734 FRANCIS H. McCRUDDEN 



of these diseases to each other. This relationship is best brought out 

 when these diseases are considered as disturbances of the calcium metab- 

 olism. From this point of view, these conditions are not distinct and 

 separate in the sense that the specific infectious diseases are distinct and 

 separate diseases, but they are very greatly exaggerated forms of conditions 

 which are not uncommon, and scarcely to be considered pathological when 

 present to but a slight degree. A person either has or has not typhoid 

 fever, for example; there are no intermediary stages. Osteomalacia and 

 rickets are more like obesity; there are all grades between the normal 

 and extreme cases of the disease. 



Bone, like other tissue, undergoes metabolism. Old bone is continu- 

 ously absorbed and new bone is continuously replacing the old. In the 

 case of growing children, as the skeleton hardens, the new bone laid down 

 is progressively richer in calcium. In addition to acting as the supporting 

 skeleton of the body, the bones act also as a storehouse of calcium salts, and 

 consequently, if for any reason calcium salts are not furnished in sufficient 

 quantities in the diet to satisfy the body requirements, or are needed else- 

 where in the body in large amounts, the new bone laid down may be 

 abnormally poor in calcium. As a result the bone becomes softer than it 

 should be. If the deficiency in calcium is great enough to result in much 

 bone softening, fragility and bending of the bone occurs, and the condition 

 is diagnosed as osteomalacia, rickets, or osteoporosis. 



This point of view has not always been held, however. Until recently 

 bone was considered practically dead tissue, not undergoing metabolism 

 once it was laid down; the decalcification of bone in osteomalacia was 

 believed to be duo to the action of an acid, an action similar to that which 

 takes place when dead bone is put into acid. 



From the time that osteomalacia was first recognized in the middle 

 of the eighteenth century, its relationship to rickets has been under dis- 

 cussion. At first the two conditions were considered one disease by some 

 authors, but clinical and anatomical differences which settled that question 

 were soon discovered (Virchow(c)). Whether or not the process going on 

 in the two conditions is essentially the same is another question. Early in 

 the nineteenth century, microscopic and chemical examination of bone in 

 osteomalacia showed decalcification similar to that which takes place when 

 dead bone is placed in dilute hydrochloric acid. This appearance sug- 

 gested that the condition is due to the action of an acid, which dissolves 

 the mineral constituents and leaves behind the soft osteoid tissue, a point 

 'of view accepted by Virchow, Lobstein, and, in fact, most pathologists 

 since. These investigators consider the processes in osteomalacia and in 

 rickets entirely different, in that in osteomalacia the lime-free bone is 

 believed to be normal bone from which the inorganic constituents have 

 been dissolved out by an acid, whereas in rickets the lime-free bone is 



