Objective:To explore the impact and predictive value of subclinical hypothyroidism on metabolic associated fatty liver disease (MAFLD).Methods:The study adopted a cross-sectional design. A total of 6 597 adults with subclinical hypothyroidism who received health check-ups in the Health Examination Center of Hebei General Hospital from 2018 to 2022 were selected as subjects. The participants were randomly divided into a modeling group (4 617) and a validation group (1 980) in a 7∶3 ratio. The basic information and serological indicators were collected in those subjects. The general clinical characteristics of the MAFLD and non-MAFLD participants were compared in the modeling group. Multivariate logistic regression analysis was used to explore the impact of thyroid hormone on MAFLD. The R language was applied to construct a nomogram prediction model, and internal validation and external validation of the model were performed to evaluate the prediction performance of the model.Results:Of the 6 597 study subjects, the prevalence of MAFLD was 31.14% (2 054/6 597). After preliminary comparison of baseline data from the modeling group, multivariate analysis showed that free triiodothyronine/free thyroxine (FT3/FT4) ( OR=20.945,95% CI: 5.862-74.838), male ( OR=1.394,95% CI: 1.109-1.752), age ( OR=1.017,95% CI: 1.009-1.025), diastolic blood pressure ( OR=1.017,95% CI: 1.004-1.021), waist circumference ( OR=1.049,95% CI:1.031-1.067), body mass index ( OR=1.236,95% CI:1.175-1.299), triglyceride ( OR=1.525,95% CI: 1.379-1.687), low density lipoprotein cholesterol ( OR=1.493,95% CI: 1.313-1.698), fasting glucose ( OR=1.173,95% CI:1.101-1.249) were risk factors for MAFLD, and high density lipoprotein cholesterol ( OR=0.243,95% CI: 0.163-0.363), aspartate aminotransferase/alanine aminotransferase ( OR=0.242,95% CI: 0.183-0.320) were protective factors for MAFLD (all P<0.05). The results showed that the two groups of calibration curves showed the consistency between MAFLD occurrence risk and actual occurrence risk. The AUCs of internal and external validation was 0.897 and 0.907, respectively. This nomogram model had a high predictive value. Conclusion:FT3/FT4 is an independent risk factor for MAFLD in the population with subclinical hypothyroidism. The prediction model incorporating thyroid function and metabolic parameters may provide clinical value for early identification of MAFLD.

Peri-implant diseases are inflammatory diseases in the spectrum of oral diseases, which are caused by the dysbiosis of peri-implant flora and the imbalance between microorganism and host. Peri-implant diseases are divided into two types: peri-implant mucositis and peri-implantitis. The diagnostic definition of peri-implant mucositis is based on presence of peri-implant signs of inflammation (redness, swelling, line or drop of bleeding/suppuration following probing) and no additional bone loss following initial healing. The clinical definition of peri-implantitis is based on not only the presence of peri-implant signs of inflammation but also radiographic evidence of bone loss following initial healing. Peri-implant diseases, like periodontitis, have clear etiology, histopathological features, clinical manifestations, and current international consensus diagnostic criteria. This article provides an overview of the etiology, histopathological features, key points of examination and diagnosis, prevention and non-surgical treatment, and surgical treatment of peri-implant diseases. The aim is to raise the awareness of dentists, especially those who specialize in oral implantology and restoration, to have a concept of periodontal and implant health, master the basic theoretical knowledge and prevention and treatment methods of peri-implant diseases, and also inform patients to control plaque and maintain their oral health.

Peri-implant disease is an oral disease that occurs with dental implant treatment. It is an inflammatory disease of peri-implant tissues caused by plaque biofilm, which can be divided into peri-implant mucositis and peri-implantitis. Peri-implant mucositis is limited in the soft tissues surrounding the implant and can be relieved through effective treatment. However if untreated, the inflammation can affect the bone around the implant and develop into peri-implantitis. Progressive resorption of supporting bone can ultimately lead to loss of osseointegration, which is the main cause of implant failure. There is a high incidence of peri-implant disease worldwide, which has become an increasingly serious public health problem. Prevention and supportive treatment of peri-implant disease is an important aspect of promoting oral health and deserves the attention of all dental professionals. This article combines literature review and relevant researches conducted by our research group in the past 15 years to introduce the control of risk factors, prevention, and supportive treatment of peri-implant disease. The aim is to raise the great attention of dentists, who engaged in oral implantation and restoration, to peri-implant and periodontal health, and master the prevention and supportive treatment methods of peri-implant disease.

