This project clarifies which mechanisms which underlie the anabolic effect of parathyroid hormone (PTH) on bones, given in intermittent treatment. This is interesting because PTH normally has a katabolic effect in the body, and by increased values can lead to osteoporosis. This project is a literary study which is centred on finding hypotheses about the anabolic effect of PTH. Following hypotheses are described and discussed; 1) The proteinkinase A pathway is essential for PTH’s anabolic effect, 2) PTH up regulates c-fos expression in bone cells, 3) IGF-I is essential for PTH’s anabolic effect because it, amongs other things, stimulates antiapoptosis and proliferation, 4) bone lining cells converts to osteoblasts, 5) mesenchymal stem cells adhere to the bone surface and form colonies under the influence of PTH, 6) PTH has an antiapoptotic effect on osteoblasts and 7) when PTH interferes with remodelling the osteoblasts over compensate. The netto formative effect of PTH given in intermittent treatment emerge through a complex network of pathways, which all results in the so called “Anabolic window”, caused by PTH activation of osteoblasts which, because of the short half-life of PTH, either do not up regulate RANKL, or up regulates this to a lesser degree. Hereby, the osteoklast precursors do not get their signal for differentiation, or get it to a lesser degree, and therefore mature osteoclasts will not be formed, while osteoblasts overcompensate. This, and the fact, that there are more bone sites where formation takes place than with resoption, gives the netto anabolic effect.