Articular cartilage consists of an extracellular matrix including many proteins as well as embedded chondrocytes. Articular cartilage formation and function are influenced by mechanical forces. Hind limb unloading or simulated microgravity causes articular cartilage loss, suggesting the importance of the healthy mechanical environment in articular cartilage homeostasis and implying a significant role of appropriate mechanical stimulation in articular cartilage degeneration. Mechanosensitive ion channels participate in regulating the metabolism of articular chondrocytes, including matrix protein production and extracellular matrix synthesis. Mechanical stimuli, including fluid shear stress, stretch, compression and cell swelling and decreased mechanical conditions (such as simulated microgravity) can alter the membrane potential and regulate the metabolism of articular chondrocytes via transmembrane ion channel-induced ionic fluxes. This process includes Ca²⁺ influx and the resulting mobilization of Ca²⁺ that is due to massive released Ca²⁺ from stores, intracellular cation efflux and extracellular cation influx. This review brings together published information on mechanosensitive ion channels, such as stretch-activated channels (SACs), voltage-gated Ca²⁺ channels (VGCCs), large conductance Ca²⁺-activated K⁺ channels (BK_Ca channels), Ca²⁺-activated K⁺ channels (SK_Ca channels), voltage-activated H⁺ channels (VAHCs), acid sensing ion channels (ASICs), transient receptor potential (TRP) family channels, and piezo1/2 channels. Data based on epithelial sodium channels (ENaCs), purinergic receptors and N-methyl-d-aspartate (NMDA) receptors are also included. These channels mediate mechanoelectrical physiological processes essential for converting physical force signals into biological signals. The primary channel-mediated effects and signaling pathways regulated by these mechanosensitive ion channels can influence the progression of osteoarthritis during the mechanosensory and mechanoadaptive process of articular chondrocytes.

Background: Previous studies had revealed that Body Mass Index (BMI) positively affected Bone Mineral Density (BMD). However, an excessively high BMI was detrimental to health, especially for the elderly. Moreover, it was elusive how much BMI was most beneficial for BMD in older adults to maintain.Objective: To investigate whether there was a BMI saturation effect value that existed to maintain optimal BMD.Methods: A cross-sectional study was conducted using the datasets of the National Health and Nutrition Examination Survey (NHANES) 2005–2006, 2007–2008, 2009–2010, 2013–2014, and 2017–2018. After adjusting for covariates, an analysis of the association between BMI and BMD in different femoral regions (Total femur, Femoral neck, Trochanter, Intertrochanter, and Ward's triangle) and lumbar spine regions (Total spine, L1, L2, L3, and L4) in the whole population was performed using the multivariate linear regression models, smoothing curve fitting, and saturation effects analysis models. Then, subgroup analyses were performed according to gender, age, and race.Results: A total of 10,910 participants (5,654 males and 5,256 females) over 50 years were enrolled in this population-based study. Multivariate linear regression analyses in the population older than 50 years showed that BMI was positively associated with femoral BMD and lumbar spine BMD (P < 0.001, respectively). Smoothing curve fitting showed that the relationship between BMI and BMD was not simply linear and that a saturation value existed. The saturation effect analysis showed that the BMI saturation value was 26.13 (kg/m²) in the total femur, 26.82 (kg/m²) in the total spine, and showed site-specificity in L1 (31.90 kg/m²) and L2 (30.89 kg/m²). The saturation values were consistent with the whole participants in males, while there was high variability in the females. BMI saturation values remained present in subgroup analyses by age and race, showing specificity in some age (60–70 years old) groups and in some races.Conclusions: Our study showed a saturation value association between BMI and BMD for people over 50 years old. Keeping the BMI in the slightly overweight value (around 26 kg/m²) might reduce other adverse effects while obtaining optimal BMD.

Tendon-bone insertion (TBI) injuries are common, primarily involving the rotator cuff (RC) and anterior cruciate ligament (ACL). At present, repair surgery and reconstructive surgery are the main treatments, and the main factor determining the curative effect of surgery is postoperative tendon-bone healing, which requires the stable combination of the transplanted tendon and the bone tunnel to ensure the stability of the joint. Fibrocartilage and bone formation are the main physiological processes in the bone marrow tract. Therefore, therapeutic measures conducive to these processes are likely to be applied clinically to promote tendon-bone healing. In recent years, biomaterials and compounds, stem cells, cell factors, platelet-rich plasma, exosomes, physical therapy, and other technologies have been widely used in the study of promoting tendon-bone healing. This review provides a comprehensive summary of strategies used to promote tendon-bone healing and analyses relevant preclinical and clinical studies. The potential application value of these strategies in promoting tendon-bone healing was also discussed.

Articular cartilage damage and wear can result in cartilage degeneration, ultimately culminating in osteoarthritis. Current surgical interventions offer limited capacity for cartilage tissue regeneration and offer only temporary alleviation of symptoms. Tissue engineering strategies are increasingly recognized as promising modalities for cartilage restoration. Currently, various biological scaffolds utilizing tissue engineering materials are extensively employed in both fundamental and clinical investigations of cartilage repair. In order to optimize the cartilage repair ability of tissue engineering scaffolds, researchers not only optimize the structure and properties of scaffolds from the perspective of materials science and manufacturing technology to enhance their histocompatibility, but also adopt strategies such as loading cells, cytokines, and drugs to promote cartilage formation. This review provides an overview of contemporary tissue engineering strategies employed in cartilage repair, as well as a synthesis of existing preclinical and clinical research. Furthermore, the obstacles faced in the translation of tissue engineering strategies to clinical practice are discussed, offering valuable guidance for researchers seeking to address these challenges.