Periodontitis has emerged as one of the most critical oral diseases, and research on this condition holds great importance for the advancement of stomatology. As the most authoritative national scientific research funding institution in China, the National Natural Science Foundation of China (NSFC) has played a pivotal role in driving the progress of periodontal science by supporting research on periodontitis. This article provides a comprehensive review of the research and development progress related to periodontitis in China from 2014 to 2023, highlighting the significant contributions of the NSFC to this field. We have summarized the detailed funding information from the NSFC, including the number of applicant codes, funded programs and the distribution of funded scholars. These data illustrate the efforts of the NSFC in cultivating young scientists and building research groups to address key challenges in national scientific research. This study offers an overview of the current hot topics, recent breakthroughs and future research prospects related to periodontitis in China.
China ; Periodontitis ; Humans ; Foundations ; Research Support as Topic ; Natural Science Disciplines ; Dental Research/economics*

Objective:By analyzing the funded projects in the field of mental disorders of the National Natural Science Foundation of China from 1987 to 2022, the study aimed to provide a reference for related research.Methods:The study accessed the website of the National Natural Science Foundation of China to search the approved projects by the Foundation with subject code H10 from 1987 to 2022, and analysed the essentia information and keywords of the projects by Excel, Origin and VOSviewer software.Results:From 1987 to 2022, 1 882 National Natural Science Foundation projects were approved for mental disorder research, with a total funding amount of 1.018076500 billion China yuan, involving 16 study categories, and 182 research centers. A total of 182 research centers were guaranteed the projects. Peking University, Central South University, Shanghai Mental Health Center and Sichuan University were the top four research centers. More than 100 projects were approved for study in Beijing, Shanghai, Hunan, Jiangsu, Guangdong, Sichuan and Zhejiang each. The projects approved in other provinces increased gradually after 2001, taking a share of 36% in 2016-2022. The researchers primarily focused on mood disorders, schizophrenia, addiction disorders, anxiety disorders and adolescent psychiatric disorders, mainly targeting genetics, neurobiochemistry, immunity, neural circuits and brain imaging. The gut flora, neuromodulation, and machine learning, have attracted significant attention in the past five years.Conclusion:The research on mental disorders in China has substantially increased and diversified. The research centers in Beijing, Shanghai, Hunan, and Sichuan have been the leading centers in China. The interest disorders in their studies reflect the prevalent features of mental conditions in China. A comprehensive research power from genetic molecules to neural networks, engaging anatomic and functioning studies, has been well established.

Objective:By analyzing the funded projects in the field of mental disorders of the National Natural Science Foundation of China from 1987 to 2022, the study aimed to provide a reference for related research.Methods:The study accessed the website of the National Natural Science Foundation of China to search the approved projects by the Foundation with subject code H10 from 1987 to 2022, and analysed the essentia information and keywords of the projects by Excel, Origin and VOSviewer software.Results:From 1987 to 2022, 1 882 National Natural Science Foundation projects were approved for mental disorder research, with a total funding amount of 1.018076500 billion China yuan, involving 16 study categories, and 182 research centers. A total of 182 research centers were guaranteed the projects. Peking University, Central South University, Shanghai Mental Health Center and Sichuan University were the top four research centers. More than 100 projects were approved for study in Beijing, Shanghai, Hunan, Jiangsu, Guangdong, Sichuan and Zhejiang each. The projects approved in other provinces increased gradually after 2001, taking a share of 36% in 2016-2022. The researchers primarily focused on mood disorders, schizophrenia, addiction disorders, anxiety disorders and adolescent psychiatric disorders, mainly targeting genetics, neurobiochemistry, immunity, neural circuits and brain imaging. The gut flora, neuromodulation, and machine learning, have attracted significant attention in the past five years.Conclusion:The research on mental disorders in China has substantially increased and diversified. The research centers in Beijing, Shanghai, Hunan, and Sichuan have been the leading centers in China. The interest disorders in their studies reflect the prevalent features of mental conditions in China. A comprehensive research power from genetic molecules to neural networks, engaging anatomic and functioning studies, has been well established.

