ABSTRACT
or=2mm and < or=6mm. Lateral window approach was used, with grafting using Bio-ceraTM only(n=1) or mixed with autogenous bone from ramus and/or maxillary tuberosity(n=13). After 6 months of healing, implant sites were created with 3mm diameter trephine and biopsies taken for histomorphometric analysis. The parameters assessed were area fraction of new bone, graft material and connective tissue. Immediate and 6 months after grafting surgery, and 6 months after implantation, computed tomography (CT) was taken and the sinus graft was evaluated morphometric analysis. After implant installation at the grafted area, the clinical outcome was checked.RESULTS:Histomorphometry was done in ten patients. Bio-ceraTM particles were surrounded by newly formed bone. The graft particles and newly formed bone were surrounded by connective tissue including small capillaries in some fields. Imaging processing revealed 24.86+/-7.59% of new bone, 38.20+/-13.19% connective tissue, and 36.92+/-14.51% of remaining Bio-ceraTM particles. All grafted sites received an implant, and in all cases sufficient bone height was achieved to install implants. The increase in ridge height was about 15.9+/-1.8mm immediately after operation (from 13mm to 19mm). After 6 months operation, ridge height was reduced about 11.5+/-13.5%. After implant installation, average marginal bone loss after 6 months was 0.3+/-0.15mm.CONCLUSION: Bio-ceraTM showed new bone formation similar with Bio-Oss(R) histomorphometrically and appeared to be an effective bone substitute in maxillary sinus augmentation procedure with the residual bone height from 2 to 6mm.
Subject(s)
Humans , Biopsy , Bone Resorption , Bone Substitutes , Calcium , Calcium Phosphates , Capillaries , Connective Tissue , Dental Implants , Floors and Floorcoverings , Maxilla , Maxillary Sinus , Osteogenesis , Sinus Floor Augmentation , TransplantsABSTRACT
No abstract available.
Subject(s)
Humans , Gingival Crevicular Fluid , Matrix Metalloproteinase 1 , Matrix Metalloproteinases , PeriodontitisABSTRACT
Osteoprotegerin (OPG), a member of the tumor necrosis factor receptor superfamily, is known to inhibit osteoclastogenesis by acting as a soluble decoy receptor for the receptor activator of NF-kB ligand (RANKL). We report the presence of OPG on the membrane of osteoclasts and the possibility of the direct action of OPG on them. Highly pure osteoclast precursors were isolated from mouse long bones and induced to differentiate into mature osteoclasts by M-CSF and soluble RANKL (sRANKL). The presence of OPG on the membrane of these cells was confirmed by western blotting and immunostaining. Furthermore, sRANKL was found to be bound to the OPG on the osteoclast precursors. These results suggest that OPG might have a new role during the differentiation of osteoclasts beyond its role as a soluble decoy receptor. The mechanism of the existence of OPG on osteoclast precursors remains to be found.
Subject(s)
Animals , Mice , Bone and Bones/cytology , Carrier Proteins/immunology , Cell Differentiation/drug effects , Cell Membrane/metabolism , Cells, Cultured , Glycoproteins/drug effects , Macrophage Colony-Stimulating Factor/pharmacology , Membrane Glycoproteins/immunology , Mice, Inbred ICR , Osteoclasts/drug effects , Receptors, Cytoplasmic and Nuclear/drug effects , Stem Cells/drug effectsABSTRACT
Macrophage colony-stimulating factor (M-CSF) is known as one of the factors essential for osteoclast development. In the present study, we examined effects of M-CSF on the apoptotic pathway of osteoclast precursors and their underlying molecular mechanisms. Osteoclast precursors underwent apoptosis in the absence of M-CSF, even in the presence of receptor activator of NF-kB ligand (RANKL). Active caspase-3 and -9 were detected in the osteoclast precursors and treatments of precursors with their specific inhibitors (Z- DEVD-FMK and Z-LEHD-FMK) decreased the apoptosis. M-CSF decreased apoptosis in a dose-dependent manner with decreasing in active caspases-3 and -9 levels and up-regulating Bcl-XL. Those effects of M-CSF on inhibiting apoptosis of osteoclasts precursor by regulating anti-apoptotic signals was more effective when combined with RANKL. These results demonstrate that M-CSF acts as a survival factor for the osteoclast precursors. Furthermore, it is believed that the apoptosis of osteoclast precursors may be involved in the activation of caspase-9 and that M-CSF may promote their survival through Bcl-XL-induced inhibition of caspase-9 activation.
