Expression of Inflammatory Markers RANK, MMP-9 and PTHrP in Chronic Apical Periodontitis from People Living with HIV Undergoing Antiretroviral Therapy

Pereira, Marcio Francisco; Pires, Fábio Ramôa; Armada, Luciana; Ferreira, Dennis Carvalho; Carrouel, Florence; Bourgeois, Denis; Gonçalves, Lúcio Souza

doi:10.3390/jcm9113611

Cited by 4 publications

(3 citation statements)

References 43 publications

(52 reference statements)

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“…MMP-9 is a gelatinase functioning in acute and chronic inflammatory diseases. During the periapical inflammatory process, the expression of MMP-9 is significantly higher than that in normal tissues [ 42 , 43 ], possibly explaining why there were more periapical mineralized tissues and neovascularization of the EndoREZ + MNP + DMADDM group in the histologic images because the expression of MMP-9 was present in osteoclasts and related to the number of neutrophils in inflammatory zones [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

The Preventive Effect of A Magnetic Nanoparticle-Modified Root Canal Sealer on Persistent Apical Periodontitis

Guo

Sun

Wang

et al. 2022

IJMS

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Persistent apical periodontitis is a critical challenge for endodontists. Developing root canal filling materials with continuous antibacterial effects and tightly sealed root canals are essential strategies to avoid the failure of root canal therapy and prevent persistent apical periodontitis. We modified the EndoREZ root canal sealer with the antibacterial material dimethylaminododecyl methacrylate (DMADDM) and magnetic nanoparticles (MNPs). The mechanical properties of the modified root canal sealer were tested. The biocompatibility of this sealer was verified in vitro and in vivo. Multispecies biofilms were constructed to assess the antibacterial effects of the modified root canal sealer. We applied magnetic fields and examined the extent of root canal sealer penetration in vitro and in vivo. The results showed that EndoREZ sealer containing 2.5% DMADDM and 1% MNP had biological safety and apical sealing ability. In addition, the modified sealer could increase the sealer penetration range and exert significant antibacterial effects on multispecies biofilms under an external magnetic field. According to the in vivo study, the apices of the root canals with the sealer containing 2.5% DMADDM and 1% MNP showed no significant resorption and exhibited only a slight increase in the periodontal ligament space, with a good inhibitory effect on persistent apical periodontitis.

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Section: Discussionmentioning

confidence: 99%

The Preventive Effect of A Magnetic Nanoparticle-Modified Root Canal Sealer on Persistent Apical Periodontitis

Guo

Sun

Wang

et al. 2022

IJMS

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“…A paracrine positive regulator of RANKL signalling in MEC, the parathyroid-hormone-related protein (PTHrP), is usually expressed in keratinocytes of the skin. Since PTHrP is known as an inflammatory marker [ 195 ], keratinocytes from MEC express more PTHrP than normal keratinocytes [ 196 ]. Most recently a study demonstrated, that not only protein expression of PTHrP in MEC epithelium is significantly increased but also positively correlated with the expression of RANKL in osteoblasts [ 197 ] and correlated to the degree of bone resorption [ 191 ].…”

