Lumbar vertebral cancellous bone is capable of responding to PGE2 treatment by stimulating both modeling and remodeling-dependent bone gain in aged male rats.

Previously we found that PGE2 3 mg/kg in 20-month-old male rats induced massive bone formation mainly by modeling dependent bone gain in cortical bone. It is not known whether cancellous bone will respond similarly; thus, we evaluated the effect of PGE2 on cancellous bone of the same aged rats. Thirty-four 20-month-old Wistar male rats were given PGE2 (3 mg/kg/day) or vehicle subcutaneously for 10 and 30 days. Double fluorescent labels were injected 9 and 2 days prior to the sacrifice. Histomorphometry was performed on 1% toluidine blue stained and unstained sagittal sections of lumbar vertebral bodies. The results demonstrated that 10-day PGE2 treatment increased osteoprogenitor cells, osteoblasts (x 2-fold), osteoid (x 4.5-fold), woven bone formation (0.04%), and 40% more trabecular area; it stimulated modeling (x 2-fold) and remodeling-dependent (x 1.5-fold) bone formation with increase of mineralization lag time (MLT, x 7.5-fold). Thirty-day treatment sustained increases in osteoblast numbers, modeling and remodeling-dependent bone formation and further stimulated woven bone formation (6.6%), turnover (x 3-fold), and trabecular area and number (x 2-fold). Osteoprogenitor cells were undetectable along with 70% less osteoid area compared with 10-day treatment 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 anabolic effect of PGE2. 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 was stimulated mainly by modeling whereas both modeling and remodeling-dependent bone gain were equally stimulated at the trabecular surface of the lumbar vertebral body.