Journal articles on the topic 'Azithromycin; periodontal disease; osteoclast'
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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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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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Jiang, Hongwei, Yongqiang Wang, Ana Viniegra, Corneliu Sima, Christopher A. McCulloch, and Michael Glogauer. "Adseverin plays a role in osteoclast differentiation and periodontal disease‐mediated bone loss." FASEB Journal 29, no. 6 (February 13, 2015): 2281–91. http://dx.doi.org/10.1096/fj.14-265744.
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Madeira, Mila Fernandes Moreira, Celso Martins Queiroz-Junior, Graciela Mitre Costa, Patrícia Campi Santos, Elcia Maria Silveira, Gustavo Pompermaier Garlet, Patrícia Silva Cisalpino, Mauro Martins Teixeira, Tarcília Aparecida Silva, and Daniele da Glória Souza. "MIF induces osteoclast differentiation and contributes to progression of periodontal disease in mice." Microbes and Infection 14, no. 2 (February 2012): 198–206. http://dx.doi.org/10.1016/j.micinf.2011.09.005.
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Komatsu, Sho, Shotaro Oshikiri, Takatoshi Nagano, Akihiro Yashima, Yuji Matsushima, Satoshi Shirakawa, Katsutoshi Komatsu, Akiko Mokubo, and Kazuhiro Gomi. "Effects of One-Stage Full-Mouth Scaling and Root Planing with Azithromycin on Diabetes and Periodontal Disease: A Randomized Controlled Trial." Antibiotics 11, no. 9 (September 18, 2022): 1266. http://dx.doi.org/10.3390/antibiotics11091266.
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Recent reports show that hemoglobin A1c (HbA1c) can be lowered by improving chronic inflammation in periodontal patients with diabetes mellitus and that full-mouth scaling and root planing (FM-SRP), in combination with azithromycin (AZM) treatment, can reduce early periodontal inflammation. However, the association of FM-SRP and AZM with periodontitis and HbA1c in patients with diabetes is largely unknown. This study investigated periodontitis and HbA1c in patients with diabetes after receiving FM-SRP and AZM to evaluate which clinical parameters most reflect the diabetic condition. Fifty-one periodontal patients with diabetes mellitus were included in this study. In total, 25 patients were assigned to the FM-SRP group in which patients were treated with FM-SRP in combination with AZM, and 26 patients were assigned to the control group in which only supragingival calculus removal was performed along with the provision of oral hygiene instructions. We evaluated periodontal parameters (probing pocket depth, periodontal inflamed surface area (PISA), bleeding on probing), and periodontal bacteria and biochemical parameters (HbA1c, high-sensitive C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1)) at baseline (BL) and 1, 3, 6, and 9 months after treatment. Compared with BL values, the FM-SRP group showed improved clinical parameters, reduced periodontal pathogens, and significantly lower HbA1c. Inflammatory cytokines (hs-CRP, TNF-α, IL-6) were significantly reduced one month after treatment and remained low thereafter. MCP-1 did not change significantly during the experimental period. PISA showed a strong correlation with HbA1c, hs-CRP, and TNF-α. FM-SRP, in combination with AZM, produced clinical, microbiological, and HbA1c improvements in periodontal patients with previously diagnosed diabetes mellitus. Additionally, PISA was shown to be a useful index for assessing the diabetic status of patients with periodontal disease.
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Mogi, M., J. Otogoto, N. Ota, and A. Togari. "Differential Expression of RANKL and Osteoprotegerin in Gingival Crevicular Fluid of Patients with Periodontitis." Journal of Dental Research 83, no. 2 (February 2004): 166–69. http://dx.doi.org/10.1177/154405910408300216.
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The receptor activator for NF-κB ligand (RANKL) plays an important role in osteoclast formation. A recent study with animal models suggests the involvement of RANKL in the pathogenesis of this periodontal disease. However, no one has examined the level of RANKL in the body fluid of human subjects. This communication reports on the in vivo concentrations of RANKL and the RANKL decoy receptor osteoprotegerin (OPG) in the gingival crevicular fluid (GCF) of periodontal subjects with severe, moderate, and mild forms of the disease. An increased concentration of RANKL and a decreased concentration of OPG were detected in GCF from patients with periodontitis (*p < 0.05 vs. control subjects). The ratio of the concentration of RANKL to that of OPG in the GCF was significantly higher for periodontal disease patients than for healthy subjects (*p < 0.01). Taken together, these data suggest that RANKL and OPG contribute to osteoclastic bone destruction in periodontal disease. Abbreviations: GCF, gingival crevicular fluid; IL, interleukin; OPG, osteoprotegerin; RANKL, receptor activator for NF-κB ligand.
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Nepokupnaia-Slobodianiuk, T. S., and P. N. Skripnikov. "Clinical efficiency of short and long-term adjuvant therapy of chronic periodontal disease with azithromycin." Stomatologiya 93, no. 6 (2014): 20. http://dx.doi.org/10.17116/stomat201493620-24.
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Teng, Yen-Tung A. "The Role of Acquired Immunity and Periodontal Disease Progression." Critical Reviews in Oral Biology & Medicine 14, no. 4 (July 2003): 237–52. http://dx.doi.org/10.1177/154411130301400402.
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Our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host’s immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system not only in fighting the virulent periodontal pathogens but also in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response—in particular, CD4+ T-cells—plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host’s tissue destruction. In particular, studies of the pathogen-specific CD4+ T-cell-mediated immunity have clarified the roles of: (i) the relative diverse immune repertoire involved in periodontal pathogenesis, (ii) the contribution of pathogen-associated Th1-Th2 cytokine expressions in periodontal disease progression, and (iii) micro-organism-triggered periodontal CD4+ T-cell-mediated osteoclastogenic factor, ‘RANK-L’, which is linked to the induction of alveolar bone destruction in situ. The present review will focus on some recent advances in the acquired immune responses involving B-cells, CD8+ T-cells, and CD4+ T-cells in the context of periodontal disease progression. New approaches will further facilitate our understanding of their underlying molecular mechanisms that may lead to the development of new treatment modalities for periodontal diseases and their associated complications. Abbreviations used in the paper are as follows: Antibody, Ab; antigen, Ag; antigen-presenting cells, APC; Actinobacillus actinomycetemcomitans, A. actinomycetemcomitans or Aa; β2-microglobulin, β2m; cytotoxic CD8+ αβ T-lymphocytes, CTL; dendritic cells, DC; delayed-type hypersensitivity, DTH; immunoglobulin, Ig; Fc receptor, Fc-R; interferon-γ, IFN-γ; receptor activator of NF-κB ligand, RANK-L; molecular weight, MW; Porphyromonas gingivalis, P. gingivalis or Pg; localized juvenile periodontitis, LJP; lipopolysaccharide, LPS; mouse mammalian tumor virus, MMTV; non-obese diabetic and severe combined immunodeficiency mice, NOD/SCID mice; osteoclast, OC; T-helper cells, Th; superantigen, SAg; transforming growth factor-β, TGF-β; secretory-IgA, s-IgA; T-cell receptor, TCR; T cytotoxic-1 cells, Tc1; and T cytotoxic-2 cells, Tc2.
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Ibraheem, Aseel J., and Aysar N. Mohammed. "Effect of Alendronate Treatment on Salivary Levels of Osteoprotegrin and TNF-α in Postmenopausal Woman with Osteoporosis and Periodontal Diseases." Journal of Baghdad College of Dentistry 30, no. 2 (June 15, 2018): 17–22. http://dx.doi.org/10.26477/jbcd.v30i2.2458.
