapp have made several 
series of experiments also of a similar nature, except that they have 
injected irritants into the anterior chamber of the eye (in rabbits), 
where both the irritant and the results of the irritation could be seen, 
and have satisfied themselves that it was impossible to produce sup- 
puration in the absence of micro-organisms. I have myself made 
some experiments, by passing broaches rendered aseptic by heat 
through the apex of the roots of teeth, from which I had just re- 
moved the pulp under aseptic conditions, into the tissues beyond, 
and tearing them up as thoroughly as was practicable. Al- 
though inflammation was sometimes produced, there was no suppu- 
ration. 
This accumulation of testimony drives us to the conclusion that 
micro-organisms are active agents in pus formation. The question 
as to how these act to produce pus, is the next important factor, and 
leads to the consideration of the second question, viz.: What is 
the cause of the liquefaction of the plastic exudate and the death of 
the ameboid cells ? 
This question had been discussed before the discovery that micro- 
organisms were in anywise related to the suppurative process, and 
the general idea of pathologists may he expressed in the phrases, 
“Over-stimulation of the part,” “Intensity of the inflammatory 
process,” Failure of nutrition,” “ Death of the cells from abnormal 
exposure,” etc. On this point there was no very satisfactory opin- 
ion, the general idea being that those cells, unfavorably placed, 
either by the intensity of the inflammatory movement, by the par- 
tial cutting off of the supply of aerated blood, or by a generally 
impoverished condition of the system, died, and that the liquefac- 
tion of the matrix or exudate was the result of this death of the 
cells, or from the same cause. All of these suppositions, except the 
last, are probably very nearly correct, and should still have due con- 
sideration, but further study of the subject seems to show that the 
liquefaction of the exudate is dependent upon other agencies, and is 
the primary lesion looking to the formation of pus. It may be 
stated as an axiomatic principle, that no portion of the animal body 
is capable of self-destruction. The changes that take place are 
under the influence of life, and life is not self-destroying. One 
part of the body may destroy another, as is seen in the solution or 
absorption of the roots of the temporary teeth by the odontoclasts, or the absorption of bone by the osteoclasts, but the roots of these 
teeth or the bone have no part, except a passive one, in the process. 
One cell may destroy another in the same way, or one group may 
destroy another group. But in no case can a cell or any individual 
component of the body destroy itself. Therefore, the liquefaction 
of the exudate cannot be regarded as an act of the exudate, nor can 
the ameboid cells destroy themselves. 
Any component of the body may die from want of nutritive sup- 
port, or may be destroyed by traumatism ; but in this event the 
material elements, the chemical forms, remain. These dead forms 
have no power in themselves to change. Long ago it was supposed, 
as was taught by Liebig, that organic matter left to itself fell into 
a state of molecular motion, in consequence of which its chemical 
form was changed. We have since learned, however, that all such 
transformations of matter are the results of life-force exhibited in 
certain micro-organisms, and that matter in itself, and by the pow- 
ers inherent in it as matter, has no power to change, except as one 
element or compound is presented to another, and that in each 
instance the action of chemical affinity thus aroused tends to self- 
satisfaction and permanent quiet, until again disturbed by forces 
extraneous to itself. Now tissue that has died is left to itself; that 
power which controlled the presentation of element to element for 
the maintenance of its changes has ceased to act, and its chemical 
affinities are satisfied. Life causes chemical combinations that are 
peculiar to its purposes, by presenting element to element under 
peculiar relations or conditions. But there is no change of the 
chemical affinities of the elements. Dead material is, therefore, 
incapable of self-movement, or of change of chemical form. This 
is continually witnessed in various parts of the body. Blood clots 
resulting from the ligation of arteries, emboli, infarctions, in which 
considerable areas of tissue are destroyed, etc., rarely suppurate. 
In these cases it is seen that a tissue that simply loses vitality,— 
dies,—does not tend to change its chemical form except as it is 
acted upon by the living tissues about it, and, being shut off from 
the approach of microbes, does not take on degenerative changes. 
