AbbreviationsCatKcathepsin KCTx‐Icarboxy‐terminal cross‐linking telopeptide of type 1 collagenE64(1S,2S)‐2‐(((S)‐1‐((4‐guanidinobutyl)amino)‐4‐methyl‐1‐oxopentan‐2‐yl)carbamoyl)cyclopropanecarboxylic acidGAGsglycosaminoglycansM‐CSFmacrophage colony‐stimulating factorOVXovariectomizedRANKLreceptor activator of NF‐κB ligandSEMscanning electron microscopyTRAcPtartrate‐resistant acid phosphataseZ‐FR‐MCAcarbobenzoxy‐phenylalanyl‐arginyl‐4‐methyl‐coumaryl‐7‐amideIntroductionCurrently, several mechanistically different approaches to treat osteoporosis are clinically utilized. Most of them are antiresorptive and include hormone replace therapy, selective oestrogen receptor modulators (SERMs), denosumab and bisphosphonates (Chen and Sambrook, ). Only parathyroid hormone‐related peptides are effective as anabolic compounds (Whitfield, ). The common feature of most antiresorptives is the suppression of osteoclast numbers. This can be achieved by replacing oestrogen in hormone‐deficient postmenopausal women where oestrogen plays a major role in osteoclast differentiation or mimicking an oestrogen effect with SERMs. Other antiresorptives directly reduce the number of osteoclasts by either interfering with osteoclastogenesis (denosumab) via neutralizing the receptor activator of NF‐κB ligand (RANKL) or by killing osteoclasts (bisphosphonates) via apoptosis (Baron et al., ). All these methods have various side effects. A common problem is that they unbalance the cooperation between bone‐forming osteoblasts and bone‐degrading osteoclasts, which ultimately leads to poor bone quality.Major efforts have been undertaken to circumvent the disruption of the crosstalk between bone cells. One promising approach is the selective inhibition of the bone‐resorbing enzyme without interfering with the viability of osteoclasts. The perfect target
British Journal of Pharmacology – Wiley
Published: Jan 1, 2018
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