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Background: All diseases concerning bone destruction such as osteoporosis and periodontal diseases share common pattern in which the osteoclast cells are absolutely responsible for bone resorption that occurred when osteoclast activity exceeds osteoblast activity. Osteoprotegrin (OPG) considered as novel soluble decoy receptor known as “bone protector” since it prevents extreme bone resorption through inhibition of differentiation and activity of osteoclast by competing for binding site. It binds to receptor activator of nuclear factor kappa-B ligand (RANKL) and prevent its interaction with receptor activator of nuclear factor kappa-B (RANK), thus inhibits osteoclast formation. TNF-α is a pro-inflammatory cytokines having a broad range of important roles in regulation of immune system and bone resorption through the stimulation of osteoclastogenesis. Alendronate (ALN) diminishes the expression of osteoclast activating factors and cytokines such as RANKL and enhances the production of decoy receptor osteoprotegerin in osteoblast cells. Moreover, it decreases the production of proinflammatory cytokines such as TNF-α by macrophage, stimulates apoptosis of monocyte-macrophage cell lines derivative and reduces inflammatory response. Aims of the Study: 1. To assess the effect of alendronate treatment on salivary levels of osteoprotegrin and TNF-α in postmenopausal women with osteoporosis and periodontal disease 2. To find any possible correlation between salivary levels of osteoprotegrin and TNF-α in control and study groups. Materials and Methods: Total sample of 90 female subjects (55-65 years) were divided into 3 groups, (30 subjects in each group): first control group involved systemically healthy subjects with healthy periodontium, second group involved postmenopausal women with osteoporosis under alendronate treatment for(3-6)months (alendronate group), third group involved postmenopausal women with osteoporosis without alendronate treatment(osteoporosis group). The last two groups were sub- divided in- to two sub –groups (15 subjects in each sub-group) of gingivitis and periodontitis subjects respectively. Salivary samples were collected from all subjects and salivary levels of osteoprotegrin and TNF- α were determined by enzyme –linked immune sorbent assay (ELISA). Results: Highest median value of salivary (OPG) was found in alendronate group followed by control group while the lowest value was found in osteoporosis group. Highest median value of TNF- α was found in osteoporosis group followed by control group and alendronate group respectively with highly significant differences between them. Spearman correlation between salivary levels of TNF-α and OPG showed non- significant correlation at all subgroups. Conclusion: Subjects with osteoporosis in this study had greater levels of TNF-α and decrease in the level of OPG comparing with patients under alendronate treatment. Alendronate treatment for women with osteoporosis and periodontal disease may have beneficial outcome.
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Ibraheem, Aseel J., and Aysar N. Mohammed. "Effect of Alendronate Treatment on Salivary Levels of Osteoprotegrin and TNF-α in Postmenopausal Woman with Osteoporosis and Periodontal Diseases." Journal of Baghdad College of Dentistry 30, no. 2 (June 2018): 17–22. http://dx.doi.org/10.12816/0049746.
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Background: All diseases concerning bone destruction such as osteoporosis and periodontal diseases share common pattern in which the osteoclast cells are absolutely responsible for bone resorption that occurred when osteoclast activity exceeds osteoblast activity. Osteoprotegrin (OPG) considered as novel soluble decoy receptor known as “bone protector” since it prevents extreme bone resorption through inhibition of differentiation and activity of osteoclast by competing for binding site. It binds to receptor activator of nuclear factor kappa-B ligand (RANKL) and prevent its interaction with receptor activator of nuclear factor kappa-B (RANK), thus inhibits osteoclast formation. TNF-α is a pro-inflammatory cytokines having a broad range of important roles in regulation of immune system and bone resorption through the stimulation of osteoclastogenesis. Alendronate (ALN) diminishes the expression of osteoclast activating factors and cytokines such as RANKL and enhances the production of decoy receptor osteoprotegerin in osteoblast cells. Moreover, it decreases the production of proinflammatory cytokines such as TNF-α by macrophage, stimulates apoptosis of monocyte-macrophage cell lines derivative and reduces inflammatory response. Aims of the Study: 1. To assess the effect of alendronate treatment on salivary levels of osteoprotegrin and TNF-α in postmenopausal women with osteoporosis and periodontal disease 2. To find any possible correlation between salivary levels of osteoprotegrin and TNF-α in control and study groups. Materials and Methods: Total sample of 90 female subjects (55-65 years) were divided into 3 groups, (30 subjects in each group): first control group involved systemically healthy subjects with healthy periodontium, second group involved postmenopausal women with osteoporosis under alendronate treatment for(3-6)months (alendronate group), third group involved postmenopausal women with osteoporosis without alendronate treatment(osteoporosis group). The last two groups were sub- divided in- to two sub –groups (15 subjects in each sub-group) of gingivitis and periodontitis subjects respectively. Salivary samples were collected from all subjects and salivary levels of osteoprotegrin and TNF- α were determined by enzyme –linked immune sorbent assay (ELISA). Results: Highest median value of salivary (OPG) was found in alendronate group followed by control group while the lowest value was found in osteoporosis group. Highest median value of TNF- α was found in osteoporosis group followed by control group and alendronate group respectively with highly significant differences between them. Spearman correlation between salivary levels of TNF-α and OPG showed non- significant correlation at all subgroups. Conclusion: Subjects with osteoporosis in this study had greater levels of TNF-α and decrease in the level of OPG comparing with patients under alendronate treatment. Alendronate treatment for women with osteoporosis and periodontal disease may have beneficial outcome.
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Hienz, Stefan A., Sweta Paliwal, and Saso Ivanovski. "Mechanisms of Bone Resorption in Periodontitis." Journal of Immunology Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/615486.
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Alveolar bone loss is a hallmark of periodontitis progression and its prevention is a key clinical challenge in periodontal disease treatment. Bone destruction is mediated by the host immune and inflammatory response to the microbial challenge. However, the mechanisms by which the local immune response against periodontopathic bacteria disturbs the homeostatic balance of bone formation and resorption in favour of bone loss remain to be established. The osteoclast, the principal bone resorptive cell, differentiates from monocyte/macrophage precursors under the regulation of the critical cytokines macrophage colony-stimulating factor, RANK ligand, and osteoprotegerin. TNF-α, IL-1, and PGE2also promote osteoclast activity, particularly in states of inflammatory osteolysis such as those found in periodontitis. The pathogenic processes of destructive inflammatory periodontal diseases are instigated by subgingival plaque microflora and factors such as lipopolysaccharides derived from specific pathogens. These are propagated by host inflammatory and immune cell influences, and the activation of T and B cells initiates the adaptive immune response via regulation of the Th1-Th2-Th17 regulatory axis. In summary, Th1-type T lymphocytes, B cell macrophages, and neutrophils promote bone loss through upregulated production of proinflammatory mediators and activation of the RANK-L expression pathways.
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Teng, Y. T. A. "Protective and Destructive Immunity in the Periodontium: Part 2—T-cell-mediated Immunity in the Periodontium." Journal of Dental Research 85, no. 3 (March 2006): 209–19. http://dx.doi.org/10.1177/154405910608500302.
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Based on the results of recent research in the field and Part 1 of this article (in this issue), the present paper will discuss the protective and destructive aspects of the T-cell-mediated adaptive immunity associated with the bacterial virulent factors or antigenic determinants during periodontal pathogenesis. Attention will be focused on: (i) osteoimmunology and periodontal disease; (ii) some molecular techniques developed and applied to identify critical microbial virulence factors or antigens associated with host immunity (with Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis as the model species); and (iii) summarizing the identified virulence factors/antigens associated with periodontal immunity. Thus, further understanding of the molecular mechanisms of the host’s T-cell-mediated immune responses and the critical microbial antigens related to disease pathogenesis will facilitate the development of novel therapeutics or protocols for future periodontal treatments. Abbreviations used in the paper are as follows: A. actinomycetemcomitans ( Aa), Actinobacillus actinomycetemcomitans; Ab, antibody; DC, dendritic cells; mAb, monoclonal antibody; pAb, polyclonal antibody; OC, osteoclast; PAMP, pathogen-associated molecular patterns; P. gingivalis ( Pg), Porphyromonas gingivalis; RANK, receptor activator of NF-κB; RANKL, receptor activator of NF-κB ligand; OPG, osteoprotegerin; TCR, T-cell-receptors; TLR, Toll-like receptors.