The cause of suppuration, when it does occur in these, will be ex- 
plained later. Were it otherwise, with the forces inherent in matter 
as such, certainly the theory of spontaneous generation might be 
maintained. 9 
That the liquefaction of the plastic exudate for the formation of 
pus is not an effect of inflamed tissue is, in the first instance, a mat- 
ter for experimental inquiry rather than for theoretic considera- 
tion. This inquiry has been had as related, and this theoretic con- 
sideration is properly the result of that inquiry. In the years that 
have passed since the discovery of the yeast plant by Schwan, in 
1838, many succeeding discoveries have combined to show that all of 
those chemical changes that had been observed to occur in the 
various forms of fermentation and putrefaction, are results of the 
life and growth of micro-organisms, and in no case has matter been 
found capable of spontaneous change. Now it is found by the 
strictest experiment that those changes which result in the forma- 
tion of pus are not due to the vital principle residing in the tissues 
of the animal, nor to physical agencies, but to the vital principle 
as exhibited in micro-organisms. It is, in fact, a species of fermen- 
tation of the plastic exudate thrown out in the act of inflammation. 
Strict experimental inquiry shows that this exudate is rendered 
fluid by a fermentative process, and is so changed in its chemical 
qualities that it no longer supports the ameboid cells. These cells 
then die, and in some of the forms of suppuration many of these 
are broken up and liquefied also. It had been supposed that con- 
tact with dead tissues was sufficient to destroy the vitality of the 
ameboid cells, but it has been found that they may wander into the 
dead tissues of infarcted regions, tissues destroyed by traumatism, 
or dead tissues placed in the body experimentally, and retain their 
vitality. 
This, then, is the explanation of the suppurative process, and is 
in strict agreement with other forms of fermentation and decompo- 
sition : Liquefaction of the plastic exudate by the operation of 
microbes, death of ameboid cells from the changed chemical character 
of their matrix—these combined, form pus. These processes pro- 
duce irritation, which extends the inflammatory movement. Hence 
the suppuration and destruction of tissue. 
This power of micro-organisms to change gelatinous material to 
the liquid form is well illustrated by artificial cultivations. A con- 
siderable number of varieties, when grown in ordinary sterilized 
gelatine in test tubes, produce liquefaction quite rapidly, at ordi- 
nary summer temperature. One variety that I have recently been 
cultivating, a film-forming, or sheet coccus, will, when planted 10 
upon the surface*of gelatine in a test tube, liquefy it progressively 
from top to bottom at the rate of about one-eighth inch per day, 
at a temperature of eighty degrees Fahr., and much more rapidly 
as the temperature is raised. Many others are found that liquefy 
gelatine similarly, but with less rapidity. It is this power of lique- 
fying substances upon which they grow that gives certain micro- 
organisms the power to produce pus, rather than any quality of 
producing irritation or inflammation.* Most of them, indeed, 
produce irritation, also, and some of them do so in a very marked 
degree, especially the ordinary streptococcus pyogenes, so generally 
found in phlegmonous abscesses. In this respect there is, accord- 
ing to my own observation, great differences among the different 
varieties of pus-producing microbes. This has been so marked in 
my experience, that I am able, generally, to say in advance that 
certain microbes are absent or present in certain qualities of ab- 
scesses. For instance, I have never found the streptococcus 
pyogenes in a white, creamy pus, in an abscess that had arisen with 
little pain, or in a wound that had not taken on a decidedly inflam- 
matory condition, etc. However, it is not now the intention to 
discuss the character of individual species, or varieties, of microbes 
that are active agents in pus formation. There are now about 
twelve varieties recognized, that are capable of producing pus, the 
greater part of which I have myself observed and cultivated. It is 
probable that additions will be made to this number in the near 
future. 
