PROF. T. WINGATE TODD ON OSTEOMALACIA. 857 



proiluced by diiferences in the setiology of the disease. For the 

 bone-changes can only be a symptom, caused, perhaps, in many 

 different ways. 



The bone-marrow in osteomalacia is much modified. The 

 marrow-cavities of the long bones are enlarged and filled with a 

 gelatinous fatty tissue and by bright red marrow. Marrow is 

 divided microscopically by Ziegler into splenoid and fine-fibred 

 constituent factors (4). Of these the latter form, is much in- 

 creased, partially filling up the marrow-cavity and penetrating 

 the bony tissue. 



In eai'ly cases the compact bone is invaded by this vascular 

 fibrous tissue, which has already replaced to a large extent the 

 spongy bone and which is not preceded by osteoclasts. The same 

 observation has been recorded by Morpurgo (3). 



In later stages the whole of the compact tissue of the shaft has 

 disappeared and is replaced by fibrous tissue, in which are to be 

 found discreet areas or islets of osseous material (see Pl.LXXXIX. 

 figs. 5, 6). Thei-e is meanwhile no subperiosteal deposit of new 

 bone. The histological picture of the bone closely resembles that 

 seen in ostitis fibrosa. The remaining islets of bone lose their 

 ossein and become transformed into a tissue which, from its 

 staining properties, appears to be hyaline in character. But, at 

 the same time, in other situations the regressing bony substance 

 exhibits a fibrillar change of the ground-substance similar to that 

 described by Retterer as the basis of normal bone (5). 



Cells with similar staining reactions to osteoblasts may still be 

 seen bordering the islets of bony tissue (see PI. LXXXIX. fig. 6). 

 In many places so-called "osteoclasts" are observed. But, on 

 examining several slides one is struck by the comparative infre- 

 quency of these cell-masses. As Gayet and Bonnet remark (1) 

 it is difiicult to believe that osteoclasts can play more than a' very 

 subsidiary part in the destruction of bone, because of their scarcity 

 when compared with the extent of the process. It would appear 

 that osteoclasts are not at all necessary for the production of 

 change in bone-siibstance. 



As the bony tissue becomes transformed or replaced by the 

 fibrous material, the Haversian ' systems disappear. The peri- 

 osteum becomes intimately united to the mass of fibrous tissue 

 which remains in place of the true bone. 1 have not observed 

 hfemorrhages in subperiosteal or other localities. The joints were 

 unaffected. At the diaphyso-epipyseal junction, changes similar 

 to those in rickets were observed. 



The theories of causation of osteomalacia have been well 

 reviewed by Morpurgo (2), who, among others, has succeeded in 

 producing the disease by inoculation of a micro-organism (6j. 



The detailed histological changes have been discussed by 

 Basset (7), whose description is amply borne out by my own 

 slides. 



The disease is one which may be secondary to some other 



