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Recent breakthroughs in identification of mutant proteins affecting bone tissue homeostasis in rare skeletal diseases have revealed novel pathways involved in skeletal development and maintenance. The characterization of new dominant, recessive and X\u2010linked forms of the rare brittle bone disease osteogenesis imperfecta (<jats:styled-content style=\"fixed-case\">OI<\/jats:styled-content>) and other<jats:styled-content style=\"fixed-case\">OI<\/jats:styled-content>\u2010related bone fragility disorders was a key player in this advance. The development of<jats:italic>in\u00a0vitro<\/jats:italic>models for these diseases along with the generation and characterization of murine and zebrafish models contributed to dissecting previously unknown pathways. Here, we describe the most recent advances in the understanding of processes involved in abnormal bone mineralization, collagen processing and osteoblast function, as illustrated by the characterization of new causative genes for<jats:styled-content style=\"fixed-case\">OI<\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">OI<\/jats:styled-content>\u2010related fragility syndromes. The coordinated role of the integral membrane protein<jats:styled-content style=\"fixed-case\">BRIL<\/jats:styled-content>and of\u00a0the secreted protein<jats:styled-content style=\"fixed-case\">PEDF<\/jats:styled-content>in modulating bone mineralization as well as the function and cross\u2010talk of the collagen\u2010specific chaperones<jats:styled-content style=\"fixed-case\">HSP<\/jats:styled-content>47 and<jats:styled-content style=\"fixed-case\">FKBP<\/jats:styled-content>65 in collagen processing and secretion are discussed. We address the significance of<jats:styled-content style=\"fixed-case\">WNT<\/jats:styled-content>ligand, the importance of maintaining endoplasmic reticulum membrane potential and of regulating intramembrane proteolysis in osteoblast homeostasis. Moreover, we also examine the relevance of the cytoskeletal protein plastin\u20103 and of the nucleotidyltransferase<jats:styled-content style=\"fixed-case\">FAM<\/jats:styled-content>46A. Thanks to these advances, new targets for the development of novel therapies for currently incurable rare bone diseases have been and, likely, will be identified, supporting the important role of basic science for translational approaches.<\/jats:p>","DOI":"10.1111\/febs.14963","type":"journal-article","created":{"date-parts":[[2019,6,20]],"date-time":"2019-06-20T20:03:04Z","timestamp":1561060984000},"page":"3033-3056","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":64,"title":["Bone biology: insights from osteogenesis imperfecta and related rare fragility syndromes"],"prefix":"10.1111","volume":"286","author":[{"given":"Roberta","family":"Besio","sequence":"first","affiliation":[{"name":"Biochemistry Unit Department of Molecular Medicine University of Pavia Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chi\u2010Wing","family":"Chow","sequence":"additional","affiliation":[{"name":"Bone and 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