Juvenile idiopathic arthritis(JIA)is the most prevalent joint disease in childhood.The disease is defined as arthritis of unknown etiology,involving one or more joints,with onset before the age of 16 years and symptomatic duration of more than 6 weeks.Temporomandibular joint(TMJ)arthritis is a common manifestation of JIA,but it often develops insidiously.Failing to diag-nose and treat it promptly may lead to maxillofacial dysfunction and dentofacial deformity,and negatively affect the patient's quality of life.Therefore,early diagnosis and disease management of TMJ arthritis are crucial.This article reviews the occurrence of JIA-TMJ arthritis and its progress in clinical diagnosis and disease treatment in recent years,aiming to provide some reference for den-tists in the clinical diagnosis and treatment of JIA.

Objective:To investigate the effect of cytoskeleton-associated protein 4 (CKAP4) gene knockout on maxillary expansion osteogenesis and its regulatory mechanism on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSC).Methods:Nineteen wild type (WT) and nineteen CKAP4 gene knockout (Ckap4 -/-) mice aged 6-8 weeks were selected to establish a mouse model of rapid maxillary expansion. Samples were taken on the 7th and 14th day after the operation. Micro-CT and HE staining were used to evaluate bone regeneration. Tissue proteins in the modeled area were collected, and Western blotting analysis (WB) was used to detect the protein expression levels of alkaline phosphatase (ALP), Runt-related transcription factor 2 (RUNX2), and osteocalcin (OCN). BMSC were isolated from WT and Ckap4 -/- mice. The expression of surface markers CD29, Sca-1, CD44, CD45, CD34, and CD11b was detected by flow cytometry, and cell proliferation ability was detected by 5-ethynyl-2'-deoxyuridine (EdU). After 7 days of osteogenic induction, real-time fluorescence quantitative PCR (RT-qPCR) and WB were used to detect the expression levels of RUXN2, ALP, OCN, protein kinase B (AKT), and phosphorylated protein kinase B (p-AKT). After 21 days, alizarin red staining and cetyl pyridine chloride quantification were used to detect the differences in mineralized nodule formation in each group. In CKAP4 gene knockout BMSC, the small-molecule AKT agonist sc79 (4 μg/ml) was added as the intervention group (Ckap4 -/- +sc79), and dimethyl sulfoxide (DMSO) treatment was used as the control group (Ckap4 -/- +DMSO). After osteogenic induction, RT-qPCR, WB, and alizarin red staining were used to compare the osteogenic differentiation differences between the two groups of cells. Results:The micro-CT results showed that at 7 days and 14 days after surgery, the new bone volume in the Ckap4 -/- group [(0.070±0.010) and (0.146±0.019) mm 3] was significantly lower than that in the WT group [(0.094±0.006) and (0.196±0.013) mm 3] (both P<0.01). HE-stained histological sections showed that the area of new bone tissue in the Ckap4 -/- group at 7 days and 14 days after surgery [(0.101±0.008) and (0.158±0.010) mm 2] was also significantly lower than that in the WT group [(0.116±0.005) and (0.183±0.008) mm 2] (both P<0.05). WB was used to detect the tissue proteins in the maxillary modeling area of mice in the two groups 7 days after surgery. The results showed that the expression levels of ALP, RUNX2 and OCN in the Ckap4 -/- group were significantly lower than those in the WT group. BMSC from wild-type mice and CKAP4 knockout mice were both positively expressed for CD29, CD44, and Sca-1, and basically not expressed for CD45, CD34, and CD11b. EdU assay showed that there was no significant difference in the proliferation ability of cells in the two groups. After 21 days of osteogenic induction of BMSC, alizarin red staining results showed that the number of mineralized nodules in the Ckap4 -/- group was significantly less than that in the WT group. After adding sc79, the number of mineralized nodules increased significantly, which was consistent with the results of cetyl pyridine chloride quantification. After 7 days of osteogenic induction, It was found that the expression levels of ALP, RUNX2, and OCN in the CKAP4 -/-group (0.751±0.066, 0.484±0.040, 0.679±0.063) were significantly lower than those in the WT group (1.000±0.113, 1.000±0.081, 1.000±0.113) (all P<0.001). The results of WB were consistent with those of RT-qPCR. At the same time, the WB results showed that the level of p-AKT protein in the CKAP4 -/-group (0.518±0.114) was significantly lower than that in the WT group (1.000±0.234) ( P<0.05). After treatment with sc79 for 7 days of osteogenic induction, RT-qPCR was used to detect the gene expression levels of ALP, RUNX2, and OCN. The results showed that the expression levels in the CKAP4 -/-+sc79 group (2.755±0.353, 4.800±0.990, 2.524±0.137) were significantly higher than those in the CKAP4 -/-+DMSO group (1.000±0.078, 1.000±0.247, 1.000±0.175) (all P<0.001). Conclusions:CKAP4 knockout inhibits the osteogenic differentiation of BMSC by reducing the activity of the PI3K/AKT signaling pathway, thereby suppressing osteogenesis in maxillary expansion.

