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A Valued correspondent requests the publication of some analyses of cereal elements, and the following tables have therefore been collated from a work on "Foods/' by Alex. Wyntner Blyth, of England.

There is a growing professional inclination in the direction of experimentation with a view to the correction or prevention of initial physical degeneracy, by the supervised production of improved human structure through prescribed alimentation, during both vanteand post-natal periods; and such scientific histogenesis would seem to be quite within the bounds of possibility.

If the pork and beans of New England, the oatmeal of Scotland, the roast beef of Old England, the black bread of Germany, and the maccaroni of Italy may be said to produce clearly discernible physical and mental characteristics in those several groups of peoples, it fairly follows that in any country the individual is, or may be made to be, the subject of distinct dietary development.

Food Elements Tabulated For The Use Of Experimenters In Special Tissue Production By Alimentation:

Wheat Flour.

Per cent. Water 14-0

Fat 1-2

Nitrogenous matter, insoluble in water 12-8

Nitrogenous matter, soluble (albumen) 1-8

Non-nitrogenous matter, soluble (dextrine) . . . . - . 7-2

Starch 59.7

Cellulose . 1-7

Ash 1-6

Wheat Bread.

Fine Bread. Coarse Bread.

Per cent. Per cent.

Water ......... 3851 4102

Nitrogenous substances 6-82 6-23

Fat -77 »22

Sugar 2-37 213

Carbo-hydrates 49.97 48-69

Woody fiber . . . . . . .38 .62

Ash M8 1-09


'Per cent.

Water 12-92

Nitrogenous matter . , 11*73

Fat 604

Sugar 2-22

Dextrine and gum 204

Starch 51-17

Fiber 10-83

Ash 305

Rye Flour.

Per cent.

Water 14-24

Nitrogenous substances 10-97

Fatty matters 1-95

Sugar 3-88

Gum 7-13

Starch 58-73

Woody fiber 1-62

Ash 1-48


Per cent.

Resin -36

Gluten 10-47

Albumen -23

Apothem 2*54

Saccharine extraction 3-08

Mucilage and gum 2-80

Starch % 52-30

Fiber 26-93

Loss 1-29

Barley Meal.

Per cent.

Water 15-06

Nitrogenous matter (1-0 to 1-7 albumen) 11-75

Fat 1-71

Carbo-hydrates (sugar 1-2, dextrine 1*7) 70-90

Woody fiber -11

Ash -47

Indian Corn.

Water .

Starch .



Dextrine and sugar



Per cent.







110 Bice.

Per cent.

Water • 1*'*1

Nitrogenous substances • .6*94

Pat .-&1;

Starch • -77-61

Woody fiber *08

Ash *45


Broad Bean. Kidney Bean.

Per cent. Per cent.

Water 14-84 18-60

Nitrogenous substances 28-66 23-12

Fat 1-63 2-28

Carbo-hydrates 49-25 53-63

Woody fiber 7-47 8-84

Ash ....... . 315 3-53


Under our "Periscope" heading will be found a valuable paper by Dr. William Henry Flower, read before the Anthropological Institute of Great Britain and Ireland, "On the Size of the Teeth as a Character of Kace." We are pleased to announce that Dr. J. L. Williams has undertaken the work in this country of measuring the skulls in the Cambridge Museum, the Peabody Museum at New Haven, and the Army Medical Museum at Washington, His examinations and measurements will be based upon Professor Flower's method, but will include observations and deductions of more especial interest to dentists. We expect to publish the results of his researches in the Dental Cosmos.


Our esteemed eotemporary, the British Journal of Dental Science, published in eleven issues of that periodical during the past year the translation from the French of Alfred Fournier's lectures on "Syphilitic Teeth," which was made expressly for the Dental Cosmos by Dr. J. William White. We have failed to discover a word of credit from first to last to the journal from which it copied. We are sure the omission was unintentional, and that the editor will be glad to give credit where credit is due.


