Deformation-Induced Calcium Signaling in Articular Chondrocytes

Abstract

Under normal physiological conditions, articular cartilage provides a nearly frictionless surface for the transmission and distribution of joint loads. The ultrastructure and composition of cartilage, which allow for this unique function, are maintained through a balance of the anabolic and catabolic activities of the chondrocyte cell population, which comprises a small fraction (1–10% by volume) of the tissue (Stockwell, 1979). Chondrocyte metabolic activity is regulated by both genetic and environmental factors, such as soluble mediators (e.g., cytokines, hormones) and physical stimuli (hydrostatic and osmotic pressures, mechanical load). This ability to regulate metabolic activity in response to the mechanical environment provides a means by which chondrocytes can alter the structure and composition, and hence the mechanical properties of the extracellular matrix, to the physical demands of the body (Gray et al., 1988; Gray et al., 1989; Guilak et al., 1994b; Helminen et al., 1987; Helminen et al., 1992; Jones et al., 1982; Sah et al., 1989; Schneiderman et al., 1986; Tammi et al., 1987; also see review by Mow et al., 1994, this volume). Under abnormal conditions, however, mechanical loads are believed to be an important factor in the initiation and progression of joint degeneration (Howell et al., 1992; Moskowitz, 1992).