Objective:To investigate the effect of cytoskeleton-associated protein 4 (CKAP4) gene knockout on maxillary expansion osteogenesis and its regulatory mechanism on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSC).Methods:Nineteen wild type (WT) and nineteen CKAP4 gene knockout (Ckap4 -/-) mice aged 6-8 weeks were selected to establish a mouse model of rapid maxillary expansion. Samples were taken on the 7th and 14th day after the operation. Micro-CT and HE staining were used to evaluate bone regeneration. Tissue proteins in the modeled area were collected, and Western blotting analysis (WB) was used to detect the protein expression levels of alkaline phosphatase (ALP), Runt-related transcription factor 2 (RUNX2), and osteocalcin (OCN). BMSC were isolated from WT and Ckap4 -/- mice. The expression of surface markers CD29, Sca-1, CD44, CD45, CD34, and CD11b was detected by flow cytometry, and cell proliferation ability was detected by 5-ethynyl-2'-deoxyuridine (EdU). After 7 days of osteogenic induction, real-time fluorescence quantitative PCR (RT-qPCR) and WB were used to detect the expression levels of RUXN2, ALP, OCN, protein kinase B (AKT), and phosphorylated protein kinase B (p-AKT). After 21 days, alizarin red staining and cetyl pyridine chloride quantification were used to detect the differences in mineralized nodule formation in each group. In CKAP4 gene knockout BMSC, the small-molecule AKT agonist sc79 (4 μg/ml) was added as the intervention group (Ckap4 -/- +sc79), and dimethyl sulfoxide (DMSO) treatment was used as the control group (Ckap4 -/- +DMSO). After osteogenic induction, RT-qPCR, WB, and alizarin red staining were used to compare the osteogenic differentiation differences between the two groups of cells. Results:The micro-CT results showed that at 7 days and 14 days after surgery, the new bone volume in the Ckap4 -/- group [(0.070±0.010) and (0.146±0.019) mm 3] was significantly lower than that in the WT group [(0.094±0.006) and (0.196±0.013) mm 3] (both P<0.01). HE-stained histological sections showed that the area of new bone tissue in the Ckap4 -/- group at 7 days and 14 days after surgery [(0.101±0.008) and (0.158±0.010) mm 2] was also significantly lower than that in the WT group [(0.116±0.005) and (0.183±0.008) mm 2] (both P<0.05). WB was used to detect the tissue proteins in the maxillary modeling area of mice in the two groups 7 days after surgery. The results showed that the expression levels of ALP, RUNX2 and OCN in the Ckap4 -/- group were significantly lower than those in the WT group. BMSC from wild-type mice and CKAP4 knockout mice were both positively expressed for CD29, CD44, and Sca-1, and basically not expressed for CD45, CD34, and CD11b. EdU assay showed that there was no significant difference in the proliferation ability of cells in the two groups. After 21 days of osteogenic induction of BMSC, alizarin red staining results showed that the number of mineralized nodules in the Ckap4 -/- group was significantly less than that in the WT group. After adding sc79, the number of mineralized nodules increased significantly, which was consistent with the results of cetyl pyridine chloride quantification. After 7 days of osteogenic induction, It was found that the expression levels of ALP, RUNX2, and OCN in the CKAP4 -/-group (0.751±0.066, 0.484±0.040, 0.679±0.063) were significantly lower than those in the WT group (1.000±0.113, 1.000±0.081, 1.000±0.113) (all P<0.001). The results of WB were consistent with those of RT-qPCR. At the same time, the WB results showed that the level of p-AKT protein in the CKAP4 -/-group (0.518±0.114) was significantly lower than that in the WT group (1.000±0.234) ( P<0.05). After treatment with sc79 for 7 days of osteogenic induction, RT-qPCR was used to detect the gene expression levels of ALP, RUNX2, and OCN. The results showed that the expression levels in the CKAP4 -/-+sc79 group (2.755±0.353, 4.800±0.990, 2.524±0.137) were significantly higher than those in the CKAP4 -/-+DMSO group (1.000±0.078, 1.000±0.247, 1.000±0.175) (all P<0.001). Conclusions:CKAP4 knockout inhibits the osteogenic differentiation of BMSC by reducing the activity of the PI3K/AKT signaling pathway, thereby suppressing osteogenesis in maxillary expansion.

