Relevant bibliographies by topics / Azithromycin; periodontal disease; osteoclast

Academic literature on the topic 'Azithromycin; periodontal disease; osteoclast'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Azithromycin; periodontal disease; osteoclast"

1

Chen, Bin, Wenlei Wu, Weibin Sun, Qian Zhang, Fuhua Yan, and Yin Xiao. "RANKL Expression in Periodontal Disease: Where Does RANKL Come from?" BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/731039.

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Periodontitis is an inflammatory disease characterized by periodontal pocket formation and alveolar bone resorption. Periodontal bone resorption is induced by osteoclasts and receptor activator of nuclear factor-κB ligand (RANKL) which is an essential and central regulator of osteoclast development and osteoclast function. Therefore, RANKL plays a critical role in periodontal bone resorption. In this review, we have summarized the sources of RANKL in periodontal disease and explored which factors may regulate RANKL expression in this disease.
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Singh, Vijendra Pal, Sangeeta Umesh Nayak, Sunil Kumar Nettemu, Sowmya Nettem, Yen Hui Lee, and Madhu B. Verma. "Azithromycin in Periodontal Therapy: Beyond the Antibiotics." Journal of Nepalese Society of Periodontology and Oral Implantology 2, no. 2 (December 31, 2018): 61–66. http://dx.doi.org/10.3126/jnspoi.v2i2.23616.

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Periodontitis is a multifactorial disease, in which microorganisms in plaque biofilm play a major role. Scaling and root planing is the primary mode of non-surgical treatment for periodontal disease. Adjunctive use of an antimicrobial is advocated in certain periodontal disease conditions. Azithromycin might be considered a promising adjunctive drug in the treatment for periodontal disease because of its distinguished characteristic of immunomodulation, anti-inflammatory and antibiotic property along with the accumulation in higher concentration into the acute reactant cells and sustained release at the site of infection. This antibiotic is popular for its very simple dosage regime and limited side effects. The objective of this literature review to highlight the mechanism and potential favourable role in the management of various form of the periodontal disease.
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Kurnia, Shafira. "BIOCOMPATIBILITY OF AZITROMICYN ON CONNECTIVE TISSUE." Indonesian Journal of Tropical and Infectious Disease 2, no. 1 (May 27, 2015): 42. http://dx.doi.org/10.20473/ijtid.v2i1.189.

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Background: periodontal disease is commonly caused by bacteria, especially actinomyces actinomycetemcomitans and porphyromonas gingivalis have an abilty enter epithelial cells objectives: to investigate systemic azithromycin as the antibiotic of choice for periodontal disease based on biocomptability test in connective tissue. Material and Methods: BHK 21 cell lines were exposed to 0.025%, 0.050%, 0.075%, and 0.1% azithromycin solution for seven times. Samples were put in incubator for 24 hours. Result: Azitrromycin 0.050%-0.1% showed significant difference between life cells percentage and control, however, azithromycin 0.025% revealed insignificant difference with control. Conclusion: 0.025% azithromycin was considered biocompatible with connective tissue and 0.050% was not.
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K, Dhivya, Yogarajan K, and Shanmugarajan T S. "EFFECT OF ORAL AZITHROMYCIN AND METRONIDAZOLE AS AN ADJUNCT TO SCALING AND ROOT PLANING ON GLYCEMIC CONTROL IN TYPE II DIABETIC PATIENTS WITH CHRONIC PERIODONTITIS." Asian Journal of Pharmaceutical and Clinical Research 10, no. 3 (March 1, 2017): 449. http://dx.doi.org/10.22159/ajpcr.2017.v10i3.16500.

