Intracortical remodeling in the adult skeleton removes and replaces ar
eas of compact bone that have sustained microdamage. Although studies
have been performed in animal species in which there is an existing ba
seline of remodeling activity, laboratory rodents have been considered
to have limited suitability as models for cortical bone turnover proc
esses because of a lack of haversian remodeling activity, Supraphysiol
ogical cyclic axial loading of the ulna in vivo was used to induce ben
ding with consequent fatigue and microdamage, Right ulnae of adult Spr
ague-Dawley rats were fatigue-loaded to a prefailure stopping point of
30% decrease in ulnae whole bone stiffness, Ten days after the first
loading, Left ulnae mere fatigued in the same may. Ulnae mere harveste
d immediately to allow comparison of the immediate response of the lef
t ulna to the fatigue loads, and the biological response of the right
leg to the fatigue challenge. Histomorphometry and confocal microscopy
of basic fuchsin-stained bone sections were used to assess intracorti
cal remodeling activity, microdamage, and osteocyte integrity. Bone mi
crodamage (linear microcracks, as well as patches of diffuse basic fuc
hsin staining within the cortex) occurred in fatigue-loaded ulnar diap
hyses, Ten days after fatigue loading, intracortical resorption was ac
tivated in ulnar cortices, Intracortical resorption occurred in prefer
ential association with linear-type microcracks, with microcrack numbe
r density reduced almost 40% by 10 days after fatigue. Resorption spac
es were also consistently observed within areas of the cortex in which
no bone matrix damage could be detected. Confocal microscopy studies
showed alterations of osteocyte and canalicular integrity around these
resorption spaces. These studies reveal that: (1) rat bone undergoes
intracortical remodeling in response to high levels of cyclic strain,
which induce microdamage in the cortex; and (2) intracortical resorpti
on is associated both with bone microdamage and with regions of altere
d osteocyte integrity. From these studies, we conclude that rats can i
nitiate haversian remodeling in long bones in response to fatigue, and
that osteocyte death or damage may provide one of the stimuli for thi
s process, (Bone 23:275-281; 1998) (C) 1998 by Elsevier Science Inc, A
ll rights reserved.