374 PATHOLOGY through, there arc not wanting indications that the same luemato- blastic function is present concurrently with the osteoblastic. Kasso- Coming, then, to the actual facts of rickets, we shall find that witz s re- those features of the process on which the greatest stress has been searches laid in the recent elaborate researches of Kassowitz are of the on nature of over-vascularization or hypencmia. In the ossification rickets, from cartilage he finds that the vessels from the perichoridium extend inwards to a greater extent and with less orderliness than usual ; then there is a development in the cartilage of colossal vessels, and finally of blood-spaces, packed full of red blood-disks, and with no very definite walls, so that it looks, at the first glance, as if hemorrhage had taken place into the bone-marrow. In many cases there is no sharp line of separation of the embryonic marrow from the contents of these blood - spaces ; it is probable that the gelatinous tissue of the former had "passed direct into hsemato- blastic substance and so into blood-corpuscles." In the periosteum also there is much more blood than usual, and the same large blood- spaces are sometimes found. These errors of vascularization Kasso witz places at the foundation of the rickety process. Deposition of calcareous salts, he points out, cannot take place where there is so much blood ; the calcification follows in an orderly way only where the movements of the blood and juices are restrained or distant, the best example of this law being the gradual reduction of the wide central space of an Haversian system to a narrow channel containing a single twig of blood-vessel. The excess of vascularity in rickets is, by Kassowitz, put down to "inflammation," or to the hypereemia of the same ; but we have seen that he also invokes, as a detail in the process, an excessive hamaatoblastic activity in the embryonic marrow-cells. The latter is a more fundamental and intelligible fact than "inflammation" (which begs all the fundamental questions), and we shall do well to give it prominence accordingly. We should then interpret the observations of Kassowitz as follows. The due regulation of the blood-supply, the restriction of it to definite and ever-narrowing channels, is necessary for the proper deposition of the earthy matter and for the building up of bone in Haversian systems. The embryonic cells surrender their indi vidual hrematoblastic function, while certain tracts of them become definite vessels for the supply of all the rest ; and in proportion as they give up individually their primitive function of blood-making they are in a position to take on individually the function of bone- making. In compact bone this change of direction is carried out most completely ; the cells become osteoblasts in successive rows, a ground - substance impregnated with earthy matter closes in around them, and they are imprisoned for ever as bone-corpuscles. In spongy bone, however, there is still a reserve of haeinatoblastic force ; only thin lamina? of bone are formed out of some of the cells, while many of them continue to be hsematoblasts and to form the familiar red marrow. Adopting, then, the figure of a struggle between the hrematoblastic and osteoblastic tendencies in embryonic cells, or the perception of a divided duty, we shall con clude that rickets is the undue preponderance of the former. It means spongy bone where there should be hard bone, and much wider spaces than usual, with much more blood in them in the proper seats of spongy bone itself ; and it means in general a retardation of the hardening process. All this enormous haematoblastic energy or local blood-forma tion is unfortunately wasted ; the child is no better for it, and is more likely than not to be anaemic. The formative powers are diverted from bone-making, and spent upon blood-making ; and the lime-salts in the organism that should have gone to make bone are actually thrown out with the urine, which has been known to have as much as four or even six times its due amount of phos phates. The organism, when rickets overtakes it, is in this fix, that it makes blood which it can no longer profit by, and has meanwhile to part with bone-salts which it will want again. The disease is, in fact, an unfortunate contretemps. Many of the facts of rickets are thus secondary to an initial error in the embryonic functions of the tissues, and the evidence seems to show that the error must have begun in most cases before birth. Although it is well known that the obvious phenomena of rickets are not usually remarked until the child is a few months old, yet, as Kassowitz has ascertained, the condition "begins much more frequently than has hitherto been assumed in the later months of intra-uterine development." The facts point very clearly to the health of the mother as being primarily at fault. "The health of the mother," says Sir William Jcnner, "has a decided influence on the development of rickets in the child. Whatever renders her delicate, whatever depresses her powers of forming good blood, that tends to produce rickets in an