OBJECTIVE: To evaluate the clinical efficacy of clear aligner therapy in patients with severe periodontitis accompanied by pathological tooth displacement in the anterior region. METHODS: This retrospective study analyzed patients diagnosed with severe periodontitis and pathological displacement in the anterior region, who visited both the Periodontics and Orthodontics Departments at Peking University School and Hospital of Stomatology between 2019 and 2022. A total of 26 eligible cases were included in this study. All the patients underwent regular periodontal maintenance throughout the treatment process, and clear aligners were used for orthodontic treatment. Intraoral scans were analyzed by dedicated software to measure and compare occlusal distribution and proximal contact scores before and after orthodontic treatment. Periodontal clinical indicators were assessed at three key time points: before periodontal treatment (T0), before orthodontic treatment (T1), and after orthodontic treatment (T2). All the cases were treated with clear aligner. RESULTS: A total of 217 pathologically displaced anterior teeth from 26 patients were analyzed. Among these, 105 teeth exhibited periodontal pockets [probing depth (PD) ≥5 mm] before periodontal treatment. After clear aligner therapy, the occlusal score improved significantly from 10.35±8.61 to 23.62±9.73 (P < 0.001), and the proximal contact score increased from 13.62±4.73 to 31.62±10.37 (P < 0.001). The median PD decreased significantly from 3.33 mm [interquartile range (IQR)=0.92] at T0 to 2.50 mm (IQR=0.67, P < 0.001) at T1 and remained stable at 2.50 mm (IQR=0.50) after treatment (T2). A significant reduction in PD was observed between T0 and T2 (P < 0.001), but no significant difference was found between T1 and T2 (P=0.948). CONCLUSION Clear aligner therapy demonstrates favorable clinical efficacy in patients with severe periodontitis and pathological anterior tooth displacement. It effectively improves occlusal distribution and proximal contact while maintaining periodontal health in these patients. However, further large-scale prospective controlled studies are needed to verify its long-term clinical outcomes.
Humans ; Retrospective Studies ; Periodontitis/therapy* ; Female ; Male ; Adult ; Tooth Migration/therapy* ; Tooth Movement Techniques/methods* ; Treatment Outcome ; Middle Aged ; Young Adult ; Orthodontic Appliances, Removable

Adenomyosis(AM)is characterized by the benign invasion of endometrial tissue and stroma into the myometrium,resulting in diffuse or localized pathological changes.Typical symptoms include increased menstrual volume,prolonged menstrual periods,and progressive dysmenorrhea.In severe cases,AM can lead to infertility.Endometrial receptivity(ER)plays a crucial role in facilitating adhesion,penetration,and implantation required for successful embryo implantation and pregnancy outcome.The impairment of ER due to AM-related factors involves complex mechanisms.This article aims to provide a comprehensive review of recent research findings on the mecha-nisms underlying ER injury caused by AM over the past three years while highlighting the latest advancements in treatment strategies.

OBJECTIVE To investigate the effects of osthole （OST） on renal interstitial fibrosis in diabetic nephropathy （DN） model mice. METHODS The diabetic mice model was established by the tail vein injection of streptozotocin once， and the DN model was established by feeding for 12 weeks after successful modeling of diabetes. Diabetic model mice were randomly divided into model group， low-dose， moderate-dose， high-dose groups （20， 40， 80 mg/kg） of OST， with 10 mice in each group. After successful modeling of diabetes， the mice were given corresponding drugs or solvent （model group） intragastrically， once a day， for consecutive 12 weeks， and the normal control group was set up at the same time. After the last administration， the levels of fasting blood glucose， 24 h urinary protein， serum creatinine （Scr） and blood urea nitrogen were tested in each group. Masson staining was used to observe the deposition of collagen fibers in renal interstitium； the expressions of E-cadherin and vimentin in renal cortex were detected by immunohistochemical staining. The protein expressions of follistatin-like protein 1 （Fstl1） and Snail family transcriptional repressor 1 （Snail1）， the phosphorylation of protein kinase B （Akt） （calculated by p-Akt/Akt） in the renal cortex were detected by Western blot. RESULTS Compared with normal control group， the levels of fasting blood glucose， 24 h urinary protein， Scr and blood urea nitrogen， collagen fiber deposition ratio of renal interstitium， the expression of vimentin， protein expressions of Fstl1 and Snail1， p-Akt/Akt in renal cortex were increased significantly （P＜0.01）， as well as the expression of E-cadherin was decreased significantly （P＜0.01）. Compared with model group， above indexes of OST groups were reversed significantly （P＜0.05 or P＜0.01）. CONCLUSIONS Preventive use of OST can effectively reduce fasting blood glucose level， protect renal function and inhibit epithelial-mesenchymal transition of DN model mice， and delay the progression of renal interstitial fibrosis ， the mechanism of which may be associated with the suppression of Fstl1/Akt/Snail1 signaling pathway.

