Molecular analysis of leptin receptor in bone tissue and some markers causing an increasing effect in bone tissue mass at lombar spinal stenosis patients who need to have surgical treatment

Leptin is a hormone that has been proven to be associated with obesity and is primarily secreted from adipose tissue. Although the amount of fat tissue is the most important marker of leptin level, changes in nutrient intake also affect leptin level. Leptin exerts its effect through leptin receptors in the central nervous system and peripheral tissues. It is reported that the leptin receptor resistance that occurs takes place in response to excessive increase in leptin levels in obesity, in which the amount of adipose tissue is increased. It has been demonstrated that leptin hormone acts directly and indirectly on bone mass. It directly affects osteoblasts and chondrocytes with mainly leptin receptors, through fibroblast growth factor 23 (FGF-23) activation mediated by osteocalcin regulation. In this way, it creates an increase in bone mass by exerting a mitogenic effect on bone tissue. In addition, leptin has a negative effect on osteoclastogenesis by stimulating stromal cells, causing osteoprotegerin increase and RANK ligand decrease. A number of pathophysiological changes occur in bone and connective tissue in patients with lumbar spinal stenosis. In these patients, mechanisms such as facet joint hypertrophy and osteophyte development in bone tissue increase pathological bone mass. Obesity has been shown as a risk factor in the development of lumbar spinal stenosis. In this study, patients diagnosed with lumbar spinal stenosis requiring surgical treatment were divided into two groups (obese and non-obese) to compare bone leptin, leptin receptor, FGF-23, osteocalcin, osteoprotegerin and RANK ligand at transcriptional level and were evaluated for the effect of leptin on bone hypertrophy in these patients.