Levels of RANKL and OPG in gingival crevicular fluid during orthodontic tooth movement and effect of compression force on releases from periodontal ligament cells in vitro.
OBJECTIVE
To determine the levels of the receptor activator of NFkB ligand (RANKL) and osteoprotegerin (OPG) in the gingival crevicular fluid (GCF) during orthodontic tooth movement. A second objective was to investigate the effect of compression force on RANKL and OPG production from human periodontal ligament (hPDL) cells.


METHODS
Ten adolescent patients were included. GCF was collected at the distal cervical margins of the experimental and control teeth 0, 1, 24, and 168 h after the retracting force was applied. Thisin vitro study was performed to examine the secretion of RANKL and OPG from hPDL cells following a compression force (0, 0.5, 1.0, 2.0, or 3.0 g/cm(2) for 48 h). Enzyme-linked immunosorbent assay (ELISA) kits were used to determine RANKL and OPG levels in the GCF and the conditioned medium.


RESULTS
GCF levels of RANKL were significantly higher, and the levels of OPG significantly lower, in the experimental canines than in the control teeth at 24 h, but there were no such significant differences at 0, 1, or 168 h. In vitro study indicated that the compression force significantly increased the secretion of RANKL and decreased that of OPG in hPDL cells in a time- and force magnitude-dependent manner. The compression-stimulated secretion of RANKL increased approximately 16.7-fold and that of OPG decreased 2.9-fold, as compared with the control.


CONCLUSIONS
The results obtained suggest that the changes of amount of RANKL and OPG may be involved in bone resorption as a response to compression force.
Nishijima
Y
Y
Department of Orthodontics, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
Yamaguchi
M
M
Kojima
T
T
Aihara
N
N
Nakajima
R
R
Kasai
K
K
D000293:Adolescent; D016301:Alveolar Bone Loss / Q000378:metabolism; D000704:Analysis of Variance; D016723:Bone Remodeling / Q000502:physiology*; D002352:Carrier Proteins / Q000096:biosynthesis*; D002478:Cells, Cultured; D019245:Compressive Strength; D003799:Dental Stress Analysis; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005347:Fibroblasts / Q000378:metabolism; D005883:Gingival Crevicular Fluid / Q000737:chemistry*; D006023:Glycoproteins / Q000096:biosynthesis*; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis*; D053244:Osteoprotegerin; D010513:Periodontal Ligament / Q000166:cytology / Q000378:metabolism*; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear / Q000096:biosynthesis*; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis*; D013314:Stress, Mechanical; D014087:Tooth Movement Techniques
D002352:Carrier Proteins; D006023:Glycoproteins; D008562:Membrane Glycoproteins; D053244:Osteoprotegerin; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C505686:TNFRSF11A protein, human; C506030:TNFRSF11B protein, human; C505688:TNFSF11 protein, human