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ABSTRACTObjective: Periodontitis, a chronic inflammatory disease characterized by destruction of the periodontal ligament and alveolar bone is the sixthcomplication of diabetes mellitus. Periodontal treatment that reduces gingival inflammation aids in the control of hyperglycemia. Therefore, thepresent study was designed to determine the effect of treating chronic periodontitis with oral antibiotics azithromycin and metronidazole on the levelof serum glycated hemoglobin in type-II diabetic patients.Methods: This prospective observational study was carried out in the dental department of a tertiary care hospital for 9 months. Clinical andbiochemistry reports of 90 patients were collected in designed case report forms. All statistical analyses were performed using IBM Statistical Packagefor Social Sciences 17 and Graph Pad Prism 7.0.Results: Significant reduction in all the clinical and dental parameters was comparatively higher in patients who received azithromycin than inpatients who received metronidazole and scaling and root planning alone.Conclusion: Periodontal therapy with oral azithromycin can be employed as a supportive strategy for the management of diabetes mellitus.Henceforth, prevention and control of periodontal disease along with antibiotics must be considered an integral part of glycemic control. However,due to the lesser sample size in this study, further investigations are required to confirm the effect of periodontal therapy on systemic diseases.Keywords: Periodontitis, Azithromycin, Metronidazole, Glycemic control, Diabetes mellitus.
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Kwack, K. H., L. Zhang, J. Sohn, V. Maglaras, R. Thiyagarajan, and K. L. Kirkwood. "Novel Preosteoclast Populations in Obesity-Associated Periodontal Disease." Journal of Dental Research 101, no. 3 (October 12, 2021): 348–56. http://dx.doi.org/10.1177/00220345211040729.

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Although there is a clear relationship between the degree of obesity and periodontal disease incidence, the mechanisms that underpin the links between these conditions are not completely understood. Understanding that myeloid-derived suppressor cells (MDSCs) are expanded during obesity and operate in a context-defined manner, we addressed the potential role of MDSCs to contribute toward obesity-associated periodontal disease. Flow cytometry revealed that in the spleen of mice fed a high-fat diet (HFD), expansion in monocytic MDSCs (M-MDSCs) significantly increased when compared with mice fed a low-fat diet (LFD). In the osteoclast differentiation assay, M-MDSCs isolated from the bone marrow of HFD-fed mice showed a larger number and area of osteoclasts with a greater number of nuclei. In the M-MDSCs of HFD-fed mice, several osteoclast-related genes were significantly elevated when compared with LFD-fed mice according to a focused transcriptomic platform. In experimental periodontitis, the number and percentage of M-MDSCs were greater, with a significantly larger increase in HFD-fed mice versus LFD-fed mice. In the spleen, the percentage of M-MDSCs was significantly higher in HFD-fed periodontitis-induced (PI) mice than in LFD-PI mice. Alveolar bone volume fraction was significantly reduced in experimental periodontitis and was further decreased in HFD-PI mice as compared with LFD-PI mice. The inflammation score was significantly higher in HFD-PI mice versus LFD-PI mice, with a concomitant increase in TRAP staining for osteoclast number and area in HFD-PI mice over LFD-PI mice. These data support the concept that M-MDSC expansion during obesity to become osteoclasts during periodontitis is related to increased alveolar bone destruction, providing a more detailed mechanistic appreciation of the interconnection between obesity and periodontitis.
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Luan, X., X. Zhou, J. Trombetta-eSilva, M. Francis, A. K. Gaharwar, P. Atsawasuwan, and T. G. H. Diekwisch. "MicroRNAs and Periodontal Homeostasis." Journal of Dental Research 96, no. 5 (January 9, 2017): 491–500. http://dx.doi.org/10.1177/0022034516685711.

