EFFECTS ON THE SKELETON 147 



The various stages in the process of healing in the rachitic skeleton have been 

 described by various authors, including Schmorl ('06, '09), Marfan and Baudouin 

 ('09), Wohlauer ('n) and Schmidt ('21) for man; by Mellanby ('21) in puppies; 

 and by Pappenheimer ('22) for rats. Calcification appears in the metaphysis 

 near the zone of proliferative cartilage, and the normal process of enchondral 

 ossification ensues. Several layers may appear, indicating alternating stages of 

 recrudescence and healing. The abnormal osteoid structures become calcified, 

 but later may be largely resorbed. A correction of minor deformities is possible. 

 Extensive deformities cannot be corrected, however, and permanent dwarfing 

 frequently results. Entire destruction of the epiphyseal cartilage (a rare occur- 

 rence) necessarily precludes the possibility of further growth in length of the long 

 bones. 



Whether the histological features above mentioned as characteristic for 

 human rickets are to be found in the somewhat similar disorders experimentally 

 produced in the lower animals is a question which has been much disputed. 

 Mouriquand ('23) claims that in human rickets the hyperemia and proliferation 

 of the bone marrow entail a decalcifying chondromyelitis which is not apparent 

 in experimental rickets in rats. There is no doubt, as Heubner ('06) and others 

 have shown, that many of the typical changes in the zone of enchondral ossifica- 

 tion in rickets can be produced in puppies by feeding calcium-poor or phos- 

 phorus-poor food. Hypertrophy of the proliferating cartilage, vascular invasion 

 of the cartilage and absence of calcification in this zone can be thus produced. As 

 to the crucial point, the production of osteoid tissue, but few investigators have 

 been successful until quite recently. Absence of excess osteoid tissue, with 

 increased absorption producing merely "pseudorachitic osteoporosis" were 

 found in experiments with calcium-poor diets (chiefly in puppies fed horse-meat 

 plus lard) by Korssakow ('92), Reimers andBoye ('05), Miwaand Stoeltzner 

 ('98), Stoeltzner ('99/08), Aron and Sebauer ('08), Dibbelt ('09), Gotting 

 ('09), and Schabad do). 



Stilling and von Mehring ('89) found that the puppies from a bitch fed 

 calcium-poor diet (horseflesh plus fat) showed no bone changes, but the 

 mother after continuing on the diet 126 days showed softening of the vertebral 

 column and pelvic skeleton. Histological examination of the affected bones 

 revealed active resorption, with bony trabeculae, covered by layers of osteoid, 

 as in human puerperal osteomalacia. 



Dibbelt ('10) fed a calcium-poor diet (rice and horseflesh, plus sodium and 

 potassium chloride) to an adult dog during pregnancy. A resected rib showed 

 considerable decalcification (halisteresis) of bone, with many osteoclasts, 

 Howship's lacunae, etc., indicating an active resorption comparable to that in 

 puerperal osteomalacia. Her 6 puppies appeared normal at birth; but 2 of the 

 puppies continued nursing the calcium-poor milk of the mother (still on the 

 calcium-poor diet). Although they increased normally in body weight, they de- 

 veloped marked skeletal lesions, so that they were scarcely able to crawl within 

 a few weeks. One of the puppies was then fed horseflesh plus calcium 

 phosphate, and improved rapidly. The other was fed horseflesh only and 

 became worse. A resected rib (on the third day of the sixth week) showed 



