Abstract:Low doses of PTH(1-34) stimulate bone formation in rats but the effect is reversed after PTH withdrawal. This study shows that this reversal is prevented when sequential PTH-APD treatment is employed. Seventy 3-month-old female wistar rats were ovariectomized, and fed with regular rodent chow and water ad libitum. Twelve weeks later they were divided into seven groups and treated as follows: GI: 3w PTH (5d/w, 20ttg/kg/d sc). G2: 3w saline (5d/w, sc). G3: lw ADP (5d/w, 250 #g/kg/d sc) -~ 3w PTH. G4: lw APD -> 3w saline. G5: 3w PTH --> 5d APD -~ 3w untreated. G6: 3w PTH -~ 5d saline --> 3w untreated. G7: 3w saline --> 5d saline -~ 3w untreated. Two tetracycline labels (2 weeks apart) were administered to each rat before killing. Static and dynamic bone histomorphometries were performed on trichrome stained and unstained sections of distal femoral metaphysis. Cancellous bone volume (Cn.BV/TV) results showed that, when compared with the osteopenie controls (G2, G7), PTH stimulated bone formation (G1) but the effect was reversed after drug withdrawal (G6) and that APD post-treatment prevented this reversal (G5). The results also showed that APD pre-treatment (G3) was as effective as APD post-treatment (GS) in building up cancellous bone, but APD alone (G4) was significantly less effective. Mineral apposition rates (MAR) showed that while APD suppressed bone formation (G4, G5), PTH was able to stimulate bone formation even after APD treatment (G3).