68 research outputs found
Denosumab and Zoledronic Acid Differently Affect Circulating Immune Subsets: A Possible Role in the Onset of MRONJ
Challenges of Periodontal Tissue Engineering: Increasing Biomimicry through 3D Printing and Controlled Dynamic Environment
In recent years, tissue engineering studies have proposed several approaches to regenerate periodontium based on the use of three-dimensional (3D) tissue scaffolds alone or in association with periodontal ligament stem cells (PDLSCs). The rapid evolution of bioprinting has sped up classic regenerative medicine, making the fabrication of multilayered scaffolds—which are essential in targeting the periodontal ligament (PDL)—conceivable. Physiological mechanical loading is fundamental to generate this complex anatomical structure ex vivo. Indeed, loading induces the correct orientation of the fibers forming the PDL and maintains tissue homeostasis, whereas overloading or a failure to adapt to mechanical load can be at least in part responsible for a wrong tissue regeneration using PDLSCs. This review provides a brief overview of the most recent achievements in periodontal tissue engineering, with a particular focus on the use of PDLSCs, which are the best choice for regenerating PDL as well as alveolar bone and cementum. Different scaffolds associated with various manufacturing methods and data derived from the application of different mechanical loading protocols have been analyzed, demonstrating that periodontal tissue engineering represents a proof of concept with high potential for innovative therapies in the near future
Senescent Markers Expressed by Periodontal Ligament-Derived Stem Cells (PDLSCs) Harvested from Patients with Periodontitis Can Be Rejuvenated by RG108
Treatment with intermittent PTH increases Wnt10b production by T cells in osteoporotic patients
Mitochondria-Targeted Doxorubicin: A New Therapeutic Strategy against Doxorubicin-Resistant Osteosarcoma
Endothelial Cells Promote Osteogenesis by Establishing a Functional and Metabolic Coupling With Human Mesenchymal Stem Cells
Bone formation involves a complex crosstalk between endothelial cells (EC) and osteodifferentiating stem cells. This functional interplay is greatly mediated by the paracrine and autocrine action of soluble factors released at the vasculature-bone interface. This study elucidates the molecular and functional responses triggered by this intimate interaction. In this study, we showed that human dermal microvascular endothelial cells (HMEC) induced the expression of pro-angiogenic factors in stem cells from human exfoliated deciduous teeth (SHED) and sustain their osteo-differentiation at the same time. In contrast, osteodifferentiating SHED increased EC recruitment and promoted the formation of complex vascular networks. Moreover, HMEC enhanced anaerobic glycolysis in proliferating SHED without compromising their ability to undergo the oxidative metabolic shift required for adequate osteo-differentiation. Taken together, these findings provide novel insights into the molecular mechanism underlying the synergistic cooperation between EC and stem cells during bone tissue renewal
LIGHT as regulator of bone homeostasis during osteolytic bone metastasis formation in non-small cell lung cancer patients
Tumor necrosis factor superfamily member 14 (TNFSF14), LIGHT
is one of the cytokines produced by tumor and immune cells, which
promotes homeostasis of lymphoid organs, liver and bone. Nonsmall cell lung cancer (NSCLC) commonly metastasizes bone, altering
bone homeostasis and causing osteolysis. Here we investigated the
role of LIGHT in NSCLC-induced osteolytic bone disease.
The LIGHT expression in monocytes was higher in patients with
metastatic bone lesions than in non-bone metastatic ones (66.5 ±
24.5 vs 43.3 ± 25.2 mean ± SD, p = 0.001), in healthy donors
(66.5 ± 24.5 vs 8.5 ± 4.6 p = 0.0002), and in non-bone metastatic
patients than in healthy donors (43.3 ± 25.2 vs 8.5 ± 4.6, p =
0.0001). Serum LIGHT levels were also significantly higher in
bone metastatic patients than in non-bone metastatic ones
(186.8 ± 191.2 pg/ml vs 115.8 ± 73 pg/ml, p = 0.04) and in healthy
donors (186.8 ± 191.2 pg/ml vs 85.7 ± 38.4 pg/ml, p = 0.04).
A neutralizing mAb anti-LIGHT added to osteoclast (OC) cultures of
both bone and non-bone metastases inhibited osteoclastogenesis, but
the decrease was statistically significant only for bone metastatic
patients (272 ± 98 vs 132 ± 74, p = 0.01). To investigate the role of
LIGHT in NSCLC- induced bone lesion in vivo, we performed an
intratibial injection of a mouse lung cancer cell line LLC-1, in wild-type
(WT) and LIGHT KO mice. The WT-injected mice displayed a significant
reduction of about 20% for BV/TV, Tb.N, Tb.Th, and Tb.Sp compared to
the WT-vehicle mice (pb 0.01). These parameters did not show
significant variation for KO-injected mice vs vehicle or for WT-injected
mice vs KO-injected mice. These data indicate LIGHT as a regulator of
bone homeostasis during NSCLC metastatic invasion, thus it may be a
novel therapeutic target in osteolytic bone metastases
CD73/Adenosine Pathway Involvement in the Interaction of Non-Small Cell Lung Cancer Stem Cells and Bone Cells in the Pre-Metastatic Niche
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