My research has explored the understudied interface between cellular responses and the environment in which cells of interest are situated in vivo. By analyzing cells maintained in their natural environment, I have been at the forefront of pathophysiological studies in both the endocrine and musculoskeletal fields. Currently I am exploring the role of bone cells in aetiology of hip fracture, with particular reference to the microarchitecture and mineral composition of the femoral neck cortex and the cellular mechanisms associated with osteocytogenesis and bone re-modelling. I am also interested in the role of osteocytes in fracture healing and the increased bone mass associated with osteoarthritis.
Reeve J, and Loveridge N. (2014) The fragile elderly hip: Mechanisms associated with age-related loss of strength and toughness.” Bone 61): 138–48.
Prideaux M, Loveridge N, Pitsillides AA, and Farquharson C. (2012) Extracellular matrix mineralization promotes E11/gp38 Glycoprotein expression and drives osteocytic differentiation. PloS One 7 (5). e36786
Power J, Poole KES, van Bezooijen R, Doube M, Caballero-Alias AM, Lowik, C, Papapoulos S, Reeve J , and Loveridge N. (2010) Sclerostin and the regulation of bone formation: Effects in hip osteoarthritis and femoral neck fracture. Journal of Bone and Mineral Research 25: 1867–76.
Loveridge N, Fletcher S, Power J, Caballero-Alias AM, Das-Gupta V, Rushton N, Parker M, Reeve J, Pitsillides AA. (2002) Patterns of osteocytic endothelial nitric oxide synthase expression in the femoral neck cortex: Differences between cases of intracapsular hip fracture and controls. Bone 30: 866–71.
Jordan GR, Loveridge N, Bell KL, Power J, Rushton N, and Reeve J. (2000) Spatial clustering of remodeling osteons in the femoral neck cortex: A cause of weakness in hip fracture? Bone 26: 305–13
Areas of expertise
human physiology,fracture, bone biomechanics, osteocytes, osteoclast, chondrocytes,osteoporosis, hip fracture