Anabolic treatment

• Osteoporosis is caused by an imbalance in the remodelling cycle with subsequent bone loss due to either enhanced osteoclastic resorption, or to a decrease in osteoblastic activity. Over time this loss of bone results in thinning and disappearance of trabeculi and to enhanced cortical porosity. With the knowledge of the pathogenetic mechanisms underlying the development of osteoporosis it is evident that there are two main strategies to develop pharmacological treatment for this condition. Either the goal is to inhibit bone resorption with e.g. bisphosphonates or RANKL interference, or alternatively to stimulate osteoblastic bone formation with anabolic treatment and thereby create new bone. Today it is well documented that intermittent injections with PTH1-34, or with full length PTH, cause a direct stimulatory effect on the osteoblastic bone formation. The treatment length is currently between 18 and 24 months and it is not known whether there is an optimal duration, called anabolic window, for this sort of treatment. The antifracture efficacy is well proven in randomised phase III trials, and real life efficacy and safety are well documented in large post marketing observational studies. When compared to antiresorptive treatment with bisphosphonates there are data that at least PTH 1–34 might be superior in some instances such as in glucocorticoid induced osteoporosis. Future development with new anabolic agents focusing on the LRP5/Wnt signalling system is under development and might bring to the clinic even more potent drugs that eventually might enable us to treat to a bone density target, and thereby in theory cure osteoporosis.

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