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Osteoporosis - Clinical research overview

This library brings together peer-reviewed studies on Mesenchymal Stem Cells (MSCs) across a wide range of medical indications. Each study contributes to a deeper understanding of how MSCs support repair, regeneration, and immune balance in the body.
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Osteoporosis

More than 200 million people live with osteoporosis, yet the condition often goes unnoticed until a fracture occurs. As researchers examine why bone resilience declines with age, current research indicates that chronic inflammation, oxidative stress and immune dysregulation play a central role in osteoporosis progression. 

Mesenchymal stem cells (MSCs) are being studied for their immunomodulatory and anti-inflammatory potential to support the aging bone environment and help limit further decline.. 

Osteoporosis

Joann L. Porter, et al.
Osteoporosis is defined as low bone mineral density caused by altered bone microstructure, ultimately predisposing patients to low-impact, fragility fractures. Osteoporotic fractures lead to a significant decrease in quality of life, increasing morbidity, mortality, and disability. Over 50% of postmenopausal white women will have an osteoporotic-related fracture. Only 33% of senior women who have a hip fracture will be able to return to independence. In white men, the risk of an osteoporotic fracture is 20%, but the one-year mortality in men who have a hip fracture is twice that of women. Black males and females have less osteoporosis than their white counterparts, but those diagnosed with osteoporosis have similar fracture risks. The aging of the American population is expected to triple the number of osteoporotic fractures.
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Oxidative stress and inflammation: roles in osteoporosis

Jing Luo, et al.
Osteoporosis (OP) is a prevalent bone disease characterized by reduced bone mineral density (BMD) and compromised microstructure, leading to an increased risk of fractures and disability. With an aging global population, OP has become a significant public health issue, affecting over 200 million people worldwide. OP can be classified into primary (type I and type II) and secondary forms, with estrogen deficiency playing a critical role in postmenopausal OP. The pathophysiology of OP involves a complex interplay of factors, including cellular senescence, oxidative stress, inflammation, and hormonal imbalances. Bone homeostasis, maintained by the balance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation, is regulated by various signaling pathways such as receptor activator of nuclear factor-κB ligand/receptor activator of nuclear factor-κB/osteoprotegerin (RANKL/RANK/OPG), interleukin-1/tumor necrosis factor-α (IL-1/TNF-α), and Notch. Disruption of these pathways, along with oxidative stress and chronic inflammation, leads to bone loss. Estrogen deficiency enhances pro-inflammatory cytokine production, increases osteoclast differentiation, and accelerates bone resorption. Furthermore, cellular senescence and oxidative stress contribute to reduced osteoblast function and increased adipogenesis in bone marrow mesenchymal stem cells (BMSCs). Chronic inflammation and oxidative stress further exacerbate the imbalance in bone remodeling, promoting osteoclast activity and impairing osteogenesis. Understanding the roles of immune dysregulation, oxidative stress, and inflammation in osteoporosis progression is crucial for developing targeted therapeutic strategies. This review discusses the molecular mechanisms underlying inflammation and oxidative stress in OP, highlights current therapeutic approaches, and proposes future research directions aimed at improving the prevention and treatment of osteoporosis.
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Safety and efficacy of Wharton's jelly-derived mesenchymal stem cells with teriparatide for osteoporotic vertebral fractures: A phase I/IIa study

JeongHyun Shim, et al.
Osteoporotic vertebral compression fractures (OVCFs) are serious health problems. We conducted a randomized, open-label, phase I/IIa study to determine the feasibility, safety, and effectiveness of Wharton's jelly-derived mesenchymal stem cells (WJ-MSCs) and teriparatide (parathyroid hormone 1-34) in OVCFs. Twenty subjects with recent OVCFs were randomized to teriparatide (20 μg/day, daily subcutaneous injection for 6 months) treatment alone or combined treatment of WJ-MSCs (intramedullary [4 × 107 cells] injection and intravenous [2 × 108 cells] injection after 1 week) and teriparatide (20 μg/day, daily subcutaneous injection for 6 months). Fourteen subjects (teriparatide alone, n = 7; combined treatment, n = 7) completed follow-up assessment (visual analog scale [VAS], Oswestry Disability Index [ODI], Short Form-36 [SF-36], bone mineral density [BMD], bone turnover measured by osteocalcin and C-terminal telopeptide of type 1 collagen, dual-energy x-ray absorptiometry [DXA], computed tomography [CT]). Our results show that (a) combined treatment with WJ-MSCs and teriparatide is feasible and tolerable for the patients with OVCFs; (b) the mean VAS, ODI, and SF-36 scores significantly improved in the combined treatment group; (c) the level of bone turnover markers were not significantly different between the two groups; (d) BMD T-scores of spine and hip by DXA increased in both control and experimental groups without a statistical difference; and (e) baseline spine CT images and follow-up CT images at 6 and 12 months showed better microarchitecture in the combined treatment group. Our results indicate that combined treatment of WJ-MSCs and teriparatide is feasible and tolerable and has a clinical benefit for fracture healing by promoting bone architecture. Clinical trial registration: https://nedrug.mfds.go.kr/, MFDS: 201600282-30937.
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Immunoporosis: Immunology of Osteoporosis-Role of T Cells

