Dental caries is the most common oral disease in children,not only impairing chewing,speech,and other functions while also impacting maxillofacial development and overall health.Recent researches have established the"ecological plaque theory",which posits that an imbalance in the oral plaque microecology leads to the demineralization of teeth hard tissues,as the widely ac-cepted etiology of dental caries.However,the significant variability in the composition and function of children's plaque microorgan-isms,influenced by primary tooth eruption and replacement,changes in diet,and increase in social interactions,makes traditional culture methods inadequate for studying this complex micro-ecosystem.Advances in multi-omics technologies have recently created new opportunities for studiing complex microecology.High-throughput sequencing technologies,such as 16S rRNA gene sequencing and metagenomics,allow for the exploration of microbial diversity and the analysis of genomic functions and their associations with dental caries.Mass spectrometry-based technologies,including metabolomics and proteomics,might elucidate the molecular mecha-nisms of dental caries by analyzing differential metabolites and pathways.This review focuses on the application of multi-omics tech-nologies to explore the relationships between the structure,function,and metabolic state of oral microbial communities and pediatric dental caries.It further discusses the future of oral microorganisms as diagnosis and therapeutic targets for caries,and is expected to provide novel strategies for the prevention and treatment of pediatric dental caries.

Dental caries is the most common oral disease in children,not only impairing chewing,speech,and other functions while also impacting maxillofacial development and overall health.Recent researches have established the"ecological plaque theory",which posits that an imbalance in the oral plaque microecology leads to the demineralization of teeth hard tissues,as the widely ac-cepted etiology of dental caries.However,the significant variability in the composition and function of children's plaque microorgan-isms,influenced by primary tooth eruption and replacement,changes in diet,and increase in social interactions,makes traditional culture methods inadequate for studying this complex micro-ecosystem.Advances in multi-omics technologies have recently created new opportunities for studiing complex microecology.High-throughput sequencing technologies,such as 16S rRNA gene sequencing and metagenomics,allow for the exploration of microbial diversity and the analysis of genomic functions and their associations with dental caries.Mass spectrometry-based technologies,including metabolomics and proteomics,might elucidate the molecular mecha-nisms of dental caries by analyzing differential metabolites and pathways.This review focuses on the application of multi-omics tech-nologies to explore the relationships between the structure,function,and metabolic state of oral microbial communities and pediatric dental caries.It further discusses the future of oral microorganisms as diagnosis and therapeutic targets for caries,and is expected to provide novel strategies for the prevention and treatment of pediatric dental caries.

A young maxillary lateral incisor of Oehlers type Ⅲ Dens invaginatus with peri-invagination periodontitis was reconstructed by CBCT,with the help of guided endodontics,the pathway to invagination was successfully established.The invaginated pseudo-root canal was treated with Vitapex mediation while preserving the pulp.After 6-month follow-up,the tooth was clinically asymptomatic.Radiological ex-amination indicated complete healing of the peri-invagination lesion with narrowed open apex,and the thickened root canal wall.

BACKGROUND: Idiopathic scoliosis (IS) affects patients' quality of life, yet there have been few reports of its morphology and epidemiological study in the southeast region of China. The aim of this study is to access the curve characteristics, prevalence, and factors associated with IS in Chaozhou city. METHODS: A cross-sectional study was performed in 2018, in which scoliosis screening was conducted among 5497 primary school students in Chaozhou city. Then, a case-control study based on the screening involving 2547 children was followed for the exploration of the associated factors. The questionnaires covering demographic characteristics, postural habits, cognition and self-sensation of scoliosis, and physical conditions were addressed for the investigation. ORs with 95%CIs were calculated based on logistic regression analysis to evaluate the factors associated with scoliosis. RESULTS: The prevalence of IS among primary school students was 6.15% in Chaozhou city, with 4.04% for males and 8.71% for females. The average Cobb angle was 15° (range 8 to 37°). Multiple logistic regression analysis suggested that female (OR=2.45), BMI (OR=0.67), having myopia (OR=1.49), self-sensation of scoliosis with symptoms (OR=5.52), insufficient sleep time (OR=2.65, 3.33), and less exercise time (OR=7.09, 7.29) were significantly associated with IS. CONCLUSIONS The prevalence of IS among primary school students in Chaozhou was at an average level, and it was significantly higher in females than in males. Lower body mass, having myopia, insufficient sleep time, and lower physical activity were associated with IS.
Case-Control Studies ; Child ; China/epidemiology* ; Cross-Sectional Studies ; Epidemiologic Studies ; Female ; Humans ; Male ; Myopia/complications* ; Risk Factors ; Schools ; Scoliosis/physiopathology* ; Students