Peri-implant diseases are inflammatory diseases in the spectrum of oral diseases, which are caused by the dysbiosis of peri-implant flora and the imbalance between microorganism and host. Peri-implant diseases are divided into two types: peri-implant mucositis and peri-implantitis. The diagnostic definition of peri-implant mucositis is based on presence of peri-implant signs of inflammation (redness, swelling, line or drop of bleeding/suppuration following probing) and no additional bone loss following initial healing. The clinical definition of peri-implantitis is based on not only the presence of peri-implant signs of inflammation but also radiographic evidence of bone loss following initial healing. Peri-implant diseases, like periodontitis, have clear etiology, histopathological features, clinical manifestations, and current international consensus diagnostic criteria. This article provides an overview of the etiology, histopathological features, key points of examination and diagnosis, prevention and non-surgical treatment, and surgical treatment of peri-implant diseases. The aim is to raise the awareness of dentists, especially those who specialize in oral implantology and restoration, to have a concept of periodontal and implant health, master the basic theoretical knowledge and prevention and treatment methods of peri-implant diseases, and also inform patients to control plaque and maintain their oral health.

Peri-implant disease is an oral disease that occurs with dental implant treatment. It is an inflammatory disease of peri-implant tissues caused by plaque biofilm, which can be divided into peri-implant mucositis and peri-implantitis. Peri-implant mucositis is limited in the soft tissues surrounding the implant and can be relieved through effective treatment. However if untreated, the inflammation can affect the bone around the implant and develop into peri-implantitis. Progressive resorption of supporting bone can ultimately lead to loss of osseointegration, which is the main cause of implant failure. There is a high incidence of peri-implant disease worldwide, which has become an increasingly serious public health problem. Prevention and supportive treatment of peri-implant disease is an important aspect of promoting oral health and deserves the attention of all dental professionals. This article combines literature review and relevant researches conducted by our research group in the past 15 years to introduce the control of risk factors, prevention, and supportive treatment of peri-implant disease. The aim is to raise the great attention of dentists, who engaged in oral implantation and restoration, to peri-implant and periodontal health, and master the prevention and supportive treatment methods of peri-implant disease.

Objective:To explore the impact and predictive value of subclinical hypothyroidism on metabolic associated fatty liver disease (MAFLD).Methods:The study adopted a cross-sectional design. A total of 6 597 adults with subclinical hypothyroidism who received health check-ups in the Health Examination Center of Hebei General Hospital from 2018 to 2022 were selected as subjects. The participants were randomly divided into a modeling group (4 617) and a validation group (1 980) in a 7∶3 ratio. The basic information and serological indicators were collected in those subjects. The general clinical characteristics of the MAFLD and non-MAFLD participants were compared in the modeling group. Multivariate logistic regression analysis was used to explore the impact of thyroid hormone on MAFLD. The R language was applied to construct a nomogram prediction model, and internal validation and external validation of the model were performed to evaluate the prediction performance of the model.Results:Of the 6 597 study subjects, the prevalence of MAFLD was 31.14% (2 054/6 597). After preliminary comparison of baseline data from the modeling group, multivariate analysis showed that free triiodothyronine/free thyroxine (FT3/FT4) ( OR=20.945,95% CI: 5.862-74.838), male ( OR=1.394,95% CI: 1.109-1.752), age ( OR=1.017,95% CI: 1.009-1.025), diastolic blood pressure ( OR=1.017,95% CI: 1.004-1.021), waist circumference ( OR=1.049,95% CI:1.031-1.067), body mass index ( OR=1.236,95% CI:1.175-1.299), triglyceride ( OR=1.525,95% CI: 1.379-1.687), low density lipoprotein cholesterol ( OR=1.493,95% CI: 1.313-1.698), fasting glucose ( OR=1.173,95% CI:1.101-1.249) were risk factors for MAFLD, and high density lipoprotein cholesterol ( OR=0.243,95% CI: 0.163-0.363), aspartate aminotransferase/alanine aminotransferase ( OR=0.242,95% CI: 0.183-0.320) were protective factors for MAFLD (all P<0.05). The results showed that the two groups of calibration curves showed the consistency between MAFLD occurrence risk and actual occurrence risk. The AUCs of internal and external validation was 0.897 and 0.907, respectively. This nomogram model had a high predictive value. Conclusion:FT3/FT4 is an independent risk factor for MAFLD in the population with subclinical hypothyroidism. The prediction model incorporating thyroid function and metabolic parameters may provide clinical value for early identification of MAFLD.

