The knee joint is a weight-bearing structure that endures varied mechanical stresses in daily and athletic activities. Its cells convert these stresses into biochemical signals through mechanotransduction, prompting changes essential for joint health, repair, and adaptation. Understanding these processes is pivotal for developing rehabilitation strategies that address injuries and degenerative conditions like osteoarthritis. Different loading modalities—compression, tension, shear, and hydrostatic pressure—impact knee tissues (cartilage, synovium, ligaments, and tendons) and their resident cells (chondrocytes, synoviocytes, and fibroblasts). Chondrocytes adjust extracellular matrix synthesis to maintain cartilage integrity, while synoviocytes regulate synovial fluid components crucial for lubrication. Fibroblasts modulate collagen production, preserving ligament and tendon strength. Underlying these activities are key signaling pathways (e.g., MAPK, NF-κB, and Wnt) that regulate gene expression and cellular metabolism in response to mechanical stimuli. By linking basic mechanobiology insights to clinical practice, clinicians can tailor therapeutic interventions—such as controlled loading, exercise regimens, manual therapy, and orthotic devices—to optimize tissue repair, restore function, and prevent further degeneration. This mechanotransduction-focused approach offers a comprehensive framework for improving knee joint health and enhancing rehabilitation outcomes.
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Mikołaj Stańczak
Bart Swinnen
Jakub Surmacz
Cellular Physiology and Biochemistry
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Stańczak et al. (Tue,) studied this question.
www.synapsesocial.com/papers/68efd921056559ef4287767a — DOI: https://doi.org/10.33594/000000818