To the dental profession, it is a fact of great interest that most of 
these fungi grow fairly well in the human saliva, and are found in 
it very frequently. I have recently made a considerable number of 
plate cultivations from the saliva of different individuals, for the 
purpose of determining how frequently these fungi might be found 
in the mouths of healthy persons. The number of cultivations 
have not been sufficient, however, to be satisfactory. In the exam- 
ination of ten persons, I found the staphlococcus pyogenes aureus 
seven times, as determined by its form of growth in broth, upon 
gelatine and upon agar-agar, staphlococcus pyogenes albus four 
times, and streptococcus pyogenes three times. These trials were 
* Note.—An organism capable of liquefying the plastic exudate, and thus producing pus, does 
not necessarily liquefy ordinary gelatine; neither does every organism that may liquefy gelatine in 
our test tubes act as a pus producer. 11 
made by simply scraping the tongue, or some portion of the mucous 
membrane of the mouth, once with a platinum wire previously 
brought to a glow. These three forms are the most wide-spread 
and prevalent of the pyogenic fungi, and my supposition is that they 
would be found in a vast majority of healthy mouths if the search 
was carefully and persistently made. In a few cases that I have 
examined repeatedly, I have found the staphlococci everywhere in 
the mouth. In other cases I have been unable to find these at all, 
after repeated efforts. 
The streptococcus pyogenes is so similar to the ordinary strepto- 
cocci of the mouth, that it cannot be distinguished by microscopic 
examination, except by one who has had much observation of these 
species together and separate ; but its colony and its surface growth 
on gelatine afford a means of distinguishing them, after its manner 
of growth has once been learned. 
Other pyogenic fungi than these three, I have found in the mouth 
only occasionally. I have also found them much less frequently in 
abscesses, and in pus from wounds, and must suppose that they are 
much less frequent in the air. It should be understood that any 
microbes in the air we breathe which are capable of growing in the 
saliva (and very large numbers grow in it), are likely to be found 
there from time to time. Besides these, there are certain species 
that are peculiar to the saliva, and are found in the mouth of almost 
every individual. These latter are comparatively few in number, 
and soon become familiar to one who spends much time in making 
cultivations from the saliva or mucous membranes of the mouth. 
As dentists, we must consider that these pyogenic fungi are gen- 
erally present in the mouth, and that every wound that we inflict 
is in danger of becoming infected by them. Under these circum- 
stances, a study of the consequences of such infection becomes im- 
portant to us and our patients. In the first place, the tissues upon 
which we operate, except it be the hard tissues of the teeth them- 
selves, are the best supplied with blood and nerves of any in the 
body, and are on tlpit account proportionately more resistant to evil 
influences of all kinds. This power of resistance applies to the en- 
croachments of microbes, as effectively as to evils resulting from 
any other form of injury. Very few of the pyogenic fungi have, 
ordinarily, any considerable power to produce inflammatory condi- 
tions, and they have practically no power of mischief in any part 12 
of the body in the absence of inflammation, and necessarily the 
least about the mouth and face, where the resistance is greatest. 
When inflammation gives them the opportunity, some of the varie- 
ties cause a very rapid liquefaction of lymph deposits in an inflam- 
matory focus, with increase of the inflammatory movement, until 
the growing fungi are surrounded by an almost solid Avail of living 
ameboid cells—the so-called pyogenic membrane of older writers. 
This increase of the living element in the wall of the abscess has the 
effect of limiting the groAvth of the fungi, and in the end they are 
expelled, followed by the healing of the abscess. 
Another reason for the abridgment of the damage is found in 
the weakening of the fungi from the accumulation of their OAvn 
waste products. If Ave plant pyogenic fungi in peptonized beef 
broth, they will make a more or less vigorous groAvth, but after a 
time they sink to the bottom of the vessel, and all groAvth ceases. 
