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Mechanisms need not be molecular ‐ tissue‐level mechanisms for drug‐induced changes to bone mechanical properties
Author(s) -
Allen Matthew
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.12.4
Subject(s) - osteoclast , mechanism (biology) , bone remodeling , bone resorption , raloxifene , mechanism of action , drug action , drug , osteoporosis , pharmacology , chemistry , neuroscience , medicine , microbiology and biotechnology , bioinformatics , biology , pathology , receptor , biochemistry , cancer , philosophy , epistemology , estrogen receptor , breast cancer , in vitro
Several pharmacological agents exist that effectively reduce fracture risk in various at‐risk populations. The most common class of agents, anti‐remodeling drugs, are known to target osteoclast‐mediated bone resorption as their main cellular mechanism of action. But for some anti‐remodeling agents, there is more to the story. Using imaging, histological, and mechanical assays, a novel mechanism of action for one particular anti‐remodeling agent, Raloxifene, has been uncovered that appears to have nothing to do with cellular activity or regulation yet helps make sense of clinical findings.