Delaissé J M, Eeckhout Y, Vaes G
Life Sci. 1985 Dec 16;37(24):2291-6. doi: 10.1016/0024-3205(85)90020-7.
When added to cultures of parathyroid hormone (PTH)-stimulated bones, dichloromethylenebisphosphonate (C12MBP) and 3-amino-1-hydroxypropydilene-1,1-bisphosphonate (AHPrBP) inhibit completely and in a parallel manner the development of resorption lacunae, the loss of calcium by the explants and their PTH-induced excretion of lysosomal hydrolases (beta-glucuronidase and N-acetyl-beta-glucosaminidase). The loss of collagen (hydroxyproline) by the bones is usually less inhibited than their loss of calcium and their heparin-induced excretion of collagenase is unaffected. To interpret these data, it is proposed that these bisphosphonates act more on the activity of osteoclasts, suppressing simultaneously their excretion of lysosomal enzymes and their erosion of mineralized bone matrix, than on that of other cell types (osteoblasts ?) responsible for collagenase production and the removal of uncalcified collagen.
当二氯亚甲基双膦酸盐（C12MBP）和3 - 氨基 - 1 - 羟基丙基 - 1,1 - 双膦酸盐（AHPrBP）添加到甲状旁腺激素（PTH）刺激的骨培养物中时，它们能完全且平行地抑制吸收陷窝的形成、外植体的钙流失以及它们由PTH诱导的溶酶体水解酶（β - 葡萄糖醛酸酶和N - 乙酰 - β - 氨基葡萄糖苷酶）的排泄。骨中胶原蛋白（羟脯氨酸）的流失通常比钙流失受到的抑制要少，且肝素诱导的胶原酶排泄不受影响。为了解释这些数据，有人提出这些双膦酸盐对破骨细胞活性的作用更大，同时抑制其溶酶体酶的排泄和对矿化骨基质的侵蚀，而对负责胶原酶产生和去除未钙化胶原蛋白的其他细胞类型（成骨细胞？）的作用较小。
