P. G.
PANDE
209
apart from its calcioprive property, exercises a
special tissue effect leading to the production of
hyperplastic changes.
These are as follows:
1. Formation of loose osseous tissue between
the periosteum and compacta of the long bones
which appears as a whitish deposit, or more
prominently as an exostosis;
2. Increased functional activity of bone as
revealed by the excessive formation of young
haversian canals, composed mainly of osteoid
tissue, in the diaphyses of long bones;
3. Development of collagenous fibrils and the
formation of new trabeculae therefrom in the
costal eppiphyses, and the presence of new and
irregularly laid trabeculae in the epiphyses of
other long bones;
4. An excessive proliferation of endosteal
cells (osteoblasts), giving rise to young haver-
sian canals in the diaphyses and syncytial
masses of osteoblasts in close apposition with
the young trabeculae in the spongiosae.
In view of these observations it seems pro-
bable that fluorine also stimulates bone forma-
tion through osteoblasts in the usual way. The
curious but the obvious double reaction of fluo-
rine on the osseous tissue may be explained on
the assumption that the calcium mobilized from
the spongiosa by its calcioprive effect is utilized
for the formation of new bony tissue under the
influence of its osteogenic property.
DISCUSSION
The main point for discussion is whether
pathologically the condition described in this
paper stimulates any known mineral deficiency
disease of the bones of cattle. Histologically,
we have observed pronounced osteoporosis in
certain mobilizable areas of bone, and as accord-
ing to Theiler [1934] osteoporosis in cattle
represents not a disease in itself, but a stage in
the development of rickets or osteomalacia,
question arises to what extent this condition
resembles osteomalacia.
Early European investigators [Bartolucci,
1912; Cristiani, 1925; Askanazy, 1930; Hupka
and Götze, 1931] have diagnosed bone changes
due to fluorine ingestion in cattle as osteo-
malacia
without
regard to the following
points:—(a) that in fluorine intoxication ani-
mals suffer from pronounced cachexia due to
toxic effects on parenchymatous organs, (b) that
the exostosis in fluorosis appears not only as a
nodular growth, but also as a continuous sheet
of secondary bone around the primary cortex
giving the bone a more or less uniformly thick-
ened appearence, (c) that the long bones show
no deformities and are not oftened and (d) that
fractures usually occur at sites of exostosis.
Thener regards osteomalacia of cattle as
aphosphorosis, a view which negatives the
identity of chronic fluorosis with osteomalacia,
uniess it can be shown, as in the case of osteo-
malacia, that under all conditions of dosage,
age, diet, duration of ingestion and the nature
of fluorine compound ingested, the blood sera
of cattle have lowered values for inorganic P.
The results of blood analyses and balance
studies in respect of Ca and P in fluorine-intoxi-
cated animals are variable. These variable
results [Greenwood et al, 1933-34; Biester et al,
1936; Du Toit et al, 1937; Phillips et al, 1934';
and Ramiah, 1940-41] may be due to varied
experimental conditions.
In the present investigation some of these
factors were adequately controlled. The experi-
mental animals, all mature hill bulls received
a diet adequate in calcium and low in its phos-
phorus contents, and were fed NaF for 9 to 10
months at the level of 3 to 4 mg. per kgm.
body weight.
There was no lowering in the
phosphorus value of blood of these animals,
[Majumdar et al, 1943], clearly indicating
thereby that the low phosphorus content of the
diet did not bring about any symptom of aphos-
phorosis during the short experimental period.
Microscopically, osteomalacia and rickets are
characterized by a superabundance of osteoid
tissues.
In fluorosis, however, although some
osteoid tissue is present, its distribution is irre-
gular and it may be absent from parts of the
skeleton where its presence
in an excessive
amount would generally be expected. This
the trabeculae composing the exostoses, the
spongiosa of the costal metaphyses
and the
diaphyses and the metaphyses of long bones are
not particularly rich in osteoid tissue, and the
small amount of osteoid in the diaphysis of long
bones only occurs as remnants of uncalcified
osseous matrix around haversian canals under-
going centrifugal calcification.
The occasional
presence of osteoid in certain easily mobiliz-
able areas of the bone may be attributed to
direct deprivation of minerals consequent on
decreased appetite.
The important features of fluorosis in these
experimental cases which distinguish it from
osteomalacia are (1) the interlacing network of
collagenous fibrils and numerous osteoblasts in
the spongiosa of the limb bones and ribs, (2) the
formation of new and irregular trabeculae from
the collagenous fibrils and osteoblasts, (3) the
absence of distinct osteoid borders around the
newly-formed trabeculae,
which are in fact