Meloxicam Temporally Inhibits the Expression of Vascular Endothelial Growth Factor Receptor (VEGFR)‐1 and VEGFR‐2 During Alveolar Bone Repair in Rats

Arantes, Ricardo Vinicius Nunes; Cestari, Tânia Mary; Viscelli, Bruno Alvares; Dionísio, Thiago José; Garlet, Gustavo; Santos, Carlos; Assis, Gérson Francisco de; Taga, Rumio

doi:10.1902/jop.2014.140259

Cited by 7 publications

(7 citation statements)

References 50 publications

(94 reference statements)

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“…The histomorphometric analysis confirms the μCT data, depicting the initial bone formation at the 7d time period, and the gradual increase in the bone mass until the alveolar socket was totally filled by newly formed bone at 21d. Accordingly, a similar kinetics of bone neoformation was previously described in a rat model [ 3 , 5 , 77 ]. The molecular data support the histomorphometric evidences of progressive bone healing at the 14d time period, since markers of advanced osteoblastic differentiation and osteocyte markers, such as PHEX (phosphate-regulating neutral endopeptidase), DMP1 (dentin matrix protein 1) and SOST (sclerostin)[ 78 , 79 ], are upregulated at this time period.…”

Section: Discussionmentioning

confidence: 87%

Intramembranous Bone Healing Process Subsequent to Tooth Extraction in Mice: Micro-Computed Tomography, Histomorphometric and Molecular Characterization

et al. 2015

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Bone tissue has a significant potential for healing, which involves a significant the interplay between bone and immune cells. While fracture healing represents a useful model to investigate endochondral bone healing, intramembranous bone healing models are yet to be developed and characterized. In this study, a micro-computed tomography, histomorphometric and molecular (RealTimePCRarray) characterization of post tooth-extraction alveolar bone healing was performed on C57Bl/6 WT mice. After the initial clot dominance (0h), the development of a provisional immature granulation tissue is evident (7d), characterized by marked cell proliferation, angiogenesis and inflammatory cells infiltration; associated with peaks of growth factors (BMP-2-4-7,TGFβ1,VEGFa), cytokines (TNFα, IL-10), chemokines & receptors (CXCL12, CCL25, CCR5, CXCR4), matrix (Col1a1-2, ITGA4, VTN, MMP1a) and MSCs (CD105, CD106, OCT4, NANOG, CD34, CD146) markers expression. Granulation tissue is sequentially replaced by more mature connective tissue (14d), characterized by inflammatory infiltrate reduction along the increased bone formation, marked expression of matrix remodeling enzymes (MMP-2-9), bone formation/maturation (RUNX2, ALP, DMP1, PHEX, SOST) markers, and chemokines & receptors associated with healing (CCL2, CCL17, CCR2). No evidences of cartilage cells or tissue were observed, strengthening the intramembranous nature of bone healing. Bone microarchitecture analysis supports the evolving healing, with total tissue and bone volumes as trabecular number and thickness showing a progressive increase over time. The extraction socket healing process is considered complete (21d) when the dental socket is filled by trabeculae bone with well-defined medullary canals; it being the expression of mature bone markers prevalent at this period. Our data confirms the intramembranous bone healing nature of the model used, revealing parallels between the gene expression profile and the histomorphometric events and the potential participation of MCSs and immune cells in the healing process, supporting the forthcoming application of the model for the better understanding of the bone healing process.

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Section: Discussionmentioning

confidence: 87%

Intramembranous Bone Healing Process Subsequent to Tooth Extraction in Mice: Micro-Computed Tomography, Histomorphometric and Molecular Characterization

et al. 2015

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“… 34 Animal studies have confirmed that the temporary inhibition of VEGFR-1 and VEGFR-2 expression by meloxicam correlated with the time of its administration, but no difference was found in VEGF expression compared to the control group. 35 …”

Section: Nsaids and Angiogenesismentioning

confidence: 99%

Positives and negatives of nonsteroidal anti-inflammatory drugs in bone healing: the effects of these drugs on bone repair

