192 THE BIOLOGICAL BASIS OF INDIVIDUALITY 



and this is true even if normal, not transplanted cartilage has reached a 

 certain thickness— the central parts may shrink and become necrotic, due 

 to their distance from the blood vessels which carry nourishment to the 

 perichondrium and to the outer layers of the cartilage. It is probably also the 

 deficiency in oxygen and other food material that causes the small, relatively 

 undifferentiated perichondrial cells to change into the large and fully dif- 

 ferentiated cartilage cells. Only in one case had a piece of cartilage, after a 

 period of serial transplantations extending over two years and ten months, 

 produced bone; bone plates were lying along the cartilage and in the bone 

 there was a development of marrow containing fat cells. 



It is the connective tissue which is active in the destruction of serially 

 transplanted cartilage. This forms a capsule around the transplant and it 

 invades, dissolves and gradually replaces the necrotic parts ; occasionally, 

 blood capillaries and some lymphocytes may penetrate with the connective 

 tissue into the areas of necrosis. But under certain conditions the connective 

 tissue may push its way also into that part of the living cartilage where 

 the cells are separated by a relatively large amount of hyaline intercellular 

 substance or by a very thick capsule. On the other hand, the connective 

 tissue is apparently unable to penetrate into living perichondrium or into 

 young perichondrial cartilage, where the cells are placed close to one another. 

 It is therefore the fargoing differentiation, the marked formation of inter- 

 cellular substance or of capsule meterial, which gives the connective tissue 

 an opportunity to exert its invasive, constrictive, and therefore injurious 

 action. Healthy young cartilage cells are safe from the attack by the host 

 connective tissue, although, as we have seen previously, they are exposed to 

 the invasion by lymphocytes. Thus a vicious circle is established: certain 

 unfavorable conditions, such as deficient nourishment, lead to the production 

 of the differentiated cellular and intercellular paraplastic substances, and 

 then the resulting ingrowth of connective tissue tends to divide the trans- 

 plant into small partitions and otherwise injure it, decreasing still further 

 its normal oxygen and food supply and preventing its normal proliferation. 

 To ensure the survival of the cartilage transplant, it is necessary to keep the 

 perichondrium surrounding it alive. The tissue equilibrium is best main- 

 tained if the resting connective tissue of the host surrounds the perichondrium 

 of the transplanted resting cartilage. But at the same time it is necessary to 

 prevent the impairment of the nourishment of the transplant by the con- 

 nective tissue capsule. If there is a deficiency in the nourishment of the 

 transplant, a necrosis in its center occurs, the tissue equilibrium is disturbed, 

 and in consequence the new formation of the perichondrial cartilage cells 

 takes place, which subsequently differentiate and produce intercellular sub- 

 stance. Thus both (1) primary injurious conditions which affect directly 

 the transplant, and (2) the activity of the host connective tissue and lympho- 

 cytes, taking place under the influence of homoiogenous individuality dif- 

 ferentials, may play a part in shortening the life of the transplant. In old 

 age, changes similar to those seen after homoiogenous transplantation occur 

 in organs, namely, a decrease in the parenchyma and an increase in the 



