Bone remodelation pathogeny in postmenopausal osteoporosis

Abstract

Osteoporosis is a progressive bone metabolic disorder with socioeconomic serious impact. Osteocytes are the most abundant bone cells. They keep the matrix calcified, and the rapid resorption of the matrix follows their death. While they share most matrix-related activities with osteoblasts, osteocytes also express many different proteins, including factors with paracrine and endocrine effects that help regulate bone remodelling. This article presents the mechanisms involved in the occurrence of postmenopausal osteoporosis based on literature review. Beyond classical mechanisms, molecular mechanisms involving Circ_0134944, pancreatic and duodenal homeobox 1 (PDX1) and S1P by sphingosine kinase 1 and 2 (SPHK1) are implicate in osteogenesis homeostasis.