Dr. Ge Zhang's Lab has an interest in understanding molecular mechanisms of musculoskeletal disorders, including osteoporosis, osteoarthritis, osteonecrosis, aged fracture repair and rheumatoid arthritis. Especially, the following histopathological events involved in the above disorders are the lab's recent research focus, i.e. reduction in bone formation during aging in osteoporosis, insufficient cartilage anabolism during cartilage degeneration in osteoarthritis, inadequate bone repair in osteonecrosis, impaired bone healing in aged bone and failure of anabolic repair for bone erosion in rheumatoid arthritis. A series of dysregulated molecules from clinical specimens recruited by the lab (Figure 1 and Figure 2) (Songlin Peng et al. Submitted to ORS 2013) would be identified as potential molecular targets toward translational medicine for preventing and even reversing those histopathological events.

Figure 1 Increased CKIP-1 protein expression level negatively associates with decrease in both osteocalcin mRNA and Smad1/5 protein levels in bone specimens from Rheumatoid Arthritis (RA) patient when compared to non-RA patients. * P<0.05 vs. non-RA patients.

Figure 2 Protein expressions of CKIP-1, Smurf-1, Smad-1 and Smad-5 in the eroded bone specimens from non-RA or RA patients.


  1. Songlin Peng, Baosheng Guo, Xiaohua Pan, Jin Liu, Miao Jiang, Lingqiang Zhang, Ge Zhang, Aiping Lu. Increased CKIP-1 protein level negatively associates with reduction in both osteocalcin mRNA and Smad1/5 protein levels in bone specimens from rheumatoid arthritis patients. Submitted to Orthopedics Research Society 2013 Annual Meeting