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Dental implantation has been the primary method for the treatment of tooth loss, but longer than 3 months healing times are generally required. Because immediate load implants are suitable only for certain categories of implant patients, it has value to develop a novel method to facilitate the implant-bone osseointegration process. Cylindrical titanium implants were implanted in the tooth sockets of beagles, and microelectrode stimulation of the sympathetic nerves in the infraorbital nerve was performed after implantation for 1 week. The authors found that one-sided nerve stimulation was shown to evoke consistent electric potential changes in both sides of the infraorbital nerves. Moreover, after 4 weeks of implantation, more new bone was clearly observed around the implants in the beagles that received electrical stimulation treatment than was observed in the control animals. Furthermore, a higher mineralization density was measured in the new peri-implant bone tissues of the stimulated beagles when compared to controls. These results demonstrate that the simple and safe physical method of microelectrode stimulation to sympathetic nerves can promote the formation of new bone and the osseointegration of implants. This technique is worth promoting and has the potential to reduce the healing time of dental implantation in future clinical cases.

The roles of nerve and neuropeptides in the process of bone formation and remolding have been studied previously. However, the effects of nervous system and neuropeptide on periodontal alveolar bone formation remained unknown. The aim of this study was to assess the effect of innervation on regeneration of alveolar bone and expression levels of calcitonin gene related peptide (CGRP) in periodontal tissues of rats, so as to have a better understanding of the effect of nerve and its related neuropeptide on periodontal tissue regeneration. Rats received transection of the left inferior alveolar nerve and a surgery to produce bilateral periodontal defect, then the alveolar tissue was obtained from animals of each group at week 1, 2, 4, 6 and 8 weeks after operation, respectively. Hematoxylin and eosin staining, and Masson staining were performed to evaluate the ability to restore and repair periodontal tissues at 4, 6 and 8 after surgery. Then new bone formation area and mineralized area were quantified using imagepro-plus6.0 software after pictures were taken under the microscope and SPSS17.0 was used for statistical analysis. Immunohistochemical staining was applied to investigate the expression of CGRP at 1, 2, 4, 6 and 8 weeks. Rats received transection of the left inferior alveolar nerve surgery and were then sacrificed at day 1, 3, 7, 14, 21, 28 after the operation. The change of CGRP expression in periodontal tissue was detected using immunohistochemical methods. The results showed that the volume of new bone formation was not significantly difference between the experimental and control groups, but the mineralized new bone area between the two groups was statistically significant. The level of CGRP expression was lower than normal at week 1, and then it began to rise in the next stage. The plateau, at higher than normal level, was reached at 6 weeks post-surgery. Results of transection of the left inferior alveolar nerve demonstrated the expression of CGRP was decreased in early stage; it reached the lowest level at day 7. Then the expression level began to increase until it returned to normal level at day 28. The results of this study suggest that nerve and its related neuropeptide CGRP are the important factors that can affect the quality of regenerated alveolar bone by reducing bone density during the mineralization process.

Background Reports of post herpetic maxillofacial complications have been very rarely documented in the literature that includes periapical lesions, calcified and devitalized pulps, resorption of roots, osteonecrosis, and spontaneous exfoliation of teeth. The atypical feature of the case of concern to the dental surgeon is the rare complication of spontaneous tooth exfoliation following herpes zoster. Case report This case reports a male patient of age 47 years who reported to the Department of Periodontology with the chief complaint of mobility in the left upper central incisor. Patient history revealed herpes zoster infection that began 11 days earlier along with underlying diabetes mellitus condition. We hereby report a known diabetic patient with history of herpes zoster infection who presented with rare complication of spontaneous tooth exfoliation involving the maxillary division of the trigeminal nerve. Discussion Limited number of cases has been reported in the literature regarding spontaneous teeth exfoliation secondary to herpes zoster. The exact pathogenesis regarding the spontaneous exfoliation of teeth in herpes zoster patient is still controversial. Thus, an oral health care provider should be aware of this rare complication while managing a case of tooth mobility with the previous history of herpes zoster of trigeminal nerve.