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Lu, Sheng-Hua, Ren-Yeong Huang, and Tz-Chong Chou. "Magnolol Ameliorates Ligature-Induced Periodontitis in Rats and Osteoclastogenesis:In VivoandIn VitroStudy." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/634095.
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Periodontal disease characterized by alveolar bone resorption and bacterial pathogen-evoked inflammatory response has been believed to have an important impact on human oral health. The aim of this study was to evaluate whether magnolol, a main constituent ofMagnolia officinalis, could inhibit the pathological features in ligature-induced periodontitis in rats and osteoclastogenesis. The sterile, 3–0 (diameter; 0.2 mm) black braided silk thread, was placed around the cervix of the upper second molars bilaterally and knotted medially to induce periodontitis. The morphological changes around the ligated molars and alveolar bone were examined by micro-CT. The distances between the amelocemental junction and the alveolar crest of the upper second molars bilaterally were measured to evaluate the alveolar bone loss. Administration of magnolol (100 mg/kg, p.o.) significantly inhibited alveolar bone resorption, the number of osteoclasts on bony surface, and protein expression of receptor activator of nuclear factor-κB ligand (RANKL), a key mediator promoting osteoclast differentiation, in ligated rats. Moreover, the ligature-induced neutrophil infiltration, expression of inducible nitric oxide synthase, cyclooxygenase-2, matrix metalloproteinase (MMP)-1 and MMP-9, superoxide formation, and nuclear factor-κB activation in inflamed gingival tissues were all attenuated by magnolol. In thein vitrostudy, magnolol also inhibited the growth ofPorphyromonas gingivalis and Aggregatibacter actinomycetemcomitansthat are key pathogens initiating periodontal disease. Furthermore, magnolol dose dependently reduced RANKL-induced osteoclast differentiation from RAW264.7 macrophages, tartrate-resistant acid phosphatase (TRAP) activity of differentiated cells accompanied by a significant attenuation of resorption pit area caused by osteoclasts. Collectively, we demonstrated for the first time that magnolol significantly ameliorates the alveolar bone loss in ligature-induced experimental periodontitis by suppressing periodontopathic microorganism accumulation, NF-κB-mediated inflammatory mediator synthesis, RANKL formation, and osteoclastogenesis. These activities support that magnolol is a potential agent to treat periodontal disease.
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Tan, Jingyi, Anna Dai, Lai Pan, Lan Zhang, Zhongxiu Wang, Ting Ke, Weilian Sun, Yanmin Wu, Pei-Hui Ding, and Lili Chen. "Inflamm-Aging-Related Cytokines of IL-17 and IFN-γ Accelerate Osteoclastogenesis and Periodontal Destruction." Journal of Immunology Research 2021 (August 4, 2021): 1–12. http://dx.doi.org/10.1155/2021/9919024.
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Periodontal disease (PD), as an age-related disease, prevalent in middle-aged and elderly population, is characterized as inflammatory periodontal tissue loss, including gingival inflammation and alveolar bone resorption. However, the definite mechanism of aging-related inflammation in PD pathology needs further investigation. Our study is aimed at exploring the effect of inflamm-aging-related cytokines of interleukin-17 (IL-17) and interferon-γ (IFN-γ) on osteoclastogenesis in vitro and periodontal destruction in vivo. For receptor activator of nuclear factor-κB ligand- (RANKL-) primed bone marrow macrophages (BMMs), IL-17 and IFN-γ enhanced osteoclastogenesis, with the expression of osteoclastogenic mRNA (TRAP, c-Fos, MMP-9, Ctsk, and NFATc1) and protein (c-Fos and MMP-9) upregulated. Ligament-induced rat models were established to investigate the role of IL-17 and IFN-γ on experimental periodontitis. Both IL-17 and IFN-γ could enhance the local inflammation in gingival tissues. Although there might be an antagonistic interaction between IL-17 and IFN-γ, IL-17 and IFN-γ could facilitate alveolar bone loss and osteoclast differentiation.
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Valerio, M. S., and K. L. Kirkwood. "Sexual Dimorphism in Immunity to Oral Bacterial Diseases: Intersection of Neutrophil and Osteoclast Pathobiology." Journal of Dental Research 97, no. 13 (September 11, 2018): 1416–23. http://dx.doi.org/10.1177/0022034518798825.
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Sex is a biological variable that affects immune responses to bacterial and other types of infectious agents. Males and females are known to have differential oral bacterial disease burden in periodontal and endodontic disease. Understanding that there is a contribution from both sex and gender to these oral diseases, we discuss in this review recent sex-based findings that provide a pathobiological basis for differences observed between males and females. Sexual dimorphism of immune responses with respect to neutrophil trafficking and osteoclast differentiation and formation is presented as a plausible mechanism to explain the sexual differences. We also emphasize that sex, as a biological variable, should be considered in these types of oral immunologic studies.
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Ramadhani, Yeka, Riski Rahayu Putri Rahmasari, Kinanti Nasywa Prajnasari, Moh Malik Alhakim, Mohammed Aljunaid, Hesham Mohammed Al-Sharani, T. Tantiana, Wisnu Setyari Juliastuti, Rini Devijanti Ridwan, and Indeswati Diyatri. "A mucoadhesive gingival patch with Epigallocatechin-3-gallate green tea (Camellia sinensis) as an alternative adjunct therapy for periodontal disease: A narrative review." Dental Journal (Majalah Kedokteran Gigi) 55, no. 2 (June 1, 2022): 114–19. http://dx.doi.org/10.20473/j.djmkg.v55.i2.p114-119.
Full textAbstract:
Background: Periodontitis is a progressive destructive periodontal disease. The prevalence of periodontal disease in Indonesia reaches 74.1% and mostly occurs in the productive age group. Most of the periodontopathogenic bacteria are gram-negative bacteria and have endotoxin in the form of lipopolysaccharide (LPS), which can penetrate the periodontal tissue and induce an inflammatory response. In inflammatory conditions, osteoclastic activity is higher than osteoblastic activity, which causes bone destruction. This results in an imbalance between osteoclast-induced bone resorption and osteoblast-induced bone formation. The current preferred treatment for periodontitis is scaling root planning (SRP), but this therapy cannot repair the damaged periodontal tissue caused by periodontitis. Purpose: To describe the possibility of using a mucoadhesive gingival patch with Epigallocatechin-3-gallate (EGCG) green tea (Camellia sinensis) as alternative adjunct therapy for periodontal disease. Review: EGCG is the main component of green tea catechins, which have antitumor, antioxidant, anti-inflammatory, anti-fibrotic, and pro-osteogenic effects. However, the weaknesses so far regarding the use of EGCG as an alternative treatment is its low oral bioavailability and the concentration of EGCG absorbed by the body decreasing when accompanied by food. EGCG can be used with a mucoadhesive gingival patch to optimise bioavailability and absorption and increase local concentration and sustained release of EGCG. EGCG encourages bone development and braces mesenchymal stem cells (MSCs) differentiation for osteoblast by enhancing the expression of bone morphogenic protein 2 (BMP2). EGCG also has been proven to increase the expression of RUNX2 and ALP activity that induces osteoblast differentiation and bone mineralisation. Conclusion: A mucoadhesive gingival patch containing EGCG Green Tea (C. sinensis) may potentially induce osteoblastic activity as an adjunct therapy to repair the periodontal tissue damage due to periodontal disease.
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Swastini, I. Gusti Agung Ayu Putu, Tjokorda Gde Bagus Mahadewa, and I. Putu Eka Widyadharma. "Alveolar Bone Osteoclast Profile in the Periodontitis Wistar Rats Model with the Snail Slime (Achatina Fulica) Application." Open Access Macedonian Journal of Medical Sciences 7, no. 10 (May 30, 2019): 1680–84. http://dx.doi.org/10.3889/oamjms.2019.451.
Full textAbstract:
BACKGROUND: Bone damage is a result of periodontal disease that occurs due to changes in osteoclast and osteoblast activity in response to local inflammation. The bacteria Aggregatibacter actinomycetemcomitans produces Lipopolysaccharide (LPS), which can increase osteoclast activity.