Objective:To analyze the histopathological characteristics of peri-implant soft tissue in re-constructed jaws and the changes after keratinized mucosa augmentation(KM A)with free gingival graft(FGG).Methods:Twenty patients were enrolled in this study.Five patients of them,who were perio-dontal and systemic healthy and referred for crown lengthening before restoration with healthy keratinized gingiva collected were enrolled as healthy controls.15 patients of them were with fibula or iliac bone flaps jaw reconstruction(10 with fibula flap and 5 with iliac flap),who were referred to FGG and implant exposures before restoration.Soft tissue was collected before FGG in reconstructed jaws,and in 5 patients(3 with fibula flap and 2 with iliac flap)8 weeks after FGG if a second surgery was conducted.Histologi-cal analysis with hematoxylin-eosin stain and immunological analysis to interlukin-1(IL-1),interlukin-6(IL-6)and tumor necrosis factor-α(TNF-α)were performed.Results:Thickness from the bottom of stratum basale to the top of stratum granulosum and thickness of keratinized layer in reconstructed jaws were significantly lower compared with that of natural healthy keratinized gingiva[0.27(0.20,0.30)mmvs.0.36(0.35,0.47)mm,P＜0.05;16.49(14.90,23.37)μm vs.26.37(24.12,31.53)μm,P＜0.05].In the reconstructed area,thickness from the bottom of stratum basale to the top of stra-tum granulosum increased after KMA with FGG[0.19(0.16,0.25)mm vs.0.38(0.25,0.39)mm,P=0.059]and the thickness of keratinized layer significantly increased after KMA with FGG[16.42(14.16,22.35)μm vs.28.57(27.16,29.14)μm,P＜0.05],which was similar to that in the con-trol group.Furthermore,the number of positive cells of IL-1,IL-6 and TNF-α significantly increased after KMA[0.67(0.17,8.93)vs.11.00(9.16,18.00);13.00(8.50,14.14)vs.21.89(15.00,28.12);0.22(0.04,0.63)vs.2.83(1.68,5.00),respectively,P＜0.05]as well as the average optical density value[0.15(0.14,0.17)vs.0.18(0.17,0.21);0.28(0.26,0.33)vs.0.36(0.33,0.37);0.23(0.22,0.29)vs.0.30(0.28,0.42),respectively,P＜0.05],which was similar to that in the healthy keratinized gingiva.Conclusion:The lack of rete pegs and inflammato-ry factors were common in soft tissue with jaw reconstruction.FGG can improve the quality of the epithe-lium and may improve the stability of the mucosa around implants.

