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knew the danger arising from the tendency of the second molar to come forward, and Mr. Edwards had shown them a method which must be of general utility.

A Case of Submental Sinus, a Sequela of Influenza, treated by Root Filling.


MR. PRESIDENT AND GENTLEMEN,-The case I wish to bring under your notice is that of a young lady, aged about 22. In December, 1899, she had a severe attack of influenza. She apparently completely recovered, but about six weeks later she noticed a swelling under the lower lip in the region of the incisive fossa. An abscess formed and pointed under the chin. This was opened in February, 1900. The teeth were not suspected as a cause of the trouble. In April, 1900, a sinus still persisted, and the patient was admitted into a hospital in order that an operation should be performed, and remained in hospital for a week.

The operation consisted, presumably, in examining the sinus and endeavouring to remove necrosed bone. In spite of this treatment the sinus did not close. In February, 1901, the patient came under the notice of Dr. Kirkpatrick, a Dublin surgeon. He at once thought that the teeth, although apparently sound, were the cause of the abscess, and took the patient to Dr. G. P. Moore, a dentist of Dublin. This gentleman, seeing that the two lower incisors were dead, had a skiagram taken in order to ascertain the length of the roots and to see whether any absorption had taken place during the prolonged suppuration. Finding that the roots were of normal length he decided that the teeth might be saved. He opened the pulp chamber and dressed the roots. As the patient was coming to London, Dr. Moore sent her to me for further treatment. When I first saw the patient on April 3, 1901, she was considerably disfigured by a mass of granulation tissue beneath the chin, and also by inflammatory swelling of the integuments, due to pus becoming pent up within the sinus.

The treatment adopted was simply to cleanse the root canals in the usual manner and fill them with gutta-percha. The sinus was opened up and packed with iodoform gauze. I was able to pass a bristle through the apex of the left central incisor, but not through that of the right incisor. I always endeavour to pass a bristle in this manner when a sinus exists in connection with a root; as, however, from the skiagram I was certain of having penetrated to very near the end of the root, I did not persist in the attempt to get through. In three weeks the sinus had distinctly shortened, and in another fortnight it had become completely closed.

In the skiagram taken after the roots had been filled and the sinus had become closed, it is noticed that the root-fillings present are not perfect, but I believe the result is as good as we generally achieve. You will see also, that the cutting edges of the teeth are separated; this I attribute to contraction having taken place upon the formation of fibrous tissue at the apices of the teeth, the alveolus between the teeth acting as a fulcrum, having led to a separation at the cutting edges. I quite recently heard from this patient that she had had no further trouble.

A short time ago Mr. F. C. Wallace communicated to the Odontological Society the record of a case in which a misplaced wisdom tooth gave rise, during an attack of influenza, to symptoms simulating necrosis of the mandible. In this case an operation was undertaken with the view that necrosis existed.

Mr. Wallace raised the question as to whether the inflammation in these cases commences in the pulp and spreads to the periodontal


membrane and bone, or whether the inflammation has origin in the tissues surrounding the tooth. He inclined to the former view, whilst Mr. Baldwin favoured the latter opinion. I think in this connection our experience teaches us that when a tooth pulp, previously healthy, becomes inflamed and dies, either from a general cause as influenza, or from a local one, as for example too large a metal filling, periodontitis does not often supervene at once. It may be that the periodontal membrane will not become inflamed for six weeks after the death of the tooth-pulp, as in the case I have mentioned; it may not do so for six months, as in a similar case I have notes of; or the tooth may remain quiescent for years, becoming gradually discoloured.

On the other hand, we know that when the vital resistance of a patient is lowered by even a slight cause, such as a common cold, and much more by a serious illness, periodontitis is very prone to occur in connection with such weak spots as unfilled or imperfectly filled dead teeth, and sometimes even with living ones. I am, therefore, inclined to think that inflammation and suppuration arising

during an illness in connection with a tooth, either normally situated or misplaced, commences not in the dental pulp but in the tissues around the tooth-namely, in the periodontal membrane if the tooth be normally situated; and either in the periosteum, or the dental follicle, or the bone, if the tooth be unerupted.