AIM: This study aimed to analyse the decrease in alveolar bone osteoclasts in periodontitis rats' model with the application of snail slime.
METHODS: Wistar rats (27) with periodontitis divided into three groups, namely the control group (debridement), P1 group (debridement and application of oral snail slime) 300 Mg/Kg Body weight, P2 group (debridement, application of topical snail slime) 0.1 Mg. Osteoclast profile analysis was carried out by HE staining procedure to determine the histological feature of osteoclasts. The statistical significance was determined using the Shapiro-Wilk Test, One Way ANOVA, and Post Hoc test (p < 0.05).
RESULTS: Osteoclast profile in rats with periodontitis applied with snail slime significantly decreased the number of osteoclasts with both oral and topical administration, there were significant differences in the number of osteoclasts between groups (one way ANOVA, p < 0.05) and there were no significant differences between groups P1 and P2 (Post Hoc, p > 0.05).
CONCLUSION: In this study, there was a decrease in the number of osteoclasts which were slipped by snail slime in Wistar rats with periodontitis; this indicates a periodontitis healing process.
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Belibasakis, G. N., A. Johansson, Y. Wang, C. Chen, S. Kalfas, and U. H. Lerner. "The Cytolethal Distending Toxin Induces Receptor Activator of NF-κB Ligand Expression in Human Gingival Fibroblasts and Periodontal Ligament Cells." Infection and Immunity 73, no. 1 (January 2005): 342–51. http://dx.doi.org/10.1128/iai.73.1.342-351.2005.
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ABSTRACT Actinobacillus actinomycetemcomitans is associated with localized aggressive periodontitis, a disease characterized by rapid loss of the alveolar bone surrounding the teeth. Receptor activator of NF-κB Ligand (RANKL) and osteoprotegerin (OPG) are two molecules that regulate osteoclast formation and bone resorption. RANKL induces osteoclast differentiation and activation, whereas OPG blocks this process by acting as a decoy receptor for RANKL. The purpose of this study was to investigate the effect of A. actinomycetemcomitans on the expression of RANKL and OPG in human gingival fibroblasts and periodontal ligament cells. RANKL mRNA expression was induced in both cell types challenged by A. actinomycetemcomitans extract, whereas OPG mRNA expression remained unaffected. Cell surface RANKL protein was also induced by A. actinomycetemcomitans, whereas there was no change in OPG protein secretion. A cytolethal distending toxin (Cdt) gene-knockout strain of A. actinomycetemcomitans did not induce RANKL expression, in contrast to its wild-type strain. Purified Cdt from Haemophilus ducreyi alone, or in combination with extract from the A. actinomycetemcomitans cdt mutant strain, induced RANKL expression. Pretreatment of A. actinomycetemcomitans wild-type extract with Cdt antiserum abolished RANKL expression. In conclusion, A. actinomycetemcomitans induces RANKL expression in periodontal connective tissue cells. Cdt is crucial for this induction and may therefore be involved in the pathological bone resorption during the process of localized aggressive periodontitis.
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Ihn, Hye-Jung, Yi-Seul Kim, Soomin Lim, Jong-Sup Bae, Jae-Chang Jung, Yeo-Hyang Kim, Jin-Woo Park, et al. "PF-3845, a Fatty Acid Amide Hydrolase Inhibitor, Directly Suppresses Osteoclastogenesis through ERK and NF-κB Pathways In Vitro and Alveolar Bone Loss In Vivo." International Journal of Molecular Sciences 22, no. 4 (February 15, 2021): 1915. http://dx.doi.org/10.3390/ijms22041915.
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Alveolar bone loss, the major feature of periodontitis, results from the activation of osteoclasts, which can consequently cause teeth to become loose and fall out; the development of drugs capable of suppressing excessive osteoclast differentiation and function is beneficial for periodontal disease patients. Given the difficulties associated with drug discovery, drug repurposing is an efficient approach for identifying alternative uses of commercially available compounds. Here, we examined the effects of PF-3845, a selective fatty acid amide hydrolase (FAAH) inhibitor, on receptor activator of nuclear factor kappa B ligand (RANKL)-mediated osteoclastogenesis, its function, and the therapeutic potential for the treatment of alveolar bone destruction in experimental periodontitis. PF-3845 significantly suppressed osteoclast differentiation and decreased the induction of nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and the expression of osteoclast-specific markers. Actin ring formation and osteoclastic bone resorption were also reduced by PF-3845, and the anti-osteoclastogenic and anti-resorptive activities were mediated by the suppression of phosphorylation of rapidly accelerated fibrosarcoma (RAF), mitogen-activated protein kinase (MEK), extracellular signal-regulated kinase, (ERK) and nuclear factor κB (NF-κB) inhibitor (IκBα). Furthermore, the administration of PF-3845 decreased the number of osteoclasts and the amount of alveolar bone destruction caused by ligature placement in experimental periodontitis in vivo. The present study provides evidence that PF-3845 is able to suppress osteoclastogenesis and prevent alveolar bone loss, and may give new insights into its role as a treatment for osteoclast-related diseases.
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Lerner, Ulf H. "New Molecules in the Tumor Necrosis Factor Ligand and Receptor Superfamilies with Importance for Physiological and Pathological Bone Resorption." Critical Reviews in Oral Biology & Medicine 15, no. 2 (March 2004): 64–81. http://dx.doi.org/10.1177/154411130401500202.
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Osteoclasts are tissue-specific polykaryon bone-resorbing cells derived from the monocyte/macrophage hematopoietic lineage with specialized functions required for the adhesion of the cells to bone and the subsequent polarization of the cell membrane, secretion of acid to dissolve mineral crystals, and release of proteolytic enzymes to degrade the extracellular matrix proteins. Most pathological conditions in the skeleton lead to loss of bone due to excess osteoclastic bone resorption, including periodontal disease, rheumatoid arthritis, and osteoporosis. In rare cases, most of them genetic, patients with osteopetrosis exhibit sclerotic bone due either to a lack of osteoclasts or to non-functional osteoclasts. Mainly because of phenotypic findings in genetically manipulated mice or due to spontaneous mutations in humans, mice, and rats, several genes have been discovered as being crucial for osteoclast formation and activation. Recent breakthroughs in our understanding of osteoclast biology have revealed the critical roles in osteoclast differentiation played by RANKL, RANK, and OPG, three novel members of the tumor necrosis factor ligand and receptor superfamilies. The further study of these molecules and downstream signaling events are likely to provide a molecular basis for the development of new drugs for the treatment of diseases with excess or deficient osteoclastic bone resorption.
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Tamura, Tetsuya, Ruoqi Zhai, Tasuku Takemura, Kazuhisa Ouhara, Yuri Taniguchi, Yuta Hamamoto, Ryousuke Fujimori, et al. "Anti-Inflammatory Effects of Geniposidic Acid on Porphyromonas gingivalis-Induced Periodontitis in Mice." Biomedicines 10, no. 12 (December 1, 2022): 3096. http://dx.doi.org/10.3390/biomedicines10123096.
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Periodontal disease is predominantly caused by the pathogenic bacterium Porphyromonas gingivalis that produces inflammation-inducing factors in the host. Eucommia ulmoides is a plant native to China that has been reported to reduce blood pressure, promote weight loss, and exhibit anti-inflammatory effects. Geniposidic acid (GPA) is the major component of E. ulmoides. Herein, we investigated the effects of GPA on P. gingivalis-induced periodontitis by measuring the inflammatory responses in human gingival epithelial cells (HGECs) after P. gingivalis stimulation and GPA addition in a P. gingivalis-induced periodontitis mouse model. We found that GPA addition suppressed interleukin (IL)-6 mRNA induction (33.8% suppression), IL-6 production (69.2% suppression), toll-like receptor (TLR) 2 induction, and mitogen-activated protein kinase (MAPK) phosphorylation in HGECs stimulated by P. gingivalis. Inoculation of mice with GPA inhibited P. gingivalis-induced alveolar bone resorption (25.6% suppression) by suppressing IL-6 and TLR2 production in the serum and gingiva. GPA suppressed osteoclast differentiation of bone marrow cells induced by M-CSF and sRANKL in mice (56.7% suppression). GPA also suppressed the mRNA expression of OSCAR, NFATc1, c-Fos, cathepsin K, and DC-STAMP. In summary, GPA exerts an anti-inflammatory effect on periodontal tissue and may be effective in preventing periodontal disease.