Objective:To analyze the concentration of formic acid,propionic acid and butyric acid in gingival crevicular fluid(GCF)of patients with stages Ⅲ and Ⅳ periodontitis,and their relationship with periodontitis.Methods:The study enrolled 37 systemically healthy patients with periodontitis and 19 healthy controls who visited Department of Periodontology,Peking University School and Hospital of Sto-matology from February 2008 to May 2011.Their GCFs were collected from the mesial-buccal site of one molar or incisor in each quadrant.Periodontal clinical parameters,including plaque index(PLI),probing depth(PD),bleeding index(BI),and attachment loss(AL).Concentrations of formic acid,propionic acid and butyric acid in the supernatant of the GCFs were analyzed by high-performance capil-lary electrophoresis(HPCE).The prediction ability of formic acid,propionic acid and butyric acid with the risk of periodontitis and the differences between grade B and grade C periodontitis were analyzed.Results:In this study,32 patients with stage Ⅲ and 5 patients with stage Ⅳ were enrolled,including 9 patients with grade B and 28 patients with grade C.Clinical periodontal variables in the patients with pe-riodontitis were significantly higher than those in the control group(P＜0.001).Formic acid was signifi-cantly lower in periodontitis than that in the control group[5.37(3.39,8.49)mmol/L vs.12.29(8.35,16.57)mmol/L,P＜0.001].Propionic acid and butyric acid in periodontitis were significantly higher than those in the control group:Propionic acid,10.23(4.28,14.90)mmol/L vs.2.71(0.00,4.25)mmol/L,P＜0.001;butyric acid,2.63(0.47,3.81)mmol/L vs.0.00(0.00,0.24)mmol/L,P＜0.001.There was no significant difference in formic acid,propionic acid and butyric acid concentrations between grade B and grade C periodontitis(P＞0.05).Propionic acid and butyric acid in the deep pocket were significantly higher than in the shallow pocket,while the concentration of formic acid decreased with the increase of PD.Propionic acid(OR=1.51,95％CI:1.29-1.75)and butyric acid(OR=3.72,95％CI:1.93-7.17)were risk factors for periodontitis,while formic acid(OR=0.87,95％CI:0.81-0.93)might be a protective factor for periodontitis.Propionic acid(AUC=0.852,95％CI:0.805-0.900),butyric acid(AUC=0.889,95％CI:0.841-0.937),f(formic acid,AUC=0.844,95％CI:0.793-0.895)demonstrated a good predictive capacity for the risk of periodontitis.Conclusion:The concentration of formic acid decrease in the GCF of periodontitis patients,which is a protective factor for periodontitis,its reciprocal have good predictive capacity.However,propionic acid and butyric acid increase,which are risk factors for periodontitis and have good predictive capacity.The concentration of formic acid,propionic acid,and butyric acid vary with probing depth,but there is no significant difference between grade B and grade C periodontitis.

The S3 level clinical practice guideline for the prevention and treatment of peri-implant diseases, developed by the European Federation of Periodontology, was published in June, 2023 (DOI: 10.1111/jcpe.13823), which culminated in the recommendations for implementation of various different interventions before, during and after implant placement/loading. Aim of the present article is to summarize and interpret the key points of this guideline and help clinicians understand this guideline better, in order to standardize the prevention and treatment of peri-implant diseases.

Objective　It is important to distinguish between motor and sensory fascicles of the peripheral nerves for nerve alignment in surgery.No biomarkers currently are available for identification of motor or sensory fascicles.The objective of this study is to search the specific proteins between sensory and motor fascicles of peripheral nerves and provide biomarkers for the identification of functional fascicles of peripheral nerves.Methods　The normal state of motor branch and saphenous nerve of femoral nerve in Wistar rats,and at 8 hours and 8 days after Sunderland V injury were respectively sampled.Five mm long samples were taken from the distal side of the broken end,and a total of 18 groups of proteins were isolated from 6 samples.After purification and quantification,differential gel electrophoresis (DIGE) was used to label the proteins,gel image was scanned,and image analysis software (DeCyder) was used to compare and identify the differentially expressed proteins in each group.Protein spots with more than 1.5 times of difference in expression were selected to prepare glue-cutting,enzyme-cutting and spot target.PMF chromatogram was analyzed and identified by MALDI-TOF-PRO mass spectrometer,and the results of proteomics were analyzed and compared by RT-PCR.Chi-square tests and t-tests were performed for comparison between motor or sensory nerve groups.Results　The data identified 6 proteins that were differentially expressed between motor and sensory fascicles (>1.5-fold,P<0.05),including Annexin V,neurofilament light polypepticle,TEC kinase,serine protease inhibitor A3N,Peroxiredoxin-2,and TPM1.The proteomic results were consistent with the mRNA expression levels of these genes as determined by quantitative reverse transcription polymerase chain reaction.Conclusion　There were significant differences in proteomic expression between the peripheral sensory and motor fascicles,and Annexin V can be used as a high-difference marker protein to distinguish the peripheral sensory from motor fascicles.