Juvenile idiopathic arthritis(JIA)is the most prevalent joint disease in childhood.The disease is defined as arthritis of unknown etiology,involving one or more joints,with onset before the age of 16 years and symptomatic duration of more than 6 weeks.Temporomandibular joint(TMJ)arthritis is a common manifestation of JIA,but it often develops insidiously.Failing to diag-nose and treat it promptly may lead to maxillofacial dysfunction and dentofacial deformity,and negatively affect the patient's quality of life.Therefore,early diagnosis and disease management of TMJ arthritis are crucial.This article reviews the occurrence of JIA-TMJ arthritis and its progress in clinical diagnosis and disease treatment in recent years,aiming to provide some reference for den-tists in the clinical diagnosis and treatment of JIA.

Objective:To investigate the preventive and therapeutic effects of epigallocatechin gallate (EGCG) on tetracycline-induced acute drug-induced liver injury (DILI) in mice.Methods:Thirty-two BALB/C mice were divided into four groups, with eight mice in each group. The normal group was raised under conventional condition. Tetracycline-induced acute DILI models were established by intraperitoneal injection of tetracycline in the model group, the blank control group was intraperitoneally injected with equivalent 0.9% NaCl soluation, and EGCG prevention/treatment group was treated with EGCG on the basis of modeling. Blood samples, feces, liver and intestinal tissues of mice were obtained and analyzed by flow cytometry, biochemical test, pathological examination, and 16S rRNA sequencing. The effects of EGCG on gut microbiota, serum lipopolysaccharides (LPS) and transaminase, CD64 expression in intestinal mucosa, hepatic macrophage typing, and hepatic steatosis were evaluated. One-way analysis of variance was performed for analysis of significant difference among groups, and independent sample t test was used for further pairwise comparison. Results:Intraperitoneal injection of tetracycline-caused disorder of gut microbiota in the model group with hepatocytes showing steatosis grade 3 in 7 mice and grade 4 in 1 mouse. The serum level of LPS in model group was significantly higher than that of normal group ( (5.50±0.20) EU/L vs. (3.96±0.19) EU/L) and by the gut-liver axis which caused M1-type macrophages in liver tissues more than that of normal group ((40.00±2.91)% vs. (36.12±2.53)%), and the differences were statistically significant( t=15.83, 2.46; P<0.001, =0.034), and CD64 expression in intestinal mucosa also increased. EGCG intervention altered the gut microbiota in mice with tetracycline-induced acute DILI. The Shannon index and Simpson index of the model group were lower than those of the normal group (4.98±0.56 vs. 5.62±0.47, 0.91±0.03 vs. 0.95±0.02), while the Shannon index (4.08±0.62) and Simpson index (0.83±0.07) of the EGCG prevention/treatment group were lower than those of the model group. The differences were statistically significant ( t=-2.30, -2.85, -2.85, 2.82; P=0.038, 0.013, 0.013, 0.014). Compared with those of the model group, liver pathological changes of EGCG prevention/treatment group improved significantly (grade 2 in 8 mice), the serum level of LPS((4.22±0.17) EU/L) decreased, and the difference was statistically significant( t=-13.63, P<0.001), but had no significant effects on the CD64 expression in intestinal mucosa. Hepatic macrophage typing was compared between EGCG prevention/treatment group and model group, M2-type macrophages promoting repair were predominant in EGCG prevention/treatment group (M2-type macrophoges ratio: (6.20±0.17)% vs. (4.74±0.48)%, t=2.84, P=0.017; M1/M2-type macrophages ratio: 6.20±1.25 vs. 8.48±0.66, t=-4.95, P=0.001). Conclusion:EGCG alleviates tetracycline-induced acute DILI by altering gut microbiota to modulate liver innate immune system.

