Thickness of labial alveolar bone overlying healthy maxillary and mandibular anterior teeth.

AIM: This study aimed to measure the thickness of labial bone overlying maxillary and mandibular anterior teeth and the distance between cementoenamel junction and bone crest in a Persian population. MATERIALS & METHODS: Two calibrated examiners evaluated tomographic data of 152 maxillary and 200 mandibular anterior teeth. Labial bone width was assessed at levels 1.0 to 5.0 mm apical to bone crest. Moreover, the distance between cementoenamel junction and bone crest was measured for both maxillary and mandibular teeth and its potential effect on the amount of labial bone thickness was assessed. RESULTS: One hundred-twenty nine maxillary central incisors, 77 lateral incisors, 70 canines, 105 mandibular central incisors, 103 lateral incisors and 81 canines were included for measurements. In maxilla, width of bone averaged 1.08mm, 1.11mm, and 1.3mm for central incisors, lateral incisors, and canines, respectively. Corresponding numbers for mandibular central incisors, lateral incisors, and canines were 0.74mm, 0.66mm and 0.40mm. High variation of cementoenamel junction to bone crest distance (range 0.5 to 5.15 mm) was detected. The mean amount of labial bone width was not statistically different in patients with different distances between cementoenamel junction and bone crest; except for mandibular lateral incisors. CONCLUSION: The mean thickness of the labial alveolar bone overlying maxillary anterior teeth was found to be between 1 to 1.2 mm and between 0.5 to 0.8 mm for mandibular anterior teeth at the first 5 mm from bone crest in a Persian population.

Response of Dental Pulp Stem Cells to Synthetic, Allograft, and Xenograft Bone Scaffolds.

Different degrees of clinical success have been reported for synthetic, allograft, and xenograft bone substitutes in human trials. Although these substitutes have been clinically investigated, their in vitro effects on cell differentiation remain unclear. Proliferation, differentiation, and attachment of dental pulp stem cells (DPSCs) to ß-tricalcium phosphate (ß-TCP), freeze-dried bone allograft (FDBA), and deproteinized bovine bone mineral (DBBM) were compared in this study. MTT assay, measurement of total DNA, and reverse transcriptase polymerase chain reaction were performed. ß-TCP had the highest potential for DPSC attachment and proliferation, while FDBA induced osteoblastic differentiation of DPSCs. Further in vivo investigations are necessary to select a clinically appropriate scaffold.

Effects of nicotine in the presence and absence of vitamin E on morphology, viability and osteogenic gene expression in MG-63 osteoblast-like cells.

BACKGROUND: Evidence shows that oxidative stress induced by nicotine plays an important role in bone loss. Vitamin E with its antioxidative properties may be able to reverse the effects of nicotine on bone. This study aimed to assess the effects of nicotine in the presence and absence of vitamin E on morphology, viability and osteogenic gene expression in MG-63 (osteosarcoma) human osteoblast-like cells. METHODS: We treated the cells with 5 mM nicotine. The viability and morphology of cells were evaluated respectively using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium (MTT) and crystal violet assays. The effect of nicotine on osteogenic gene expression in MG-63 cells was assessed by real-time reverse-transcription polymerase chain reaction of osteoblast markers, namely, alkaline phosphatase, osteocalcin and bone sialoprotein. RESULTS: The results revealed that survival and proliferation of MG-63 cells were suppressed following exposure to nicotine, and cytoplasm vacuolization occurred in the cells. Nicotine significantly down-regulated the expression of osteogenic marker genes. Such adverse effects on morphology, viability and osteogenic gene expression of MG-63 cells were reversed by vitamin E therapy. CONCLUSIONS: In conclusion, vitamin E supplementation may play a role in proliferation and differentiation of osteoblasts, and vitamin E can be considered as an anabolic agent to treat nicotine-induced bone loss.