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Gonçalves, Vinícius de Paiva, Marta Liliana Musskopf, Angeliz Rivera-Concepcion, Christina Yu, Sing Wai Wong, Stephen A. Tuin, Yizu Jiao, Cristiano Susin, Luís Carlos Spolidorio, and Patricia Almeida Miguez. "Systemic Dietary Hesperidin Modulation of Osteoclastogenesis, Bone Homeostasis and Periodontal Disease in Mice." International Journal of Molecular Sciences 23, no. 13 (June 26, 2022): 7100. http://dx.doi.org/10.3390/ijms23137100.
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This study aimed to evaluate the effects of hesperidin (HE) on in vitro osteoclastogenesis and dietary supplementation on mouse periodontal disease and femoral bone phenotype. RAW 264.7 cells were stimulated with RANKL in the presence or absence of HE (1, 100 or 500 µM) for 5 days, and evaluated by TRAP, TUNEL and Western Blot (WB) analyses. In vivo, C57BL/6 mice were given HE via oral gavage (125, 250 and 500 mg/kg) for 4 weeks. A sterile silk ligature was placed between the first and second right maxillary molars for 10 days and microcomputed tomography (μCT), histopathological and immunohistochemical evaluation were performed. Femoral bones subjected or not to dietary HE (500 mg/kg) for 6 and 12 weeks were evaluated using μCT. In vitro, HE 500 µM reduced formation of RANKL-stimulated TRAP-positive(+) multinucleated cells (500 µM) as well as c-Fos and NFATc1 protein expression (p < 0.05), markers of osteoclasts. In vivo, dietary HE 500 mg/kg increased the alveolar bone resorption in ligated teeth (p < 0.05) and resulted in a significant increase in TRAP+ cells (p < 0.05). Gingival inflammatory infiltrate was greater in the HE 500 mg/kg group even in the absence of ligature. In femurs, HE 500 mg/kg protected trabecular and cortical bone mass at 6 weeks of treatment. In conclusion, HE impaired in vitro osteoclastogenesis, but on the contrary, oral administration of a high concentration of dietary HE increased osteoclast numbers and promoted inflammation-induced alveolar bone loss. However, HE at 500 mg/kg can promote a bone-sparing effect on skeletal bone under physiological conditions.
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Garlet, Gustavo P., Walter Martins, Benedito A. L. Fonseca, Beatriz R. Ferreira, and Joao S. Silva. "Matrix metalloproteinases, their physiological inhibitors and osteoclast factors are differentially regulated by the cytokine profile in human periodontal disease." Journal of Clinical Periodontology 31, no. 8 (August 2004): 671–79. http://dx.doi.org/10.1111/j.1600-051x.2004.00545.x.
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Jimi, Eijiro, Nana Takakura, Fumitaka Hiura, Ichiro Nakamura, and Shizu Hirata-Tsuchiya. "The Role of NF-κB in Physiological Bone Development and Inflammatory Bone Diseases: Is NF-κB Inhibition “Killing Two Birds with One Stone”?" Cells 8, no. 12 (December 14, 2019): 1636. http://dx.doi.org/10.3390/cells8121636.
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Nuclear factor-κB (NF-κB) is a transcription factor that regulates the expression of various genes involved in inflammation and the immune response. The activation of NF-κB occurs via two pathways: inflammatory cytokines, such as TNF-α and IL-1β, activate the “classical pathway”, and cytokines involved in lymph node formation, such as CD40L, activate the “alternative pathway”. NF-κB1 (p50) and NF-κB2 (p52) double-knockout mice exhibited severe osteopetrosis due to the total lack of osteoclasts, suggesting that NF-κB activation is required for osteoclast differentiation. These results indicate that NF-κB may be a therapeutic target for inflammatory bone diseases, such as rheumatoid arthritis and periodontal disease. On the other hand, mice that express the dominant negative form of IκB kinase (IKK)-β specifically in osteoblasts exhibited increased bone mass, but there was no change in osteoclast numbers. Therefore, inhibition of NF-κB is thought to promote bone formation. Taken together, the inhibition of NF-κB leads to “killing two birds with one stone”: it suppresses bone resorption and promotes bone formation. This review describes the role of NF-κB in physiological bone metabolism, pathologic bone destruction, and bone regeneration.
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Vinchurkar, Urjita, Gunvant Parmar, Yogita Mistry, and Summaiya Mullan. "Antimicrobial susceptibility profile of aerobic bacterial strains isolated from periodontal lesions." International Journal of Research in Medical Sciences 10, no. 11 (October 28, 2022): 2403. http://dx.doi.org/10.18203/2320-6012.ijrms20222834.
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Background: Periodontitis or gum disease is a serious gum disease that damages soft tissue and without treatment can destroy the bone that support the teeth. It is because of consequences of specific or non specific bacterial infections. bacteria Drug resistance is a major concern in treatment of periodontitis also. So this study was planned to isolate, identify aerobic bacteria and to characterize the antibiotic sensitivity pattern of this isolate from periodontal lesions and to analyze host/patient related factors.Methods: Patients coming to dental OPD with signs and symptoms of periodontitis were selected for the study. samples were collected from periodontal lesions using bent swab stick to collect proper sample from periodontal lesion pocket. Samples were processed only for aerobic culture, antibiotic susceptibility test. Data will be entered in Excel sheet and analyzed using SPSS software version 23.Results: Total 71 aerobic isolates were found out of 100 aerobic culture. In E.coli isolates 83% resistance was found for ceftriaxone and ceftazidime. K.oxytoca isolates show 75% resistance to ceftazidime. K.pneumonaie shows 75% resistance to ceftazidime, 50% to amoxiclav, 29% to minocyclin. S.viridans shows 22% resistance to azithromycin, 19% to tetracycline and erythromycin. In present study higher drug resistance was found in K.pneumonaie followed by E.coli, K.oxytoca, and S.viridans. There is significant association between dental hygiene and the culture result (chi-square=20.771, df=8. p<0.01) and no significant association between age and the culture result (chi-square=44.032, df=40, p=0.305).Conclusions: Periodontitis patients shows drug resistant to commonly used antibiotics for the same. Also, there is an association between dental hygiene and culture positivity. So proper dental hygiene can prevent periodontitis.
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Zhang, Xufang, Chen Fan, Yin Xiao, and Xueli Mao. "Anti-Inflammatory and Antiosteoclastogenic Activities of Parthenolide on Human Periodontal Ligament CellsIn Vitro." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/546097.
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Periodontitis is an inflammatory disease that causes osteolysis and tooth loss. It is known that the nuclear factor kappa B (NF-κB) signalling pathway plays a key role in the progression of inflammation and osteoclastogenesis in periodontitis. Parthenolide (PTL), a sesquiterpene lactone extracted from the shoots ofTanacetum parthenium, has been shown to possess anti-inflammatory properties in various diseases. In the study reported herein, we investigated the effects of PTL on the inflammatory and osteoclastogenic response of human periodontal ligament-derived cells (hPDLCs) and revealed the signalling pathways in this process. Our results showed that PTL decreased NF-κB activation, I-κB degradation, and ERK activation in hPDLCs. PTL significantly reduced the expression of inflammatory (IL-1β, IL-6, and TNF-α) and osteoclastogenic (RANKL, OPG, and M-CSF) genes in LPS-stimulated hPDLCs. In addition, PTL attenuated hPDLC-induced osteoclastogenic differentiation of macrophages (RAW264.7 cells), as well as reducing gene expression of osteoclast-related markers in RAW264.7 cells in an hPDLC-macrophage coculture model. Taken together, these results demonstrate the anti-inflammatory and antiosteoclastogenic activities of PTL in hPDLCsin vitro. These data offer fundamental evidence supporting the potential use of PTL in periodontitis treatment.