Objective To investigate the effects and mechanisms of glutamine (Gln) supplementation on oxidative stress,autophagy response and neurobehavioral outcome after traumatic brain injury (TBI) in rats.Methods TBI animal models were established using Feeney's method.Eighty SD rats were randomly divided into 4 groups:sham operation group (group Sham),Sham + glutamine supplementation group (group Sham+ GLN),traumatic brain injury group (group TBI),and TBI + glutamine supplementation group (group TBI+ GLN).We measured rat behavioral outcomes by modified neurologic severity score (mNSS) tests at day 1,3,7 and 14 after TBI.The apoptosis neurons in TBI cerebral cortex were determined by TUNEL staining.The expression of reactive oxygen species (ROS) was tested by ROS kits.Oxidative stress and autophagy related cytokines (HO-1,NQO1,Nrf2,LC3-Ⅱ and Beclin-1) were tested with Western blotting.Results Compared with the TBI group,the neurological function was improved [(9.79±0.43) vs.(8.43±0.30),F =6.775,P =0.010] and the apoptosis rate decreased (19.88％ ± 1.60％ vs.15.35％ ± 1.28％,P =0.013) in the TBI+ GLN group after 7-day treatment.Compared with the Sham group,the protein expression of ROS increased (P=0.000),and the expression of anti-oxidative stress factors (HO-1,NQO1) and Nrf2 pathway significantly decreased in the TBI group.After glutamine supplementation was given,the expression of ROS decreased and the expressions of HO-1 and NQO1 increased.The Nrf2 pathway and autophagy response also were activated with the expressions of Nrf2,LC3-Ⅱ and Beclin-1 increasing.Conclusion Glutamine supplementation can markedly reduce neuron apoptosis and improve neurological outcomes after TBI,thus has the protective effect on nerves by inhibiting TBI-induced oxidative stress response,activating Nrf2 pathway and autophagy response.

Objective: To investigate the protective effect of propofol on neurological function in rats after traumatic brain injury (TBI) and its possible mechanism. Methods: A total of 96 SD rats were randomly divided into sham operation group, sham operation+ propofol group, TBI group and TBI + propofol group, with 24 rats in each group. The TBI model was prepared by modified Feeney method. The sham operation+ propofol group and the TBI+ propofol group were given 50 mg/kg of propofol once daily. The sham operation group and the TBI group were injected with the same amount of normal saline. Modified neurobehavioral functional scores (mNSS) were evaluated at 1, 3, 7 and 14 days after injury; dry-wet specific gravity method was used to detect brain water content in injured area; TUNEL staining was used to detect neuronal apoptosis; chemiluminescence was used to detect activity of Oxygen cluster (ROS) content; Western blot was used to determine the expressions of inositol requirement enzyme 1 (IRE-1), enhancer binding protein homolog protein (CHOP), heme oxygenase 1 (HO-1), quinone oxidoreductase 1 (NQO1) and nuclear factor E2 related factor 2 (Nrf2) protein. Results: Compared with the sham operation group and the sham operation + propofol group, the mNSS, brain tissue water content, apoptosis number and ROS increased at 1, 3, 7 and 14 days after TBI in the TBI group and TBI + propofol group (P<0.05). Compared with TBI group, mNSS in TBI+ propofol group decreased significantly [(9.3±1.4)points ∶(10.9±1.2)points] 7 days after injury (P<0.05); the brain tissue water content decreased significantly [(81.0±0.8)%∶(82.1±0.8)%] 3 days after injury (P<0.05); the number of apoptotic cells decreased significantly 7 days after injury[(14.1±1.4)%∶(15.6±1.6)%], with the most significant decrease at 14 days after injury [( 10.4±1.5)%∶(13.2±1.4)% (P<0.05); and ROS decreased significantly 7 days after injury [(61.5±4.0)RFU∶(77.3±5.5)RFU](P<0.05). Compared with the sham operation group and the sham operation+ propofol group, the expressions of IRE-1 and CHOP were significantly up-regulated in the TBI group and the TBI+ propofol group (P<0.05); the expressions of HO-1, NQO1 and Nrf2 in the TBI group were significantly decreased (P<0.05); the expressions of HO-1 and NQO1 in TBI+ propofol group were increased (P<0.05) while the expression of Nrf2 were decreased slightly (P<0.05). Compared with the TBI group, the expressions of IRE-1 and CHOP in TBI+ propofol group were decreased (P<0.05), while the expressions of HO-1, NQO1 and Nrf2 were significantly increased (P<0.05). Conclusion After TBI in rats, propofol can reduce oxidative stress by activating the Nrf2-antioxidant element (ARE) pathway, reduce brain edema, and inhibit neuronal apoptosis, thus playing a neuro-protective role.

