BACKGROUND:The exact pathogenesis of temporomandibular joint osteoarthritis is currently unclear.Traditional clinical treatment strategies for temporomandibular joint osteoarthritis are symptomatic treatments such as pain relief and reduction of inflammation,which can stop the progression of the disease to a certain degree but cannot reverse the destruction of the cartilage.Cartilage degeneration,as one of the most prominent pathologic features in the development of temporomandibular joint osteoarthritis,has been the subject of an increasing number of studies that focus on its pathogenesis.Consequently,we hope to provide an ideal radical solution for the regeneration of the temporomandibular joint.OBJECTIVE:To review the progress of research on cartilage degeneration in temporomandibular joint osteoarthritis.METHODS:The search terms were"temporomandibular joint osteoarthritis,degradation of cartilage matrix,synovitis,oxidative stress,chondrocyte hypertrophy,chondrocyte apoptosis,ferroptosis,autophagy,angiogenesis,extracellular vesicles"in Chinese and English.Literature search was conducted in PubMed database and CNKI,and the time limit for the search was from January 2004 to October 2024.Screening was performed by analyzing and reading the literature,and according to the inclusion and exclusion criteria,81 papers were finally included for review.RESULTS AND CONCLUSION:(1)Increased secretion of cartilage matrix degrading enzymes causes degradation of the cartilage matrix,leading to cartilage degeneration.(2)Synovitis promotes cartilage degeneration through macrophage M1-type polarization and production of inflammatory mediators.(3)Oxidative stress promotes cartilage degeneration by exacerbating the inflammatory response through overproduction of reactive oxygen species.(4)Chondrocyte phenotypic changes and death lead to the decrease of cartilage matrix synthesis,resulting in cartilage degeneration.(5)Blood vessels of subchondral bone penetrate the calcified cartilage layer to reach the superficial cartilage layer,which destroys the cartilage structure and leads to cartilage degeneration.(6)Bioactive substances carried by serum-derived extracellular vesicles in inflammatory states also promote cartilage degeneration in temporomandibular joint osteoarthritis.

BACKGROUND:The exact pathogenesis of temporomandibular joint osteoarthritis is currently unclear.Traditional clinical treatment strategies for temporomandibular joint osteoarthritis are symptomatic treatments such as pain relief and reduction of inflammation,which can stop the progression of the disease to a certain degree but cannot reverse the destruction of the cartilage.Cartilage degeneration,as one of the most prominent pathologic features in the development of temporomandibular joint osteoarthritis,has been the subject of an increasing number of studies that focus on its pathogenesis.Consequently,we hope to provide an ideal radical solution for the regeneration of the temporomandibular joint.OBJECTIVE:To review the progress of research on cartilage degeneration in temporomandibular joint osteoarthritis.METHODS:The search terms were"temporomandibular joint osteoarthritis,degradation of cartilage matrix,synovitis,oxidative stress,chondrocyte hypertrophy,chondrocyte apoptosis,ferroptosis,autophagy,angiogenesis,extracellular vesicles"in Chinese and English.Literature search was conducted in PubMed database and CNKI,and the time limit for the search was from January 2004 to October 2024.Screening was performed by analyzing and reading the literature,and according to the inclusion and exclusion criteria,81 papers were finally included for review.RESULTS AND CONCLUSION:(1)Increased secretion of cartilage matrix degrading enzymes causes degradation of the cartilage matrix,leading to cartilage degeneration.(2)Synovitis promotes cartilage degeneration through macrophage M1-type polarization and production of inflammatory mediators.(3)Oxidative stress promotes cartilage degeneration by exacerbating the inflammatory response through overproduction of reactive oxygen species.(4)Chondrocyte phenotypic changes and death lead to the decrease of cartilage matrix synthesis,resulting in cartilage degeneration.(5)Blood vessels of subchondral bone penetrate the calcified cartilage layer to reach the superficial cartilage layer,which destroys the cartilage structure and leads to cartilage degeneration.(6)Bioactive substances carried by serum-derived extracellular vesicles in inflammatory states also promote cartilage degeneration in temporomandibular joint osteoarthritis.

