Maureen J. Devlin

Research Interests

Although it's well known that growing bones respond to mechanical loading, many of the mechanisms involved are poorly understood. Skeletal robusticity varies among human populations, suggesting that osteogenic responses to mechanical loading also vary, but the biological basis is unknown. How does strain stimulate bone growth? Does individual physiology affect skeletal growth in response to strain?

These are complex questions, because many interacting stimuli influence bone growth--including genes, hormones, climate, nutrition, disease, and mechanical loading. My current research tests how interactions between estradiol levels and mechanical loading affect diaphyseal bone growth. Estradiol is best known as a reproductive hormone, but it is also a major regulator of bone growth. More importantly, its primary receptor, estrogen receptor alpha (ERalpha), is necessary for osteoblasts (bone cells) to sense mechanical loading. Estradiol increases the transcription of ERalpha.

Using controlled experiments, I have shown that variation in estradiol levels during skeletal growth affects the capacity of bone to respond to mechanical loading. In both sheep and mice, individuals with higher E2 levels have greater ERalpha expression, and more bone growth in response to bone strain, than individuals with lower E2 levels.

Current Projects

Thesis Research

Estradiol level affects osteogenic response to strain via estrogen receptor-alpha. Supported by NSF Doctoral Dissertation Improvement Grant BCS-0434894

Committee: Dan Lieberman, Peter Ellison, David Pilbeam, Noreen Tuross, Andy Biewener

Other Projects

Trabecular orientation in flexed versus extended postures in guinea fowl: a test of Wolff’s Law (with Herman Pontzer and Dan Lieberman)

Effects of food processing on masticatory strain and craniofacial growth in a retrognathic face (with Dan Lieberman, Gail Krovitz, Franklin Yates)