Objective To observe periventricular white matter changes and matrix metalloproteinase-3 (MMP-3) expression after two-vessel occlusion in rats.Methods A total of 40 Wistar rats were randomly divided into four groups:sham operation group,model group 1 (20 days after operation),model group 2 (40 days after operation),model group 3 (60 days after operation)(n =10 per group).Model of chronic cerebral hypoperfusion was induced by permanent ligation of the bilateral common carotid arteries in the rat.The change of periventricular white matter was observed by electron microscope.The myelin basic protein (MBP) levels was determined by Western blotting,and the expression of MMP-3 was analysed by immunohistochemical stain and Western blotting.Results Permanent ligation of the bilateral common carotid arteries resulted in demyelination in the corpus callosum and internal capsule in rats.The expressions of MMP-3 in model groups were markedly elevated compared with sham group (model group 1,39.17± 4.167; model group 2,43.33±3.502; model group 3,54.16±2.787; sham group,26.67±3.830; all P＜0.01).The content of MBP in model groups was gradually decreased compared with sham group (model group 1,54.50±4.087; model group 2,47.83±4.875; model group 3,36.50±4.231; sham group,65.01±7.688; all P＜0.01).Additionally,the upregulation of MMP-3 had significant correlation with the loss of MBP in the periventricular white matter (r =-0.883,P＜0.01).Conclusions Chronic cerebral hypoperfusion induces progressive periventricular white matter demyelination,and the upregulation of MMP-3 may involve in the pathological process.

Objective To observe the effects of histone deacetylases inhibitor (HDACi) on cognitive performance and cerebral tau phosphorylation in transgenic mice coexpressed five familial Alzheimer' s disease mutations (5XFAD).Method The total 12 5XFAD-CC and 12 wild type (WT) mice were administrated with suberoylanilide hydroxamic acid ( SAHA,n =7) and vehicle ( n =5 ),respectively.The cognitive performance was assessed by Y-maze and Morris water maze.The protein levels of acetylated α-tubulin,total tau and phosphorylated tau and phosphorylated glycogen synthase kinase-3β (GSK3β) were determined by Western blotting.Results SAHA ameliorated learning and memory deficits in 5XFAD-CC mice (39.10％ ±2.25％,t =2.688,P =0.0312 for total numbers of entrance in novel arm; 26.81％ ±0.78％,t =3.271,P =0.017 for time spending in novel arm; F =5.936,P =0.045 for hidden platform;31.70％ ±4.21％,t =2.317,P =0.049 for probe trial).Administration of SAHA significantly increased acetylated α-tubulin in hippocampus of WT and 5XFAD-CC mice (26.42％ and 29.64％,respectively).Additionally,SAHA attenuated tau-pSer396,tau-pSer404 and tau-pThrThr231 in hippocampus of 5XFAD-CC mice (24.22％,48.98％ and 26.95％,respectively). Moreover,hippocampal phosphorylated GSK3β was markedly reduced in SAHA-treated 5XFAD-CC mice (31.29％). Conclusion SAHA may improve cognitive performance in 5XFAD-CC mice, which is associated with its significant effects on the phosphorylation of tau and GSK3β.

Objective To investigate the relationship between the neuroprotective effect of epigallocatechin gallate ( EGCG ) for PC12 cells induced by 1-methyl-4-phenyl-pyridinium ( MPP+ ) and activating nuclear factor-related factor 2 ( NRF2 ).Methods Well differentiated PC12 cells treated with MPP+ were used as the in vitro cell models,and PC12 cells were pretreated with different concentrations of EGCG.MTT assay was used to investigate the cell viability.Western blot was used to observe the expression of NRF2 in cells and distribution in the nucleus and the cytoplasm.Real-time PCR was used to observe the antioxidant enzymes,HO-1 and NQO1 mRNA expression.Results Pretreatment of PC12 cells with different concentrations of EG CG for an hour could restore cell viability.Western blot showed that expression of NRF2 in cells treated with MPP+ for 24 hours was increased 148％ +5％ compared with the control group (t =6.102,P ＜0.01 ).The level of NRF2 in EGCG pretreated group was 188％ + 6％ compared with the control group(t =11.172,P ＜0.01 ).Moreover the NRF2 protein level in the nuclear was also increased.Western blot showed that the NRF2 protein level in the nuclear was 258％ +2％ compared with the control group (t =21.995,P ＜ 0.01 ).Further research found U 120,an inhibitor of ERK,could inhibit the effect of EGCG.The levels of NRF2 in both samples were 148％ ± 15％ and 158％ ± 1％ compared with their respective control groups(t =6.118,8.058,both P ＜0.01 ).In accordance with the NRF2 data,real-time PCR indicated that the levels of HO-1 and NQO1 mRNA expression increased obviously in the group pretreated with EGCG.Likewise,U120 could also inhibit HO-1 and NQO1 mRNA expression induced by EGCG.Conclusions EGCG can repair oxidative damage to PC12 cells induced by MPP+.The protective effect may be related through the ways to activate ERK-NRF2 and induce downstream of antioxidant enzyme expression,such as HO-1 and NQO1.