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Queiroz-Junior, Celso Martins, Marcelo José Barbosa Silva, Jôice Dias Corrêa, Mila Fernandes Moreira Madeira, Thiago Pompermaier Garlet, Gustavo Pompermaier Garlet, Fernando Queiroz Cunha, Mauro Martins Teixeira, and Tarcília Aparecida da Silva. "A Controversial Role for IL-12 in Immune Response and Bone Resorption at Apical Periodontal Sites." Clinical and Developmental Immunology 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/327417.
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Periapical lesions are inflammatory conditions of tooth periapical tissues, triggered by dental pulp infection and characterized by exudation of immune cells to the affected tissues and production of inflammatory mediators such as cytokines. The inflammatory periapical reaction is mainly driven by Th1, Th2, and Th17 responses, and such polarization may modulate progression of the disease and expression of bone proresorptive cytokines. IL-12 is a potent inducer of IFN-γproduction, which stimulates Th1 effector cells. Many evidences have shown a positive correlation between the bone resorptive cytokine IL-1βand the production of IL-12 and IFN-γ. Furthermore, IL-12 may have a potential role in the release of bone resorptive mediators and blockade of Th2 cytokines, affecting the progression of periapical bone loss. Nevertheless, IL-12 and IFN-γhave also been described as suppressors of osteoclast differentiation and activation, favoring bone maintenance. This paper focuses on the controversial roles of IL-12 in periapical lesions.
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Suzuki, Yuki, Takeshi Kikuchi, Hisashi Goto, Yuhei Takayanagi, Shotaro Kawamura, Noritaka Sawada, Yoshikazu Naiki, et al. "Porphyromonas gingivalis Fimbriae Induce Osteoclastogenesis via Toll-like Receptors in RAW264 Cells." International Journal of Molecular Sciences 23, no. 23 (December 4, 2022): 15293. http://dx.doi.org/10.3390/ijms232315293.
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The effect of Mfa1 fimbriae of Porphyromonas gingivalis on the progression of bone resorption remains unclear, especially compared with another fimbriae, FimA. We investigated the effect of Mfa1 on osteoclastogenesis together with FimA. We also investigated the role of Toll-like receptors (TLRs) in Mfa1 recognition during osteoclast differentiation. Receptor activator of nuclear factor κβ ligand (RANKL)-prestimulated RAW264 cells were used to examine the effects of purified Mfa1 fimbriae. The number of osteoclasts was examined by tartrate-resistant acid phosphate (TRAP) staining, osteoclast activation was investigated by bone resorption assays, and gene expression of differentiation markers was examined by quantitative real-time PCR. Transfection of Tlr2 and Tlr4 siRNAs into RAW264 cells was also employed and their role in Mfa1 recognition was investigated. Mfa1 effectively induced the formation of TRAP-positive multinucleated cells and activated osteoclasts. Mfa1 also increased gene expression of Acp5, Mmp9, and Ctsk in RANKL-prestimulated RAW264 cells compared with the control. The osteoclastogenesis induced by Mfa1 was significantly decreased in cells transfected with Tlr2 or Tlr4 siRNAs compared with control siRNA. Our results revealed the role of Mfa1 fimbriae in osteoclastogenesis that may contribute to the partial elucidation of the mechanisms of periodontal disease progression and the development of new therapeutic strategies.
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Gemmell, E., K. Yamazaki, and G. J. Seymour. "Destructive Periodontitis Lesions are Determined by the Nature of the Lymphocytic Response." Critical Reviews in Oral Biology & Medicine 13, no. 1 (January 2002): 17–34. http://dx.doi.org/10.1177/154411130201300104.
Full textAbstract:
It is now 35 years since Brandtzaeg and Kraus (1965) published their seminal work entitled "Autoimmunity and periodontal disease". Initially, this work led to the concept that destructive periodontitis was a localized hypersensitivity reaction involving immune complex formation within the tissues. In 1970, Ivanyi and Lehner highlighted a possible role for cell-mediated immunity, which stimulated a flurry of activity centered on the role of lymphokines such as osteoclast-activating factor (OAF), macrophage-activating factor (MAF), macrophage migration inhibition factor (MIF), and myriad others. In the late 1970s and early 1980s, attention focused on the role of polymorphonuclear neutrophils, and it was thought that periodontal destruction occurred as a series of acute exacerbations. As well, at this stage doubt was being cast on the concept that there was a neutrophil chemotactic defect in periodontitis patients. Once it was realized that neutrophils were primarily protective and that severe periodontal destruction occurred in the absence of these cells, attention swung back to the role of lymphocytes and in particular the regulatory role of T-cells. By this time in the early 1990s, while the roles of interleukin (IL)-1, prostaglandin (PG) E2, and metalloproteinases as the destructive mediators in periodontal disease were largely understood, the control and regulation of these cytokines remained controversial. With the widespread acceptance of the Th1/Th2 paradigm, the regulatory role of T-cells became the main focus of attention. Two apparently conflicting theories have emerged. One is based on direct observations of human lesions, while the other is based on animal model experiments and the inability to demonstrate IL-4 mRNA in gingival extracts. As part of the "Controversy" series, this review is intended to stimulate debate and hence may appear in some places provocative. In this context, this review will present the case that destructive periodontitis is due to the nature of the lymphocytic infiltrate and is not due to periodic acute exacerbations, nor is it due to the so-called virulence factors of putative periodontal pathogens.
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Souza, Joao AC, Marcell C. Medeiros, Fernanda RG Rocha, Sabrina G. de Aquino, Mario J. Ávila-Campos, Luis C. Spolidorio, Dario S. Zamboni, Dana T. Graves, and Carlos Rossa. "Role of NOD2 and RIP2 in host–microbe interactions with Gram-negative bacteria: insights from the periodontal disease model." Innate Immunity 22, no. 8 (September 22, 2016): 598–611. http://dx.doi.org/10.1177/1753425916666652.
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NOD2 is a member of the NLR family of proteins that participate in the activation of the innate immune response. RIP2 is a downstream kinase activated by both NOD1 and NOD2. There is scarcity of information regarding the relevance of NOD2 in periodontitis, a chronic inflammatory condition characterized by inflammatory bone resorption. We used NOD2-KO and RIP2-KO mice in a model of microbial-induced periodontitis. Heat-killed Aggregatibacter actinomycetemcomitans was injected in the gingival tissues three times/wk for 4 wk. Bone resorption was assessed by μCT analysis; osteoclasts were identified by immunohistochemical staining for TRAP and inflammation was assessed using a severity score system in H/E-stained sections. In vitro studies using primary macrophages assessed the response macrophages using qPCR-based array and multi-ligand ELISA. Bone resorption and osteoclastogenesis were significantly reduced in NOD2-KO mice. Severity of inflammation was not affected. qPCR-focused arrays and multi-ligand ELISA showed that expression of pro-inflammatory mediators was reduced in NOD2- and RIP2-deficient cells. RANKL-induced osteoclastogenesis was impaired in NOD2- and RIP2-deficient macrophages. We conclude that NOD2 is important for osteoclast differentiation and inflammatory bone resorption in vivo and also for the macrophage response to Gram-negative bacteria.
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Zubery, Yuval, Colin R. Dunstan, Beryl M. Story, Lakshmyya Kesavalu, Jeffrey L. Ebersole, Stanley C. Holt, and Brendan F. Boyce. "Bone Resorption Caused by Three Periodontal Pathogens In Vivo in Mice Is Mediated in Part by Prostaglandin." Infection and Immunity 66, no. 9 (September 1, 1998): 4158–62. http://dx.doi.org/10.1128/iai.66.9.4158-4162.1998.
