428 RETROGRESSIVE CHANGES 



take either acid or basic stains strongly, are usually called "colloid." 

 We may properly consider that pathological hyalin can be divided 

 into two chief classes according to its origin: (1) connective-tissue 

 hyahn; (2) epithelial hyahn. 



Connective=tissue hyalin is characterized, like amyloid, by be- 

 ing deposited in or among the fibrillar substance of connective tissues, 

 and not within the cells themselves, but there are undoubtedly several 

 different sorts of chemical substances responsible for various forms of 

 connective-tissue hyalin. One form is closely associated with amyloid, 

 being found in organs showing amyloid degeneration, or in other tis- 

 sues in the same body. In experimentally produced amyloidosis in 

 animals it has been shown that such a hyahne substance may appear 

 before the amyloid, which eventually replaces it; hence, it has been 

 suggested that hyalin is a precursor of amyloid. ^^ Such hyalin differs 

 from true amyloid only in its failure to give the characteristic stain- 

 ing reaction of amyloid; in all other respects, e. g., cause, location, 

 termination, it is the same. As it has been shown (see preceding sec- 

 tion) that the staining properties of amyloid are very inconstant, it 

 is probable that the above-described variety of hyahn is merely an in- 

 completely developed, or occasionally a retrogressively altered amy- 

 loid. However, it is probably not necessary, as some authors have 

 thought, that amyloid should always pass through this hyaline stage 

 in its formation. 



Quite different, without doubt, is the form of hyalin observed in 

 scar tissue. This variety develops almost constantly in any scar-tissue 

 after the blood-supply has been reduced to a minimum through con- 

 traction, and is seen characteristically in the corpora fibrosa of the 

 ovary, fibroid glomerules in chronic nephritis, thickened pleural, peri- 

 cardial, and episplenitis scars, etc. Such hyahne substance occurs 

 independent of the usual causes of amyloid, affects only abnormal 

 fibrous tissue, never changes into amyloid, and is prone to undergo 

 calcification — it surely has no close chemical relation to the form of 

 hyalin that does become amyloid. Presumably, it is similar in na- 

 ture to the collagen of normal fibrous tissue intercellular substance, 

 which has undergone physical rather than chemical changes into a 

 homogeneous hyaline substance. For its physiological prototype it 

 has the thick "collagenous" fibers of the subcutaneous connective tis- 

 sue. 



Probably of quite different origin is the hyalin that develops from 

 elastic tissue, as seen best in the thick-walled, partly obliterated 

 arteries of the senile spleen; and less characteristically in the early 

 stages of arteriosclerosis, since here the preceding form of connective- 

 tissue hyalin may also occur. Although arterial elastic tissue is 

 related chemically to amyloid, these hj^alinc vessels do not develop the 

 usual amyloid reaction, but retain more or less of the specific, clastic 



" SeeLubarsch, Cent. f. Pathol., 1910 (21), 97. 



