Lumbar vertebral cancellous bone is capable of responding to PGE(2) treatment by stimulating both modeling and remodeling-dependent bone gain in agedmale rats
H. Zhou et al., Lumbar vertebral cancellous bone is capable of responding to PGE(2) treatment by stimulating both modeling and remodeling-dependent bone gain in agedmale rats, CALCIF TIS, 68(3), 2001, pp. 179-184
Previously we found that PGE(2) 3 mg/kg in 20-month-old male rats induced m
assive bone formation mainly by modeling dependent bone gain in cortical bo
ne. It is not known whether cancellous bone will respond similarly; thus, w
e evaluated the effect of PGE(2) on cancellous bone of the same aged rats.
Thirty-four 20-month-old Wistar male rats were given PGE(2) (3 mg/kg/day) o
r vehicle subcutanously for 10 and 30 days. Double fluorescent labels were
injected 9 and 2 days prior to the sacrifice. Histomorphometry was performe
d on 1% toluidine blue stained and unstained sagittal sections of lumbar ve
rtebral bodies. The results demonstrated that 10-day PGE(2) treatment incre
ased osteoprogenitor cells, osteoblasts (x2-fold), osteoid (x4.5-fold), wov
en bone formation (0.04%), and 40% more trabecular area; it stimulated mode
ling (x2-fold) and remodeling-dependent (x1.5-fold) bone formation with inc
rease of mineralization lag time (MLT, x 7.5-fold). Thirty-day treatment su
stained increases in osteoblast numbers, modeling, and remodeling-dependent
bone formation and further stimulated woven bone formation (6.6%), turnove
r (x3-fold), and trabecular area and number (x2-fold). Osteoprogenitor cell
s were undetectable along with 70% less osteoid area compared with 10-day t
reatment but still was 1.5-fold higher than aging controls. MLT returned to
aging control level. It was concluded that the aged cancellous bone of 20-
month-old male Wistar rat retains a capability of responding to the anaboli
c effect of PGE(2). Osteoblastogenesis and enhanced modeling and remodeling
-dependent woven or lamellar formation contribute to this anabolic action.
Bone formation differed in that the endocortical surface of cortical bone w
as stimulated mainly by modeling whereas both modeling and remodeling-depen
dent bone gain were equally stimulated at the trabecular surface of the lum
bar vertebral body.