Objective To compare cortical bone screwing and Endobutton plating for the treatment of ankle joint fracture complicated with injury to the distal tibiofibular syndesmosis. Methods Fifty-eight pa-tients with ankle joint fracture and injury to the distal tibiofibular syndesmosis were treated at Department of Orthopedic Surgery, The Affiliated Hospital to Guangdong Medical University from January 2014 to June 2016. Half of them were treated by conventional cortical bone screwing. They were 16 males and 13 females with an average age of 43.2 ± 4.1 years. The other half were treated by Endobutton plating. They were 15 males and 14 females with an average age of 44.1 ± 3.9 years. The 2 groups were compared in terms of intraoperative bleed-ing, operation time, tibiofibular clear space ( TBCS ) , tibiofibular overlap ( TBOL ) , the American Orthopedic Foot Ankle Society (AOFAS) ankle-hindfoot scale and complications. Results The cortical bone screwing group needed significantly shorter operation time (63.4 ± 5.4 min) than the plating group (89.6 ± 6.2 min) ( P ＜0.05) . There were no significant differences between the 2 groups in intraoperative bleeding ( 68.9 ± 6.3 mL versus 67.4 ± 6.4 mL ) , TBCS ( 4.6 ± 0.3 mm versus 4.7 ± 0.3 mm) , TBOL ( 7.5 ± 0.4 mm versus 7.4 ± 0.4 mm ) , good to excellent rate by AOFAS score ( 72.4% versus 75.9%) , or rate of complications ( 6.9% versus 10.3%) ( P ＞ 0.05 ). Conclusion Since cortical bone screwing and Endobutton plating show no signifi-cant difference for the treatment of ankle joint fracture complicated with distal tibiofibular syndesmosis injury, a proper surgical procedure should be decided according to the specific conditions of the patient.

Objective To investigate the effects of glutamine (Gln) supplementation on neurologica severity score,brain edema,neuron apoptosis,and endoplasmic reticulum stress (ERS) response after traumatic brain injury (TBI) in rats.Methods TBI rat models were established using modified Feeney's method.Eighty Sprague-Dawley rats were divided into 4 groups with a random number table:sham operation group (Sham group),TBI group,Gln supplementation group (TBI + Gln group) and ERS inducer 2-deoxy-D-glucose group (TBI +Gln + 2-DG group).We measured the rats' neurobehavioral outcomes by modified neurologic severity score (mNSS) on day 1,3,7 and 14 after TBI.Neuron apoptosis was detected using TUNEL staining.Brain water content was measured with wet-dry weight method.The apoptosis-related protein (caspase-12,caspase3,and Bcl-2) and ERS-related cytokines [inositol-requiring enzyme 1 (IRE-1),C/EBP homologous protein (CHOP)] expressions in TBI cerebral cortex were determined by immunohistochemistry staining and Western blot.Results Compared with the Sham group,the levels of brain edema,mNSS,apoptosis-related protein (caspase-12,caspase-3,Bcl-2) and ERS-related proteins (IRE-1,CHOP) were significantly increased in the other three groups (all P =0.00).Compared with the TB1 group,the TBI +Gln group showed significant lower brain water content [3 d:(81.39±0.59)％ vs.(83.54±0.52)％,P=0.04;7 d:(74.86±0.38)％ vs.(77.32±0.66)％,P=0.03],improved mNSS (8.63 ±0.22 vs.10.37±0.29,P=0.03),suppressed expressions of apoptosis-and ERS-related proteins (caspase-12,caspase-3,IRE-1,and CHOP)(P =0.01,P ＜ 0.01),and increased expression of anti-apoptotic protein Bcl-2 (P =0.02).Compared withthe TBI + Gln group,the expression of ERS-related factors (IRE-1 and CHOP),brain edema level,and neurological severity were increased in the TBI + Glu + 2-DG group.Conclusion Glutamine supplementation may have neuroprotection function,demonstrated as reducing brain edema and neuron apoptosis,and improving neurobehaviroal outcomes after TBI,possibly mediated by inhibiting TBI-induced ERS response.