In case of the acid-forming fungi, Ave have learned by direct experi- 
ment that this cessation of groAvth is not on account of the exhaus- 
tion of the pabulum, but on account of the accumulation of the 
Avaste product, the acid, and that if this is neutralized by the addi- 
tion of a proper amount of an alkaline base, forming a salt, answer- 
ing the end of elimination of this product, growth will again pro- 
ceed. This accumulation of the Avaste products of the pyogenic 
fungi occurs in the pus of abscesses, rendering it unfit for the con- 
tinued growth of the fungi which produced it. The operations of 
the fungus thus become limited to the fresh exudates thrown in 
from the abscess Avail. This is in turn limited as the Avails become 
more solidly packed with ameboid cells—living matter—which is not 
so readily attacked. 
This seems to be the explanation of the sharp rise and subsidence 
of suppuration, Avhich may be said to be the common course of 
eA'ents when a focus of inflammation, arising from direct trauma- 
tism or other cause, is infected with pyogenic fungi alone. This is 
A'aried by tAvo factors: first, the vital poAvers of the tissues; second, 
the activity or vital energy of the fungus. Acpording as the one 
or the other is greater or less, will the course of suppuration be pro- 
longed or abridged. If, hoAvever, the focus of inflammation be 
contaminated also with those species of fungi which produce active 
inflammatory condition, such as the cocci of erysipelas, or others of 
similar nature, the injury may be Avide-spread and grave. Happily, 13 
such is but rarely the case in the class of lesions which we are called 
upon to treat. 
Thus far we have considered open wounds only, or abscesses 
which may possibly have been infected from the surface. But 
microbes are found in all pus, whether the locality of its formation 
has had the opportunity of infection from the surface or not. The 
question now comes as to the possibility of infection by other chan- 
nels, or what I shall designate as indirect infection. The ablest 
experimentation, perhaps, on the subject of indirect infection, has 
been performed by Becker and Krause. It having been observed 
that pus was occasionally formed in case of simple fracture of the 
limbs, in which the wound was in a position which rendered direct 
infection impossible, and yet that this pus contained the usual 
cocci, these gentlemen instituted experiments for the purpose of 
determining whether or not microbes could be conveyed to the spot 
by the blood streams, a theory that had been widely entertained 
soon after the introduction of the Lister dressings. This had led 
to a search of healthy tissues for micro-organisms, and the results 
satisfied bacteriologists that such tissues did not ordinarily contain 
them. Still, the question as to whether micro-organisms gaining 
access to the blood by accident might be so carried, was an open 
one. In this view of the case, the gentlemen named began their 
experiments by breaking the limbs of healthy rabbits, and found 
them to heal readily without the formation of pus. Then, after 
breaking the bone of the leg, the experiment was varied by inject- 
ing into a vein of the ear a fluid containing pus-forming microbes. 
In this case it was found that suppuration followed regularly, and 
that the same species of microbes injected appeared in the pus. 
These experiments, together with others of a like nature, estab- 
lished the fact that microbes may be carried by the blood to a focus 
of inflammation, and there set up suppuration. Dr. Knapp’s ex- 
periments also show that pus-forming microbes gain entrance to 
the blood from wounds that are infected experimentally, for in his 
experiments with double operations on the eyes of rabbits (see New 
York Medical Record of December 25, 1886), one of which was 
infected and the other not, he occasionally found the same order of 
microbes used in the infection had gained access to the eye that 
was not infected, showing that direct infection into the blood 
streams is not absolutely necessary to the infection of an internal 14 
focus of inflammation. This teaches us that an internal focus of 
inflammation may become infected from a remote focus of suppura- 
tion upon the surface, or upon the mucous membranes. There- 
fore, it behooves the surgeon to examine his patient critically for 
minor points of suppuration before performing any important sur- 
gical operation. 
It also serves to clear up another point. It is very well known 
that inflammation may arise in internal parts, notably in the joints, 
and continue for a considerable time without suppuration, but 
sooner or later suppuration will occur, though no direct infection 
has been possible. The explanation simply is that microbes have 
gained access to the blood through some breach, or possibly small 
and unimportant focus of suppuration. This class of cases may 
often be noted in teeth that have lost their pulps. They may go 
on for months together without suppurating, but finally suppura- 
tion occurs. 
