1. The experimental evidence presented shows that in the presence of non-union of short fibular defects an associated conical bone atrophy, which in some cases was extreme, occurred in the fragment ends. The bone was removed both by lacunar absorption, produced by giant-cell osteoclasts, and by smooth absorption, produced by mononuclear cells. The atrophy is explained on the basis of disuse, caused by an interrupted bony continuity, which resulted in a lack of functional stimulus.

2. When atrophy and absorption of bone ends occurred it was bilateral in practically the same degree and rate despite the fact that on one side there was a circulatory change, produced either by lumbar sympathectomy or by vein ligation. Hence circulatory changes (arterial hyperaemia or venous congestion) per se had no essential effect on bone atrophy or on absorption.

3. Non-union occurred in seventeen of forty-four subperiosteal fibular defects (one and five-tenths millimeters), despite the presence in each case of an intact periosteal tube which bridged the defect. This failure of union is explained by non-apposition and excessive motion of the fragment ends, for in twenty-eight linear subperiosteal osteotomies in fibulae where the fragment ends were opposed only one case of non-union occurred.