Rupesh K Srivastava, et al.
The role of immune system in various bone pathologies, such as osteoporosis, osteoarthritis, and rheumatoid arthritis is now well established. This had led to the emergence of a modern field of systems biology called as osteoimmunology, an integrated research between fields of immunology and bone biology under one umbrella. Osteoporosis is one of the most common inflammatory bone loss condition with more than 200 million individuals affected worldwide. T helper (Th) cells along with various other immune cells are major players involved in bone homeostasis. In the present review, we specifically discuss the role of various defined T lymphocyte subsets (Th cells comprising Th1, Th2, Th9, Th17, Th22, regulatory T cells, follicular helper T cells, natural killer T cells, γδ T cells, and CD8+ T cells) in the pathophysiology of osteoporosis. The study of the specific role of immune system in osteoporosis has now been proposed by our group as "immunoporosis: the immunology of osteoporosis" with special emphasis on the role of various subsets of T lymphocytes. The establishment of this new field had been need of the hour due to the emergence of novel roles of various T cell lymphocytes in accelerated bone loss observed during osteoporosis. Activated T cells either directly or indirectly through the secretion of various cytokines and factors modulate bone health and thereby regulate bone remodeling. Several studies have summarized the role of inflammation in pathogenesis of osteoporosis but very few reports had delineated the precise role of various T cell subsets in the pathobiology of osteoporosis. The present review thus for the first time clearly highlights and summarizes the role of various T lymphocytes in the development and pathophysiology of osteoporosis, giving birth to a new field of biology termed as "immunoporosis". This novel field will thus provide an overview of the nexus between the cellular components of both bone and immune systems, responsible for the observed bone loss in osteoporosis. A molecular insight into the upcoming and novel field of immunoporosis would thus leads to development of innovative approaches for the prevention and treatment of osteoporosis.
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The Rising Era of "Immunoporosis": Role of Immune System in the Pathophysiology of Osteoporosis

Rupesh K Srivastava, et al.
Discoveries in the last few years have emphasized the existence of an enormous breadth of communication between bone and the immune system in maintaining skeletal homeostasis. Originally, the discovery of various factors was assigned to the immune system viz. interleukin (IL)-6, IL-10, IL-17, tumor necrosis factor (TNF)-α, receptor activator of nuclear factor kappa B ligand (RANKL), nuclear factor of activated T cells (NFATc1), etc., but now these factors have also been shown to have a significant impact on osteoblasts (OBs) and osteoclasts (OCs) biology. These discoveries led to an alteration in the approach for the treatment of several bone pathologies including osteoporosis. Osteoporosis is an inflammatory bone anomaly affecting more than 500 million people globally. In 2018, to highlight the importance of the immune system in the pathophysiology of osteoporosis, our group coined the term "immunoporosis". In the present review, we exhaustively revisit the characteristics, mechanism of action, and function of both innate and adaptive immune cells with the goal of understanding the potential of immune cells in osteoporosis. We also highlight the Immunoporotic role of gut microbiota (GM) for the treatment and management of osteoporosis. Importantly, we further discuss whether an immune cell-based strategy to treat and manage osteoporosis is feasible and relevant in clinical settings.
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Rejuvenation of Bone Marrow Mesenchymal Stem Cells: Mechanisms and Their Application in Senile Osteoporosis Treatment

Rui-Chuan Tian, et al.
Bone marrow mesenchymal stromal cells (BM-MSCs) are multipotent cells present in bone marrow; they play a crucial role in the process of bone formation. Cellular senescence is defined as a stable state of cell cycle arrest that impairs the functioning of cells. Research has shown that aging triggers a state of senescence in BM-MSCs, leading to a reduced capacity for osteogenic differentiation and the accumulation of senescent cells, which can accelerate the onset of various diseases. Therefore, it is essential to explore mechanisms and strategies for the rejuvenation of senescent BM-MSCs. Senile osteoporosis (SOP) is a metabolic bone disease characterized by reduced bone formation. The senescence of BM-MSCs is considered one of the most important factors in the occurrence and development of SOP. Therefore, the rejuvenation of BM-MSCs for the treatment of SOP represents a promising strategy. This work provides a summary of the functional alterations observed in senescent BM-MSCs and a systematic review of the mechanisms that facilitate the rejuvenation of senescent BM-MSCs. Additionally, we analyze the progress in and the limitations associated with the application of rejuvenated senescent BM-MSCs to treat SOP, with the aim of providing new insights for the prevention and treatment of SOP.
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