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MicroRNAs (miRNAs) are a group of small RNAs that control gene expression in all aspects of eukaryotic life, primarily through RNA silencing mechanisms. The purpose of the present review is to introduce key miRNAs involved in periodontal homeostasis, summarize the mechanisms by which they affect downstream genes and tissues, and provide an introduction into the therapeutic potential of periodontal miRNAs. In general, miRNAs function synergistically to fine-tune the regulation of biological processes and to remove expression noise rather than by causing drastic changes in expression levels. In the periodontium, miRNAs play key roles in development and periodontal homeostasis and during the loss of periodontal tissue integrity as a result of periodontal disease. As part of the anabolic phase of periodontal homeostasis and periodontal development, miRNAs direct periodontal fibroblasts toward alveolar bone lineage differentiation and new bone formation through WNT, bone morphogenetic protein, and Notch signaling pathways. miRNAs contribute equally to the catabolic aspect of periodontal homeostasis as they affect osteoclastogenesis and osteoclast function, either by directly promoting osteoclast activity or by inhibiting osteoclast signaling intermediaries or through negative feedback loops. Their small size and ability to target multiple regulatory networks of related sets of genes have predisposed miRNAs to become ideal candidates for drug delivery and tissue regeneration. To address the immense therapeutic potential of miRNAs and their antagomirs, an ever growing number of delivery approaches toward clinical applications have been developed, including nanoparticle carriers and secondary structure interference inhibitor systems. However, only a fraction of the miRNAs involved in periodontal health and disease are known today. It is anticipated that continued research will lead to a more comprehensive understanding of the periodontal miRNA world, and a systematic effort toward harnessing the enormous therapeutic potential of these small molecules will greatly benefit the future of periodontal patient care.
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Sefton, A. M., J. P. Maskell, D. Beighton, A. Whiley, H. Shain, D. Foyle, S. R. Smith, F. C. Smales, and J. D. Williams. "Azithromycin in the treatment of periodontal disease Effect on microbial flora." Journal of Clinical Periodontology 23, no. 11 (November 1996): 998–1003. http://dx.doi.org/10.1111/j.1600-051x.1996.tb00527.x.

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8

Li, Qiyan, Michael S. Valerio, and Keith L. Kirkwood. "MAPK Usage in Periodontal Disease Progression." Journal of Signal Transduction 2012 (January 23, 2012): 1–17. http://dx.doi.org/10.1155/2012/308943.

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In periodontal disease, host recognition of bacterial constituents, including lipopolysaccharide (LPS), induces p38 MAPK activation and subsequent inflammatory cytokine expression, favoring osteoclastogenesis and increased net bone resorption in the local periodontal environment. In this paper, we discuss evidence that the p38/MAPK-activated protein kinase-2 (MK2) signaling axis is needed for periodontal disease progression: an orally administered p38α inhibitor reduced the progression of experimental periodontal bone loss by reducing inflammation and cytokine expression. Subsequently, the significance of p38 signaling was confirmed with RNA interference to attenuate MK2-reduced cytokine expression and LPS-induced alveolar bone loss. MAPK phosphatase-1 (MKP-1), a negative regulator of MAPK activation, was also critical for periodontal disease progression. In MPK-1-deficient mice, p38-sustained activation increased osteoclast formation and bone loss, whereas MKP-1 overexpression dampened p38 signaling and subsequent cytokine expression. Finally, overexpression of the p38/MK2 target RNA-binding tristetraprolin (TTP) decreased mRNA stability of key inflammatory cytokines at the posttranscriptional level, thereby protecting against periodontal inflammation. Collectively, these studies highlight the importance of p38 MAPK signaling in immune cytokine production and periodontal disease progression.
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Taubman, M. A., and T. Kawai. "Involvement of T-Lymphocytes in Periodontal Disease and in Direct and Indirect Induction of Bone Resorption." Critical Reviews in Oral Biology & Medicine 12, no. 2 (March 2001): 125–35. http://dx.doi.org/10.1177/10454411010120020301.