The PRESIDENT thought that Mr. May had raised a very important pathological question by the way in which he accounted for the condition of the patient, and had advanced a novel theory for the separation which so often took place in the lower incisors. It would be interesting to know whether the author attributed the separation of apparently healthy lower incisors to the contraction of tissue at their roots and the fulcrum of the bone between. It was an everyday occurrence in practice to see perfectly healthy teeth moving from one another. Mr. May's explanation seemed a very good solution in the case of dead teeth, but he did not quite see how it applied to perfectly healthy teeth.

Mr. T. A. COYSH said he had had an identical case with that of Mr. May in a girl of 16, with the exception that one incisor only was dead. Practically there had been no uncomfortable symptoms at all. When he saw her, there was a slight swelling from the sinus below the chin, which the patient and the dentist she had formerly seen had apparently not paid much attention to. Obviously one of the lower incisors was dead, and it was drilled into, the root treated and filled, and the sinus then healed up without any trouble. In that case the incisor died from a blow. He saw the patient about twelve months ago, four or five years after the root was filled; there was then no separation of the incisors, everything being perfectly normal.

Mr. E. LLOYD-WILLIAMS said the communication was especially interesting to him from the fact that at the Dental Hospital that very day they had had a patient, a man of 26, with a sinus which had existed for twelve years, with apparently no lesion of the teeth. On carefully examining the teeth, one was found to have lost its translucency, and was supposed to be dead. It was drilled into and their conclusion found to be accurate. It had been treated exactly on the lines suggested by Mr. May. He was glad to have heard of the case because it promised well for the other one, which had existed for such a long time. The pathological question was an interesting one, a discussion of which might take up a whole evening. He was inclined to disagree with the author on the point, thinking that the inflammation started in the pulp itself. He also argued from analogy. The analogous cases that were common were those of pyorrhoea, where it was known that a suppurative periodontitis had existed for a very long time. It was perfectly well known that in these cases the pulp retained its vitality for an enormous time after the suppuration of the socket had taken place. He therefore thought it was more likely that the inflammation started in the pulp in the same way as an inflammation of any other part of the body. The point with regard to the separation was also an interesting question. He believed it was due to pathological changes in the bone itself rather than to granulation tissue, because there was no granulation tissue in cases where there were healthy teeth, and yet they were always seeing them separated. He saw no reason why the bone should not undergo patho

logical change resulting in interstitial growth which tended to separate any teeth existing in the immediate neighbourhood.

Mr. W. HERN thought the case illustrated the importance of examining the teeth to see whether they were living or dead in all cases of sinuses of obscure origin opening into the mouth or on to the face. He had come across cases on more than one occasion in which hospital patients been had sent up from the country to a general hospital with which he was connected to have some surgical interference for the cure of sinuses about the jaws. Such cases had usually been sent on to the dental department before any operative procedure was undertaken, in order to eliminate any causes from the teeth, and it frequently happened that such cases had been sent home cured without any more serious operation than the extraction of a dead tooth or buried root. With regard to the pathological question, he agreed with Mr. Williams that in these cases they were due to septic apical inflammation, set up by some of the septic contents of the pulp cavity being extruded from the point of the root. No doubt any depression of the general health, even a cold, would start an inflammation in a dead tooth with septic contents, but he considered that only a secondary cause, the primary cause being the presence of septic material in the tooth. He thought Mr. May's allusion to the last Odontological meeting, in regard to a remark made by Mr. Baldwin, did not apply to the present case. Mr. Baldwin was speaking of buried living teeth, or teeth in which inflammation commenced around the crown and not around the root. He thought the history of odontomes showed that buried teeth which were normal, or odontomes, usually remain quiescent as long as the soft tissues overlying them were unopened, and that the inflammation starts coincidentally with this communicating opening into the mouth by infection of the tooth sac with mouth organisms.