Subject(s)
Animals , Female , Mice , Apoptosis/drug effects , Carrier Proteins/pharmacology , Caspases/antagonists & inhibitors , Cell Survival/drug effects , Cells, Cultured , Cysteine Proteinase Inhibitors/pharmacology , Enzyme Activation/drug effects , Macrophage Colony-Stimulating Factor/pharmacology , Membrane Glycoproteins/pharmacology , Mice, Inbred ICR , Oligopeptides/pharmacology , Osteoclasts/cytology , Proto-Oncogene Proteins c-bcl-2/drug effects , Stem Cells/cytology , Up-RegulationABSTRACT
Orthodontic tooth movement requires remodelling of periodontal tissues, especially alveolar bone. Fluoride is known to be a potent inhibitor of osteoclastic bone resorption. The purpose of this study was to examine the effects of a consumption of fluoride on osteoclast numbers appearing on the pressure side of alveolar bones at experimental tooth movement. 40 male rats were exposed to 0, 10, 25 mg/kg/day of sodium fluoride(NaF) in their drinking water for up to 60 days. Orthodontic appliance were activated to mesially tip maxillary first molar with 50-70g. The rats were sacrificed at 1, 2, 4 days after initial activation. The number of osteoclast was counted in a 450 x 700 micrometer2 area interradicular septum on the pressure side of the maxillary first molar. The results were as follows, 1. There was significantly different osteoclast number between control group and 25 mg/kg/day group at all measured time. (p<0.05) 2. There was significantly different active bone-resorption area between control group and 25 mg/kg/day group except at 96 hours post activation. (p<0.05) 3. There was slight reduction of active bone-resorption area in control group from 48 hours to 96 hours but in both 10 mg/kg/day group and 25 mg/kg/day group a slight increase was observed from 48 hours to 96 hours.
Subject(s)
Animals , Humans , Male , Rats , Bone Resorption , Drinking Water , Fluorides , Molar , Orthodontic Appliances , Osteoclasts , Sodium , Tooth Movement TechniquesABSTRACT
This paper describes a new method to create an animal model for TMJ internal derangement in the New Zealand white rabbits and the light and electron microscopical changes of posterior attachment of them. Twenty six rabbits(2.5-3.0kg), four normal and twenty two experimental, were used. The right disc of experimental animal was displaced anteriorly without sectioning the posterior attachment and tied to the zygomatic arch with nylon not to be reduced to the original position. The left TMJ was sham-operated to be compared with its right experimental one. Normal animals were sacrificed one day and eight weeks after experiment. Experimental animals were sacrificed one day, ten days, three weeks, five weeks and eight weeks after surgery respectively. They were fixed intravenously with 2% glutaldehyde under general anesthesia and the samples of them were processed for light and electron microscopic examination. The purpose of this experiment is to make a suitable animal model of disc displacement without reduction for studying and understanding the cellular and morphologic events in posterior attachment of TMJ including early changes which were difficult to be observed in human TMJs. The results of this investigation suggest the following conclusions: 1. Authors induced anterior disc displacement surgically in rabbits with new method to examine histologic changes of posterior attachment. Tissue reactions of this model seem to be similar to those observed in human disc displacement. We think this animal model for anterior disc displacement may be used to explore and evaluate objectively the effects of many treatment modalities in disc displacements. 2. The animal disease model showed inflammation at early stage(one and ten days). At this stage there were mild-to-severe mononuclear inflammatory cell infiltration, numerous newly formed vessels, vessel dilatation and engormement and many fibroblasts. 3. At middle stage(three weeks), fibrosis occurred, where fibroblasts decreased in number, but their cytoplasm was profuse indicating high activity. Collagen fibers increased in number and the tissue looked more dense. 4. At late stage(five weeks and eight weeks) showed degenerative changes including perforation of posterior attachment, disintegration of collagen fiber bundles, degeneration of fibroblasts, metastatic ossification, and dystrophic calcification.