Section: Applicable Targets In Precision Medicine For Mec Therapymentioning

confidence: 99%

Review of potential medical treatments for middle ear cholesteatoma

2022

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Middle ear cholesteatoma (MEC), is a destructive, and locally invasive lesion in the middle ear driven by inflammation with an annual incidence of 10 per 100,000. Surgical extraction/excision remains the only treatment strategy available and recurrence is high (up to 40%), therefore developing the first pharmaceutical treatments for MEC is desperately required. This review was targeted at connecting the dysregulated inflammatory network of MEC to pathogenesis and identification of pharmaceutical targets. We summarized the numerous basic research endeavors undertaken over the last 30+ years to identify the key targets in the dysregulated inflammatory pathways and judged the level of evidence for a given target if it was generated by in vitro, in vivo or clinical experiments. MEC pathogenesis was found to be connected to cytokines characteristic for Th1, Th17 and M1 cells. In addition, we found that the inflammation created damage associated molecular patterns (DAMPs), which further promoted inflammation. Similar positive feedback loops have already been described for other Th1/Th17 driven inflammatory diseases (arthritis, Crohn’s disease or multiple sclerosis). A wide-ranging search for molecular targeted therapies (MTT) led to the discovery of over a hundred clinically approved drugs already applied in precision medicine. Based on exclusion criteria designed to enable fast translation as well as efficacy, we condensed the numerous MTTs down to 13 top drugs. The review should serve as groundwork for the primary goal, which is to provide potential pharmaceutical therapies to MEC patients for the first time in history.

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“…Osteoporosis, a metabolic skeletal disease reflected by decreased bone mineral density, microarchitectural deterioration, and impaired bone strength, leads to an increased risk of fragility fracture. The development of osteoporosis and bone diseases is influenced significantly by aging, estrogen deficiency, and inflammation [3][4][5]. The fundamental etiology of osteoporosis involves an imbalance in bone turnover, characterized by a higher rate of bone resorption mediated by osteoclasts compared to the rate of bone formation mediated by osteoblasts.…”

Section: Introductionmentioning

confidence: 99%

Nrf2 Mitigates RANKL and M-CSF Induced Osteoclast Differentiation via ROS-Dependent Mechanisms

Yang,

Liu,

et al. 2023

Antioxidants

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Nuclear factor-erythroid 2-related factor 2 (Nrf2) has been shown to be a negative regulator of osteoclast differentiation, but the precise mechanisms have not yet been established. We examined the precise roles of Nrf2 in regulating antioxidants and reactive oxygen species (ROS) levels, especially the cytoplasmic and mitochondrial ROS during osteoclastogenesis in vitro. In the current study, we found that the absence of Nrf2 promotes osteoclast differentiation in bone-marrow-derived macrophages (BMMs) and RAW 264.7 cells. The receptor activator of NF-κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) significantly lowered the levels of Nrf2 and its downstream antioxidant enzymes at mRNA and/or protein levels during osteoclast differentiation in the BMMs of mice and RAW 264.7 mouse leukemic monocytes. Compared to the wild-type cells, Nrf2-deficient cells exhibited heightened sensitivity to both transient RANKL-induced cytoplasmic ROS and prolonged RANKL and M-CSF-induced cytoplasmic and mitochondrial ROS accumulation. Furthermore, exogenous antioxidant agents, including N-acetyl-cysteine (NAC), diphenyleneiodonium chloride (DPI), and mitoquinone mesylate (MitoQ), exhibited substantial capability to suppress the elevation of ROS levels during osteoclast differentiation induced by Nrf2 deficiency, and they consequently inhibited osteoclast differentiation augmented by the lack of Nrf2. The activation of phosphorylated c-FOS resulting from elevated ROS promoted osteoclast differentiation. The inhibition of c-FOS blocked osteoclast differentiation, which was elevated by Nrf2-deficiency. Taken together, these data reveal that Nrf2 effectively decreased the accumulation of intracellular ROS and the phosphorylation of c-FOS during osteoclastic differentiation by regulating antioxidant enzymes and subsequently inhibited RANKL-induced osteoclast differentiation.

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Expression of Inflammatory Markers RANK, MMP-9 and PTHrP in Chronic Apical Periodontitis from People Living with HIV Undergoing Antiretroviral Therapy

Cited by 4 publications

References 43 publications

The Preventive Effect of A Magnetic Nanoparticle-Modified Root Canal Sealer on Persistent Apical Periodontitis

The Preventive Effect of A Magnetic Nanoparticle-Modified Root Canal Sealer on Persistent Apical Periodontitis

Review of potential medical treatments for middle ear cholesteatoma

Nrf2 Mitigates RANKL and M-CSF Induced Osteoclast Differentiation via ROS-Dependent Mechanisms

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