Objective:To investigate the preventive and therapeutic effects of epigallocatechin gallate (EGCG) on tetracycline-induced acute drug-induced liver injury (DILI) in mice.Methods:Thirty-two BALB/C mice were divided into four groups, with eight mice in each group. The normal group was raised under conventional condition. Tetracycline-induced acute DILI models were established by intraperitoneal injection of tetracycline in the model group, the blank control group was intraperitoneally injected with equivalent 0.9% NaCl soluation, and EGCG prevention/treatment group was treated with EGCG on the basis of modeling. Blood samples, feces, liver and intestinal tissues of mice were obtained and analyzed by flow cytometry, biochemical test, pathological examination, and 16S rRNA sequencing. The effects of EGCG on gut microbiota, serum lipopolysaccharides (LPS) and transaminase, CD64 expression in intestinal mucosa, hepatic macrophage typing, and hepatic steatosis were evaluated. One-way analysis of variance was performed for analysis of significant difference among groups, and independent sample t test was used for further pairwise comparison. Results:Intraperitoneal injection of tetracycline-caused disorder of gut microbiota in the model group with hepatocytes showing steatosis grade 3 in 7 mice and grade 4 in 1 mouse. The serum level of LPS in model group was significantly higher than that of normal group ( (5.50±0.20) EU/L vs. (3.96±0.19) EU/L) and by the gut-liver axis which caused M1-type macrophages in liver tissues more than that of normal group ((40.00±2.91)% vs. (36.12±2.53)%), and the differences were statistically significant( t=15.83, 2.46; P<0.001, =0.034), and CD64 expression in intestinal mucosa also increased. EGCG intervention altered the gut microbiota in mice with tetracycline-induced acute DILI. The Shannon index and Simpson index of the model group were lower than those of the normal group (4.98±0.56 vs. 5.62±0.47, 0.91±0.03 vs. 0.95±0.02), while the Shannon index (4.08±0.62) and Simpson index (0.83±0.07) of the EGCG prevention/treatment group were lower than those of the model group. The differences were statistically significant ( t=-2.30, -2.85, -2.85, 2.82; P=0.038, 0.013, 0.013, 0.014). Compared with those of the model group, liver pathological changes of EGCG prevention/treatment group improved significantly (grade 2 in 8 mice), the serum level of LPS((4.22±0.17) EU/L) decreased, and the difference was statistically significant( t=-13.63, P<0.001), but had no significant effects on the CD64 expression in intestinal mucosa. Hepatic macrophage typing was compared between EGCG prevention/treatment group and model group, M2-type macrophages promoting repair were predominant in EGCG prevention/treatment group (M2-type macrophoges ratio: (6.20±0.17)% vs. (4.74±0.48)%, t=2.84, P=0.017; M1/M2-type macrophages ratio: 6.20±1.25 vs. 8.48±0.66, t=-4.95, P=0.001). Conclusion:EGCG alleviates tetracycline-induced acute DILI by altering gut microbiota to modulate liver innate immune system.

