The use of crevicular fluid to assess markers of inflammation and angiogenesis, IL-17 and VEGF, in patients with solid tumors receiving zoledronic acid and/or bevacizumab

Papadopoulou, Erofili; Nicolatou‐Galitis, Ourania; Papassotiriou, Ioannis; Linardou, Helena; Karagianni, Aikaterini; Tsixlakis, Konstantinos; Tarampikou, A.; Michalakakou, Kelly; Vardas, Emmanouil; Bafaloukos, Dimitrios

doi:10.1007/s00520-019-04793-2

Cited by 6 publications

(2 citation statements)

References 25 publications

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“…Bone becomes necrotic without adequate blood supply [ 56 ]. In the case of MRONJ, bisphosphonates can contribute to the pathogenesis of MRONJ due to their ability to reduced blood vessel formation causing delayed mucosal healing [ 57 ]. It has been reported that various antiangiogenic agents, such as VEGF antibodies and tyrosine kinase inhibitors, can also cause jaw necrosis and therefore the development of MRONJ [ 15 ].…”

Section: Pathogenesismentioning

confidence: 99%

Medication-Related Osteonecrosis of the Jaw: A Critical Narrative Review

Lorenzo-Pouso

Bagán

et al. 2021

JCM

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Background: Nearly two decades have passed since a paradoxical reaction in the orofacial region to some bone modifying agents and other drugs was recognized, namely medication-related osteonecrosis of the jaw (MRONJ). Purpose: The aim of this manuscript was to critically review published data on MRONJ to provide an update on key terminology, concepts, and current trends in terms of prevention and diagnosis. In addition, our objective was to examine and evaluate the therapeutic options available for MRONJ. Methods: The authors perused the most relevant literature relating to MRONJ through a search in textbooks and published articles included in several databases for the years 2003–2021. Results and conclusions: A comprehensive update of the current understanding of these matters was elaborated, addressing these topics and identifying relevant gaps of knowledge. This review describes our updated view of the previous thematic blocks, highlights our current clinical directions, and emphasizes controversial aspects and barriers that may lead to extending the accumulating body of evidence related to this severe treatment sequela.

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Section: Pathogenesismentioning

confidence: 99%

Medication-Related Osteonecrosis of the Jaw: A Critical Narrative Review

Lorenzo-Pouso

Bagán

et al. 2021

JCM

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“…They produce IL-17, attract myeloid-derived suppressor cells (MDSCs), and promote their own proliferation and development ( 135 , 136 ). The concentration of VEGF is positively correlated with the concentration of IL-17 ( 137 ), and IL-17 can increase tumor angiogenesis, thus enhancing tumor proliferation and metastasis. Meanwhile, the anti-abscopal extracellular nucleotidase CD39 and CD73 on the surface of Th17 cells decompose ATP into AMP to achieve an immunosuppressive effect ( 117 ).…”

Section: Roles Of Tumor-associated Molecular Patternsmentioning

confidence: 99%

Mechanism of exosomes in the tumor microenvironment in the abscopal effect (Review)

et al. 2022

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Previously, the abscopal effect, which is an antitumor therapeutic effect on untreated tumor locations elsewhere in the body as a result of treatment of the targeted region, was rarely reported, and its mechanism remains unknown. Increasing evidence has shown that the immune system is implicated in the abscopal effect, and that combining immunotherapy and radiation can assist to improve its frequency. Understanding how different types of cells and cell-derived exosomes cause the abscopal effect in the tumor microenvironment (TME) is crucial to increasing the clinical occurrence of the abscopal effect in the TME. Contents 1. Introduction 2. Immune mechanism of the abscopal effect 3. Role of tumor cells 4. Roles of tumor-associated molecular patterns 5. Clinical application 6. Conclusions

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