*Corresponding author:
Yang Gu, Assistant Professor and Oral Pathologist, Director of Oral Pathology Clinic, Department of Oral and Maxillofacial Sciences, Faculty of Dentistry, Dalhousie University, CanadaReceived: June 26, 2018; Published: July 03, 2018
DOI: 10.26717/BJSTR.2018.06.001332
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Aim: The paper reorganized new findings in the field of osteoblastogenesis and osteoclastogenesis for clinicians to identify systemic and local risks of oral and maxillofacial osteogenic conditions (OMOCs) that are not related to genetic diseases.
Method: The non-systemic review was undertaken by searching pertinent key wards in English literature. Case report and publications with weak levels of evidence were excluded.
Results: Coupling factors from endocrine and paracrine systems affect osteoblastogenesis and osteoclastogenesis in different pathways. Levels of hormones change with age or by medical conditions. Cytokine accumulations are triggered by the local mechanical force or ischemia. Osteoblasts take a leading role in the maturation of osteoclasts, while the activity of osteoclasts could be an initial event in a local osteogenic lesion. The entangling relation between osteoblasts and osteoclasts derives some patterns for OMOCs radiographically.
Discussion: A triple-hit frame composited by timings, coupling factors from endocrine and paracrine systems is an approachable method to explore local and systemic risks for OMOCs.
Keywords: Osteoblast; Osteoclast; Hormone; Cytokine; Radiolucency; Radiopacity
Abbreviations: OPG: Osteoprotegerin; RANKL: Nuclear Factor-kB Ligand; GI: Gastrointestinal System; S1P: Sphingosine 1-Phosphate; TNF: Tumor Necrosis Factor; IL: Interleukin; FasL: Fas Ligand; PDGF: Platelet-Derived Growth Factor; VEGF: Vascular Endothelial Growth Factor
Abstract| Introduction| Method| Results| Discussion| Acknowledgement| References|