Development of a peri-implantitis model in the rat.

OBJECTIVES: The aim of the present study was to establish a rodent peri-implantitis model induced by a mixed bacterial infection characterized by bone loss and semi-quantitative graduation of peri-implant inflammation in histological sections. MATERIALS AND METHODS: Two titanium implants were implanted in Sprague-Dawley rats, bilaterally in each maxilla. After 3 weeks healing, the rats were randomized into three groups according to different treatments over the next 3 months: Antibiotic-Group with oral lavage of antibiotics; Bacteria-Group with oral lavage of Streptococcus oralis and Aggregatibacter actinomycetemcomitans; and Untreated Group with standard housing and no additional treatment. Maxillae were dissected to perform microscopic and histological analysis of bone height and peri-implant tissues. RESULTS: The bone level, measured at one implant site per animal, in the Bacteria-Group (2.60 ± 0.39 mm) was significantly reduced compared to the Antibiotic-Group (2.29 ± 0.32 mm) after 3 months. The differences of bone height in the Bacteria-Group and the Untreated Group (2.46 ± 0.27 mm) did not reach statistical significance. The inflammatory response with respect to the number of inflammatory cells and fibrous tissue compartments of the peri-implant tissues in the Bacteria-Group was significantly increased compared with the Antibiotic-Group (p < .05). S. oralis and A. actinomycetemcomitans DNAs were detected in the Bacteria-Group. CONCLUSIONS: This rat model of peri-implantitis used oral bacterial lavage for the induction of an inflammatory host response and bone loss. Additional bacterial treatment enhances the peri-implant phenotype, so that significant differences to a reduced bacterial load similar to the human peri-implantitis disease can be identified.

Investigation of Cuprizone Inactivation by Temperature.

Animal models, such as cuprizone (bis-cyclohexanone oxaldihydrazone) feeding, are helpful to study experimental demyelination and remyelination in the context of diseases like multiple sclerosis. Cuprizone is a copper chelator, which when supplemented to the normal food of C57BL/6J mice in a concentration of 0.2% leads to oligodendroglial loss, subsequent microglia and astrocyte activation, resulting in demyelination. Termination of the cuprizone diet results in remyelination, promoted by newly formed mature oligodendrocytes. The exact mode of cuprizone's action is not well understood, and information about its inactivation and cleavage are still not available. The knowledge of these processes could lead to a better understanding of cuprizone's mode of action, as well as a safer handling of this toxin. We therefore performed experiments with the aim to inactivate cuprizone by thermal heating, since it was suggested in the past that cuprizone is heat sensitive. C57BL/6J mice were fed for 4 weeks with 0.2% cuprizone, either thermally pretreated (60, 80, 105, 121 °C) or not heated. In addition, primary rat oligodendrocytes, as a known selective toxic target of cuprizone, were incubated with 350 µM cuprizone solutions, which were either thermally pretreated or not. Our results demonstrate that none of the tested thermal pretreatment conditions could abrogate or restrict the toxic and demyelinating effects of cuprizone, neither in vitro nor in vivo. In conclusion, the current study rebuts the hypothesis of cuprizone as a heat-sensitive compound, as well as the assumption that heat exposure is a reason for an insufficient demyelination of cuprizone-containing pellets.

Mortality Due to Porcine Reproductive and Respiratory Syndrome Virus in Immunocompromised Göttingen Minipigs (Sus scrofa domestica).

Porcine reproductive and respiratory syndrome virus (PRRSV) infection was diagnosed in 6 Göttingen minipigs (Sus scrofa domestica) with severe interstitial pneumonia. The virus was defined as a North American (NA) subtype virus, which is common in the commercial pig population and might be derived from a widely used attenuated live-virus vaccine in Europe. The ORF5 sequence of the isolated PRRSV was 98% identical to the vaccine virus. The affected pigs were part of a lung transplantation model and received tacrolimus and steroids as well as irradiation or CD8 antibody for immunosuppression. The likely source of the infection was pigs that were shedding the identified PRRSV, which were housed in a separate room of the same building. This case report provides evidence that a virus closely related to an attenuated live vaccine might cause severe pneumonia and death in PRRSVseronegative pigs receiving immunosuppressive treatment. We recommend strict barrier housing for immunocompromised pigs.

A mutation in Myo15 leads to Usher-like symptoms in LEW/Ztm-ci2 rats.

The LEW/Ztm-ci2 rat is an animal model for syndromal deafness that arose from a spontaneous mutation. Homozygous animals show locomotor abnormalities like lateralized circling behavior. Additionally, an impaired vision can be observed in some animals through behavioral studies. Syndromal deafness as well as retinal degeneration are features of the Usher syndrome in humans. In the present study, the mutation was identified as a base substitution (T->C) in exon 56 of Myo15, leading to an amino acid exchange from leucine (Leu) to proline (Pro) within the carboxy-terminal MyTH4 domain in the proteins' tail region. Myo15 mRNA was expressed in the retina as demonstrated for the first time with the help of in-situ hybridization and PCR. To characterize the visual phenotype, rats were examined by scotopic and photopic electroretinography and, additionally, histological analyses of the retinas were conducted. The complete loss of sight was detected along with a severe degeneration of photoreceptor cells. Interestingly, the manifestation of the disease does not solely depend on the mutation, but also on environmental factors. Since the LEW/Ztm-ci2 rat features the entire range of symptoms of the human Usher syndrome we think that this strain is an appropriate model for this disease. Our findings display that mutations in binding domains of myosin XV do not only cause non-syndromic hearing loss but can also lead to syndromic disorders including retinal dysfunction.