Etiology and Measurement of Peri-Implant Crestal Bone Loss (CBL).

The etiology of peri-implant crestal bone loss is today better understood and certain factors proposed in the past have turned out to not be of concern. Regardless, the incidence of crestal bone loss remains higher than necessary and this paper reviews current theory on the etiology with a special emphasis on traditional and innovative methods to assess the level of crestal bone around dental implants that will enable greater sensitivity and specificity and significantly reduce variability in bone loss measurement.

Ten-year survival of immediate-loading implants in fully edentulous mandibles in the Japanese population: a multilevel analysis.

PURPOSE: To evaluate the long-term clinical results of and risk factors for immediate-loading implant treatment of completely edentulous mandibles. METHODS: We retrospectively studied 220 implants in 52 patients who received immediate-loading implants in fully edentulous mandibles. Kaplan-Meier survival analyses, log-rank tests, and multilevel mixed-effects parametric survival analysis was used for statistical analyses. RESULTS: Thirteen of implants in seven patients failed, and the 10-year cumulative implant survival rate was 93.9 % and significantly (p=0.049) higher in women than in men. None of the predictor variables were significantly associated with implant survival, although sex tended to be associated with implant survival. CONCLUSIONS: Immediate-loading implant treatment for completely edentulous mandibles had acceptable clinical results in the long term. Although we could not identify significant risk factors, we established a multilevel mixed-effects parametric survival analysis with the immediate-loading implant survival data.

Histomorphometric and immunohistochemical analysis of human maxillary sinus-floor augmentation using porous ß-tricalcium phosphate for dental implant treatment.

OBJECTIVES: This study utilized the constitution and expression of Runx2/Cbfa1 to conduct 6-month-post-operation histomorphometrical and histochemical analysis of osteocalcin in bone regeneration following sinus-floor augmentation procedures using ß-tricalcium phosphate (ß-TCP) and autogenous cortical bone. MATERIAL AND METHODS: Thirteen sinuses of nine patients were treated with sinus-floor augmentation using 50% ß-TCP and 50% autogenous cancellous bone harvested from the ramus of the mandible. Biopsies of augmented sinuses were taken at 6 months for histomorphometric and immunohistochemical measurements. RESULTS: Runx2/Cbfa1- and osteocalcin-positive cells were found around TCP particles and on the bone surface. Approximately 60% of cells found around TCP particles stained positive for Runx2/Cbfa1. Fewer cells stained positive for osteocalcin. These positive cells decreased apically with increasing vertical distance from the maxillary bone surface. Histomorphometric analysis showed that the augmented site close to residual bone and periosteum contained approximately 42% bony tissue and 42% soft connective tissue, and the remaining 16% consisted of TCP particles. On the other hand, the augmented bone far from residual bone and periosteum contained 35% bony tissue and 50% soft connective tissue. CONCLUSIONS: Our data suggest that TCP particles attract osteoprogenitor cells that migrate into the interconnecting micropores of the bone-substitute material by 6 months. The augmented site close to residual bone contained a higher proportion of bony tissue and a lower proportion of soft connective tissue than did the augmented site far from residual bone.

Heparin inhibits BMP-2 osteogenic bioactivity by binding to both BMP-2 and BMP receptor.

Heparin demonstrates several kinds of biological activities by binding to various extracellular molecules and plays pivotal roles in bone metabolism. However, the role of heparin in the biological activity of bone morphogenetic protein (BMP) remains unclear. In the present study, we examined whether heparin has the effects on osteoblast differentiation induced by BMP-2 in vitro and also elucidated the precise mechanism by which heparin regulates bone metabolism induced by this molecule. Our results showed that heparin inhibited alkaline phosphatase (ALP) activity and mineralization in osteoblastic cells cultured with BMP-2. Heparin was found to suppress the mRNA expressions of osterix, Runx2, ALP and osteocalcin, as well as phosphorylation of Smad1/5/8 and p38 MAPK. Further, heparin bound to both BMP-2 and BMP receptor (BMPR). These results suggest that heparin suppresses BMP-2-BMPR binding, and inhibits BMP-2 osteogenic activity in vitro.

Heparin inhibits osteoclastic differentiation and function.

We investigated the effects of Glycosaminoglycans (GAGs) on mouse monocytic cell line in regard to their differentiation, proliferation, and function in vitro. RAW 264.7 cells were cultured with receptor activator of NF-kappaB ligand (RANKL) and various GAGs. Osteoclastic cells were visualized by staining for tartrate-resistant acid phosphatase (TRAP) and detected using a phenyl-phosphate substrate method. RAW 264.7 cells were also cultured with stimulants contained in BD BioCoat OSTEOLOGIC(TM) kit, and bone resorption activity was assessed by counting the numbers of resorption pits. We also examined the effect of heparin on cell growth using MTT assay, while the expression level of c-Src protein was determined by immunoblot analysis. Heparin suppressed TRAP-positive multinucleated cell formation and TRAP activity induced by RANKL, whereas the other GAGs showed no effects on osteoclast differentiation. Heparin also inhibited the formation of resorption pits, while the others did not. In the MTT assay, none of the tested GAGs had an influence on RAW 264.7 cell proliferation. However, heparin reduced the level of c-Src protein in RAW 264.7 cells stimulated with RANKL. To determine the affinity of heparin and RANKL, they were subjected by HiTrap heparin column chromatography and each fraction was collected. Western blotting analysis revealed the expression of RANKL in the fraction bound to heparin. The binding of RANKL and heparin was confirmed by quartz-crystal microbalance. These results indicate that the inhibitory effect of heparin toward osteoclastogenesis induced by RANKL is due to the binding of heparin to RANKL.

Dermatan sulfate inhibits osteoclast formation by binding to receptor activator of NF-kappa B ligand.

Dermatan sulfate (DS) is a major component of extracellular matrices in mammalian tissues. In the present study, DS demonstrated a high level of binding activity to receptor activator of NF-kappaB ligand (RANKL) and obstructed the binding of RANK to RANKL, determined using a quartz-crystal microbalance (QCM) technique. Further, when mouse bone marrow cells were cultured with RANKL and macrophage colony-stimulating factor, DS suppressed tartrate-resistant acid phosphatase-positive multinucleated cell formation in a dose-dependent manner. In addition, immunoblot analyses revealed that DS reduced the levels of phosphorylation of p38 mitogen-activated protein kinase and extracellular signal-regulated kinase protein in mouse osteoclast progenitor cells stimulated with RANKL. Together, these results indicate that DS regulates osteoclast formation through binding to RANKL and inhibition of signal transduction in osteoclast progenitor cells, suggesting that it has an important role in bone metabolism in pathological conditions.