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ABSTRACT Gingival inflammation, bacterial infection, alveolar bone destruction, and subsequent tooth loss are characteristic features of periodontal disease, but the precise mechanisms of bone loss are poorly understood. Most animal models of the disease require injury to gingival tissues or teeth, and the effects of microorganisms are thus complicated by host responses to tissue destruction. To determine whether three putative periodontal pathogens, Porphyromonas gingivalis, Campylobacter rectus, andFusobacterium nucleatum, could cause localized bone resorption in vivo in the absence of tissue injury, we injected live or heat-killed preparations of these microorganisms into the subcutaneous tissues overlying the calvaria of normal mice once daily for 6 days and then examined the bones histologically. We found that all three microorganisms (both live and heat killed) stimulated bone resorption and that the strain of F. nucleatum used appeared to be the strongest inducer of osteoclast activity. Treatment of the mice concomitantly with indomethacin reduced but did not completely inhibit bone resorption by these microorganisms, suggesting that their effects were mediated, in part, by arachidonic acid metabolites (e.g., prostaglandins). Our findings indicate that these potential pathogens can stimulate bone resorption locally when placed beside a bone surface in vivo in the absence of prior tissue injury and support a role for them in the pathogenesis of bone loss around teeth in periodontitis.
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Rahmitasari, Fitria, Retno Pudji Rahayu, and Elly Munadziroh. "The potential of chitosan combined with chicken shank collagen as scaffold on bone defect regeneration process in Rattus norvegicus." Dental Journal (Majalah Kedokteran Gigi) 49, no. 1 (December 5, 2016): 22. http://dx.doi.org/10.20473/j.djmkg.v49.i1.p22-26.
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Background: In the field of dentistry, alveolar bone damage can be caused by periodontal disease, traumatic injury due to tooth extraction, cyst enucleation, and tumor surgery. One of the ways to regenerate the bone defect is using graft scaffold. Thus, combination of chitosan and collagen can stimulate osteogenesis. Purpose: The aim of this study was to examine the potential of chitosan combined with chicken shank collagen on bone defect regeneration process. Method: Twelve Rattus norvegicus were prepared as animal models in this research. A bone defect was intentionally created at both of the right and left femoral bones of the models. Next, 24 samples were divided into four groups, namely Group 1 using chitosan – collagen scaffold (50:50), Group 2 using chitosan collagen-scaffold (80:20), Group 3 using chitosan scaffold only, and Control Group using 3% CMC-Na. On 14th day, those animals were sacrificed, and histopathological anatomy examination was conducted to observe osteoclast cells. In addition, immunohistochemistry examination was also performed to observe RANKL expressions. Result: There was a significant difference in RANKL expressions among the groups, except between Group 3 using chitosan scaffold only and control group (p value > 0.05). The highest expression of RANKL was found in Group 1 with chitosan – collagen scaffold (50:50), followed by Group 2 with chitosan-collagen scaffold (80:20). Moreover, there was also a significant difference in osteoclast generation, except between Group 1 using chitosan – collagen scaffold (50:50) and Group 2 using chitosan-collagen scaffold (80:20), p value < 0.05; and between Group 3 using chitosan scaffold only and control group, p value > 0.05. Less osteoclast was found in the groups using chitosan – collagen scaffold (Group 1 and Group 2). Conclusion: Combination of chitosan and chicken shank collagen scaffold can improve regeneration process of bone defect in Rattus novergicus animals through increasing of RANKL expressions, and decreasing of osteoclast.
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Yang, Wenbin, Zheng Zhu, Longjiang Li, Abigail McVicar, Ning Gao, Lin Wang, Yi-Ping Li, and Wei Chen. "Silencing of Ac45 Simultaneously Inhibits Osteoclast-Mediated Bone Resorption and Attenuates Dendritic Cell-Mediated Inflammation through Impairing Acidification and Cathepsin K Secretion." Infection and Immunity 89, no. 1 (October 19, 2020): e00436-20. http://dx.doi.org/10.1128/iai.00436-20.
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ABSTRACTEndodontic disease is characterized by inflammation and destruction of periapical tissues, leading to severe bone resorption and tooth loss. ATP6AP1 (Ac45) has been implicated in human immune diseases, yet the mechanism underlying how Ac45 regulates immune response and reaction in inflammatory diseases remains unknown. We generated endodontic disease mice through bacterial infection as an inflammatory disease model and used adeno-associated virus (AAV)-mediated Ac45 RNA interference knockdown to study the function of Ac45 in periapical inflammation and bone resorption. We demonstrated that the AAV small hairpin RNA targeting Ac45 (AAV-sh-Ac45) impaired cellular acidification, extracellular acidification, and bone resorption. Our results showed that local delivery of AAV-sh-Ac45 in periapical tissues in bacterium-induced inflammatory lesions largely reduced bone destruction, inhibited inflammation, and dramatically reduced mononuclear immune cells. T-cell, macrophage, and dendritic cell infiltration in the periapical lesion was dramatically reduced, and the periodontal ligament was protected from inflammation-induced destruction. Furthermore, AAV-sh-Ac45 significantly reduced osteoclast formation and the expression of proinflammatory cytokines, such as tumor necrosis factor alpha, interleukin-10 (IL-10), IL-12, IL-1α, IL-6, and IL-17. Interestingly, AAV-sh-Ac45 impaired mature cathepsin K secretion more significantly than that by AAV-sh-C1 and AAV-sh-CtsK. Unbiased genome-wide transcriptome sequencing analysis of Ctsk−/− dendritic cells stimulated with lipopolysaccharide demonstrated that the ablation of Ctsk dramatically reduced dendritic cell-mediated inflammatory signaling. Taken together, our results indicated that AAV-sh-Ac45 simultaneously inhibits osteoclast-mediated bone resorption and attenuates dendritic cell-mediated inflammation through impairing acidification and cathepsin K secretion. Thus, Ac45 may be a novel target for therapeutic approaches to attenuate inflammation and bone erosion in endodontic disease and other inflammation-related osteolytic diseases.
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Jing, L., S. Kim, L. Sun, L. Wang, E. Mildner, K. Divaris, Y. Jiao, and S. Offenbacher. "IL-37- and IL-35/IL-37-Producing Plasma Cells in Chronic Periodontitis." Journal of Dental Research 98, no. 7 (May 3, 2019): 813–21. http://dx.doi.org/10.1177/0022034519847443.
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Periodontitis is one of the most prevalent chronic inflammatory diseases and is induced by the interaction between oral microorganisms and the host immune system. Plasma cells are of special interest in chronic periodontitis (CP), as they represent ~50% of infiltrated immune cells in periodontal lesions. Plasma cells constitute the only known cell type capable of antibody production; however, recent evidence supports an emerging role for distinct sets of plasma cells in cytokine production. However, the presence of cytokine-producing plasma cells in CP is unknown. In this study, we used immunohistochemistry to detect significantly elevated levels of IL-35 and IL-37 (2 recently identified anti-inflammatory cytokines) in CP gingival tissue as compared with healthy tissue. Remarkably, we demonstrate that CD138+ CD38+ plasma cells are the major immune cell type in CP gingival tissues and that these cells produce IL-35 and IL-37. We used immunofluorescence and confocal microscopy analysis to identify a subset of plasma cells with robust cytoplasmic expression of IL-37—we denote this subset as IL-37-producing plasma cells (CD138+CD38+PIL-37). Another subset of plasma cells coproduces IL-35 and IL-37 and is denoted as IL-37/IL-35-coproducing plasma cells (CD138+CD38+PIL-35/IL-37). We determined that these 2 plasma cell subsets are IgG+plasma cells. Moreover, we show that human recombinant IL-35 and IL-37 exhibit a dose-dependent inhibition of osteoclast formation in vitro (~78.9% and 97.7% inhibition in 300 ng/mL of IL-35 and IL-37, respectively, P < 0.05). Overall, our findings suggest that PIL-37 and PIL-35/IL-37 exist as subsets of plasma cells in CP lesions and that these 2 new types of plasma cells may regulate periodontitis pathogenesis by inhibiting alveolar bone loss through directly blocking osteoclast formation. Importantly, these data suggest a novel role of plasma cells and offer potential new mechanistic and regulatory targets to be investigated in the context of periodontal health and disease.
