Effects of Mechanical Loading and Interstitial Fluid Pressure on Bone Remodeling
Charles H. Turner
Abstract
Charles H. Turner
Abstract
Abstract Mechanical loading clearly affects bone remodeling (by remodeling, I refer to the process of removal and replacement of bone tissue rather than bone shape changes). Bone remodeling is minimal under normal physiological conditions, but becomes elevated under disuse or extreme overuse (Figure 1). In each case, the mechanism for elevated remodeling is probably quite different. Elevated bone remodeling in overuse is probably caused by microdamage accumulation in the bone tissue. Microdamage causes site-directed bone remodeling [1,2], preceded by osteocyte apoptosis [3]. Conversely, elevated bone remodeling in disuse is not due to tissue microdamage but probably diminished tissue perfusion. In bone subject to disuse, osteocytes show signs of hypoxia within three days and remodeling becomes elevated a few days later [4]. Therefore elevated bone remodeling is preceded by osteocyte distress regardless of whether it is caused by disuse or overuse, suggesting that osteocytes play an important role in the signal cascade leading to elevated bone remodeling. Osteocytes form a highly interconnected network within the bone matrix which has signal processing capabilities, yet is unclear how osteocytes process information, e.g., microdamage. In this paper some effects of disuse and overuse on bone remodeling are discussed with the goal of outlining the key mechanical parameters important for bone remodeling.
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Abstract Mechanical loading clearly affects bone remodeling (by remodeling, I refer to the process of removal and replacement of bone tissue rather than bone shape changes). Bone remodeling is minimal under normal physiological conditions, but becomes elevated under disuse or extreme overuse (Figure 1). In each case, the mechanism for elevated remodeling is probably quite different. Elevated bone remodeling in overuse is probably caused by microdamage accumulation in the bone tissue. Microdamage causes site-directed bone remodeling [1,2], preceded by osteocyte apoptosis [3]. Conversely, elevated bone remodeling in disuse is not due to tissue microdamage but probably diminished tissue perfusion. In bone subject to disuse, osteocytes show signs of hypoxia within three days and remodeling becomes elevated a few days later [4]. Therefore elevated bone remodeling is preceded by osteocyte distress regardless of whether it is caused by disuse or overuse, suggesting that osteocytes play an important role in the signal cascade leading to elevated bone remodeling. Osteocytes form a highly interconnected network within the bone matrix which has signal processing capabilities, yet is unclear how osteocytes process information, e.g., microdamage. In this paper some effects of disuse and overuse on bone remodeling are discussed with the goal of outlining the key mechanical parameters important for bone remodeling.
Key concepts: Osteocyte, Bone remodeling, Bone remodeling period, Bone tissue, Bone matrix, Bone cell, Chemistry, Medicine