ABSTRACT
OBJECTIVE@#To summarize the research progress on the role of macrophage-mediated osteoimmune in osteonecrosis of the femoral head (ONFH) and its mechanisms.@*METHODS@#Recent studies on the role and mechanism of macrophage-mediated osteoimmune in ONFH at home and abroad were extensively reviewed. The classification and function of macrophages were summarized, the osteoimmune regulation of macrophages on chronic inflammation in ONFH was summarized, and the pathophysiological mechanism of osteonecrosis was expounded from the perspective of osteoimmune, which provided new ideas for the treatment of ONFH.@*RESULTS@#Macrophages are important immune cells involved in inflammatory response, which can differentiate into classically activated type (M1) and alternatively activated type (M2), and play specific functions to participate in and regulate the physiological and pathological processes of the body. Studies have shown that bone immune imbalance mediated by macrophages can cause local chronic inflammation and lead to the occurrence and development of ONFH. Therefore, regulating macrophage polarization is a potential ONFH treatment strategy. In chronic inflammatory microenvironment, inhibiting macrophage polarization to M1 can promote local inflammatory dissipation and effectively delay the progression of ONFH; regulating macrophage polarization to M2 can build a local osteoimmune microenvironment conducive to bone repair, which is helpful to necrotic tissue regeneration and repair to a certain extent.@*CONCLUSION@#At present, it has been confirmed that macrophage-mediated chronic inflammatory immune microenvironment is an important mechanism for the occurrence and development of ONFH. It is necessary to study the subtypes of immune cells in ONFH, the interaction between immune cells and macrophages, and the interaction between various immune cells and macrophages, which is beneficial to the development of potential therapeutic methods for ONFH.
Subject(s)
Humans , Femur Head/pathology , Osteonecrosis/therapy , Macrophages/pathology , Inflammation , Femur Head Necrosis/pathologyABSTRACT
[Objective] The retrospective study was designed to analyze the dynamic relationship between the Apolipoprotein A 1,B100 and the progression of coronary artery lesion.[Methods] Patients who underwent the second coronary angiography or coronary 320-slice CTA at a minimum review interval of 6 months after their first examinations in the Third Affiliated Hospital of Sun Yat-sen University from 2010 to 2015 (n =245),were divided into non progress group (n =114) and progress group (n =131).We compared the differences of clinical and Biochemical data between two groups,and tried to find out the relationship by Logistic Regression analysis.[Results] The baseline levels of APOA1 (1.33 ± 0.29 vs 1.24 ± 0.25,P =0.015),APOA1/AOPB100(1.56 ± 0.65 vs 1.38 ± 0.44,P =0.014)in non progress group were higher than those in progress group.The baseline levels of APOB 100 were similar in both groups.The follow-up levels of APOA1 were higher than the baseline levels in both groups,the variation was significant in progress group (1.24 -± 0.25 vs 1.31 ± 0.28,P =0.006).The levels of APOA1 and APOA1/APOB100 were correlated with progression of coronary artery lesion negatively in single-variate logistic regression analysis.The level of APOA 1 (OR =0.245,P =0.005) was correlated with progression of coronary artery lesion negatively in multivariate logistic regression analysis.[Conclusions] APOA1 may has the effect of delaying the progression of coronary artery lesion,and may predict the progression of coronary artery lesion.