Page 873 - My FlipBook

CHANGES IN THE ODONTOBLASTS. 883
of dentine soon begin to show a failure as to the normal number of the
tubes, has led me into the study of the condition of these cells in the
varying conditions of the pulp as regards secondary deposits. I have,
however, found this an exceedingly difficult study. In cases of calci-
fication it is very difficult to get good sections without decalcifying the
hard tissues, and in so doing the tissue is so deranged and otherwise
injured as to be of little use. Again, in removing the pulp from its
chamber the layer of odontoblasts so often remains clinging to the den-
tinal walls, either as a whole or in part, as to cause much vexation.
Witli all of these troubles in the way it is not surprising that the study
of this layer of cells in its diseases has made so little progress.
I have already alluded to the fact that this layer of cells seems to
persist unchanged in acute inflammations of the pulp until it is under-
mined by the processes of suppuration. This, however, does not argue
the greater vitality of these cells, but rather the reverse, for it shows
that they are less susceptible to changes of form than the other cells
of the organ. The facts already given speak plainly of the atrophy of
the odontoblasts before the death of the pulp as a whole. Indeed, some
of my observations seem to indicate that the pulp may remain alive for
a considerable time after the atrophy of a large proportion of the odon-
toblasts. In many of my sections of pulps that had been long in a
state of disease the peculiar structure of the margin of the pulp in which
the odontoblasts lie has been present, but without the odontoblasts, or
with one here and there only, or with patches from which they Avere
missing, very much the same as we often see in secondary dentine where
the tubes fliil in patches or become fewer in number and finally disap-
pear. Again, I have found in some sections that all signs of the nor-
mal periphery of the pulp were missing, and yet along the margin
there was an occasional odontoblast which took the stain in a very
unusual manner, as though profoundly clianged in its chemical con-
dition.
In Figs. 479 and 480 are given illustrations of these changes. These
can be better appreciated by comparison with Fig. 440, in which the
full number of odontoblasts that occupy the periphery of the pulp are
present. This form of failure of these cells seems to accompany the
degenerative changes of the tissues of the pulp that have been described,
and, taken together with the evident persistence of these cells during
the changes due to acute inflammations, show us plainly that it is in the
cln-onic diseases that we must expect the atrophy of this layer. This
agrees also with what is seen in secondary dentine. It seems that these
cells are profoundly affected by irritation of the distal ends of the
fibrils, for we often find them depositing secondary dentine in cases of
abrasion, as has been indicated, and in connection with tliis perform-
ance the cells disappear. Not only this, but they disappear in many
cases in which there has been no deposit of secondary dentine whatever.
This has appeared prominently in two cases in which there had been
long-continued inflammation, accomjmnied with hypertrophy of the
pulp which was projected into the cavity of decay, as shown in Fig. 454.
In neither of these cases were there any secondary deposits except a few
pulp-nodules and a few masses of calcoglobulin ; but over a consider-