Abstract
Osteoporosis is a progressive skeletal disease characterized by reduced bone density leading to bone fragility and an elevated risk of bone fractures. In osteoporotic conditions, decrease in bone density happens due to the augmented osteoclastic activity and the reduced number of osteoblast progenitor cells (mesenchymal stem cells, MSCs). We investigated a new method of cell therapy with membrane-engineered MSCs to restore the osteoblast progenitor pool and to inhibit osteoclastic activity in the fractured osteoporotic bones. The primary active sites of the polymer are the N-hydroxysuccinimide and bisphosphonate groups that allow the polymer to covalently bind to the MSCs’ plasma membrane, target hydroxyapatite molecules on the bone surface and inhibit osteolysis. The therapeutic utility of the membrane-engineered MSCs was investigated in female rats with induced estrogen-dependent osteoporosis and ulnar fractures. The analysis of the bone density dynamics showed a 27.4% and 21.5% increase in bone density at 4 and 24 weeks after the osteotomy of the ulna in animals that received four transplantations of polymer-modified MSCs. The results of the intravital observations were confirmed by the post-mortem analysis of histological slices of the fracture zones. Therefore, this combined approach that involves polymer and cell transplantation shows promise and warrants further bio-safety and clinical exploration.
Highlights
Osteoporosis is a chronic progressive metabolic bone disease that predisposes patients to an increased risk of bone fracture
There are more than 9 million fractures associated with osteoporosis, including 1.6 million hip fractures, 1.7 million of the forearm, and 1.4 million clinical vertebral fractures [1]
It is expected that in 30 years, the incidence of osteoporosis-related hip fracture will rise by 310% among men and 240% among women [3]
Summary
Osteoporosis is a chronic progressive metabolic bone disease that predisposes patients to an increased risk of bone fracture. There are more than 9 million fractures associated with osteoporosis, including 1.6 million hip fractures, 1.7 million of the forearm, and 1.4 million clinical vertebral fractures [1]. Of all these fractures, 51% are attributed to Europe and the Americas, while the rest belong to the Western Pacific region and Southeast Asia [1,2]. The decrease in bone density is called osteopenia and it is caused by aging-associated bone resorption, decline in the number of osteoblasts and reduced calcium absorption. A number of studies have been performed on developing strategies aiming to preserve bone mass and decrease the risks of the fractures. Fewer efforts have been made to explore osteoporosis-associated fracture-healing strategies [5]
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