ABSTRACT
Abstract The roles and molecular mechanisms of tumor necrosis factor-α-induced protein 8-like 2 (TIPE2) in periodontitis remain largely unknown. Objective This study aimed to determine the expression of TIPE2 and NF-κB p65 in rat Porphyromonas gingivalis-induced periodontics in vivo. Methodology Periodontal inflammation and alveolar bone resorption were analyzed using western blotting, micro-computed tomography, TRAP staining, immunohistochemistry, and immunofluorescence. THP-1 monocytes were stimulated using 1 μg/ml Pg. lipopolysaccharide (Pg.LPS) to determine the expression of TIPE2 in vitro. TIPE2 mRNA was suppressed by siRNA transfection, and the transfection efficiency was proven using western blotting and real-time PCR. The NF-κB pathway was activated by treating the cells with 1 μg/ml Pg.LPS to explore related mechanisms. Results The expression of both TIPE2 and NF-κB p65 was increased in the gingival tissues of rat periodontitis compared with normal tissues. Positive expression of TIPE2 was distributed in inflammatory infiltrating cells and osteoclasts in the marginal lacunae of the alveolar bone. However, strong positive expression of TIPE2 in THP-1 was downregulated after Pg.LPS stimulation. TIPE2 levels negatively correlated with TNF-α and IL-1β. Decreased TIPE2 in THP-1 further promoted NF-κB p65 phosphorylation. Mechanistically, TIPE2 knockdown upregulated NF-κB signaling pathway activity. Conclusions Taken together, these findings demonstrate that TIPE2 knockdown aggravates periodontal inflammatory infiltration via NF-κB pathway. Interventions aimed at increasing TIPE2 may help in the therapeutic applications for periodontitis.
ABSTRACT
Abstract Characterizations of rat mandibular second molar extraction socket with significantly different buccal and lingual alveolar ridge width remain unclear. Objective: To observe alterations in the alveolar ridge after extraction of mandibular second molars, and to examine processes of alveolar socket healing in an experimental model of alveolar ridge absorption and preservation. Methodology: Eighteen Wistar rats were included and divided into six groups regarding healing time in the study. Bilateral mandibular second molars were extracted. The rats with tooth extraction sockets took 0, 1.5, 2, 3, 4 and 8 weeks of healing. Histological observation, tartrate-resistant acidic phosphatase (TRAP) staining, Masson's trichrome staining, immunohistochemical staining and micro-computed tomography (micro-CT) were applied to estimate alterations in the alveolar ridge. Results: Different buccal and lingual alveolar ridge width led to different height loss. Lingual wall height (LH) decreased significantly two weeks after tooth extraction. Buccal wall height rarely reduced its higher ridge width. From two to eight weeks after extraction, bone volume (BV/TV), density (BMD), and trabecular thickness (Tb.Th) progressively increased in the alveolar socket, which gradually decreased in Tb.Sp and Tb.N. LH showed no significant change during the same period. Osteogenic marker OCN and OPN increased during bone repair from two to eight weeks. The reduced height of the lingual wall of the tooth extraction socket was rarely repaired in the later repair stage. Osteoclast activity led to absorption of the alveolar ridge of the alveolar bone wall within two weeks after operation. We observed positive expression of EMMPRIN and MMP-9 in osteoclasts that participated in the absorption of the spire region. Conclusion: Extraction of rat mandibular second molars may help the study of alveolar ridge absorption and preservation. The EMMPRIN-MMP-9 pathway may be a candidate for further study on attenuating bone resorption after tooth extraction.
ABSTRACT
Objective @#To learn the passive smoking exposure and hazard awareness among the residents aged 18 years and over in Zhengzhou,so as to provide evidence for tobacco control. @*Methods@#By multi-stage stratified and clustered sampling method,the residents aged 18 years and over in Zhengzhou were selected. From June to October in 2018,a questionnaire for risk factors of non-communicable diseases,designed by Chinese Center for Disease Control and Prevention,was used to collect their passive smoking exposure and hazard awareness and then analyzed.@*Results @#A total of 6 793 questionnaires were qualified in 6 809 questionnaires and the effective rate was 99.77%. Among 5 387 non-smokers,2 131 people were exposed to passive smoking,and the crude and standardized rate was 39.56% and 40.14%. The standardized rate of passive smoking exposure was higher in men than in women（42.44% vs. 38.67%,P<0.05）,in rural residents than in urban residents（43.90% vs. 36.62%,P<0.05）,and it decreased with the age increase（P<0.05）. The standardized rate of passive smoking exposure in family,indoor workplace and indoor public place was 30.99%,36.99% and 68.02%,respectively. The standardized awareness rate of “passive smoking exposure may lead to heart disease,lung disease in children and lung cancer in adults” was 56.63%,which was higher in urban rural residents than in rural residents（75.69% vs. 36.33%,P<0.05）. @*Conclusions@#The passive smoking exposure rate was high in Zhengzhou,especially in indoor public places. The awareness of the hazards of passive smoking exposure was scarce, especially in rural residents.