METABOLISM IN DISEASES OF BONES AND JOINTS 765 



The disease appeared in almost epidemic form in the Saxon Erzege- 

 birge in 1909-1910; analysis of the hay eaten by the horses showed an 

 extremely low calcium content ( Schennert, Schattke, Lotsche) . The losses 

 of calcium through excessive lactation in cows is very great (Meigs, 

 Blatherwick and Gary, also Forbes, Beegle, Fritz, Morgan and Rhue(a) 

 (&)), and if upon this are superimposed other unfavorable conditions 

 unfertile, sandy soil, granitic soil, insufficiently fertilized soil, season 

 of drought, overstocked pastures, deficient food supply malnutrition of 

 bone may develop. The animals suffering from this condition readily 

 respond to improved nutrition, especially if bone meal or chalk be added 

 to the diet (Forbes, Beegle, Fritz, Morgan and Rhue(a)). 



What has been said about the cause or causes of calcium inadequacy 

 in non-puerperal osteomalacia applies to rickets, osteitis deformans and 

 other forms of disturbed bone metabolism. Many different factors may 

 contribute. A survey and analysis of all the conflicting evidences on 

 the subject, especially in the case of rickets, would be out of place here. 

 The important fact to bear in mind is the active and continuous nature 

 of bone metabolism. It is then easy to understand that different fac- 

 tors may contribute to the depletion of the calcium store in the 

 bones. 



The same kind of factors which produce osteomalacia in adults may 

 give rise to rickets in children. Pregnancy and arteriosclerosis do not 

 of course come into consideration in the case of rickets, but renal calculi 

 do, as already pointed out (Daires-Colley), and myositis ossificans pro- 

 gressiva, which in adults may give rise to osteomalacia, may be accom- 

 panied in childhood by rickets (Rabek). Eustace Smith has pointed out 

 that in rickets the process of ossification is not only retarded; it is also 

 perverted; calcium salts are deposited in abnormal situations (Smith). 

 The muscles especially seem to be a storing place for calcium in rickets. 

 Pritchard has described in some detail how rickets develops as the result 

 of a need for calcium more urgent than that of the calcifying bones. 



Dr. Charles F. Painter, the Boston orthopedic surgeon, has called 

 my attention to the occurrence of .a late variety of non-rachitic bow legs, 

 occurring in children about the time the epiphyses begin to harden; the 

 flux of calcium to the hardening epiphyses may be responsible for the 

 decalcification elsewhere. 



Osteitis deformans occurs late in life, and is undoubtedly a localized 

 form of osteomalacia. It is practically always accompanied by arterio- 

 sclerosis (Higbee and Ellis; Emerson). In such cases the areas of bone 

 rarefaction and intense arterial calcification can be seen side by side in 

 skiagrams. Here again we have a demand for calcium (on the part of 

 the arteries) followed by a loss of calcium by the bones. 



Careful examination of the bone in osteogenesis imperfecta has shown 

 that the process is of the same nature as that in osteomalacia; in this 