Dental Caries: A Critical Summary; and the Prevention of Dental Caries. By Henry Sewill, M.R.C.S. and L.D.S. London: Bailliere, Tindall & Cox, 20 King William street, Strand, 1884. Under the above title the author publishes in permanent form a series of papers reprinted from the Journal of the British Dental Association. It is an effort to show that "caries is a process of disintegration, commencing invariably at the surface, proceeding inwards, and due entirely to external agents. Enamel and dentine are perfectly passive under this process of disintegration, and manifest neither pathological action nor vital reaction of any kind.'" We have italicized the latter portion of the author's proposition concerning dental caries because his efforts are mainly directed towards establishing this clause, and because of the inevitable futility of any attempt to maintain such a manifestly absurd and impossible hypothesis. While there may be some difference of opinion concerning just what is implied in the use of that somewhat questionable expression, "vital reaction," yet there can be no difference of opinion among those who have had any considerable practical observation regarding the reaction of those organic forces which serve to maintain all parts of the body in the condition which we call health. Whether it is possible for a true inflammatory reaction to be exhibited in dentine depends entirely upon the definition of inflammation. If increased or exalted sensibility, appearing in a tissue as the result or sequence of injuries wrought by agencies foreign to the tissue or organ, be accepted as evidence of the existence of an inflammatory condition; if the existence of a well-defined line of demarkation between the external dead layer of dentine in a carious tooth and the more internal healthy tissue, as has been clearly demonstrated by Prof. Mayr and others, in which line or zone there is nearly always much greater sensitiveness than in the healthy dentine beneath it, can be considered as an evidence of inflammatory reaction, then dentine is capable of no insignificant degree of inflammation, and it would seem, to a rational mind, a self-evident proposition, requiring no objective evidence, that any tissue capable of presenting a condition of exalted sensibility is also one in which molecular, and therefore nutritive, changes are possible. But if there are minds incapable of perceiving this truth on a priori grounds, it is only necessary to open one's eyes to see abundant and incontrovertible proof of its existence. The author admits that he has made no original research of importance, and that his deductions are based largely on the labors of Tomes and Wedl. But his irrational and radical position is hardly warranted by the guarded and carefully qualified statements of these authors. I quote from page 413 of Wedl's "Pathology of the Teeth:"

"Since we know that an interchange of material takes place in the dentine and cement during life, as is proved by the occurrence of atrophies, hypertrophies, and new formations, and that the dentine possesses a degree of sensibility, we cannot reject absolutely the idea of a reaction on the part of both hard tissues against the effects of external agents. * * * There can be no doubt that the sensibility, sometimes increasing to actual pain, of the dentine when deprived of its protective covering is a vital action [the Italics are ours], and that this becomes diminished when the most sensitive, the peripheral, portion is destroyed by an external agent."

Now, accepting, with our author, Dr. Burdon Sanderson's definition, that "inflammation is the aggregate of those results which manifest themselves in an injured part as the immediate consequences of the injurious action to which it has been exposed," we submit that he is without reasonable excuse for the following utterances:

"Dentine being perfectly passive under every form of injury, * * * must, I repeat, be considered incapable of inflammation—a term which we may now note includes morbid action of every kind due to injury" Italics are ours. "We know that dentine violently broken or lacerated does not inflame; we know that a broken exposed surface of dentine, on application of an irritant like solid nitrate of silver, does not inflame; and we know that we may drill a hole into healthy dentine, or expose a surface of healthy dentine after excavating a carious cavity, and forcibly wedge on to that bare surface a foreign metallic mass, a filling, and leave it there, and the dentine will not manifest inflammatory action of any kind." Keeping in mind Dr. Sanderson's definition of inflammation, as given above, we may ask what practical dentist does not know that very decided changes in the dentinal tissue occur beneath fillings? - While these changes may sometimes be attributed to the chemical action of the material of which the filling is composed, in very many instances no such explanation is possible. What operator of experience does not know that an inflammatory condition of the dentine sometimes supervenes on grinding the cutting edges of incisors? What operator does not know that the sensitiveness of dentine is often increased by the application of dilute chloride of zinc? Instances of the above character are too common to call for more than a mere reference to them. While it is undoubtedly true that teeth poorly organized in the beginning may never be changed into teeth of faultless structure, yet it is within the limits of indisputable demonstration that such teeth may be vastly improved. This would not be possible

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