RANK/RANKL/OPG role in distraction osteogenesis

Distraction osteogenesis is a fundamental pillar for craniomaxillofacial reconstruction processes. Nonetheless, although the clinical, biomechanical, and histologic changes associated with distraction osteogenesis have been widely described, this is not the case with the molecular mechanisms that re...

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Published in:Oral surgery, oral medicine, oral pathology, oral radiology and endodontics oral medicine, oral pathology, oral radiology and endodontics, 2010-05, Vol.109 (5), p.679-686
Main Authors: Pérez-Sayáns, Mario, DDS, Somoza-Martín, José Manuel, DDS, PhD, Barros-Angueira, Francisco, PhD, Rey, José Manuel Gándara, MD, DDS, PhD, García-García, Abel, MD, PhD
Format: Article
Language:English
Subjects:
Biological and medical sciences
Bone Regeneration - physiology
Bone Remodeling - physiology
Bone Resorption - prevention & control
Cell physiology
Dentistry
Fundamental and applied biological sciences. Psychology
Humans
Medical sciences
Mineralization, calcification
Molecular and cellular biology
Osteoblasts - physiology
Osteoclasts - physiology
Osteogenesis, Distraction
Osteoprotegerin - physiology
Otorhinolaryngology. Stomatology
RANK Ligand - physiology
Receptor Activator of Nuclear Factor-kappa B - physiology
Skeleton and joints
Stromal Cells - physiology
Surgery
Vertebrates: osteoarticular system, musculoskeletal system
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Summary:Distraction osteogenesis is a fundamental pillar for craniomaxillofacial reconstruction processes. Nonetheless, although the clinical, biomechanical, and histologic changes associated with distraction osteogenesis have been widely described, this is not the case with the molecular mechanisms that regulate bone synthesis in the interfragmentary gap resulting from the gradual separation of bone segments. Recent studies have attributed a decisive role to the RANK/RANKL/OPG system in regulating bone metabolism and osteoclastogenesis. Receptor activator of nuclear factor kappa β (RANK), belonging to the tumor necrosis factor superfamily, is present in the osteoclasts. It promotes osteoclastogenesis when it binds to RANK ligand (RANKL), which is produced by the osteoblasts and other stromal cells. Osteoprotegerin (OPG) acts as a decoy receptor by binding to RANKL and preventing RANK signaling. Osteoclast activation is thus blocked and apoptosis induced. The aim of this review is to analyze the influence of the RANK/RANKL/OPG system on the bone healing and remodeling processes that occur in distraction osteogenesis, with a view to possibly developing molecular mechanisms that stimulate bone regeneration and inhibit resorption, thereby improving the clinical outcome for distraction osteogenesis.
ISSN:1079-2104
1528-395X
DOI:10.1016/j.tripleo.2009.10.042