We need not here go into the details of this process. It will suffice that we bear in mind that enamel and dentine are simultaneous in their formation, or nearly so, and proceed from the same points of deposit; the enamel from within outwards, the dentine from without inwards; the dentine in globules, layer upon layer, upon the external surface of the gradually receding pulp, until it reaches the proper pulp size,—nature's type,—that wonderful limitation to further progress which appears alike in the crystals of inorganic and the perfected forms of organized matter.

The deposit as a formative process may now be said to have ceased, but it has become a, pulp function, and is continuous through life,—so greatly lessened, however, as to be almost inappreciable normally; but under abnormal excitation it may be increased to a rapidity that will soon result in entire obliteration of the pulp.

The enamel cells or columns are the internal epithelium of the enamel organ, and it is in these cells that the deposit takes place.* Beginning at the end of the column contiguous to the pulp, and at the periphery of the cell, it extends towards its centre or axis, and simultaneously towards the distal end of the prism, uniting with adjoining cells that are undergoing the same process. The axial portion of the column does not calcify as rapidly as the periphery, and at eruption has not attained the same hardness.

Enamel when first formed has a chalky appearance, and is not hard and glassy as when erupted.

The time at which calcification begins, as indicated by the appearance of the "dentine-cap/' is for the temporary teeth during the sixteenth and seventeenth weeks of intra-uterine life. In the permanent set calcification appears as follows: In the incisors, cuspids, and bicuspids, the first month after birth; in the first molars, the sixth month of fetal life; in the second molars at the third, and in the third molars at the twelfth, year of age.f With the exception, therefore, of the third molar, all the permanent teeth are in process of calcifying during the first five years of childhood, a period especially subject to infantile disorders.

The place of first deposit is in all incisors at the cutting-edge of the tooth, and appears as a line of dentine extending across the matrix. In all teeth having cusps these become the points of first deposit. From these first points calcification extends throughout the matrix.

Description Of Abnormalities.—Errors of calcification present varied appearances, from a microscopical pit to an almost entire absence of enamel. Pits or depressions in the enamel surface are exceedingly common. They may be deep with abrupt sides, or shallow and "scooped" in appearance. They occur singly or in groups, but in the latter case usually extend horizontally across the tooth. The bottoms are usually covered with enamel. When very extensive, the tooth is said to be "honeycombed."

Grooves extending across the face of or encircling a tooth are also common, and may be accompanied by a corresponding elevation or wrinkling up of the adjoining enamel. There may be several parallel grooves at regular intervals with elevations between, giving tbe so-called "stepped" appearance.

Fissures or breaks in the continuity of the enamel differ from the above in extending entirely through the enamel and in being of irregular appearance. They occur upon the masticating surfaces of the molars and bicuspids, and at the cingulum (when developed) in incisors and cuspids. They are usually regarded as examples of arrested development, but I think incorrectly. They are rather instances of imperfect union between portions of enamel. I have said that calcification began in the cusps of these teeth (bicuspids and molars), and from these points they extend throughout the matrix. Take, for example, a qudracuspid molar,—the four points would extend towards each other until, meeting, they would coalesce. On a flat surface their union would probably be perfect, but the surface is not flat, and in the angular concavity the prisms are brought in nearly end to end contact, and imperfect coalescence could easily result.*

The same condition exists when the cingulum or basal ridge is developed upon an incisor.

It is probable that the fissure on the buccal surfaces of lower molars is formed by coalescence, hence its liability to be imperfectly calcified.

Patches of brownish or yellowish color and of greater or less extent often appear upon the molars and bicuspids. They are of much softer texture than normal enamel. They are an exaggeration of a normal condition, namely, the imperfect hardening of the central portion of the enamel prisms. Although predisposing to caries, they have less influence than might be supposed.

Leber and Eottensteinf describe two cases of congenital white patches in enamel, accompanied by greatly diminished consistence.

Notches sometimes appear upon the edges of the incisors, usually the upper centrals. I do not think they are often tbe seat of caries.

A very peculiar condition is sometimes seen in the enamel of the bicuspids and first molars. At a certain height on the surface of the tooth a shoulder is formed, and the tooth is then continued, but diminished in size, looking like "a small tooth growing out of a large one." (Fournier.) I have seen but one case of this kind. In that the lesion was well marked upon all the bicuspids and first molars. Upon the latter the shoulder was about the middle of the tooth, while upon the bicuspids it was close to the articulating surface. All the teeth were of inferior organization, and more or less carious. The gentleman was a transient patron, and I could obtain no history.

Mr. Tomes describes a granular condition of enamel in which the normal prismatic calcification is wanting.

Defects of dentine can hardly be called predisposing causes of caries, as the enamel must first be penetrated ere this tissue can be acted upon, but they accelerate the disease, and have thus far a causative relation.

The interglobular spaces of Czermack are inclosures between unusually large dentine corpuscles, or aggregations of corpuscles, filled with a substance resembling bone plasma,* or, acording to Tomes,f the globules may coalesce so as to isolate an unimpregnated portion of the matrix, which is therefore simply a cavity containing soft tissue.