The time, in the course of a suppuration, at which the blood is 
most likely to contain microbes, is important. I do not know that 
there has, as yet, been any direct experimentation upon this point, 
but it is reasonable to suppose that after the formation of granula- 
tions, or the limitation of an abscess by the formation of a so-called 
pyogenic membrane, the danger of internal infections will be greatly 
diminished. This is also in harmony with what is known of the 
occurrence of septicemia and pyemia from wounds. 
Such being the teaching of the facts now at our disposal, it be- 
comes important that we inquire into the circumstances and condi- 
tions under which infection with these fungi is liable to occur in 
dental operations, and the circumstances and localities which favor 
the continued activity of the fungi after infection has occurred. 
The great prevalence of alveolar abscess, and the frequency with 
which the dentist is called upon to operate under conditions which 
favor the infection of the apical space, renders it the best example 
for the illustration of the principles taught by the facts recited. 
Since we have learned that we can only have alveolar abscess after 
infection of the apical space with pus-forming organisms, we have 
an incentive to the performance of aseptic operations which we 
never felt before. e have also learned that the enemy is in the 
saliva of our patients, and the facts at our disposal point to this as 
not only the most probable source of infection, but as surely the 15 
almost universal source—except infected instruments. It therefore 
follows that this source of infection should always be eliminated 
before a pulp chamber is opened. To do this it is necessary to put 
on the rubber-dam, and disinfect the tooth or teeth included, and 
to disinfect all instruments used in the operation. For this pur- 
pose suitable disinfectants should always be on the operating table. 
It may appear to some that in case a pulp chamber is already open, 
and infected, this precaution will be of little avail. Xot so, for if 
the canals are already infected the first object will be to thoroughly 
disinfect them, and to do this the source of infection should first 
be eliminated. Then, and not until then, should we expect to suc- 
cessfully disinfect the canals. The fact that many root canals have 
been successfully disinfected without this precaution, only shows 
the power of the disinfectants employed. It does not serve to rec- 
ommend such procedures, since the source of infection has become 
so thoroughly known. Very foul roots should be cleaned and dis- 
infected with the rubber-dam in position, and the last of the opera- 
tion should be done with freshly disinfected instruments. The 
cavity should then be perfectly sealed with a temporary filling of 
gutta-percha, or other suitable material.• In no case should this 
filling be removed at a subsequent sitting, before the readjustment 
of the rubber-dam and disinfection of the included parts. In those 
cases in which the pulp chamber is opened for the first time, as in 
the removal of a living pulp, or a pulp destroyed by the operator, 
we should never have abscess occur; indeed, it should be impossible, 
except by indirect infection. This also is a matter that should 
always receive our attention. Unless the exigencies of the case 
especially demand it, we should not open a pulp chamber at a time 
when there is an active focus of suppuration in progress anywhere 
in the body of the patient. In this statement I do not include 
chronic discharges, though these must in every case be regarded as 
unfavorable. 
If we have found the conditions favorable, abscess following the 
removal of the tooth’s pulp should be impossible. We may pass 
our broach through the apical foramen and wound and lacerate the 
tissues, and possibly provoke an inflammatory movement, but if the 
root canal and the instrument be aseptic, abscess cannot occur. 
This I have tried experimentally in a sufficient number of instances 
to be convinced that it is practically true, as well as theoretically 16 
true. In several cases I have, in this way, aroused a considerable 
degree of inflammation, but in no case did abscess occur. These 
experiments were made with broaches cleaned by heat. 
