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end ; but in a relatively long absence of preventivemeasures it showed no tendency to a violent flare-upor even to a slow serious extension. This is a

phenomenon that has been previously observed-for instance, in Melbourne-and is clearly of epidemio-losdcal imnortancc.

THE INNERVATION OF DENTINE

FOR many years the destination of the abundantnerve-supply of the dental pulp has interested workersin dental histology. The extreme sensitiveness ofdentine-so obvious both to dentists and theirpatients-made it seem likely that dentine possessesa nerve-supply. But the proof or otherwise of thisby histological methods was far from easy, owing tothe technical difficulties of preparing sections of hardand soft tissues in their normal relations. The lateHoward Mummery, a histologist of unsurpassedtechnique, after many years’ patient.work, claimed tohave shown that nerve-fibres entered the dentinaltubules. In a later paper he described a layer of nerve-cells, just below the odontoblast layer, round whichthe nerves entering the pulp aborised ; from thesecells axons passed into the dentine and could betraced nearly up to the enamel. But this work,though it seemed to have solved the problem, has notpassed unchallenged, and while some at least ofMummery’s conclusions may be true, the generalproblem is still unsettled. D. Stewart 2 approachedit from another angle. He severed the inferior dentalnerve in a cat on one side and later compared the pulpsof the teeth with those of the opposite side. He foundthat histologically the fibres which Mummery hadassumed to be nerve-fibres showed no difference intheir staining reactions from those on the normal side ;he concluded that if they were nerve-fibres some

change would be visible and that they must thereforebe connective tissue fibres. But this work, significantthough it be, does not take into account the possibilityof some nerve-supply through the sympathetic fibresaccompanying the blood-vessels. Another possiblefallacy is that little is known of the changes in thestaining reactions of non-medullated nerve-fibres aftersection of the parent axon, and an absence of anydemonstrable change in fibres passing into the dentinemight not necessarily mean that they were connective ’

tissue fibres and not nerves. The latest contributionto the subject has been made by 0. W. Tiegs 3 ofMelbourne. Using the Bielschowsky method, he hasexamined the pulps of young molar teeth, and findsthat from the deeper layers of the pulp nerves can befollowed through the odontoblast layer into the sub-dentinal zone. These fibres pass as fine filamentsunder the dentine and often run for a considerabledistance among the odontoblast processes, on whichthey terminate in definite end-organs attached totheir surface. Nerve filaments may also end byminute swellings on the odontoblast cells. Tiegs wasunable to find any evidence of the existence of nerve-cells in the pulp as described by Mummery, nor couldhe trace the fibres into the dentinal tubes. He con-cludes that the odontoblast cells must act as receptororgans for the nerve-endings, and that it is unnecessaryto infer a special innervation of the dentine when thehistological findings do not support it. It is to be notedthat the odontoblast cells which according to Tiegsact as receptors of painful impulses, are mesodermaland not epiblastic. But on this point he remarks thatthere is no a priori reason why sense organs should be

1 Microscopic Anatomy of the Teeth, London, 2nd ed., 1924.2 Jour. of Anat., 1927, lxi., 439.

3 Ibid., 1932, lxvi., 622.

exclusively epiblastic ; they are predominantly so

because this layer is most likely to come into contactwith the outer world.The careful character of this piece of work and the

excellent illustrations which accompany it make itan important contribution to an interesting thoughslightly academic subject. In the absence of anyconfirmation by other workers of Mummery’s layerof nerve-cells in the pulp, this portion of his findingslooks as though it must be abandoned as untenable.An examination of Mummery’s original sections, nowin the museum of the Royal College of Surgeons ofEngland, leaves no doubt that whatever their naturethe fibres which he demonstrated as passing into thedentinal tubes are not artefacts ; though whetherthey are nerve-fibres as he assumed or whether theyare connective tissue fibres remains uncertain.

