
According to the WHO, osteoporosis is one of the most common bone diseases and is the main cause of vertebral body and hip fractures in older patients.
It is characterized by impaired bone homeostasis, increased bone resorption and is defined by reduced bone density and structure. Women are much more frequently affected by osteoporosis. After the menopause in particular, hormonal changes lead to a decline in bone structure and bone density. The risk of osteoporotic fractures increases as a result of changes in the microarchitecture of the bone. Typical osteoporotic fractures are found in the forearm and wrist, vertebrae, shoulder and hip. A reduced expression of osteoprotegerin (OPG), which is secreted by osteoblasts, is partly responsible for the increased bone resorption. OPG is a soluble receptor that intercepts the ligand Receptor Activator of Nuclear Factor-κappa B (RANK-L), which is also secreted by osteoblasts. If there is an imbalance in favor of RANK-L, this ligand binds more strongly to the RANK receptor of the osteoclasts, so that they are excessively activated, which causes increased bone resorption.
Angiogenesis is also essential for maintaining bone homeostasis. It has already been demonstrated that a reduced blood supply to the bone was associated with osteoporosis, in the sense of reduced bone density. This indicates that bone density is directly related to the supply of minerals in the bloodstream.
With the help of our own preliminary work, we were able to identify various angiogenesis-relevant cytokines, such as IL-6 and angiogenin, which were differentially expressed in osteoblasts of patients diagnosed with osteoporosis compared to patients with normal bone density.
The influence of the differential expression of these parameters on factors such as OPG and RANK-L and also on endothelial cells is the subject of our research work.
Furthermore, the influence of the other identified factors on osteogenesis- and osteoporosis-relevant factors will also be analyzed.
The aim of our work is to analyze age-dependent or dysfunctional effects of osteoblasts in osteoporosis patients in more detail. The results should serve to further clarify the multifactorial pathogenesis of osteoporosis and, if possible, offer new treatment options.