Mr. BALDWIN said that when he spoke at the Odontological Society recently, he only referred to buried teeth which developed an abscess round them. He thought in the majority of those cases the teeth were not dead and the suppuration commenced around the crowns of the teeth. Whenever the teeth were dead, as in Mr. May's case, he thought the most likely explanation of the inflammation was that it was septic inflammation set up by the escape of septic material from the pulp canal into the soft tissue. When teeth were killed by a blow, as probably front teeth generally were, the pulp became absolutely diffluent and decomposed in some way, and might or might not set up abscess. They much more frequently did so when it was a lower incisor, probably because the force of gravity helped the escape of septic material, and that result would naturally be assisted by any disease, such as influenza, which would lower the general tone, and increase the number of micro-organismis circulating in the blood.

Mr. W. HERN asked the reader of the paper to state whether the patient was affected with any pyorrhoea. If so, that would explain the separation of the teeth.

Mr. ASHLEY DENSHAM recorded a case which had come under his own notice, in which there was submental inflammation followed by a sinus in a child of 6. The surgeons who treated the case removed, through an opening made by enlarging the sinus, two imperfectly developed permanent lower incisors. The temporary incisors had become absorbed, and had recently fallen out. There did not appear to be any communication at all between the oral

cavity and the crowns of the forming permanent incisors. In that case there was a very considerable amount of inflammation, evidently septic, and there was a very large swelling underneath the chin, which eventually discharged through a sinus. He quite agreed with Mr. Hern and Mr. Baldwin that the inflammation in most cases of buried teeth came from some communication with the mouth.

Mr. CLARK asked if it was quite clear that the teeth were alive before the attack of influenza took place.

The PRESIDENT thought the communication ought to provide the Branch with two very interesting papers in the future. Firstly, on "How does septic inflammation occur in a perfectly sound tooth without any caries in it?" and secondly, "How do perfectly healthy teeth separate?" He hoped the members who had taken part in the discussion would bear that suggestion in mind.

Mr. FARMER referred to a case where there was a small abscess at the apices of two lower incisors, with a great deal of swelling, but no submental sinus. The patient, a flautist, a professor at the Royal Academy of Music, complained of tenderness when he placed the flute to his lips. At the apex of the right lower central and right lower lateral incisor were two small abscesses. The electric light revealed that the pulps were alive, and that there was no dental cause of the trouble. Mr. Bland-Sutton saw the case, but seemed dubious as to the cause. After the pus was evacuated, some spicules of dead bone came away and the parts healed up. Since this happened, three years ago, the patient had had no recurrence and was still teaching. There was no apparent lesion either in the teeth or mucous membrane, and no signs of the pus burrowing. Could any member account for, the presence of pus under these conditions?

Mr. MAY, in reply to the President's question, said he had not the faintest idea why teeth moved in the extraordinary manner they sometimes did. He only stated that in his particular case, where the apices of the teeth were embedded in fibrous tissue, that accounted for the separation of the teeth. At any rate they did not begin to separate at the cutting edges until the fibrous tissue was formed and contracted. A gentleman had asked him how he knew that the teeth died through influenza, and whether they were alive before. He did not definitely know that, but he argued it was so from the analogy of other cases. The teeth were only beginning to discolour, and if the teeth had been dead for five or six years he should have expected to find them more discoloured. Mr. Hern and Mr. Lloyd-Williams, he believed, agreed with him, although he would have a difficulty in showing why. They said that the inflammation commenced in the pulp. He argued that in cases where previously healthy teeth died from influenza or other cause, periostitis and suppuration did not supervene in the majority of cases for some weeks or months, and then commenced in the tissues around the tooth, as a dead pulp obviously could not become inflamed. Supposing the patient had an attack of influenza, with swelling and necrosis arising during the attack, he would say that the teeth had been dead or unhealthy for some time previously, and that the lowered vitality of the patient had set up the inflammation and suppuration again in the tissues around the tooth.

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