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Periodontal disease is a peripheral infection involving species of Gram-negative organisms. T-lymphocytes can be found in the dense inflammatory infiltrate in this disease. CD4+ and CD8+ T-cells are present in periodontal lesions, as are memory/activated T-lymphocytes. In addition, Th1- and Th2-type T-lymphocytes and their associated cytokines with a subtle polarization to Th 1 may be present. Th1-type T-cells up-regulate the production of pro-inflammatory cytokines IL-1 and TNF-α, which can induce bone resorption indirectly by promoting differentiation of osteoclast precursors and subsequently by activating osteoclasts. Such osteoclast differentiation is dependent on stimulation of osteoprotegerin ligand (OPG-L) production by osteoblastic cells. By contrast, activated T-cells, by virtue of direct production and expression of OPG-L, can directly promote osteoclast differentiation. OPG-L appears to be predominantly expressed on Th1-type cells. The direct and indirect T-cell involvement in periodontal bone resorption appears to be dependent on the degree of Th 1-type T-cell recruitment into inflamed gingival tissues. This T-cell recruitment is regulated by adhesion molecules and chemokines/chemokine receptors. The adhesion molecules involved include a4 and a6 integrins, LFA-1, and ICAM-1. The Th1-type T-cells preferentially express CCR5 and CXCR3, which are found prominently in diseased gingivae. By contrast, little CCR4, expressed by Th2-type T-cells, can be detected. Also, the chemokine ligands RANTES, MIP1-α (both CCR5), and IP-10 (CXCR3 ligand) were elevated in inflamed periodontal tissues. The T-cell features in diseased periodontal tissues can be compared with those in rheumatoid arthritis, wherein bone resorption often attributed to Th1-type T-cell involvement has also been demonstrated.
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Arredondo, Alexandre, Vanessa Blanc, Carolina Mor, José Nart, and Rubén León. "Azithromycin and erythromycin susceptibility and macrolide resistance genes inPrevotellafrom patients with periodontal disease." Oral Diseases 25, no. 3 (February 7, 2019): 860–67. http://dx.doi.org/10.1111/odi.13043.

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Dissertations / Theses on the topic "Azithromycin; periodontal disease; osteoclast"

1

Gannon, Siobhan Catherine. "Azithromycin suppresses human osteoclast formation and activity in vitro." Thesis, 2013. http://hdl.handle.net/2440/80998.

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Azithromycin is an antibiotic with anti-inflammatory properties used as an adjunct in the treatment of periodontitis, a common inflammatory mediated condition featuring pathologic alveolar bone resorption. The aim of this study was to determine the effect of azithromycin on human osteoclast formation and resorptive activity in vitro. Osteoclasts were generated from peripheral blood mononuclear cells stimulated with macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor kappa B (RANK) ligand. The effects of azithromycin at concentrations ranging from 0.5 μg/mL to 40 μg/mL were tested. Osteoclast formation and activity, acidification, actin ring formation and expression of mRNA and protein encoding for key osteoclast genes were assessed. The results demonstrated that azithromycin reduced osteoclast resorptive activity at all concentrations tested with osteoclast formation being significantly reduced at the higher concentrations (20μg/mL and 40μg/mL). mRNA and protein expression of the key osteoclast transcription factor Nuclear Factor of Activated T cells (NFATc1) was significantly reduced by azithromycin at later stages of osteoclast development (day 17). Azithromycin also reduced tumour necrosis factor receptor associated factor-6 (TRAF6) mRNA expression at day 14, and cathepsin K mRNA expression at day 14 and 17. Integrin β3 and MMP-9 mRNA expression was reduced by azithromycin at day 17 in osteoclasts cultured on dentine. The osteoclast proton pump did not appear to be affected by azithromycin, however formation of the actin ring cytoskeleton was inhibited. This study demonstrates that azithromycin inhibits human osteoclast function in vitro, which may account for at least some of the beneficial clinical effects observed with azithromycin treatment in periodontitis.
Thesis (D. Clin. Dent.) -- University of Adelaide, School of Dentistry, 2013
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Lopes, Paulo Alexandre Mascarenhas. "The effect of azithromycin as an adjunct to non-surgical periodontal therapy in smokers this thesis was submitted in fulfillment ... for the degree of Master of Science in Periodontics ... /." 2004. http://catalog.hathitrust.org/api/volumes/oclc/68962658.html.

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