While all of this is true, it is absolutely essential that both the 
canal and the broach be aseptic. Few men who have not had prac- 
tical experience in the cultivation of microbes can form an adequate 
idea of the readiness with which they may be carried into the tis- 
sues of the apical space by the broach. I have often passed a sur- 
geon’s platinum suture wire, after having brought it to a glow to 
completely disinfect it, into a foul root canal, and then into stiff 
gelatine cultivating media, four, five and six inches, and have seen 
the development of microbes along the track of the wire from end 
to end. If these organisms may be carried into a stiff gelatine in 
this way with a perfectly smooth platinum wire, what may we ex- 
pect from a barbed broach thrust through a foul root canal into 
the tissue beyond ? If this does not produce abscess, it will be be- 
cause the root canal happened not to contain pus-forming microbes. 
I have myself, as I think, produced abscess in this manner many 
times, and from what I know of the practice of others I am satis- 
fied that such an accident is of very frequent occurrence. In the 
cleaning of contaminated canals, and all root conals to which the 
saliva has had access should be regarded as contaminated, no at- 
tempt should be made to reaoh the apex before the introduction of 
a reliable disinfectant. The danger of forcing microbes through, 
into the tissues of the apical space, is so great that they should be 
destroyed before the attempt to reach the end of the canal is made. 
Then we may risk passing the broach to the very end of the canal, 
and not before. The rule is simple enough. To have alveolar 
abscess, we must first have microbes in the tissues. If the canals 
have been exposed to the fluids of the mouth, we must not risk 
forcing its contents through the apex until it has been rendered 
aseptic. Then if the aseptic material is forced through, it may pro- 
duce a transient inflammation, but it will not beget abscess. 
What is the teaching of the facts developed in case of infection 
of the tissues ? 
First, I may say that it is clear that there are many infections 
that are successfully resisted by the tissues, and the microbes elim- 
inated without the formation of abscess. Second, where the area 
of abscess is small and the general condition of the patient 17 
good, the tissues, by their own unaided powers, will expel the in- 
truders with the pus first formed, or very soon thereafter, if proper 
opportunity is presented. This only requires free discharge of the 
pus, with care that there is not continuous reinfection. It should 
be stated that pus itself should be regarded in the same light as a 
stale cultivating medium, in which the organism which produced 
this condition is incapable of growing until transferred to fresh 
media; hence, when the central focus of the inflammation, or of 
the lymph deposit, is broken down, the organisms have become 
greatly depressed from the presence of their own products, and are 
readily expelled by the young connective tissue cells, which have 
formed themselves into a compact wall about the abscess. There- 
fore, the source of continuous reinfection, if such exist, should be 
eliminated, for this is the factor which begets chronicity. In case of 
simple chronic alveolar abscess, this source is the pulp canal. In 
this space the micro-organisms are out of .reach of the tissues, and 
a new growth occurs, with a reinfection about the apex of the root, 
every time fresh pabulum has entered the root canal, and these 
infect any fresh lymph deposits about the apex of the root. Hence 
the abscess becomes chronic. Dead bone, with its Haversian 
canals, offers the same opportunity for growth of organisms in a 
harbor beyond the reach of the tissues. If, on the other hand, this 
bone be aseptic, it will be absorbed by the tissues, and removed. 
With the root of the tooth this sometimes occurs to our sorrow, but 
in case the root of the tooth becomes denuded of its tissues, this 
tendency is here largely counteracted by another, which is the 
tendency to the reinvestment of the root with cementum. But in 
order that either of these can occur, the part must be aseptic, or 
free from microbes. In any such cases the microbes, if present, 
have a wall to lie against, and are to that extent protected. The 
active tissue is on one side only, instead of surrounding them. 
Experience teaches us that in this case a chronic condition of ab- 
scess is in many instances maintained. This requires antiseptic 
treatment to dislodge the microbes, but in all ordinary cases of 
alveolar abscess, the elimination of the source of continuous rein- 
fection from the root canal is sufficient to cure chronic alveolar abscess. 
As a rule, the microbes of pus formation are unable to maintain 
themselves continuously when surrounded by living tissues.