This condition of the dentine presents under the microscope a granular appearance, that is normal beneath the cementum, but abnormal beneath the enamel. Defects of enamel are usually accompanied by defects of dentine.

In describing these lesions, I have not referred to those conditions common to all, which we will now consider.

First, homologous teeth are usually affected alike.

Second, teeth calcified at the same time have the blemish at the same level, and those calcified at different times may have the same blemish, but at a different level, represented by their differing degrees of calcification; as, for example, a groove appearing upon the cuspid near the point would appear upon the incisors several lines nearer the gum; the latter being earlier in development than the former.

The first consideration points to a systemic cause. The second points to a definite time at which that cause was active,—namely, the time that the affected portion of the tooth was undergoing calcification. We are, therefore, irresistibly forced to the conclusion that these lesions are due to arrest of development.

I have already given the cause of fissures. They differ from other defects in being errors of union rather than due to arrest of devel

* Wedl, "Pathology," page 45. f " Dental Surgery," page 283.

opment. We find them in normally-formed enamel, showing no signs of developmental errors. They are not due to systemic disease, and occur alike upon all teeth having more than one point of calcification.

Causation.—We have now reached "deep water." If but one tooth show defects of calcification, while its homologue is free from such defects, then we must assume a local cause; as, possibly, an abscessed temporary tooth. Such cases are not common, and a systemic cause must be invoked to explain an evident arrest of development.

The temporary teeth do not so frequently show these lesions. When defective, the cause must be sought in parental influence, because these teeth are calcified prior to birth, and are beyond future influences.

The first molar begins to calcify during the sixth month of intrauterine life, and would be to a slight extent subject to the same conditions as the temporary teeth.

As might be expected, the second and third molars, are almost free from these defects, showing the limitation of the cause to the earlier years of childhood. We must look, therefore, to those diseases incident to this period.

Hereditary Syphilis.—The potency of this influence is undoubted. Indeed, it is the only recognized cause affecting the temporary denture. In regard to the permanent denture, it is questionable if we have not given it too much prominence. It should never be assumed to be the cause, save when it can be demonstrated to have been existent, and when no other causative influence is visible.

The bulk of testimony is to the effect that this disease is not only a cause, but the principal cause, of defects of calcification, and that certain defects, as the Hutchinson notch, and the peculiar condition affecting the bicuspids and molars above described, are specific. As to the latter claim, the syphilographers are probably correct, but the former is too sweeping an assertion. Hundreds of cases are seen where syphilis is out of the question, and where there is not the slightest history to indicate it. There is another reason for doubt in this matter. Lesions of calcification are almost always abrupt, and indicate plainly the commencement and termination of the influence. Syphilis is a continuous disease, and ought to produce usually a continuous effect; hence I cannot regard those lesions which indicate a short-lived cause as due to syphilis directly, and should suspect some other cause, although I could not find it. It is common to assume that the syphilitic taint can do anything bad, and, once its existence is determined, no further effort is made to find the origin of anything obscure.

Eclampsia.—According to the observations of Magitot, infantile convulsions are a common cause of erosions. In a large number of cases he traced the defects to convulsions occurring at the time when the tooth was in formation, and found no other assignable cause.

In my own practice I have seen two cases traceable to this cause. It is exceedingly difficult for the dentist to investigate this subject, and but few have done so. Much depends upon the parent's memory, which is quite commonly inexact.

Rachitis.—At first glance it would seem, from the nature of this disease, that it would be certain to cause dental imperfections. It is a bone disease. It is caused by arrest of development. It comes at the formative period of the teeth. Still, it is doubtful if it has much effect. Certainly it cannot often be a cause, because it is a comparatively rare disease. We cannot deny its influence, but regard it as infrequent. It is well known that it retards the eruption of the teeth, and this fact becomes one of the diagnostic signs of the disease. It is also true that rickety children quite often have good teeth.

Eruptive Fevers and Skin Diseases.—The teeth are dermal appendages, and it is reasonable to suppose that they are more or less directly affected by those influences which act upon dermal structure, supposing such influences existent during their formative period. The hair and nails are affected in this manner; why not the teeth? Many skin diseases are of syphilitic origin, and could thus account for the effect of that disease at a stated interval, the subordinate lesion being abrupt and of short duration. Many of the eruptive fevers, as scarlatina, are very depressing in their effects, and require the whole vital force to throw them off.

Scrofula has been mentioned in this connection. There is not the slightest evidence that it has any influence.

Rheumatism, Diphtheria, and Fevers.—Many times no adequate cause can be found for these lesions, unless we consider as such some prostrating disease. When we bear in mind the fact that often in these diseases the system of the little sufferer is doing work, represented by consumption of tissue, much greater than any day laborer, we will recognize that all its vitality is used in combating the disease. Often these diseases leave serious sequelae, and there is for a long time a general stunted condition of the child. I do not think it is assuming too much to say that their potency extends to the forming teeth.

Conclusions.—I have shown that this condition has probably many causes, and that we are not justified in attributing to any one apparent cause all cases alike. Rather we should by patient search endeavor to verify our observations. Unfortunately, dentists have