Objective To investigate the effects of omega-3 polyunsaturated fatty acids (ω-3 PUFA) supplementation on neuron apoptosis,brain edema,activation of microglia,inflammatory response and neural function after traumatic brain injury (TBI) in rats,so as to understand the protection of ω-3 PUFA in rats following TBI and its mechanism.Methods TBI model was established using Feeney's method.Ninety SD rats were randomly divided into 5 groups:sham operation group (sham group),TBI group,TBI + selective activator of c-Jun N-terminal kinase (JNK) anisomycin group (TBI + Aniso group),TBI + ω-3 PUFA supplementation group (TBI + ω-3 group),and TBI + ω-3 PUFA supplementation + JNK activation group (TBI + ω-3 + Aniso group).We measured rat behavioral outcomes by modified neurological severity score (mNSS) on day 1,3,and 7 after TBI.Brain water content was measured with wet-dry weight method.The neuron apoptosis and microglial activation (identified by specific marker IBA-1) in TBI cerebral cortex were determined by TUNEL staining and immunofluorescence.Inflammatory cytokines [tumor necrosis factor-α (TNF-α),interleukin (IL)-1α,IL-1β,and IL-6] and the JNK signaling pathway (JNK,pJNK) were tested with reverse transcription-polymerase chain reaction and Western blot,respectively.Results Compared with the sham group,the levels of brain cell apoptosis,brain edema,neuron apoptosis,and inflammatory-relatived factors (TNF-α,IL-1 α,IL-1β,and IL-6) were significantly increased in the other four groups (P ＜ 0.05).Compared with the TBl group,ω-3 PUFA supplementation reduced brain water content following TBI,especially on day 3 after TBI [(78.14 ± 0.57) ％ vs.(82.31 ± 0.81) ％,P ＜ 0.01],and improved neurological function score (P ＜ 0.05).Meanwhile,ω-3 PUFA supplementation suppressed neuron apoptosis,the activation of microglia,and the mRNA and protein expressions of inflammatory cytokines (TNF-α,IL-1α,IL-1 β,IL-6).The activation of JNK signaling pathway was also inhibited by ω-3 PUFA.Conclusion ω-3 PUFA supplementation may markedly reduce brain edema,suppress neuron apoptosis,and improve neurological outcomes after TBI in rats,possibly mediated by inhibiting JNK signaling pathway and microglial activation,reducing microglia-induced cerebral inflammatory responses,demonstrated as down-regulated expression of TNF-α,IL-1α,IL-1β,and IL-6.

As a transmembrane protein, β-amyloid precursor protein(β-APP) distributes extensively in the central nervous system, has the effect of neurotrophic, and neuroprotective, promote neurite growth and synaptogenesis, β-amyloid(Aβ) is the digestion products of its precursor-APP in the pathological conditions, and it is the main component of senile plaques-the main pathological changes of Alzheimer' s disease (AD), its toxic effects can also induce neuronal apoptosis, The expression of the two proteins after brain injuried has a close relationship with the injury, cognitive dysfunction, Alzheimer' s disease and the pathophysiological changes of central nervous system. To explore its expression in the brain after traumatic brain injury can determine the degree of injury, assess the prognosis and open up new avenues for the treatment of traumatic brain injury.