The Mechanobiology of Articular Cartilage: Bearing the Burden of Osteoarthritis

Abstract

Articular cartilage injuries and degenerative joint diseases are responsible for progressive pain and disability in millions of people worldwide, yet there is currently no treatment available to restore full joint functionality. As the tissue functions under mechanical load, an understanding of the physiologic or pathologic effects of biomechanical factors on cartilage physiology is of particular interest. Here we highlight studies that have measured cartilage deformation at scales ranging from the macroscale to the microscale, as well as the responses of the resident cartilage cells, chondrocytes, to mechanical loading using in vitro and in vivo approaches. From these studies, it is clear that there exists a complex interplay between mechanical, inflammatory, and biochemical factors that can either support or inhibit cartilage matrix homeostasis under normal or pathologic conditions. Understanding these interactions is an important step toward developing tissue engineering approaches and therapeutic interventions for cartilage pathologies.

In vivo cartilage strain increases following medial meniscal tear and correlates with synovial fluid matrix metalloproteinase activity

“…However, despite the increasing evidence of altered stress and strain distributions in the joint following injury, how these changes relate to mechanical and other physical factors experienced at the cellular and molecular compositional level is less clear (Halloran et al, 2012). In this regard, in vivo strain data, in combination with experimental measures of contact stress (Bedi et al, 2010) and computational models of the knee (Pena et al, 2006; Wilson et al, 2003; Zielinska and Donahue, 2006) may provide important insights into the mechanobiologic response of cartilage to altered loading (Sanchez-Adams et al, 2014). In this study, we have shown the effects of a meniscal tear on cartilage strain but it is also important to note that the altered mechanical loading in the joint following a meniscal injury likely affects other joint tissues including the meniscus, bone, ligaments, and synovium.…”

Stratification of knee osteoarthritis: two major patient subgroups identified by genome wide expression analysis of articular cartilage

“…Chondrocytes therefore have mechanosensitive homeostatic mechanisms that regulate the assembly and maintenance of cartilage matrix. 29 The increases in less chondrogenic genes in Group B may reflect a response to a changed pattern of mechanical stress across the joint causing altered loading on chondrocytes. 30 31 Mechanosensors, ion channels, calcium control, water balance and cytoskeletal tensing are all implicit in chondrocyte load responses, 29 31 32 and these show a spectrum of changes, which are more pronounced in Group B.…”

Consequences of metabolic and oxidative modifications of cartilage tissue

“…Hyaline cartilage and fibrocartilage are exquisitely designed for the purpose of distributing mechanical forces across articulating surfaces, absorbing shock and minimizing friction during joint motion. 10,25,98 In this respect, articular cartilage is able to remodel itself to achieve a best-fit articulation that optimally distributes mechanical stresses to subchondral bone. 99 …”