OBJECTIVE To study the effects of the Mongolian medicine Sugemule-4 on the metabolism of insomnia rats， and to preliminarily explore its possible mechanisms for improving insomnia. METHODS The rat model of chronic stress insomnia was established by tail clipping stimulation and intraperitoneal injection of p-chlorophenyl alanine solution. Twenty-four male rats were randomly divided into the normal group， model group， diazepam group （positive control， 0.92 mg/kg）， and Sugemule-4 group （5.2 g/kg）， with 6 rats in each group. Since the 7th day of tail clipping stimulation， the Sugemule-4 group and diazepam group began to be intragastrically administered with relevant medicine； the normal group and model group were intragastrically administered with an equal volume of distilled water， once a day， for 14 consecutive days. The learning and memory abilities of rats were tested using a water maze experiment， and the non-invasive sleep activity monitoring system was used to monitor the 24- hour sleep time of rats. A metabolomics study was conducted on rat serum and hippocampal tissue by using ultra-high-performance liquid chromatography-tandem mass spectrometry. The multivariate statistical analysis method was adopted to analyze the differential metabolites in serum and hippocampal tissue of rats， and screen for differential metabolites and metabolic pathways among those groups. RESULTS Compared with the normal group， the escape latency of rats in the model group was significantly increased， the times of crossing platforms were significantly reduced， and the percentage of average 24-hour sleep time was significantly reduced （P＜0.05）. Compared with the model group， the levels of the above indicators were significantly reversed in the diazepam group and Sugemule-4 group （P＜0.05）. Metabolomics studies found that a total of 9 differential metabolites were identified in rat serum and hippocampal tissue， including 5-hydroxyindoleacetic acid， canine urate， canine urinary quinolinic acid， 5-hydroxytryptamine， phenol sulfate， 1-carboxyethyltyrosine， 3-（4-hydroxyphenyl） lactate， N-acetyl tyrosine， tyrosine and phenol sulfate， mainly involving 2 metabolic pathways of tryptophan and tyrosine.CONCLUSIONS Sugemule-4 can improve the sleep time and behavioral performance of insomnia rats， and its mechanism may be associated with affecting amino acid metabolic pathways such as tryptophan and tyrosine.

Objective To determine the value of differential time to positivity ( DTTP ) of blood culture for the diagnosis of catheter-related bloodstream infection ( CRBSI ) in patients with solid tumors in intensive care unit ( ICU ). Methods A retrospective study was conducted. 615 pairs of peripheral vein blood cultures and instantaneous catheter tip blood culture of 615 patients admitted to ICU of Tianjin Medical University Cancer Institute and Hospital were collected from August 2011 to March 2014. The DTTP method and ( or ) semi quantitative culture of catheter tip were compared. CRBSI was diagnosed when both cultures were positive for the same microorganism and DTTP ≥2 hours ( 120 minutes ). The result of this procedure was compared with that of organism obtained using the semi quantitative culture of blood at catheter tip with≥15 cfu. Based on the clinical diagnosis, the reliability of two kinds of laboratory examination was compared for the diagnosis of CRBSI by plotting receiver operator characteristic curve ( ROC curve ). Results The result of 615 cases suspected of having CRBSI were analyzed during the study period. Of these, 440 episodes were excluded because cultures were negative for blood obtained through peripheral vein and central vein. Eight episodes were excluded because only peripheral vein blood culture was positive and 57 episodes were excluded because of only central vein blood culture was positive, 68 pairs of blood cultures were excluded due to the presence of multiple catheters and repeated blood withdrawals. Two cases of polymicrobial cultures were excluded from the final analysis due to the difficulty in determining the time of positive result for each individual microorganism. Ten cases in 42 cases of suspected cases of CRBSI were excluded from analysis because catheter was not removed, therefore culture from catheter tip could not be obtained. Using the DTTP method, 14 out of 17 CRBSI cases were diagnosed with DTTP≥120 minutes, while 3 cases were missed;the semi quantitative catheter tip culture was positive in 13 cases, and in 4 cases it was neglected. In 2 cases of CRBSI it was missed by both methods. The area under the ROC curve ( AUC ) of DTTP, catheter tip culture and the combination method was 0.912, 0.882 and 0.941 for diagnosis of CRBSI, respectively. Validity values for the diagnosis of CRBSI for DTTP were:sensitivity 82.35%, specificity 92.31%, positive predictive value 93.33%and negative predictive value 80.00%, and they were higher than those of the catheter tip culture method only ( 76.47%, 84.62%, 86.67% and 73.33%). The specificity and positive predictive CRBSI combination of the two methods in the diagnosis value were up to 100%, the sensitivity ( 88.24%) and negative predictive value ( 86.67%) was also increased, but no significant differences were found with DTTP method (χ2=0.00, P=1.00;χ2=0.00, P=0.98;χ2=0.00, P=0.98;χ2=0.00, P=0.98 ). Conclusions DTTP can be a valid method recommended for CRBSI diagnosis in critically ill patients with acceptable sensitivity, good specificity as well as positive predictive value. DTTP combined with other clinical symptoms can not only avoid unnecessary catheter withdrawal, but it also can help obtain the optimal treatment time and strategy.