Abstract
Diphosphonates are of pharmacological interest because they act on bone (1). In animals they decrease the performance of osteoclasts and of osteoblasts and can hinder the mineralization of osteoid (2,3,4). The first two properties have been used to reduce bone turnover in patients with Paget’s disease by treatment with Ethane-l-hydroxy-1,1-diphosphonate (EHDP) (5). But, whilst the desired decrement of activity of the disease was often achieved, the hindrance of mineralization has caused excesse of unmineralized osteoid in the diseased bones (6). This is probably why patients treated with EHDP have had an increased incidence of pathological fractures (7,8,9). Is undermineralization a necessary price to pay for reduction of bone formation and resorption in Paget’s disease by diphosphonates?
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References
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Lemkes, H.H.P.J., Reitsma, P.H., Frijlink, W., Verlinden-Ooms, H., Bijvoet, O.L.M. (1978). A New Diphosphonate: Dissociation Between Effects on Cells and Mineral in Rats and a Preliminary Trial in Paget’s Disease. In: Massry, S.G., Ritz, E., Rapado, A. (eds) Homeostasis of Phosphate and Other Minerals. Advances in Experimental Medicine and Biology, vol 103. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7758-0_47
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DOI: https://doi.org/10.1007/978-1-4684-7758-0_47
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