THE ÆTIOLOGY OF GOITRE

Colonel R. McCarrison’s report to the Bernecongress of 1927 summarised the knowledge of theaetiology of goitre at that time, but left many gapsto be filled. " The Life Line of the Thyroid Gland " *is a further memoir, written in association withProf. K. B. Madhava, of Madras, which describeswork done by the senior author during the past fiveyears. Before further progress could be made inanalysis of the factors which tend to produce goitreit was necessary, he says, to answer the question,What is the normal The material of research was astock of albino rats, living under such healthy con-ditions in the laboratory that for three years therehad been no illness or death from natural causes.The thyroid gland was removed from large numbersof animals of this stock and was weighed, glandsbeing taken from both sexes at different seasons ofthe year, some from those living a normal life andothers from those sexually isolated. The figures thusobtained served as controls for further observations.Similar investigations were also made in pigeons,guinea-pigs, and rabbits, and this mass of accumulateddata, together with previous observations on manand animals, was subjected to statistical study byProf. Madhava and forms the basis of the presentmemoir. The conclusions reached are of no littleinterest. In early life, it is found, the normal thyroidgland grows more rapidly than the body as a whole,and it is then that it specially needs all the elementsnecessary for normal nutrition. The maximum

weight of the thyroid relative to the body is attainedjust before puberty, and thereafter it gradually fallsin both sexes, though in females there are secondaryrises associated with reproduction. It is noteworthythat these results obtained in animals are in agreement

,

with those of Percy Stocks for children, and that thisnormal enlargement of the thyroid gland at pubertyis often mistaken for goitre in surveys of school-children. Of the influences which lead to goitre the

, memoir especially emphasises faulty diet. According,

to Colonel McCarrison a diet may be goitrogenic.

because it contains excess of certain substancesnormally present, such as fats, fatty acids, and lime ;

B because it is deficient in certain substances such as0 vitamins A and C, or iodine, or has a relative deficiency: of phosphates to lime ; or, lastly, because it containsL certain positive goitre-producing substances which’

are present in cabbage, ground-nut, bran, and maize,’ and possibly in certain other cereals. Lack of vitamin B

4 Indian Med. Research Mem., No. 23, 1932. Published forthe Indian Research Fund Association, by Thacker, Spink andCo., Ltd., Calcutta. Pp. 378. Rs. 12/12 (19s.).

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is also possibly another cause. After diet, factorsof importance are insanitary conditions of life whichinvolve contamination of food and drink with excreta,and iodine insufficiency. The interaction of thesethree is complicated ; for example, contaminationof food and drink can only produce goitre when thediet is in some degree faulty, and this would explain,why races living under the worst possible conditionsof sanitation may entirely escape it. Similarly alow iodine intake, although favourable to goitre,almost always produces its effect in association witha diet which is also deficient in other respects. Theeffect of iodine-lack is most noticeable just beforepuberty when the demand for iodine is greatest.

PLAGUE IN EGYPTFROM its situation as a half-way house between

east and west, Egypt has been visited by more thanits share of pestilences. There are many referencesto plague in the ancient Egyptian writings. TheIsraelites, in very early times, probably suffered fromthe disease, and later, some three thousand years ago,Sennacherib’s army is said to have incurred severelosses from an outbreak, in which field mice playedan important part. Rufus of Ephesus, the famousphysician and historian, who lived two centuriesB.C., also refers unmistakably to plague. In morerecent times, three great outbreaks of plague areknown to have occurred in Egypt as part of

general pandemics ; these are the subjects of a

monograph by Dr. A. W. Wakil, assistant pro-fessor of hygiene and preventive medicine in theUniversity of Cairo.’ The first of the three was knownas the plague of Justinian, which was supposed to haveoriginated in Egypt in the sixth century. The second,which commenced in Asia and spread over the wholeworld as then known, reached its zenith in A.D. 1347 ;from its peculiarly fatal character, it earned thedesignation of black death. The third, believed tohave originated in China, reached Egypt, presumablyvia India, in 1899. In the wake of each of thesegreat outbreaks, a series of minor epidemics hasoccurred, but history has enabled us to define thefirst two pandemics with some precision, and theprobabilities are that the third will die a naturaldeath like them, accelerated, one may hope, by modernmethods of sanitation and prophylaxis. It is now

