// <![CDATA[ $('.header-date').hide();$('#titleAuthors').hide();$('#abstractHeader').hide(); // ]]> Hui Li1, *, Yanyan Xu2, *, Hua Mei3, Liang Peng4, Xiaojie Li5 and Jianzhou Tang4, 5 1Department of Microbiology and Immunology, Medical School of Jishou University, Jishou 416000, Hunan, China 2Department of Molecular Pathology, Guangzhou Kingmed Center for Clinical Laboratory, Guangzhou 510000, China 3Department of Somatic Stem Cell, Hunan Guangxiu Hospital, Changsha 410002, Hunan, China 4Department of Biological and Environmental Engineering, Changsha University, Changsha 410003, Hunan, China 5College of Animal Science and Technology of Hunan Agriculture University, Changsha 410128, Hunan, China *These authors have contributed equally to this work and should be considered as co-first authors Correspondence to: Jianzhou Tang, email: Z20050711@ccsu.edu.cn Keywords: TERT, cancer, risk, meta-analysis, telomerase Received: December 27, 2016 Accepted: February 15, 2017 Published: March 17, 2017

‘Oral bone’ primarily refers to the bones within the mouth, specifically the jawbones and the alveolar bone that supports teeth. Oral bone tissue defects are commonly caused by trauma, inflammation and surgical excision and their repair represents one of the core challenges in the field of oral medicine. The use of functional biomaterials for tissue regeneration has become a research focus in the field of damaged tissue treatment. However, following the implantation of biomaterials, the immune response induces the generation of reactive oxygen species (ROS) and the open and susceptible environment of oral bone predisposes it to redox imbalance, resulting in ROS accumulation and compromised repair. In response to this challenge, ROS-regulating biomaterials have developed into an effective platform for restoring redox balance. Despite this progress, current research lacks a systematic framework for the mechanism and design of biomaterials specifically addressing the special metabolism of oral bone. This review focuses on the physiological and pathological characteristics of oral bone, explores the interaction mechanisms between the oxidative stress and oral bone defects and provides a functional classification of regulation mechanisms. In addition, this review provides several corresponding suggestions for the development of targeted biomaterials according to the problems of existing ROS-regulating materials applied in oral bone repair.

Background: The plasminogen activator inhibitor-1 (PAI-1) was found in many types of tumor cells, which involved in tumorigenesis. Some studies investigated the associations between PAI-1 polymorphisms and various cancers, but the results were inconsistent. So this study did a meta-analysis to assess the strength of relationship between PAI-1 and cancer. Methods: Articles that meet the requirements were searched from PubMed, EMBASE, MEDLINE, Scopus, CNKI, Wanfang and SinoMed electronic databases before June 17th 2021. Stata version 11.2 was performed to merge the odds ratios (ORs) values and calculate 95% confidence intervals (CIs). Stratified analyses were assessed on the basis of types of cancer, ethnicity and source of the control group. Heterogeneity and sensitivity analysis were tested, and publication bias was also estimated. A meta-regression analysis was applied to explore sources of heterogeneity. The false-positive report probabilities (FPRP) and the Bayesian False Discovery Probability (BFDP) test were used to assess the credibility of statistically significant associations. Results: Ultimately, in this study, 33 eligible reports were included with 9550 cases and 10431 controls for the rs1799889 polymorphism, 5 reports with 2705 cases and 3168 controls for the rs2227631 polymorphism, and 4 reports with 2799 cases and 4011 controls for the rs2227667 polymorphism. The ORs and 95% CIs showed a statistically significant relationship between rs1799889 4G>5G polymorphism and cancer risk, especially in feminine cancer. The term refers to cancers that occur in the female reproductive system, such as ovarian, breast, endometrial and cervical cancer. Moreover, there was no association observed for the PAI-1 promoter A>G polymorphism (rs2227631 and rs2227667). In further subgroup analyses of 4G>5G polymorphism (rs1799889), an increased susceptibility to cancer was observed in Caucasians group and some types of cancer groups. Conclusions: This article comes to a conclusion that the rs1799889 polymorphism might help to increase the risk of cancer; moreover, the susceptibility to feminine cancer is more evident.