1910-11.] Bone Growth in absence of Functioning Testicles. 133 
fact, that soon after the cartilage cells attain to their maximum size they 
begin to exhibit indications of impaired vitality. Their protoplasm shrinks, 
their nuclei degenerate, and in a little while they are dead. 
As the cartilage cells die out, the neighbouring matrix, no longer kept 
healthy by its guardian cells, has lime salts deposited in it. This interpre- 
tation of the meaning of the calcification of the cartilaginous matrix brings 
it into line with the pathological calcifications which occur in degenerating, 
dying, or dead tissue. 
So soon as these changes are established, the cells of the osteogenetic 
layer of the primitive periosteum begin to multiply, to absorb the debris of 
the cartilage, and to eat out a space, the primitive marrow cavity, which they 
occupy, and in which they proliferate to form a tissue, the primitive 
marrow. From the primitive marrow the osteoblasts arise. 
Around the primitive marrow cavity the surfeit and death of the 
cartilage cells continue, but before the cartilage cells undergo their fatal 
hypertrophy they provide for the safety of their race, temporarily at least, 
by dividing. One of the daughter cells apparently always escapes to the 
side furthest from the area of the greatest cell hypertrophy. 
The deductions rendered inevitable by a study of these phenomena of 
endochondral ossification are — 
1. That high states of nutrition compel the cartilage cells to proliferate 
rapidly. This determines growth in length of long bones, for such growth 
necessarily waits upon and follows cartilaginous proliferation. 
2. That, assuming the composition of the blood to be uniform and the 
amount of growth in different parts of the body unequal, the inequality 
must be directly dependent upon an inequality in the absorptive power of 
the cartilage cells. 
2. The Physiological Meaning of the ascertained Facts with 
Regard to Castrated Men and Animals. 
As a result of the anatomical and anthropological survey undertaken 
in section 1 of this paper, it was found that — 
1. The effect of castration is to stimulate and to prolong the period of 
endochondral ossification. 
2. This stimulation and prolongation tends to be especially marked in 
the more distal segments of the limbs. 
These generalisations can now be replaced by the statements — 
1. The effect of castration is to determine a markedly anabolic type of 
nutrition which increases the liability of the cartilage cells to death by 
surfeit. 
