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Background: One of the rare but serious complications observed with deoxycholic acid administration is damage to the marginal mandibular nerve. In this study, we evaluated if deoxycholic acid directly induces histologic damage to fresh cadaveric marginal mandibular nerve., Methods: A segment of marginal mandibular nerve was harvested from 12 hemifaces of 6 fresh cadavers. The nerve specimen was exposed to either 0.9% sterile saline for 24 h, deoxycholic acid (10 mg/ml) for 20 min, or deoxycholic acid (10 mg/ml) for 24 h. The nerve specimens were then fixed in glutaraldehyde for a minimum of 24 h. Toluidine blue stained sections were evaluated for stain intensity using light microscopy and color deconvolution image analysis. Supraplatysmal fat was harvested as a positive control and exposed to the same treatments as the marginal mandibular nerve specimens, then evaluated using transmission electron microscopy., Results: Toluidine blue staining was less in the marginal mandibular nerve exposed to deoxycholic acid when compared to saline. The specimen exposed to deoxycholic acid for 24 h showed less toluidine blue staining than that of the nerve exposed to deoxycholic acid for 20 min. Transmission electron microscopy of submental fat exposed to deoxycholic acid revealed disruption of adipocyte cell membrane integrity and loss of cellular organelles when compared to specimens only exposed to saline., Conclusions: Deoxycholic acid (10 mg/ml) damages the marginal mandibular nerve myelin sheath in fresh human cadaver specimens. Direct deoxycholic acid neurotoxicity may cause marginal mandibular nerve injury clinically., No Level Assigned: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

(1) Misoprostol, a synthetic prostaglandin E1 analogue, is used to treat gastric and duodenal ulcers, and, in combination with mifepristone, for medical abortion. (2) The French and American summaries of product characteristics, based on data submitted to the relevant regulatory agencies, mention no teratogenicity in animals. However, some studies showed malformations in rats and rabbits. (3) Severe malformations have been reported in countries where misoprostol is frequently used for abortion without medical supervision despite its poor efficacy when used alone. The malformations included cranial nerve defects (especially pairs 6 and 7, characteristic of the Möbius syndrome) and various limb abnormalities. (4) Malformations, including one case of Möbius syndrome, have been reported in France after medically supervised use of misoprostol. (5) In practice, when a patient wishes to continue a pregnancy after a failed attempt at drug-induced abortion, she needs to be informed of the risk to her unborn child. Cranial nerve defects are rarely detectable by sonography, however thorough. In addition, misoprostol has a negative risk-benefit balance in the prevention or treatment of gastro-duodenal ulcers in young women.

Damage to the inferior alveolar nerve is a relatively infrequent complication in dental practice. When root canal treatment of a lower molar or premolar surpasses and/or overextends beyond the apical foramen and invades the periapical zone, the foreign material introduced within such a sensitive anatomical space may mechanically or even chemically affect the inferior alveolar nerve. We describe a case of endodontic treatment of a permanent right lower first molar in which the sealer cement overextended in large amounts and damaged the right inferior alveolar nerve. The condition reverted a few months after the surgical removal of the material. Evaluation of the removed material, using powder x-ray diffraction and scanning electron microscopy with coupled dispersive energy spectroscopy, showed it to consist of calcium tungstate (scheelite [CaWO4]) and zirconium oxide (baddeleyite [ZrO2]), which were chemical components of the sealer cement.

The present study describes a case of endodontic paste (Endomethasone) penetration within and along the mandibular canal from the periapical zone of a lower first premolar following endodontic treatment of the latter. The clinical manifestations comprised anesthesia of the right side of the lower lip and paresthesia of the gums in the fourth quadrant, appearing immediately after endodontic treatment. The lip anesthesia was seen to decrease, with persistence of the gingival paresthesia, after 7 months.

Although retinoic acid (RA), the active form of vitamin A, is required for normal embryonic growth and development, it is also a powerful teratogen. Infants born to mothers exposed to retinoids during pregnancy have a 25-fold increased risk for malformations, nearly exclusively of cranial neural crest-derived tissues. To characterize neural crest cell responses to RA, we exposed murine crest cultures to teratogenic levels of RA and subjected their RNA to microarray-based gene expression profile analysis using Affymetrix MG-U74Av2 GeneChips. RNAs were isolated from independent cultures treated with 10(-6) M RA for 6, 12, 24, or 48 h. Statistical analyses of gene expression profile data facilitated identification of the 205 top-ranked differentially regulated genes whose expression was reproducibly changed by RA over time. Cluster analyses of these genes across the independently treated sample series revealed distinctive kinetic patterns of altered gene expression. The largest group was transiently affected within the first 6 h of exposure, representing early responding genes. Group 2 showed sustained induction by RA over all times, whereas group 3 was characterized by the suppression of a time-dependent expression increase normally seen in untreated cells. Additional patterns demonstrated time-dependent increased or decreased expression among genes not normally regulated to a significant extent. Gene function analysis revealed that more than one-third of all RA-regulated genes were associated with developmental regulation, including both canonical and noncanonical Wnt signaling pathways. Multiple genes associated with cell adhesion and cell cycle regulation, recognized targets for the biological effects of RA, were also affected. Taken together, these results support the hypothesis that the teratogenic effects of RA derive from reprogramming gene expression of a host of genes, which play critical roles during embryonic development regulating pathways that determine subsequent differentiation of cranial neural crest cells.