Lisowska

Kosson

Domaracka

2018

DDDT

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Tissue damage following injury triggers the processes of coagulation, inflammation and healing. In tissues surrounding the bone, the result of the healing process is a scar, while bone tissue has a unique ability to achieve shape, strength and pre-injury function. Bone healing is a process of regeneration rather than classic recovery. The result of this process is the formation of new, healthy bone tissue instead of a scar. Many factors can inhibit or impair the bone healing process, and their influence is critical during the stages of inflammation and angiogenesis and finally on the clinical outcome. Nonsteroidal anti-inflammatory drugs (NSAIDs) play an essential role associated with their analgesic potency and anti-inflammatory effects. NSAIDs are also the most often used drugs in patients who require pain control and inflammation reduction due to musculoskeletal diseases or injures. Although their analgesic effect is well documented, NSAIDs also interfere with bone healing; therefore, the relative benefits and disadvantages connected with their administration should be taken into consideration. Despite the negative effect, NSAIDs have beneficial properties, but their clinical benefits in relation to dose and time of use are still unclear. Therefore, in this review, we focus on bone healing with relation to the impact of NSAIDs.

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“…VEGFR-2 contains 19 tyrosine residues. [22] The extent to which the multitude of tyrosines in its cytoplasmic tail is differentially phosphorylated remains unclear. The binding mechanism of different SH2 domain-containing proteins, which leads to activation of gene induction patterns and receptor-specific intracellular signaling, is also unclear.…”

Section: Effect Of Vascular Endothelial Growth Factor On Endothelial mentioning

confidence: 99%

Pivotal micro factors associated with endothelial cells

Meng

Zhang

Shan

et al. 2019

Chinese Medical Journal

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Objective: Recent studies have shown the important influence of various micro factors on the general biological activity and function of endothelial cells (ECs). Vascular endothelial growth factor ( VEGF ) and angiogenin ( ANG ) are classic micro factors that promote proliferation, differentiation, and migration of ECs. The underlying pathophysiological mechanisms and related pathways of these micro factors remain the focus of current research. Data sources: An extensive search was undertaken in the PubMed database by using keywords including “micro factors” and “endothelial cell.” This search covered relevant research articles published between January 1, 2007 and December 31, 2018. Study selection: Original articles, reviews, and other articles were searched and reviewed for content on micro factors of ECs. Results: VEGF and ANG have critical functions in the occurrence, development, and status of the physiological pathology of ECs. Other EC-associated micro factors include interleukin 10, tumor protein P53, nuclear factor kappa B subunit, interleukin 6, and tumor necrosis factor. The results of Gene Ontology analysis revealed that variations were mainly enriched in positive regulation of transcription by the RNA polymerase II promoter, cellular response to lipopolysaccharides, negative regulation of apoptotic processes, external side of the plasma membrane, cytoplasm, extracellular regions, cytokine activity, growth factor activity, and identical protein binding. The results of the Kyoto Encyclopedia of Genes and Genomes analysis revealed that micro factors were predominantly enriched in inflammatory diseases. Conclusions: In summary, the main mediators, factors, or genes associated with ECs include VEGF and ANG . The effect of micro factors on ECs is complex and multifaceted. This review summarizes the correlation between ECs and several micro factors.

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Meloxicam Temporally Inhibits the Expression of Vascular Endothelial Growth Factor Receptor (VEGFR)‐1 and VEGFR‐2 During Alveolar Bone Repair in Rats

Abstract: In rat alveolar bone repair, meloxicam did not affect VEGF expression but downregulated VEGFR expression, which may cause a delay in the bone repair/remodeling process.

Cited by 7 publications

References 50 publications

Intramembranous Bone Healing Process Subsequent to Tooth Extraction in Mice: Micro-Computed Tomography, Histomorphometric and Molecular Characterization

Intramembranous Bone Healing Process Subsequent to Tooth Extraction in Mice: Micro-Computed Tomography, Histomorphometric and Molecular Characterization

Positives and negatives of nonsteroidal anti-inflammatory drugs in bone healing: the effects of these drugs on bone repair

Pivotal micro factors associated with endothelial cells

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