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骨关节炎膝关节中的炎症生物标志物与胫股关节状态:一项叙述性综述

Inflammatory biomarkers and state of the tibiofemoral joint in the osteoarthritic knee: a narrative review.

作者信息

Kennedy Mitchell Iung, Olson Conner P, DePhillipo Nicholas N, Tagliero Adam J, LaPrade Robert F, Kennedy Nicholas I

机构信息

Elson S. Floyd College of Medicine, Spokane, WA, USA.

University of Minnesota Medical School, Minneapolis, MN, USA.

出版信息

Ann Jt. 2024 Jun 11;9:27. doi: 10.21037/aoj-23-59. eCollection 2024.

Abstract

BACKGROUND

The healing process is initiated by injurious stimuli in response to cellular damage. Upon recruiting proinflammatory biomarkers to the tissue site of injury, the release of additional biomarkers occurs, including the likes of cytokines, matrix molecules, macrophages, neutrophils, and others. This influx of immune system mediators can occur for chronic periods, and though its intention is for healing the original injurious stimuli, it is also suspected of causing long term cartilage impairment following internal structure damage. The objective of this narrative review is to identify which inflammatory factors have the leading roles in the progression of osteoarthritis (OA) following knee injuries and how they fluctuate throughout the healing process, both acutely and chronically.

METHODS

This narrative review was performed following a computerized search of the electronic database on PubMed in May 2023. Abstracts related to the inflammatory biomarkers of the post-traumatic knee were included for review.

KEY CONTENT AND FINDINGS

The chronic low-level inflammation that leads to OA leads to the destruction of the cartilage extracellular matrix, which new and developing orthopedic research is still attempting to find resolve for. Some of this damage is attributed to the biomechanical alterations that occurs following injury, though with most procedures capable of joint biomechanical restoration, focus has rather been shifted toward the environment of inflammatory biomarkers.

CONCLUSIONS

Future studies will be aiming to improve the diagnostics of OA, focusing on a consistent correlation of inflammatory biomarkers with imaging. Additionally, biochemical treatments will need to focus on validating reproducible modulation of signaling molecules, in attempts to lessen the chronic elevations of destructive biomarkers.

摘要

背景

愈合过程由针对细胞损伤的有害刺激引发。在将促炎生物标志物募集到损伤组织部位后,会释放其他生物标志物,包括细胞因子、基质分子、巨噬细胞、中性粒细胞等。免疫系统介质的这种涌入可能会持续很长时间,尽管其目的是愈合最初的有害刺激,但也有人怀疑它会在内部结构损伤后导致长期软骨损伤。本叙述性综述的目的是确定哪些炎症因子在膝关节损伤后骨关节炎(OA)的进展中起主导作用,以及它们在整个愈合过程中(急性和慢性)如何波动。

方法

本叙述性综述于2023年5月在PubMed电子数据库进行计算机检索后完成。纳入与创伤后膝关节炎症生物标志物相关的摘要进行综述。

关键内容与发现

导致OA的慢性低水平炎症会导致软骨细胞外基质的破坏,新出现的骨科研究仍在试图找到解决办法。这种损伤部分归因于损伤后发生的生物力学改变,不过由于大多数手术能够恢复关节生物力学,研究重点已转向炎症生物标志物的环境。

结论

未来的研究将旨在改进OA的诊断,重点是炎症生物标志物与影像学的一致相关性。此外,生化治疗将需要专注于验证信号分子的可重复调节,以试图减轻破坏性生物标志物的慢性升高。

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