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On July 16, 2010, the bone biology community suffered a tremendous loss with the passing of Charles H Turner, who lost a 2-year battle with colorectal cancer at the much-too-young age of 48. He died peacefully at home, surrounded by his loving family.

Charles graduated from Texas Tech in 1983 with a BS in mechanical engineering and subsequently earned a PhD from Tulane in 1987 under the tutelage of Dr Stephen Cowin. His PhD years at Tulane were spent developing a mathematical model for the relationship between cancellous bone elastic properties and its structure. After graduating, Charles spent four years at Creighton University as a faculty member in the Osteoporosis Research Center. In 1991, he moved to Indianapolis to join the skeletal biology group at the Indiana University School of Medicine, which at that time was largely clinically oriented. Charles spent a significant portion of his 19-year tenure at the Indiana University School of Medicine and Indiana University–Purdue University at Indianapolis (IUPUI) selflessly building up the bone group with personnel, resources, and international recognition. He played a central role in establishing and developing the Biomedical Engineering Program, of which he was associate director. He also was the director of the Biomechanics and Biomaterials Research Center, which later became a Signature Center of the University under his leadership. While at IUPUI, Charles earned many honors and awards, including the ASBMR's Fuller Albright Award in 2001, the Abraham M. Max Distinguished Professor Award from IUPUI in 2006, and election as a fellow of the American Institute for Medical and Biological Engineering, also in 2006. He was awarded IUPUI's highly coveted title of Chancellor's Professor in 2008 in recognition of his outstanding scientific and educational achievements.

Early in his career, Charles recognized that two concepts were very important to the future of bone metabolism research, particularly in the area of bone mechanotransduction: (1) The rodent was becoming the model workhorse for biomedical applications of skeletal biologic research, and (2) there was a great need for noninvasive in vivo models of mechanotransduction. Around 1990, available in vivo models of enhanced mechanical loading involved surgical implantation of Steinman pins in or around long bones of interest in rabbits, turkeys, and chickens. The pins were secured in a materials testing device and pulled to deform the bone in a predictable manner, allowing histologic study of the adaptive response. Other studies would surgically remove a portion of the diaphysis in a limb segment typically supported by two bones (eg, ulnar resection to overload the radius). Charles set his sights on developing the first model of well-controlled mechanical stimulation in vivo that did not require surgical intervention (and the potential experimental artifacts associated with it), and he had the foresight to use the rat as the animal model platform.

In 1991, he published his description of the rat tibia four-point bending model, which applies mediolateral pressure to the rat tibia through misaligned padded upper and lower force platens. Further, Charles exercised the scientific rigor to design a sham loading configuration to his model that was capable of applying similar pressure to the leg but induced negligible bending. To date, that model has been used to study adaptation in rats and mice in over 50 publications in many labs worldwide. A few years later, Lance Lanyon's group in the United Kingdom published an alterative model of well-controlled noninvasive in vivo loading that was in many respects superior to the model that Charles developed, at least for studying periosteal responses. Rather than pridefully adhering to his own model, Charles was quick to set up and institute the rodent ulna axial loading model developed by Lanyon and essentially retired his four-point model, except for rare cases in which its use was justified. In this and many other cases, Charles was a quintessential scientist whose aim was to facilitate proper execution of the most informative experiments possible, whether by himself or by others, and regardless of whether the models used were his or those of others.

Charles also was instrumental during the 1990 s in elucidating the deleterious effects of fluoride on bone material properties. He played a key role in developing a report for a US Environmental Protection Agency (EPA) panel regarding fluoride in drinking water. Charles was invited to address the panel on his cell- and animal-based data. He reported that although bone mass appeared to be increased, bone strength was diminished, and he attributed this to alteration of the crystal structure of the bone induced by fluoride. Charles' arguments were scientifically strong, and his data were valuable to the panel's eventual conclusions regarding fluoride's effects. His data were cited widely in the bone fluoride chapter in the EPA report, which dealt with all aspects of water fluoridation, from the cellular level through multiple stages of human skeletal fluorosis. Several years later, Charles was instrumental in evaluating the biomechanical consequences of teriparatide treatment for Lilly's preclinical exploration of Forteo, the first and only anabolic therapy approved by the Food and Drug Administration for severe osteoporosis.

In the earlier part of this decade, as the Human Genome Project was nearing completion, Charles began realizing the potential power of genomics to tackle questions in metabolic bone disease and fracture susceptibility. However, with no formal training in genetics, he knew that he had his work cut out for him. Undeterred, he began reading as many genetics textbooks, primers, and articles as he could get his hands on. After several years of in-depth study (in addition to carrying on his established research program), he set out to screen approximately 15 inbred lines of rats for bone strength at several skeletal sites. On identifying high- and low-strength lines, he began a classic genetics study by crossing two inbred rat lines with extreme bone strength phenotypes (one high and one low) and then phenotyping and genotyping the resulting F2 rats. He was able to identify a number of quantitative trait loci (QTLs) for bone strength that are still being pursued to this day to identify the individual genes that contribute to bone strength/geometry. Those studies led to support for his work on the genetics of bone fragility from the US National Institutes of Health (NIH) and a few years later earned him an individual project on a bone genetics Program Project Grant organized by Dr Michael Econs in the Endocrinology Division here at Indiana University. In the meantime, Charles had the insight to begin looking at the genetics of mechanotransduction using similar approaches. He collaborated with Dr Wesley Beamer at the Jackson Laboratories to begin screening congenic mouse lines for their ability to respond to mechanical loads. Those seminal studies have been capitalized on by other labs to narrow several QTLs into viable candidate genes.

Beyond these and other precious contributions to orthopedic science, bioengineering, and bone biology, Charles was an unmatched asset to have as a collaborator, mentor, and friend. He was always eager to go out for a beer on Friday afternoons to informally discuss new ideas and synthesize and grow existing ideas. It was truly a privilege to have spent time with someone so genuinely excited by science and the possibilities that it holds. He was exceptionally generous with his time, resources, ideas, and knowledge, and he was always the biggest cheerleader for his students and postdoctoral trainees at meetings and other events. On a personal level, Charles was gregarious yet reserved, and all who knew him well would attest to his fairness (sometimes at his own peril). Charles was a remarkable scientist, and we will miss him dearly.