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Free Radical Biology and Aging Research Program

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Weight is not the only factor in osteoarthritis

Timothy M. Griffin, Ph.D. Assistant Member, Free Radical Biology and Aging Research Program Adjunct Assistant Professor, Department of Biochemistry and Molecular Biology,   University of Oklahoma Health Sciences Center

Research Interests
Osteoarthritis is a disease characterized by cartilage destruction and abnormal bone growth resulting in joint pain and severe disability. It is the primary cause of disability in the United States, and it contributes significantly to reductions in health that occur with aging. Although osteoarthritis is often considered an inevitable consequence of aging, numerous genetic and environment risk factors have been identified that mediate its occurrence and severity. One of the most significant and modifiable risk factors is obesity.

Our laboratory uses integrative and interdisciplinary approaches to study how obesity dysregulates biomechanical, inflammatory, and metabolic processes that are associated with the development of osteoarthritis. We are seeking to determine how dietary fats, adipokines (e.g., leptin), and altered joint loading regulate articular cartilage homeostasis via effects on chondrocyte mitochondrial function and free radical biology. We are particularly interested in the role of nitric oxide as a signaling molecule for genes that regulate cell metabolism and oxidative stress responses, such as peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1α).

We are also interested in understanding how physical activity interacts with obesity-related phenotypes to regulate these processes in healthy and diseased tissue. Therefore, we use a variety of models spanning multiple levels of organization (e.g., cell, tissue, and animal) to study the effect of voluntary exercise (in vivo) and controlled biomechanical loading regimes (in vitro) on inflammatory, metabolic, and anti-oxidant processes in cartilage.

By studying the interaction of diet and physical activity (i.e., two modifiable risk factors for obesity), we hope to reveal novel pathways that regulate cartilage matrix homeostasis. Furthermore, by examining behavioral outcomes in our animal models that are associated with altered motor function and pain, we seek to identify the pathologic mechanisms linking obesity to clinically relevant outcome measures. These studies will also provide a basis for examining how therapeutic interventions that target inflammatory and oxidative processes affect joint-specific pathophysiology and behavioral outcomes.

Joined OMRF Scientific Staff in 2008.

Mailing Address
Free Radical Biology and Aging Research Program, MS 21
Oklahoma Medical Research Foundation
825 N.E. 13th Street
Oklahoma City, Oklahoma 73104

Contact Information
Phone: (405) 271-7579
Fax: (405) 271-1437
E-mail: Tim-Griffin@omrf.org