This study is to observe the effect of ilexonin A (IA) on the expression of basic fibroblast growth factor (bFGF) and growth associated protein-43 (GAP-43), and neurogenesis after cerebral ischemia-reperfusion in rats and explore its possible mechanism of protecting neuronal injury. Models of middle cerebral artery occlusion (MCAO) were established in SD rats. Before and after two hours ischemia-reperfusion, IA (20 and 40 mg x kg(-1)) was injected immediately and on 3, 7, 14, and 28 d once a day. The neurological severity was evaluated by neurological severity scores (NSS); neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Niss1 staining. The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blotting and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively. After treatment with IA, the NSS of treatment groups were lower than that of the models (3 and 7 d). The number of TUNEL positive neurons decreased and Nissl positive neurons increased at the same time (3 d). The expressions of bFGF and GAP-43 increased significantly in the boundary zone of the infarction area when compared to model group. Moreover, IA markedly enhanced the neurogenesis in the brain after ischemia-reperfusion, which revealed an increase of Brdu/NeuN positive cells in the boundary zone of the infarction area. The possible mechanism of protecting neuronal injury of IA may be related to inhibition on neuronal apoptosis, upregulation of bFGF and GAP-43, and neurogenesis in boundary zone of infarction after cerebral ischemia-reperfusion.

This study is to explore whether the Wnt/beta-catenin signaling pathway is involved in the process of tripchlorolide (T4) protecting against oligomeric Abeta(1-42)-induced neuronal apoptosis. Primary cultured cortical neurons were used for the experiments on day 6 or 7. The oligomeric Abeta(1-42) (5 micromol x L(-1) for 24 h) was applied to induce neuronal apoptosis. Prior to treatment with Abeta(1-42) for 24 h, the cultured neurons were pre-incubated with T4 (2.5, 10, and 40 nmol x L(-1)), Wnt3a (Wnt signaling agonists) and Dkk1 (inhibitors) for indicated time. Then the cell viability, neuronal apoptosis, and protein levels of Wnt, glycogen synthase kinase 3beta (GSK3beta), beta-catenin and phospho-beta-catenin were measured by MTT assay, TUNEL staining and Western blotting, respectively. The result demonstrated that oligomeric Abeta(1-42) induced apoptotic neuronal cell death in a time- and dose-dependent manner. Pretreatment with T4 significantly increased the neuronal cell survival and attenuated neuronal apoptosis. Moreover, oligomeric Abeta(1-42)-induced phosphorylation of beta-catenin and GSK3beta was markedly inhibited by T4. Additionally, T4 stabilized cytoplasmic beta-catenin. These results indicate that tripchlorolide protects against the neurotoxicity of Abeta by regulating Wnt/beta-catenin signaling pathway. This may provide insight into the clinical application of tripchlorolide to Alzheimer's disease.

Objective To explore the characteristics of gross motor development in 1～6-year-old children with cerebral palsy at different levels. Methods 708 children (487 males and 221 females, age range: 1～6 years, from 6 rehabilitation centers in Shanghai) with cerebral palsy (CP) were assessed with Chinese version of Gross Motor Function Classification System （GMFCS） and Gross Motor Function Measure (GMFM). Distributions of GMFM scores at different GMFCS levels in children with cerebral palsy were analyzed. Results The GMFM-66 scores increased most in children with GMFCS Level Ⅰ, and more than 75% of them would be greater than 67 points in GMFM-66 score after the age of 48～50 months. The children with GMFCS Level Ⅱ～Ⅳ appeared similar increasing range of GMFM-66 scores in 1～6 years old. Less than 25% of the children at GMFCS Level Ⅱ would be greater than 67 points in GMFM-66 score before the age of 6 years, more than 50% of those at GMFCS Level Ⅲ would be less than 56 points, more than 75% of those at GMFCS Level Ⅳ couldn't exceed 46 points （except groups of 54～56 months and 66～68 months）. Compared with the children with other GMFCS levels, the GMFM-66 scores were always at very low level in children with GMFCS Level V, and trended to decrease with time after 5 years old. Conclusion The characteristics of gross motor development are different in children with cerebral palsy at different GMFCS levels.

Objective To investigate the development and the risk factor of hip dislocation about children with cerebral palsy. Methods 90 children with cerebral palsy were divided with Chinese version of Gross Motor Function Classification System （GMFCS） and type of cerebral palsy. Their femoral head migration percentage was measured. Results The quadriplegia children were in the biggest risk of hip dislocation, hemiplegia children were the minimum; GMFCS Ⅰ children were in the lowest risk of hip dislocation, GMFCS Ⅴ children were the highest. Conclusion The abnormal development of the hip is correlative with the type of cerebral palsy and motor function in spastic cerebral palsy children.