Root canal adhesive filling in dogs' teeth with or without coronal restoration: a histopathological evaluation

The purpose of this study was to evaluate in vivo the response of the periradicular tissues after endodontic treatment and root filling with Epiphany/Resilon (Penntron Clinical Technologies, LLC, Wallingford, CT) or gutta percha and new Sealapex (SybronEndo, Glendora, CA) in dogs' teeth with or without coronal restoration. Teeth without coronal restorations were used to assess the influence of continuous exposure to the oral environment on the periradicular tissues. Sixty root canals with vital pulps in three dogs were instrumented and obturated in a single session and randomly assigned to one of four groups as follows. group 1: root canal filling with Epiphany/Resilon with coronal restoration, group 2: root canal filling with Sealapex sealer and gutta percha with restoration, group 3: root canal filling with Epiphany/Resilon without restoration, and group 4: root canal filling with Sealapex sealer and gutta percha without coronal restoration. After 90 days, the animals were euthanized, and the maxillas and mandibles were removed and submitted for histologic processing. Longitudinal sections were obtained and stained with hematoxylin and eosin, Mallory's trichrome, and Brown and Brenn stains and examined under light microscopy. There were significant differences found between the four groups (p < 0.05). The results showed that roots canals filled with Epiphany/Resilon, with coronal restoration, had significantly less periradicular inflammation than roots canals filled with gutta percha and Sealapex, with coronal restoration (p = 0.021). No significant difference was observed in the intensity of inflammation between roots canals filled with Epiphany/Resilon with no restoration and roots filled with gutta percha and Sealapex with restoration (p = 0.269). Roots canals filled with gutta percha and Sealapex sealer without coronal restoration showed the greatest degree of periradicular inflammation.     

Vestibular evoked myogenic potentials in Bell’s palsy

The aim of the present study was to evaluate vestibular nerve involvement in patients with Bell’s palsy with ocular and cervical vestibular evoked myogenic potentials (oVEMP and cVEMP). Ten patients who were diagnosed with Bell’s palsy and ten healthy controls were included. All patients underwent VEMP recordings within 6 days after their initial presentation. Patients with Bell’s palsy had greater oVEMP asymmetry ratio comparing to healthy controls (?38.4 ± 28.7 % vs ?1.3 ± 19.3 %, p = 0.005). As well N10 latencies of the oVEMP response were prolonged comparing to healthy controls (11.575 vs 9.72 ms). There was no difference in cVEMP asymmetry ratio or latencies between groups. We found no correlation between House–Brackmann grading scale and oVEMP asymmetry ratio (r = 0.003, p = 0.994). There are three possible explanations for increased oVEMP amplitudes on the affected side: (1) oVEMP response on the ipsilateral eye could be contaminated by facial nerve activity (blink reflex); (2) the amplitude of N10-P33 could be affected through the stapedial reflex; and (3) increased oVEMP amplitude could be the consequence of the vestibular nerve dysfunction itself, with prolonged latencies of the N10 oVEMP further supporting this explanation. The results of this study indicate possible involvement of the superior branch of the vestibular nerve in patients with Bell’s palsy.     

Nonredundant roles of antibody,cytokines, and perforin in the eradication of established Her-2/neu carcinomas

Since the mechanisms by which specific immunity destroys Her-2/neu carcinoma cells are highly undetermined, these were assessed in BALB/c mice vaccinated with plasmids encoding extracellular and transmembrane domains of the protein product (p185(neu)) of the rat Her-2/neu oncogene shot into the skin by gene gun. Vaccinated mice rejected a lethal challenge of TUBO carcinoma cells expressing p185(neu). Depletion of CD4 T cells during immunization abolished the protection, while depletion of CD8 cells during the effector phase halved it, and depletion of polymorphonuclear granulocytes abolished all protection. By contrast, Ig mu-chain gene KO mice, as well as Fcgamma receptor I/III, beta-2 microglobulin, CD1, monocyte chemoattractant protein 1 (MCP1), IFN-gamma, and perforin gene KO mice were protected. Only mice with both IFN-gamma and perforin gene KOs were not protected. Although immunization also cured all BALB/c mice bearing established TUBO carcinomas, it did not cure any of the perforin KO or perforin and IFN-gamma KO mice. Few mice were cured that had knockouts of the gene for Ig mu-chain, Fcgamma receptor I/III, IFN-gamma, or beta-2 microglobulin. Moreover, vaccination cured half of the CD1 and the majority of the MCP1 KO mice. The eradication of established p185(neu) carcinomas involves distinct mechanisms, each endowed with a different curative potential.