Open Access

ARTICLE

Aging-Related Differences in Chondrocyte Viscoelastic Properties

by

* Shiley Center for Orthopaedic Research and Education at Scripps Clinic, La Jolla, CA
† University of California, San Diego, La Jolla, CA
‡ Corresponding Author. Shiley Center for Orthopaedic Research and Education at Scripps Clinic, 11025 North Torrey Pines Road, Suite 140, La Jolla, CA 92037. Tel: 858-332-0166; Fax: 858-332-0140; Email: ddlima@scripps.edu

Molecular & Cellular Biomechanics 2009, 6(2), 113-119. https://doi.org/10.3970/mcb.2009.006.113

Abstract

The biomechanical properties of articular cartilage change profoundly with aging. These changes have been linked with increased potential for cartilage degeneration and osteoarthritis. However, less is known about the change in biomechanical properties of chondrocytes with increasing age. Cell stiffness can affect mechanotransduction pathways and may alter cell function. We measured aging-related changes in the biomechanical properties of chondrocytes. Human chondrocytes were isolated from knee articular cartilage within 48 hours after death or from osteochondral specimens obtained from knee arthroplasty. Cells were divided into two age groups: between 18 and 35 years (18 -- 35); and greater than 55 years (55+) of age. The 55+ group was further subdivided based on visual grade of osteoarthritis: normal (N) or osteoarthritic (OA). The viscoelastic properties of the cell were measured using the previously described micropipette cell aspiration technique. The equilibrium modulus, instantaneous modulus, and apparent viscosity were significantly higher in the 55+ year age group than in the 18 -- 35 age group. On the other hand, no differences were found in the equilibrium modulus, instantaneous modulus, or apparent viscosity between the N and OA groups. The increase in cell stiffness can be attributed to altered mechanical properties of the cell membrane, the cytoplasm, or the cytoskeleton. Increased stiffness has been reported in osteoarthritic chondrocytes, which in turn has been attributed to the actin cytoskeleton. A similar mechanism may be responsible for our finding of increased stiffness in aging chondrocytes. With advancing age, changes in the biomechanical properties of the cell could alter molecular and biochemical responses.

---