EFFECTS ON THE SKELETON 145 



Knochensubstanz bilden sollte, existirt ein ganz ungewohnlich dichtes osteoides 

 Gewebe; die mikroskopische Untersuchung weist dann noch des Genaueren 

 nach, wie alle diese Vorgange auf das bunteste durch einander gehen, kurz wir 

 haben die Rachitis, wie sie im Buche steht." 



Wegner stated that his work confirms the theory that rickets is due to two 

 factors: (1) insufficient supply of inorganic salts (due to defective intake or 

 excessive excretion); and (2) a constitutional stimulus upon the osteogenic tissue. 



Lehmann ('78) and E. Voit ('77, '80) produced experimental rickets 

 in puppies. Voit stated: "Ich will es unternehmen, jeden jungen Hund 

 grosser Rasse in 3-4 Wochen durch Futterung mit kalkarmen Muskelfleisch 

 und reinem Fett ohne Abmagerung hochgradig rachitisch zu machen." Voit 

 ('80) based his diagnosis upon the characteristic softening and deformity of the 

 various bones, with broadening of the epiphyseal cartilage and marked 

 histological irregularities in the process of ossification. 



While it was early recognized that rickets involves an abnormal widening of 

 the epiphyseal cartilage and a disturbance of the normal process of enchondral 

 ossification (Rufz '34; Guerin '39; Beylard '52; Friedleben '60) the exact 

 histology of this disorder was somewhat neglected until comparatively recent 

 times. Meyer ('49) described the structure of rachitic bone as similar to that 

 decalcified by acids. A detailed and accurate histological description was given 

 by Broca ('52), whose excellent work has usually been overlooked by later inves- 

 tigators. He recognized that the "spongoid tissue" described by Guerin in 

 human rickets is essentially an uncalcified osteoid layer, a transition between the 

 epiphyseal cartilage and the calcified diaphyseal bone, normally present in small 

 amount, but accumulating in large quantity when the ossification process is 

 interrupted in rickets. 



The existence of osteoid substance (uncalcified bone) in rickets was also 

 recognized by Friedleben ('60), Wegner ('72), Kassowitz ('82-'85) and others, 

 but its significance was not fully appreciated until later. Pommer ('85) empha- 

 sized the formation of excessive osteoid substance as a cardinal point in true 

 rickets. This distinguishes it from osteoporosis, which is due merely to exces- 

 sive absorption of already formed bone. Halisteresis, or decalcification of 

 formed bone, is less frequent, but may occur (as was noted by Broca), especially 

 in adults. The gross appearance and consistency of bone may be very similar 

 in rickets and osteoporosis, and the two conditions may be coincident. 

 Osteomalacia is now generally considered as a form of late rickets arising after 

 growth has ceased, and hence not involving the phenomena in the zone of 

 enchondral ossification (Pommer '85; Wild '01; Schmorl '05; Looser '05, '08, '09, 

 '20; Schmidt '09; Ribbert '09; Stoeltzner '09; v. Recklinghausen '10; Boehme 

 '19; Higier '22; Korenchevsky '22; Maxwell '23; et al.). This view was held 

 long ago by Beylard ('52) and others. 



It is impracticable to mention here the large number of papers (chiefly 

 German) dealing with the histology of rickets, which appeared in the pre-vitamin 

 epoch, chiefly between 1885 and 1910. Detailed reviews of this literature will 

 be found in the works of Rievel ('07), Schmorl ('09b), Lehnerdt ('10), and 

 v. Recklinghausen ('10). The chemical phases of rickets are reviewed by 



