Osteocytes remedy bone loss by balancing RANKL/OPG expression in osteoporotic sheep modelWednesday (10.05.2017) 15:00 - 15:20 Part of:
Osteoporosis is a systemic skeletal disease generating a lower bone density resulting in a higher risk of bone fracture.
The current study reveals the changes on RANKL/OPG expression in bone cells using, ovariectomized sheep and combined diet beside steroid administration to induce osteoporosis. Therefore, lumbar vertebra of female merino sheep were investigated after 8 months post induction. The study utilized 32 skeletally mature female merino sheep with an average age of 5.5 years were divided into 4 groups (n=8 each): control group (C), bilateral ovariectomized (OVX), OVX and a calcium- and vitamin-D2/3-deficient diet (OVXD), and OVX, diet and corticosteroids (OVXDS). After 8M (M=months) samples were stained with Movat pentachrom for descriptive and histomorphometrical analysis. Immunohistochemical and Enzymohistochemical were performed to visualize osteoclasts and osteoblasts (TRAP and ALP). RANKL and OPG were detected in the osteocyte lacuna, erosion tunnel, and resorption pits. Osteocytes number and morphology were detected using silver nitrate and Rhodamine stains.
Noticeably inferior bone quality and bone mass of the animals in the OVXDS after 8M in comparison with the C group. However, lower osteoclasts numbers in the OVXDS at 8M compared to all groups. ALP positive area were higher in the OVXDS at 8M compared to the controls. Furthermore, spindle-shaped osteocytes were less in treated groups when compared to control.
OVXDS group reflects structural and cellular symptoms of osteoporotic bone after 8M. Increased nonmineralized tissue and ALP positive areas with decreased TRAP positive cells indicate unbalanced RANKL/OPG at the erosion tunnels and resorption pits. Interestingly, the expression RANKL and OPG by osteocytes was lower with treatment progression. Importantly the ratio of RANKL/OPG in osteocytes was comparable between OVXDS and control. The results suggests a controlling role of osteocyte upon bone weakening through RANKL/OPG to bring bone homeostasis to a healthy-like status.