oifspring. . . . The child of an ill-nourished mother is disposed to become rickety when placed under unfavourable circumstances after birth, or even under favourable circumstances in some cases." The disposition must be in most cases, and in the worst cases, congenital in the child s tissues. We should therefore seek in the intra-uterine con nexion between mother and child for some defect on the maternal side which would induce that which would appear to be essential to rickets in the child, namely, a preponderance of the luemato- blastic function of embryonic cells over the osteoblastic, a reversion in the cell-life of the growing frame towards independent blood- making. In seeking for this source of error, it will be necessary to recall for a moment the nature of the intra-uterine connexion between mother and child, or the part played by the placenta. Placental Function in Congenital Disorders. The embryo makes its own blood and establishes the connexion with the mother by its own blood-vessels. Its blood is carried to the placenta to be aerated, as the phrase goes ; but it is much more than aerated. The placenta is a glandular or secreting organ of the mother, inasmuch as the maternal blood, flowing slowly through the sponge- like tissue of thick-walled vessels, receives additions of mucus-like drops from the deliquescence of the large nuclei in the proto plasmic vessel-walls (tig. 40). This mucus-like addition is clearly an adaptation for the foetus ; and the sur faces of the placenta, where the foetal ves sels touch it, are further adapted, through a thick-set cap of nuclei, for exuding it where it can be taken up by the plasmatic tissue of the chorion. This placental contribu tion is the "uterine milk " furnished by the mother for the use of the foetus, so that, although the latter makes its own blood (and blood vessels), it receives material additions to its blood from the mother. It is obvi ous, therefore, that FIG. 40. Secreting structure of placenta (guinea-pig); the secretion of the the wa ^ s f the maternal blood-channels are them- i , , , ( selves the secreting structure, their substance yield- piacenia is eiy es- j n g cu . p s O f mucus a , which mix with the blood l>. sential to the foetus, and the due endowment of the latter must depend greatly upon the structural and functional sufficiency of that organ. It sup plies the foetus with much of the fluid that circulates in the latter s vessels ; it may be said to spare the foetus to that extent the need of producing such fluid itself, or to dispense with the ha inato- blastic activity of its tissues, so that they may take other formative directions, such as bone-making. Or it may be contended that there are ingredients in the normal placental secretion which are specially adapted to bone-making. Now, if there should be any interference with these placental contributions, we are left to sup pose that there must then be a reversion on the part of the fa-tul cells to self-helping tendencies, and especially to local blood-making. The excessive blood-making of rickets, and the retardation of bone- making consequent thereon, would thus be traced to failure in the placental function. But, if there be such a change in the direction of the formative processes of the foetus as an adaptation to its special intra-uterine conditions, why should rickets not become declared until several months after birth ? In the first place, we have the evidence col lected by Kassowitz that there are plain indications of the rickety process to be observed where death of the child has occurred before the full term ; and, further, there are analogies to show that it requires all the extra-uterine functions to have been in action for some little time before a congenitally-acquircd tendency manifests itself. Although the intra-uterine life comes to an end, and the child ceases to be dependent on the placental function of the mother, yet the acquired tendency, or the adaptation to a deficient performance of that function, remains for a certain time longer. It comes to an end, however, from the second to the fourth year ; the bone-forming tissues cease to follow the devious direction, the bone- salts present in the organism are put to their proper use, ossification resumes its normal course, and, as the soft formative material of bone had accumulated in excess, the bones of the once rickety child are in the end harder and thicker than those of normal growth. There is an assumption in the foregoing which calls for remark, the assumption, namely, that the placental function has been in adequate on the mother s side or that the requisite additions to the blood have not been made. Our almost complete ignorance of the pathology of the placenta is the reason why the above-mentioned facts and principles have to be eked out by an assumption. We do, indeed, know that the placenta suffers in syphilis of the parent ; and we know that in congenital syphilis of the child the growth of the bones is affected in many ways analogous to the shortcomings of rickets, and that, as in rickets, the error of growth may not show Plac- tal i ! nexi and lick