OBJECTIVE： To study on the effects of prophylactic administration of Ramulus mori polysaccharides （RMP） on inflammatory response of renal ischemia reperfusion injury （RIRI） model mice and to explore its possible mechanism. METHODS： Totally 60 C57BL/6 mice were randomly divided to sham operation group， model group， atorvastatin group （positive control， 15 mg/kg）， RMP low-dose， medium-dose and high-dose groups （300， 600， 1 200 mg/kg）. Except for sham operation group， RIRI model was induced in other 5 groups. 24 h before surgery， they were given relevant medicine intragastrically， once a day， for consecutive one week. 24 h after reperfusion， the mice were sacrificed. The serum levels of Scr and BUN were detected. The morphological changes of renal tissue were observed under optical microscope. The serum levels of IL-1β， IL-6， IL-10 and TNF-α were determined by ELISA. Western blot assay was used to determine the protein expressions of Toll-like receptor 4 （TLR4）， p38 mitogen-activation protein kinase （p38MAPK） and p-p38MAPK. RESULTS： Compared with sham operation group， the serum levels of Scr and BUN were significantly elevated in model group  （P＜0.01）. RIRI led to typical inflammatory response of renal tissue， widespread renal tubular epithelial cell degeneration and necrosis， and inflammatory cells infiltration. Serum levels of IL-1β， IL-6， IL-10 and TNF-α were increased significantly （P＜0.01）. The protein expressions of TLR4， p38MAPK and p-p38MAPK were increased significantly in renal cortex （P＜0.01）. Compared with model group， serum levels of Scr and BUN were decreased significantly in administration groups （P＜0.05 or P＜0.01）. The pathological damage of renal tissue was improved in varying degrees， especially in the RMP medium-dose and high-dose groups. Serum levels of IL-1β and IL-6 were decreased significantly in administration groups （P＜0.05 or P＜0.01）. Serum levels of IL-10 were further increased in atorvastatin group and RMP high-dose group （P＜0.01）， and serum level of TNF-α was decreased significantly in atorvastatin group and RMP medium-dose and high-dose groups （P＜0.05 or P＜0.01）. The protein expressions of TLR4 and p-p38MAPK in renal cortex were decreased significantly in administration groups （P＜0.05 or P＜0.01）. CONCLUSIONS： RMP prophylactic administration can improve RIRI of mice， the mechanism of which may be associated with relieving the inflammatory response through inhibition of TLR4/p38MAPK signaling pathway.

Objective: To examine the proliferating cell nuclear antigen (PCNA) expression in submandibular gland of diabetic mice and to investigate the influence of fibroblast growth factor 1 (FGF-1) on PCNA expression and its possible mechanism. Methods: Sixteen db/db diabetic male mice were randomly divided into diabetic group and diabetic-FGF-1 group (n=8). Eight age-matched db/m mice served as a control group. After FGF-1 was administered intraperitoneally to diabetic-FGF-1 group continuously for 16 weeks, blood glucose and body weight of each mouse in the three groups were detected at 0, 4, 8, 12, 16 weeks. Then the flow rate of saliva in three groups was compared at 0, 8, 16 weeks. At 16 week, bilateral submandibular glands were resected. Then HE staining was performed to observe the histological morphology of submandibular gland and PCNA expression was examined by immunohistochemical staining. Results: Four weeks after administration, the blood glucose in diabetic-FGF-1 group decreased markedly, close to the control group (P>0.05). Weight loss in diabetic-FGF-1 group was noticeable at 8 weeks after administration, but still higher than that in the control group (P<0.05). The flow rate of saliva in diabetic-FGF-1 group increased gradually after administration, which was higher at 8, 16 weeks ([260.1±43.3], [308.5±34.0] mg·min^-1·kg^-1) respectively than that in the diabetic group at the same time point ([181.8±37.5], [194.9±49.8] mg·min^-1·kg^-1) (P<0.05). Compared with the control group, submandibular glands in diabetic group significantly atrophied and the glandular atrophy in diabetic-FGF-1 group was alleviated. The submandibular gland index in the control group, diabetic group and diabetic-FGF-1 group were (7.45±0.63), (2.23±0.26), (3.97±0.15) mg/g, respectively (P<0.05). HE staining showed that the histological morphology of submandibular gland in diabetic-FGF-1 group was clearer, and acinar and ductal atrophy were less significant than diabetic group. Immunohistochemistry showed that the rate of PCNA-positive cells in the control group, diabetic group and diabetic-FGF-1 group were (45.23±7.78)%, (11.50±1.69)%, (36.98±6.53)% respectively (P<0.05). Conclusions FGF-1 can up-regulate the expression of PCNA in submandibular gland of diabetic mice. This effect may be one of the important mechanisms of FGF-1 reversing the structural atrophy and dysfunction of submandibular gland caused by diabetes mellitus.