Periodontitis is a chronic inflammatory disease primarily triggered by dysregulation of microbial communities and altered host immune response.It is clinically presented by alveolar bone resorption,which is one of the main causes of loosening of teeth and tooth loss.Cathepsin K(CTSK)is a highly expressed collagenase produced by osteo-clasts and can directly degrade matrix collagen proteins and indirectly increase osteoclast activity.The expression level of CTSK fluctuates in response to the progression of periodontal inflammation.The expression of Toll-like receptors is upregu-lated in periodontitis lesions.Pathogen-associated molecular pattern binds to relevant TLRs,initiating downstream im-mune pathways that promote receptor activator of nuclear factor-κB ligand-dependent osteoclastogenesis,along with in-creased expression of CTSK.Intervening in the process of alveolar bone resorption can be achieved through the regulation of CTSK.This paper provides a summary of the pathogenic mechanism of CTSK in periodontitis and highlights the research progress regarding the use of CTSK as a therapeutic target.The aim is to offer insights and references for the treatment of periodontitis.

Periodontitis is a chronic inflammatory disease primarily triggered by dysregulation of microbial communities and altered host immune response.It is clinically presented by alveolar bone resorption,which is one of the main causes of loosening of teeth and tooth loss.Cathepsin K(CTSK)is a highly expressed collagenase produced by osteo-clasts and can directly degrade matrix collagen proteins and indirectly increase osteoclast activity.The expression level of CTSK fluctuates in response to the progression of periodontal inflammation.The expression of Toll-like receptors is upregu-lated in periodontitis lesions.Pathogen-associated molecular pattern binds to relevant TLRs,initiating downstream im-mune pathways that promote receptor activator of nuclear factor-κB ligand-dependent osteoclastogenesis,along with in-creased expression of CTSK.Intervening in the process of alveolar bone resorption can be achieved through the regulation of CTSK.This paper provides a summary of the pathogenic mechanism of CTSK in periodontitis and highlights the research progress regarding the use of CTSK as a therapeutic target.The aim is to offer insights and references for the treatment of periodontitis.

Objective To explore the occurrence and related factors of diarrhea in the early stage of enternal nutrition in critically ill patients, therefore providing guidance for the optimization of enteral nutrition. Methods A prospective cross-sectional study was conducted in 29 ICUs of 28 general hospitals of Zhejiang Province between June 1 and October 1, 2016. Patients who were admitted to ICU required for enteral nutrition were included and continuously observed for over 7 days or till discharged from ICU. The patient's general characteristics, severity of disease, enteral nutrition, diarrhea-related and prognostic indicators were recorded. Multivariable logistic regression was performed to analysis risk factors associated with diarrhea and in-hospital mortality. Results A total of 533 critically ill patientswere enrolled in this study. The overall incidence of diarrhea was 30.8％ (n = 164). Diarrhea occurred most frequently on the three days after EN, with a median duration of 2 (1, 3) days. The daily incidence of diarrhea were significantly different between groups (all P< 0.05), which were gradually reduced on day 7. Multivariable logistic regression analysis showed that prokinetic drugs (OR=1.82; 95％ CI: 1.24-2.65), APACHE II score (OR=1.04; 95％ CI: 1.02-1.07), post-pylorus enteral feeding (OR=1.90; 95％ CI:1.11-3.36) were independent risk factors for diarrhea, while interruption of EN (OR=3.74; 95％ CI: 1.85-7.54), APACHE II score (OR=1.07; 95％ CI: 1.04-1.11), vasoactive agent (OR=2.31; 95％ CI: 1.42-3.77), and timing (>48 h) (OR=2.00; 95％ CI: 1.08-3.70) were independent risk factors for in-hospital mortality. Conclusions Our study showed that APACHE II score, the use of prokinetic drugs, and post-pylorus enteral feeding were risk factors for diarrhea. Patients suffering diarrhea experienced increased ICU length of stay, increased the time of mechanical ventilation and in-hospital mortality compared with patients without diarrhea. Interruption of EN induced by diarrhea significantly increased the risk of in-hospital mortality.