Regulation of biomechanical signals by NF-kappaB transcription factors in chondrocytes.
Physical therapies and exercise are beneficial not only for physiological recovery in inflamed or injured joints, but also for promoting a homeostatic equilibrium in healthy joints. Human joints provide the pivot points and physiological hinges essential for ambulation and movement to the body, and it is this mobility that in return promotes the health of the joints. But how mobilization regulates the joint microenvironment at the molecular level has remained enigmatic for many years. Recent advances in joint biomechanics and molecular approaches have facilitated an enriched understanding of how joints operate. Consequently, the mechanisms active during joint inflammation that lead to arthritic conditions, both in vivo in animal models, and in vitro at cell and tissue levels, have become increasingly detailed and defined. These efforts have produced mounting evidences supporting the premise that biomechanical signals play a fundamental role in both the etiopathogenesis of arthritic diseases and in the physiological restoration of joints. This report aims to summarize current peer-reviewed literature and available experimental data to explain how the signals generated by mechanical forces/joint mobilization generate beneficial effects on inflamed articular cartilage, and to propose the basis for using appropriate physical therapies for the optimal benefit to the patient suffering from joint associated injuries.
Laboratory of Biomechanics and Tissue Engineering, The Ohio State University, Columbus, OH 43210, USA.
Mirela
M
Anghelina
Danen
D
Sjostrom
Priyangi
P
Perera
Jin
J
Nam
Thomas
T
Knobloch
Sudha
S
Agarwal
D001696:Biomechanical Phenomena / Q000502:physiology; D002356:Cartilage / Q000166:cytology; D002358:Cartilage, Articular / Q000378:metabolism*; D019902:Chondrocytes / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism*; D007596:Joints / Q000378:metabolism; D040542:Mechanotransduction, Cellular / Q000235:genetics; D016328:NF-kappa B / Q000378:metabolism*; D015398:Signal Transduction; D013314:Stress, Mechanical; D014157:Transcription Factors / Q000378:metabolism*
D053583:Interleukin-1beta; D016328:NF-kappa B; D014157:Transcription Factors