THE SKELETON AND ITS JOINTS 361 
Heredity has been held responsible in seven per cent, of 
the cases in human beings. 
That some inflammatory factor is partly responsible 
seems plausible when one considers the active growth of 
fibrocellular tissue in the endo- and periosteum. The 
more interesting theories go back to perversions of 
internal secretions, pituitary, parathyroid etc., (Macallum 
& Vogtlein). Higbee and Ellis (9) say in relation to the 
neurotrophic theory that if the neurotrophic mechanism 
governs metabolism and is influenced by the activity of the 
ductless glands, there is considerable likelihood that its 
disturbance may possibly be found to be the cause. 
Da Costa(lO) believed the disease to be a disorder of 
bone metabolism probably dependent on the absence or 
perversion of some internal secretion. There is much 
evidence on hand to indicate that disorders of the ductless 
glands do influence bone metabolism, and changes in these 
glands have been reported in cases of Paget 's disease, 
although the findings and lesions have been far from uni- 
form or distinctive or even confined to one gland. Eight 
cases were reported as possibly due to a hypothyroid con- 
dition; pituitary changes were found in three; adrenal 
changes in one; parathyroid reported missing in two; 
three had sclerotic thyroids. Many case reports make no 
mention whatever of the glands of internal secretion. 
Da Costa interprets the retention of calcium, phos- 
phorus and magnesium, with the sulphur loss found in 
these cases, as indicating a stimulated osseous or osseoid 
formation accompanying the resorption of a highly sul- 
phurized organic matrix. In the course of this calcifica- 
tion procedure we suppose a certain quota of the sulphur 
of the matrix is replaced by other elements, a process 
which must entail retention of calcium, phosphorus and 
magnesium and increased elimination of sulphur. He 
shows the close parallelism between the mineral metabo- 
(9) Jour. Med. Res., Vol. 24, 43, 1911. 
(10) Publ. Jefferson Med. College, Vol. 6, 1, 1915. 
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