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Supplemental Material, sj-pdf-1-ojs-10.1177_23259671231174476 for Open Versus Arthroscopic Latarjet for Recurrent Anterior Shoulder Instability: A Systematic Review and Meta-analysis by Zhenhan Deng, Yizi Zheng, Jingyue Su, Siyu Chen, Zhiqin Deng, Weimin Zhu, Yusheng Li and Wei Lu in Orthopaedic Journal of Sports Medicine

Persistent hypotonic and inflammatory conditions in the joint cavity can lead to the loss of cartilage matrix and cell death, which are the important mechanisms of osteoarthritis (OA) onset. Previous studies have confirmed that the existence of a hypotonic environment is a red flag for inflammation, as hypotonic environment induces the opening of the chloride channel of the cell and promotes chloride ion efflux, which prompts the cell volume to increase. Chloride channels play an important role in the regulation of mineralization and chondrocyte death. Here, we reported that OA chondrocytes showed a significant increase of cell death rate and the imbalance of cartilage matrix catabolism. We found that the distribution of skeleton protein F-actin was disordered. In addition, the volume-sensitive chloride current of OA chondrocytes decreased significantly with the increase of the expression levels of inflammation-related proteins caspase-1, caspase-3, and NLRP3. Moreover, interleukin-1β (IL-1β) showed a potential to activate the chloride current of normal chondrocytes. These results indicate that IL-1β-induced chloride channel opening in chondrocytes may be closely related to the occurrence of OA. This chloride channel opening process may therefore be a potential target for the treatment of OA.

Huankun Fang,1,2,* Zhiqin Deng,1,* Jianquan Liu,1,* Siyu Chen,3 Zhenhan Deng,3 Wencui Li1 1Hand and Foot Surgery Department, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, Shenzhen, Guangdong, 518035, People’s Republic of China; 2Medical College, Shantou University, Shantou, Guangdong, 515041, People’s Republic of China; 3Department of Sports Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, Shenzhen, Guangdong, 518035, People’s Republic of China*These authors contributed equally to this workCorrespondence: Zhenhan Deng, Department of Sports Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, 3002 Sungang West Road, Shenzhen City, 518025, People’s Republic of China, Tel +86 13928440786, Fax +86 755-83366388, Email dengzhenhan@email.szu.edu.cn Wencui Li, Department of Hand and Foot Surgery, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, 3002 Sungang West Road, Shenzhen City, 518025, People’s Republic of China, Tel +86 13923750767, Email wencuilisz@126.comAbstract: Senescence mainly manifests as a series of degenerative changes in the morphological structure and function of the body. Osteoporosis is a systemic bone metabolic disease characterized by destruction of bone microstructure, low bone mineral content, decreased bone strength, and increased brittleness and fracture susceptibility. Osteoblasts, osteoclasts and osteocytes are the main cellular components of bones. However, in the process of aging, due to various self or environmental factors, the body’s function and metabolism are disordered, and osteoporosis will appear in the bones. Here, we summarize the mechanism of aging, and focus on the impact of aging on bone remodeling homeostasis, including the mechanism of ion channels on bone remodeling. Finally, we summarized the current clinical medications, targets and defects for the treatment of osteoporosis.Keywords: aging, osteoporosis, bone formation, epigenetics, autophagy, chlorine channel

Zicong Lin,1,* Zhiqin Deng,1,* Jianquan Liu,1,* Zhongshi Lin,2 Siyu Chen,3 Zhenhan Deng,3 Wencui Li1 1Hand and Foot Surgery Department, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, Shenzhen, Guangdong, 518035, People’s Republic of China; 2Shenzhen Institute for Drug Control (Shenzhen Testing Center of Medical Devices), Shenzhen, Guangdong, 518057, People’s Republic of China; 3Department of Sports Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, Shenzhen, Guangdong, 518035, People’s Republic of China*These authors contributed equally to this workCorrespondence: Zhenhan Deng, Department of Sports Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, 3002 Sungang West Road, Shenzhen City, 518025, People’s Republic of China, Tel +86 13928440786, Fax +86 755-83366388, Email dengzhenhan@email.szu.edu.cn Wencui Li, Department of Hand and Foot Surgery, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, 3002 Sungang West Road, Shenzhen City, 518025, People’s Republic of China, Tel +86 13923750767, Email liwencui@email.szu.edu.cnAbstract: Articular cartilage allows the human body to buffer and absorb stress during normal exercise. It is mainly composed of cartilage cells and the extracellular matrix and is surrounded by the extracellular microenvironment formed by synovial fluid and various factors in it. Studies have shown that chondrocytes are the metabolic center of articular cartilage. Under physiological conditions, the extracellular matrix is in a dynamic balance of anabolism and catabolism, and various factors and physical and chemical conditions in the extracellular microenvironment are also in a steady state. This homeostasis depends on the normal function of proteins represented by various ion channels on chondrocytes. In mammalian chondrocyte species, ion channels are mainly divided into two categories: cation channels and anion channels. Anion channels such as chloride channels have become hot research topics in recent years. These channels play an extremely important role in various physiological processes. Recently, a growing body of evidence has shown that many pathological processes, abnormal concentration of mechanical stress and chloride channel dysfunction in articular cartilage lead to microenvironment disorders, matrix and bone metabolism imbalances, which cause partial aseptic inflammation. These pathological processes initiate extracellular matrix degradation, abnormal chondrocyte death, hyperplasia of inflammatory synovium and bony. Osteoarthritis (OA) is a common clinical disease in orthopedics. Its typical manifestations are joint inflammation and pain caused by articular cartilage degeneration, but its pathogenesis has not been fully elucidated. Focusing on the physiological functions and pathological changes of chloride channels and pathophysiology of aseptic inflammation furthers the understanding of OA pathogenesis and provides possible targets for subsequent medication development.Keywords: osteoarthritis, chondrocyte, ion channel, inflammatory factors