CSF3 or granulocyte colony stimulating factor (GCSF) has clinically documented effects on bone homeostasis in health, pathology, and accompanying therapeutic applications by either directly or indirectly acting on mature osteoclasts or precursors. GCSF appears to stimulate osteoclasts (OC), impair osteoblasts (OB), elevated in tissue and serology of periodontitis, mobilise haematopoetic stem cells (HSC) and alter tumour burden in particular by disrupting the CXCR4:CXCL12 axis [8,9,11,12,13,14,15,16,18].
Our research group detected 11.8-fold up-regulation of GCSF receptor in human osteoclasts derived from adherent Peripheral Blood Mononuclear Cells (PBMC) [1] and indicated increased expression and involvement of C-C chemokine receptors and ligands (CCR2/CCL2 & CCL5) within OC and monocyte derived multinuclear cell fusion [1,2,3,4,5]. The involvement of GCSF in modulating CCL2 in neutrophil differentiation, neuropathic pain pathways, and Craniocervical Instability (CCI) supports further investigation of GCSF in musculoskeletal biology, pathology, and the potential as a broader therapeutic target [9,10,17].
Initial results of GCSF-treatment in models of osteoclast differentiation and mature OC function will be presented, including gene expression, dentine resorption, and cell morphology profiles of osteoclast models derived from human peripheral blood and mouse bone marrow monocytes (wild type, CCL2 -/-; CCR2 -/-) with either "continuous", "early" (0h to pre-osteoclast or fused polykaryons), and "late" (polykaryon to activated/mature) treatment [1,2,3,4,5,6,7].