532 SECTIONAL TRANSACTIONS .—I. 
Dr. H. D. Kay. 
The work of Robison and his collaborators has shown clearly the import- 
ance of phosphatase in the deposition of bone salts, and has incidentally 
called attention to the fact, apparently forgotten for many years, that phos- 
phorification as well as calcification takes place in growing bone. The 
phosphatase mechanism is also probably concerned with bone resorption ; 
in vitro experiments have shown that under certain conditions bone salts 
can be transformed again into soluble phosphoric esters in the presence of 
phosphatase. 
Changes in the phosphoric ester content of the tissues in experimentally 
induced abnormal bony conditions have been observed. The marked 
increase in phosphatase content of the blood, which is frequently associated 
with diseases involving the skeleton, has been shown to be reversible after 
adequate therapeutic measures have been taken. 
The production of experimental rickets in rats, on a normal diet containing 
vitamin D, by adding small quantities of beryllium carbonate to the diet 
has enabled evidence to be brought forward in support of the view that one 
of the major activities of vitamin D is to stimulate the uptake of phosphate 
through the intestinal wall. 
Dr. LesLiz J. Harris. Vitamin action and bone formation. 
The following theory of the mode of action of vitamin D explains the 
known facts and has enabled predictions to be made which were subse- 
quently verified : vitamin D acts primarily by raising the blood Ca x P, 
causing increased absorption of Ca and/or P from the gut and diminished 
excretion into the gut (i.e. increased ‘net absorption’); the increased 
calcification in the bone is secondary to the blood change. It has been 
shown that this theory accounts for the following known facts :— 
(1) The association of rickets with high fecal and (2) low blood 
Ca and/or P and (3) low bone Ca and P ; 
(4) The rectification of these errors with vitamin D, (5) the rise in 
blood Ca X P preceding the new calcification ; 
(6) The influence of the dietary acid-base balance ; (7) dietary Ca-P 
ratio ; (8) Be, etc. 
(9) Differences in species susceptibility. 
(10) Calcification im vitro (proportional to Ca x P). 
The writer predicted from this theory that overdoses should cause 
hypercalcemia and/or hyperphosphatemia, and hence excessive calcifica- 
tion, e.g. at growing end of bone. These effects were duly found and have 
since been confirmed by others, the bones and teeth in hypervitaminosis 
showing highly characteristic abnormalities. (With maximal overdoses and 
insufficient Ca and P available in the gut, some of the extra Ca and P may 
be drawn from parts of the bony store.) 
The widely advocated theory that vitamin D acts by stimulating the para- 
thyroid has been disproved by showing that the latter, in contrast with 
vitamin D, does not increase ‘ net absorption,’ and acts by withdrawing Ca 
from bone, causing loss to the body. 
The primary effect of vitamin C deficiency is to cause degeneration of 
osteoblasts, odontoblasts, ameloblasts, etc. ; hence cessation of osteogenesis. 
Other effects in the hard tissues are secondary. 
Dr. DonaLD HUNTER. 
The clinical worker is in a position to study ossification in patients under 
treatment. Progress is followed by estimations of the blood chemistry and 
. 
