[Effect of human PTH on steroid-induced osteopenia: a histomorphometric study of decalcified and undecalcified trabecular bone sections in rat].
Serum and urine chemical analyses were combined with a bone histomorphometrical study of rat metaphyses to evaluate the osteogenetic effect of intermittent administration of human parathyroid hormone (h-PTH) on steroid-induced osteopenia. Seven-month-old female Wistar rats were divided into the following 4 groups: (1) a control group: age-matched and untreated; (2) a baseline control group (BL group): given 2.5 mg/kg prednisolone subcutaneously 6 times/week for 8 weeks, at the end of which the animals were sacrificed; (3) a PTH group: in the 9th week of continuous steroid administration, 6.0 micrograms/kg h-PTH was added to the regimen; and the animals were sacrificed in the 12th week; (4) a vehicle group, as a control for the h-PTH group: only the vehicle was administered instead of PTH. At the necropsy at the end of the experiment, both tibias were collected. The undecalcified sections were stained by Villanueva bone stain and labelled with tetracycline, and the decalcified sections were stained by TRAP, and examined histomorphometrically. Serum Ca and P were not changed by any treatment. Serum 1,25 (OH)2D3 values were significantly increased in rats treated with h-PTH. There was no significant change in urinary Ca, P, or hydroxyproline excretion in any group. Histomorphometrically, the parameters related to bone formation--osteoid surface, mineralized surface and bone formation rate--were all reduced in the BL group and in the vehicle group. The bone volume was significantly lower in these group than in controls. The PTH group, on the other hand, showed increases in the osteoid surface, mineral apposition rate, and bone formation rate and the bone volume was significantly higher than in controls. The PTH group showed no increases in the osteoclast number or in the osteoclast surface. These results suggested that intermittent administration of h-PTH activated bone formation only, and increased bone volume.
Unoki
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E
Department of Orthopedic Surgery, Akita University School of Medicine, Japan.
D000818:Animals; D015519:Bone Density / Q000187:drug effects; D001851:Bone Diseases, Metabolic / Q000139:chemically induced* / Q000473:pathology* / Q000503:physiopathology; D001842:Bone and Bones / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D010012:Osteogenesis / Q000187:drug effects; D010281:Parathyroid Hormone / Q000008:administration & dosage / Q000494:pharmacology*; D011239:Prednisolone / Q000009:adverse effects*; D051381:Rats; D017208:Rats, Wistar
D010281:Parathyroid Hormone; D011239:Prednisolone