Background: Mental foramen (MF) is an anatomical structure of particular importance in local anesthesia and surgical procedures in terms of achieving effective mandibular nerve blocks and avoiding injuries to the neurovascular bundles. Aim: To determine the morphometry and morphology of MF in south Andhra population of India, hitherto unreported. Materials and Methods: Ninety dry dentulous mandibles of both sexes were examined for position, size, shape and number of MF. Results: Various parameters investigated are, the horizontal distance between (1) symphysis menti and MF was 27.2 mm on right and 27.7 mm on the left, (2) MF and posterior border of ramus was 70.7 mm on both sides, vertical distance between (3) MF and inferior border of mandible was16.5 mm on right and 14.3 mm on left, (4) alveolar crest and MF was 13.7 mm on right and 16.4 on left, (5) distance between the MF and below the apex of premolar socket was +2.8 mm on right and +3.5 mm on left and above the socket was -2.8 mm on right and -2.7 mm on left. Occurrence of MF below the second premolar tooth was found to be highest (73.2%). Average size of MF was larger on left and its way of exit was in postero-superior direction. Shape of MF was round in 79% and oval in 21% and double MF was found in 8.9% of mandibles. Conclusions: In the present study, most common position of MF was found below the apex of second premolar in 73.2% and between the second premolar and first molar in 19% of mandibles. The other morphometrical findings of this study may be implicated by dental practitioners and maxillofacial surgeons

Dexamethasone causes extensive physiologic reactions including the reduction of inflammation and pain. Here, we asked whether it also affected dental or periodontal cells or dental innervation by altering voltage-gated sodium channel Na(v)1.6 immunoreactivity (IR) or neural synaptophysin. Daily dexamethasone (0.2 mg/kg) given for 1 week to rats caused 12-fold increased intensity of Na(v)1.6-IR in dendritic pulpal cells of normal molars and incisors compared with vehicle treatment. These cells also co-localized monocyte (ED-1) or dendritic cell (CD11b/Ox42) markers, and their location in molars expanded during dexamethasone treatment to include deeper pulp. Furthermore, dexamethasone caused a 10-fold decrease in the number of Na(v)1.6-immunoreactive multinucleate osteoclasts along the alveolar bone of molar root sockets. No changes occurred for neural Na(v)1.6 at axonal nodes of Ranvier, even though IR for calcitonin gene-related peptide was greatly decreased, as expected, and neural synaptophysin-IR was decreased 59% by dexamethasone. At 4 days after tooth injury, pulpal vasodilation and increased Na(v)1.6-immunoreactive pulp cells were similar for all groups. Thus, dexamethasone changes dental pulp cell and alveolar osteoclast Na(v)1.6-IR in normal teeth, but different mechanisms occur after tooth injury when tissue reactions were similar for dexamethasone- and vehicle-treated rats. Steroid-induced alterations of dental pain and inflammation coincide with altered exocytic capability in dental nerve fibers as shown by synaptophysin-IR and with altered pulp cell Na(v)1.6-IR and osteoclast number, but not with any changes in Na(v)1.6-IR for nodes of Ranvier in myelinated dental axons.

Dexamethasone causes extensive physiologic reactions including the reduction of inflammation and pain. Here, we asked whether it also affected dental or periodontal cells or dental innervation by altering voltage-gated sodium channel Nav1.6 immunoreactivity (IR) or neural synaptophysin. Daily dexamethasone (0.2 mg/kg) given for 1 week to rats caused 12-fold increased intensity of Nav1.6-IR in dendritic pulpal cells of normal molars and incisors compared with vehicle treatment. These cells also co-localized monocyte (ED-1) or dendritic cell (CD11b/Ox42) markers, and their location in molars expanded during dexamethasone treatment to include deeper pulp. Furthermore, dexamethasone caused a 10-fold decrease in the number of Nav1.6-immunoreactive multinucleate osteoclasts along the alveolar bone of molar root sockets. No changes occurred for neural Nav1.6 at axonal nodes of Ranvier, even though IR for calcitonin gene-related peptide was greatly decreased, as expected, and neural synaptophysin-IR was decreased 59% by dexamethasone. At 4 days after tooth injury, pulpal vasodilation and increased Nav1.6-immunoreactive pulp cells were similar for all groups. Thus, dexamethasone changes dental pulp cell and alveolar osteoclast Nav1.6-IR in normal teeth, but different mechanisms occur after tooth injury when tissue reactions were similar for dexamethasone- and vehicle-treated rats. Steroid-induced alterations of dental pain and inflammation coincide with altered exocytic capability in dental nerve fibers as shown by synaptophysin-IR and with altered pulp cell Nav1.6-IR and osteoclast number, but not with any changes in Nav1.6-IR for nodes of Ranvier in myelinated dental axons.