@article{9376ea21c5204640afb14d50d38917d8,
title = "Effect of a growth hormone treatment on bone orthotropic elasticity in dwarf rats",
abstract = "A refinement of the current ultrasonic elasticity technique was used to measure the orthotropic elastic properties of rat cortical bone as well as to quantify changes in elastic properties, density, and porosity of the dwarf rat cortex after a treatment with recombinant human growth hormone (rhGH). The ultrasonic elasticity technique was refined via optimized signal management of high-frequency wave propagation through cubic cortical specimens. Twenty dwarf rats (37 days old) were randomly assigned to two groups (10 rats each). The dwarf rat model (5-10% of normal GH) was given subcutaneous injections of either rhGH or saline over a 14-day treatment period. Density was measured using Archimedes' technique. Porosity and other microstructural characteristics were also explored via scanning electron microscopy and image analysis. Statistical tests verified significant decreases in cortical orthotropic Young's (-26.7%) and shear (-16.7%) moduli and density (-2.42%) concomitant with an increase in porosity (+125%) after rhGH treatments to the dwarf model (p<0.05). A change in material symmetry from orthotropy toward planar isotropy within the radial-circumferential plane after GH treatments was also noted. These results demonstrate some alteration in bone properties at this time interval. Structural implications of these changes throughout physiological loading regimens should be explored.",
keywords = "Cortical bone, Dwarfism, Growth hormone, Rat model, Ultrasonic elasticity",
author = "Kohles, {Sean S.} and Martinez, {Daniel A.} and Bowers, {James R.} and Vailas, {Arthur C.} and Ray Vanderby",
note = "Funding Information: Administration of exogenous recombinant human growth hormone (rhGH) has been shown to elicit a re- Acknowledgment--Partial funding provided by the National Aeronautic and Space Administration (NAG-2568) and the Veteran's Administration. Recombinant hGH and dwarf male rats were provided by Ge-nentech, San Francisco, CA. Scanning electron microscopy was completed at the University of Wisconsin Integrated Microscopy Resource. Presented in part at the ASME Summer Bioengineering Conference in Breckenridge, CO, June, 1993, the Second World Congress of Biomechanics in Amsterdam, The Netherlands, July, 1994, and the Orthopaedic Research Society Meeting in Orlando, FL, February, 1995 (New Investigator Research Award finalist). Address correspondence to Sean S. Kohles, Department of Exercise and Movement Science, University of Oregon, Eugene, OR 97403-1240, U.S.A. (Received 13Nov95, Revised 26Jun96, Revised 15Mar96, Accepted 25Mar96) sponse at both the structural and tissue levels. A structural response has been measured through increased limb length via a stimulatory effect on the prechondrocytes in the epiphyseal growth plate (19,37). GH has further been shown to augment bone formation and regulation in growth-disrupted (hypophysectomized) rats, thus restoring the growth rate toward that of normal bone (17,18,31,34). On a tissue level, decreased bone growth due to hypophysectomy generally results in a greater abundance of mature (stable) collagen cross-links (30) as well as a decrease in osteoblastic activity (9). Mature intermolecular and intramolecular cross-links are thought to stabilize the molecular matrices of the bone collagen fibrils by ensuring collagen fiber spacing and affecting crystal size via mineralization and resorption, thus potentially increasing the tissue's mechanical tensile strength and decreasing collagen solubility (3,13,41). The possibility then exists that rhGH may alter the mechanical characteristics of mature bone via an up-regulation in bone formation and a decrease in bone maturity. Presumably restoration or augmentation of growth would have an effect on both the quantity and quality of cortical bone as measured on either a structural or tissue level.",
year = "1997",
doi = "10.1007/BF02738540",
language = "English (US)",
volume = "25",
pages = "77--85",
journal = "Annals of Biomedical Engineering",
issn = "0090-6964",
publisher = "Springer Netherlands",
number = "1",
}