generally admitted that the real home of plague liesin central and northern Asia, and that the formertendency to saddle Egypt with the responsibility forthe first two pandemics was unjustified. With regardto the third, the outbreak which is now petering out,there is of course no doubt that it was imported intoEgypt from outside. A virulent epidemic occurredin the first part of the nineteenth century, but mostauthorities are agreed that after 1844 Egypt wascompletely free from plague until 1899, the year ofthe commencement of the present outbreak, whichfollowed those in India and China. As soon as thedisease obtained a firm footing in Bombay (1896),it was realised that extension to new areas could onlybe a matter of time, and many governments des-patched research commissions to investigate on thespot. The Egyptian government was fully alive tothe possibilities, and it was probably owing tomeasures recommended by their commission thatinfection of Egypt was postponed for some threeyears. It was in May, 1899, at Alexandria, that thefirst local case was discovered. The patient was a

1 The Third Pandemic of Plague in Egypt. Published by theEgyptian University.

Greek, and the next 19 cases were of the same nation-ality—mostly living in or about groceries, wineshops,and bakeries. The mode of entry was not easy toascertain, and the question is still a matter of contro-versy. The people affected did not live near the har-bour, and dock labourers remained free for quite along time. Rival theories at the time were that infec-tion arose from used sacks, which were imported inlarge numbers from Bombay via Suez by rail, or fromthe baggage of Greek merchants, from Jeddah. Asthe primary outbreaks were of the bubonic type,it seems clear that infected rats must have obtainedentry in some way. It is curious that Alexandriawas affected before Suez and Port Said, and otherplaces lying nearer to India. As a matter of factSuez was not declared infected until 1904, thoughcases were discovered in Port Said early in 1900.Meanwhile the disease was spreading irregularlyinland, especially in the thickly populated region ofthe Nile delta. The outlook was now very bad, andmust have given rise to gloomy forebodings. Inprevious epidemics, plague had been extremely fatalin Egypt. Fortunately, in the present epidemic, theincidence has been extraordinarily low. The totalnumber of cases registered during the thirty-two yearsof its duration is only 19,386. That the virulencehas not been correspondingly slight is shown by thefact that deaths numbered 10,272. The largesttotal of deaths (1041) in any one year was in1911, when the population was estimated at nearlytwelve millions. Allowing for some fallacies innotification and diagnosis, the disease thereforehas not exercised any considerable influence on

the total mortality figures. It has been suggestedthat this comparatively small incidence may havebeen due to hereditary immunity of the rat popula-tion, following the last epidemic. But there are

some other remarkable circumstances which cannot beaccounted for in that way. Incidence of all types wasfive times greater in upper than lower Egypt, and thepneumonic form occurred about five times more

frequently, in proportion, in the former than thelatter , Cairo, contrary to expectations, has through-out been almost immune ; and it is stated that nota single case of plague has been recorded in the variousoases, nor in the Sinai peninsula, nor on the Red Sealittoral below Suez. It remains for research on bio-logical, climatic, and other possible factors, which isstill proceeding, to throw light on these and otherproblems. ____

PEPTIC ULCER AND THE HYPOTHALAMUS

MENTION has been made in these columns ofProf. Harvey Cushing’s suggestion that functionalderangement of the autonomic centres of the hypo-thalamus may play some part in the causation ofpeptic ulcer. In a more recent paper 2 he sets forththe circumstances which prompted this surmise. The

neurogenic hypothesis of ulcer, as he points out, is byno means new. As early as 1841 Carl Rokitanskycommented on the frequent association betweengelatinous softening of the stomach and intracranialdisease, and suggested that the vagus might be atfault. Rokitansky’s views, however, though stilltaught in Vienna, were forgotten when his influencewas supplanted by the less speculative philosophy ofhis successor, Virchow. Cushing’s attention was

directed to the question by the disturbing experienceof losing three patients from acute perforations of the

1 THE LANCET, 1932, i., 848, 1058.2 Surg., Gyn., and Obst., July, 1932, p. 1.