Elevated levels of 8-OHdG and PARK7/DJ-1 in peri-implantitis mucosa

BackgroundReactive oxygen species contribute to periodontal tissue homeostasis under control of anti-oxidative responses. Disruption in this balance induces severe inflammation and extended tissue degradation.PurposeAim of this study was to identify the expression levels of nuclear factor, erythroid 2 like 2 (NFE2L2/NRF2), Parkinsonism associated deglycase (PARK7/DJ-1), kelch-like ECH associated protein 1 (KEAP1), and 8-hydroxy-deoxyguanosine (8-OHdG) in peri-implant mucosal tissues affected by peri-implantitis, and to compare the levels to those of periodontally diseased and healthy tissue samples.MethodsTissue biopsies were collected from systemically healthy, non-smoking 12 peri-implantitis patients, 13 periodontitis patients, and 13 periodontally healthy controls. Expression levels of NFE2L2/NRF2, PARK7/DJ-1, KEAP1, and 8-OHdG in tissue samples were analyzed immunohistochemically. Statistical analysis was performed by one-way ANOVA with Tukey's HSD test.ResultsInflammatory cell infiltration in the connective tissue and loss of architecture in the spinous layer of the epithelium were prominent in peri-implantitis. Proportions of 8-OHdG and PARK7/DJ-1 expressing cells were elevated in both peri-implantitis (P = .025 for 8-OHdG and P = .014 for PARK7/DJ-1) and periodontitis (P = .038 for 8-OHdG and P = .012 for PARK7/DJ-1) groups in comparison with controls. Staining intensities of 8-OHdG and PARK7/DJ-1 were higher in the periodontitis and peri-implantitis groups than in the control (P < .01) groups. There was no difference in the expression levels of NFE2L2/NRF2 between the groups. KEAP1 was not observed in any tissue sample.ConclusionsPeri-implantitis is characterized by severe inflammation and architectural changes in the epithelium and connective tissue. The expressions of 8-OHdG and PARK7/DJ-1 are elevated in both peri-implantitis and periodontitis

Olfactory stem cells reveal MOCOS as a new player in autism spectrum disorders

International audienceWith an onset under the age of 3 years, autism spectrum disorders (ASDs) are now understood as diseases arising from pre-and/or early postnatal brain developmental anomalies and/or early brain insults. To unveil the molecular mechanisms taking place during the misshaping of the developing brain, we chose to study cells that are representative of the very early stages of ontogenesis, namely stem cells. Here we report on MOlybdenum COfactor Sulfurase (MOCOS), an enzyme involved in purine metabolism, as a newly identified player in ASD. We found in adult nasal olfactory stem cells of 11 adults with ASD that MOCOS is downregulated in most of them when compared with 11 age-and gender-matched control adults without any neuropsychiatric disorders. Genetic approaches using in vivo and in vitro engineered models converge to indicate that altered expression of MOCOS results in neurotransmission and synaptic defects. Furthermore, we found that MOCOS misexpression induces increased oxidative-stress sensitivity. Our results demonstrate that altered MOCOS expression is likely to have an impact on neurodevelopment and neurotransmission, and may explain comorbid conditions, including gastrointestinal disorders. We anticipate our discovery to be a fresh starting point for the study on the roles of MOCOS in brain development and its functional implications in ASD clinical symptoms. Moreover, our study suggests the possible development of new diagnostic tests based on MOCOS expression, and paves the way for drug screening targeting MOCOS and/or the purine metabolism to ultimately develop novel treatments in ASD