146 INANITION AND MALNUTRITION 



Schabad ('10). The essential structural features which were established for 

 rickets may be summarized briefly as follows (Schmidt '21, p. 204) : 



"Die anatomische Grundlage dieser Veranderungen ist sehr kompliziert. 

 Sie besteht erstens im Auftreten osteoider Substanz in einer das normale Mass 

 in Dicken- und Flachenausdehnung weit uberschreitender Menge, und oft in 

 einer mit starker Hyperamie verbundenen, iibermassigen knochenbildenden 

 Tatigkeit des Periostes und Endostes, welche zu Verdickung und Verdichtung 

 der Knochen fdhrt; zweitens in einer Storung der enchondralen Ossifikation, 

 namlich in iibermiissiger Proliferation, mangelnder Verkalkung und unegelmas- 

 siger Vaskularisierung und Ossifikation des Knorpels." 



Associated with the endosteal proliferation, especially in the long bones, 

 the marrow may be extensively replaced by a fibrous connective tissue. Pri- 

 mary lesions in the marrow have been described by Marfan and Baudouin 

 ('09), Marfan, Baudouin and Feuille ('09), confirmed by Hutinel and Tixier 

 ('09). There is apparently an early stage of proliferation in the various types of 

 marrow cells, followed later by their regression and replacement by fibrous 

 marrow. Networks of osteoid trabeculae may be formed in this fibrous marrow, 

 or may arise by decalcification of pre-existing bone (halisteresis). The decalci- 

 fied, osteoid structures may later be resorbed through the activity of the osteo- 

 clasts (Morpurgo '09), giving rise to a variable degree of osteoporosis. 



In the region of enchondral ossification, the proliferative zone of the epiphy- 

 seal cartilage becomes abnormally wide. According to Pommer ('85), Schmorl 

 ('06) and Heubner ('06), this is due not to increased proliferation of the cartilage, 

 but to lack of its removal as occurs in the normally succeeding stages in the 

 ossification process. Provisional calcification fails to occur in the adjacent zone. 

 Schmorl ('09) considers this defective calcification of the cartilage primarily 

 responsible for the further irregularities in the process of ossification. The 

 vascularization of the cartilage is excessive, with vessels coming not only from 

 the marrow, but also (largely) from the adjacent perichondrium or periosteum. 

 Kassowitz ('78, '82-'85, '12) has long maintained that this hyperemia is inflam- 

 matory in character and of primary importance in rachitis. Owing to the irregu- 

 lar invasion of the cartilage, the normally even plane of ossification is replaced 

 by a wide irregular "spongoid zone" or "metaphysis," composed of cartilagi- 

 nous masses of variable size, intermingled with osteoid substance (uncalcified 

 bone) and vascular marrow. This occasions the widening of the zone between 

 the epiphysis and diaphysis, as seen by the Roentgen-rays or in gross 

 preparations. 



According to Strelzoff ('73), Kassowitz ('82-'85), Schmidt ('09), and 

 Wohlauer ('n), the osteoid substance (at least in part) is formed by direct meta- 

 plasia of the persistent cartilage. Although this metaplasia theory is doubted 

 by Schmorl ('06, '09), it has recently been supported by McCollum and his 

 co-workers. Ribbert ('13) described necrosis of the cartilage cells, which he 

 considered evidence of a toxic agent in rickets. Simultaneous with the forma- 

 tion of the osteoid metaphysis, osteoid substance is also deposited under the 

 periosteum of the bone. The osteoblasts become surrounded by matrix, as 

 normally, but the latter fails to become calcified. 



