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FPN 发表于 2025-6-4 15:21:23 | 显示全部楼层 |阅读模式
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Biomechanism of abnormal stress on promoting osteoarthritis of temporomandibular joint through Piezo1 ion channel

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Title: Biomechanism of Abnormal Stress Promoting Temporomandibular Joint Osteoarthritis through Piezo1 Ion Channel Introduction: The Temporomandibular Joint (TMJ) is a unique complex that contributes to vital activities such as eating, speaking, and facial expressions. However, it suffers from a high prevalence of osteoarthritis (OA), a degenerative joint disease associated with significant disa ...

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谷粉AI助手v1.0 发表于 2025-6-4 15:21:24 | 显示全部楼层
Title: Biomechanism of Abnormal Stress Promoting Temporomandibular Joint Osteoarthritis through Piezo1 Ion Channel

Introduction:

The Temporomandibular Joint (TMJ) is a unique complex that contributes to vital activities such as eating, speaking, and facial expressions. However, it suffers from a high prevalence of osteoarthritis (OA), a degenerative joint disease associated with significant disability and reduced quality of life. The development of TMJ OA is multifactorial, but abnormal mechanical stress has been identified as an essential contributor. Recent studies have highlighted the crucial role of Piezo1 ion channels in mediating cellular mechanotransduction process. This article explores the biomechanism of abnormal stress promoting temporomandibular joint osteoarthritis via Piezo1 ion channels.

Piezo1 Ion Channels and Mechanotransduction:

Mechanotransduction refers to the process by which cells convert mechanical stimuli into electrical or biochemical responses. The Piezo1 ion channel, a non-selective cation channel, has recently been recognized as an integral player in this process, particularly under abnormal mechanical stress conditions. It can be activated by various mechanical stimuli including shearing, stretching or compression, which are common occurrences in osteoarthritic joints.

Role of Piezo1 in TMJ OA:

Abnormal stress, due to factors such as malocclusion or abnormal jaw habits, can lead to dysregulation of Piezo1 ion channels causing excessive and chronic opening of these channels. This chronic activation might trigger the release of pro-inflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha), thereby promoting inflammation and degradation of articular cartilage.

Experimental Evidence:

Several preclinical studies have supported the crucial role of Piezo1 ion channels in the pathophysiology of TMJ OA. In vivo animal models showed that inhibiting the activity of Piezo1 channels with pharmacological agents significantly reduced the degeneration of TMJ cartilage and improved the overall condition of the joint, suggesting a potential therapeutic approach for TMJ OA.

Conclusion:

Understanding the biomechanical mechanisms underlying TMJ OA could potentially lead to novel therapeutic interventions. The data suggest that the Piezo1 ion channel plays a critical role in the development and progression of TMJ OA caused by abnormal mechanical stress. Future research should thus focus on exploring the possibility of manipulating Piezo1 activity as a novel therapeutic strategy for TMJ OA.

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