Objective: To compare the effects of surgical and conservative therapy in the treatment of orbital blow-out fracture. Methods: 90 cases of obital blow-out fracture were treated by surgical(n = 40) and conservative(n = 50) trerapy respectively, the patients were fllowed up for 12 months. The treatment outcome was retrospectively analysed. Results: Of the 40 patients managed surgically 39 were with complete follow up data, 19 had diplopia in peripheral gaze before surgery, 13 (33％) had at 3-month and 12 (31％) had at 6-month follow-up. 31 had enophthalmus before surgery and 3(8％) had at 3-month and 6-month follow-up. Of the 50 patients managed conservatively 26 were with complete follow-up data, 11 had diplopia in peripheral gaze initially, 9(35％) had at 3-month and 8(31％) had at 6-month follow-up. 15 had enophthalmus initially and 13(50％) had at 3-month and 6-month followup. Conclusion: Surgical therapy is more effective for the treatment of enophthalmus. The effects tend to be stable 3 months after treatment, the ratio of diplopia in peripheral gaze after treatment by the 2 treatments is similar(about 30％ of the total cases).

Objective To identify the role of phosphatidylinositol-3-kinase(PI3K) in mediating necroptosis induced by tumor necrosis factor alpha (TNFα) and the involved mechanism.Methods Knockdown of p110α,receptor-interacting protein 1(RIP1) or both p110αand RIP1 was mediated by the specific short hairpin RNA (shRNA) lentivirus and verified by RT-PCR or Western blotting .In addition , Western blotting was used to detect phosphorylation of mixed lineage kinase domain-like protein(MLKL) and protein kinase B(AKT) or tetramerization of MLKL.Cell death was measured by micros-copy and flow cytometry.Results AKT phosphorylation and TNFα-induced necroptosis of L929 cells were suppressed by the inhibitors of PI3K or AKT, as well as p110αknockdown.Moreover, RIP1 knockdown did not inhibit L929 cell death induced by TNFαplus Z-VAD, but the RIP1-independent necroptosis was inhibited by p 110αknockdown.In addition, p110αknockdown suppressed MLKL phosphorylation and tetramerization induced by TNFαwith Z-VAD in L929 cells. Conclusion PI3K mediates necroptosis of L929 cells induced by TNFαby activating AKT and MLKL, respectively.

It was reported that pancreatic arteries constricted during the early phase of bile salt-induced acute pancreatitis (AP), leading to pancreatic microcirculatory disturbance. We conducted this experiment to verify whether the above-mentioned finding was true. AP was induced with intraductal injection of taurodeoxyholate. Small pancreatic artery pressure in dogs was recorded. Functional capillaries were counted and calibrated by multiplying wet weight of pancreas. Pancreatic perfusion was measured with Laser Doppler flowmeter. Pancreatic arterioles of rats dilated during the initial 20 min of AP, and pancreatic arterial pressure declined during the early phase of AP in dogs (from 104.5 +/- 4.8 mmHg to 54.6 +/- 5.6 mmHg). The hematocrit of blood from inferior vena cava was significantly lower than that of portal vein at 5 min after pancreatitis induction. The "true" pancreatic functional capillary density increased. The early pancreatic microcirculatory disturbance coincided with a marked increase of portal vein pressure (PVP) as high as 9.18 +/- 0.78 mmHg. Reduction of PVP to baseline level was followed by a marked increase of pancreatic perfusion (by 1.4-fold). Arterial dilatation, but not constriction, occurred during the early phase of bile salt-induced AP. The pancreatic microcirculatory disturbance was due to a marked rise in PVP that greatly reduced the pressure difference in the pancreatic blood vessels and increased plasma extravasation which led. to local hemoconcentration.
Animals ; Bile Acids and Salts ; adverse effects ; Hypertension, Portal ; complications ; Male ; Microcirculation ; drug effects ; physiology ; Pancreas ; blood supply ; Pancreatitis ; etiology ; physiopathology ; Portal Pressure ; Portal Vein ; physiopathology ; Rats ; Rats, Sprague-Dawley