Synthetic Peptide CK2.3 Enhances Bone Mineral Density in Senile Mice
Osteoporosis is a silent disease caused by low bone mineral density that results in bone fractures in 1 out of 2 women and 1 in 4 men over the age of 50. Although several treatments for osteopenia and osteoporosis are available, they have severe side effects and new treatments are desperately needed. Current treatments usually target osteoclasts and inhibit their activity or differentiation. Treatments that decrease osteoclast differentiation and activity but enhance osteogenesis and osteoblast activity are not available. We recently developed a peptide, CK2.3, that induces bone formation and increases bone mineral density as demonstrated by injection over the calvaria of 6 to 9-day-old mice and tail vein injection of 8-week-old mice. CK2.3 also decreased osteoclast formation and activity. However, these studies raise questions: does CK2.3 induce similar results in old mice and if so, what is the effective CK2.3 concentration and, is the bone mineral density of vertebrae of the spinal column increased as well? Calcaneal fracture is that the commonest website of injury among tarsal bones and Intra-articular fractures accounted for regarding seventy fifth of all bone fractures. Bone remodeling is a dynamic process and the balance between osteoclast and osteoblast activity is key to the normal bone remodeling. Changes in this balance may cause many bone diseases, including osteoporosis.