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Brito, Victor Gustavo Balera, Mariana Sousa Patrocinio, Maria Carolina Linjardi Sousa, Ayná Emanuelli Alves Barreto, Sabrina Cruz Tfaile Frasnelli, Vanessa Soares Lara, Carlos Ferreira Santos, and Sandra Helena Penha Oliveira. "Mast cells contribute to alveolar bone loss in Spontaneously Hypertensive Rats with periodontal disease regulating cytokines production." PLOS ONE 16, no. 3 (March 4, 2021): e0247372. http://dx.doi.org/10.1371/journal.pone.0247372.
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Mast cells (MCs) play a pivotal role in inflammatory responses and had been studied in inflammatory bone disorders, however, their role in alveolar bone loss induced by periodontal disease (PD) is not yet fully understood. We, therefore, aimed to evaluate the effects of MCs depletion in the PD-induced alveolar bone loss in Wistar (W) and Spontaneously Hypertensive Rats (SHRs). PD was induced by ligating the lower first molars with silk thread one day after the MCs depletion, by the pre-treatment with compound 48/80 for 4 days. After 15 days of PD induction, the hemi-mandibles were surgically collected for qRT-PCR, histological analyses, immunostaining, and ELISA. Systolic blood pressure (SBP) was verified by tail plethysmography to confirm the hypertensive status, and SHR presented SBP >150 mmHg, and previous MC depletion alone or associated with PD did not alter this parameter. SHRs showed a more severe alveolar bone loss compared to W, and MC depletion significantly inhibited this response in both strains, with a more significant response in SHRs. MCs were less abundant in 48/80+PD groups, thus validating the previous MCs depletion in our model. PD increased the number of MC in the gingival tissue of SHR. Cytokine production (TNF-α, IL-6, IL-1β, and CXCL3) was constitutively higher in SHR and increased further after PD, which was also significantly reduced in the MCs-depleted animals. PD led to an increased expression of Opn, Rankl, Rank, Vtn, Itga5, Itgb5, Trap, and Ctsk in the mandible of W and SHRs, which was reversed in MCs-depleted animals. These results suggest that MCs significantly contributes to the PD-induced alveolar bone resorption, especially in the SHR, which is associated with a more severe PD progression compared to Wistar, partly explained by these cells contribution to the inflammatory status and mediator production, stimulating osteoclast-related response markers, which were reduced after MC depletion in our experimental model.
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Aung, Kyaw Thu, Kentaro Akiyama, Masayoshi Kunitomo, Aung Ye Mun, Ikue Tosa, Ha Thi Thu Nguyen, Jiewen Zhang, et al. "Aging-Affected MSC Functions and Severity of Periodontal Tissue Destruction in a Ligature-Induced Mouse Periodontitis Model." International Journal of Molecular Sciences 21, no. 21 (October 30, 2020): 8103. http://dx.doi.org/10.3390/ijms21218103.
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Mesenchymal stem cells (MSCs) are known to play important roles in the repair of lost or damaged tissues and immunotolerance. On the other hand, aging is known to impair MSC function. However, little is currently known about how aged MSCs affect the host response to the local inflammatory condition and tissue deterioration in periodontitis, which is a progressive destructive disease of the periodontal tissue potentially leading to multiple tooth loss. In this study, we examined the relationship between aging-induced impairment of MSC function and the severity of periodontal tissue destruction associated with the decrease in host immunomodulatory response using a ligature-induced periodontitis model in young and aged mice. The results of micro computerized tomography (micro-CT) and histological analysis revealed a more severe bone loss associated with increased osteoclast activity in aged (50-week-old) mice compared to young (5-week-old) mice. Immunostaining analysis revealed that, in aged mice, the accumulation of inflammatory T and B cells was higher, whereas the percentage of platelet-derived growth factor receptor α (PDGFRα)+ MSCs, which are known to modulate the apoptosis of T cells, was significantly lower than in young mice. In vitro analysis of MSC function showed that the expression of surface antigen markers for MSCs (Sca-1, CD90, CD146), colony formation, migration, and osteogenic differentiation of aged MSCs were significantly declined compared to those of young MSCs. Moreover, a significantly higher proportion of aged MSCs were positive for the senescence-associated β galactosidase activity. Importantly, aged MSCs presented a decreased expression of FAS-L, which was associated with a lower immunomodulatory property of aged MSCs to induce T cell apoptosis in co-cultures compared with young MSCs. In summary, this is the first study showing that aging-induced impairment of MSC function, including immunomodulatory response, is potentially correlated with progressive periodontal tissue deterioration.
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Wang, Pao-Li. "Roles of Oral Bacteria in Cardiovascular Diseases — From Molecular Mechanisms to Clinical Cases: Treatment of Periodontal Disease Regarded as Biofilm Infection: Systemic Administration of Azithromycin." Journal of Pharmacological Sciences 113, no. 2 (2010): 126–33. http://dx.doi.org/10.1254/jphs.09r25fm.
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Ramadan, Doaa Elsayed, Ninuk Hariyani, Retno Indrawati, Rini Devijanti Ridwan, and Indeswati Diyatri. "Cytokines and Chemokines in Periodontitis." European Journal of Dentistry 14, no. 03 (June 23, 2020): 483–95. http://dx.doi.org/10.1055/s-0040-1712718.
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AbstractPeriodontitis is a common inflammatory periodontal disease affecting a wide range of population all over the world. The causing bacteria releases chemicals which activate the innate immune system to release proinflammatory cytokines contributing to more progression. This activates the acquired immune system leading to more progression of periodontitis. As the immune response goes on, released cytokines and chemokines can damage the periodontal ligaments, gingiva, and alveolar bone. There are many types of cytokines and chemokines in periodontitis. Cytokines are peptide mediators who are responsible for cell signaling and communication. Chemokines are a large subfamily of cytokines having the ability to coordinate leukocyte recruitment and activation. This paper is a narrative review of the literature.This review ensures that inflammatory mediators in the case of periodontitis can cause a noticeable damage in the whole apparatus of the periodontium. It causes soft tissue inflammation and bone damage affected by the mediators of both innate and acquired immune system.The inflammatory process is accompanied by large network of cytokines and chemokines. There is high expression of proinflammatory cytokines such as interleukin (IL)-1α, IL-1β, IL-6, IL-12, tumor necrosis factor (TNF)-α, and regulatory cytokines such as IL-4, IL-1(RA) receptor antagonist, IL-10, and induced protein (IP)-10. There is also increased production of cytokines IL-10, IL-12, interferon-γ, IP-10, IL-1RA, and IL-4. Cytokines IL-17, IL-6, IL-1β, TNF-α, macrophage colony-stimulating factor, and prostaglandin E2 trigger the osteoclast activity causing bone resorption.
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Yuan, G., C. Fu, S. T. Yang, D. Y. Yuh, G. Hajishengallis, and S. Yang. "RGS12 Drives Macrophage Activation and Osteoclastogenesis in Periodontitis." Journal of Dental Research 101, no. 4 (November 19, 2021): 448–57. http://dx.doi.org/10.1177/00220345211045303.
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Periodontitis is a complex inflammatory disease affecting the supporting structures of teeth and is associated with systemic inflammatory disorders. Regulator of G-protein signaling 12 (RGS12), the largest protein in the RGS protein family, plays a crucial role in the development of inflammation and bone remodeling. However, the role and mechanism(s) by which RGS12 may regulate periodontitis have not been elucidated. Here, we showed that ablation of RGS12 in Mx1+ hematopoietic cells blocked bone loss in the ligature-induced periodontitis model, as evidenced morphometrically and by micro–computed tomography analysis of the alveolar bone. Moreover, hematopoietic cell-specific deletion of RGS12 inhibited osteoclast formation and activity as well as the production of inflammatory cytokines such as IL1β, IL6, and TNFα in the diseased periodontal tissue. In the in vitro experiments, we found that the overexpression of RGS12 promoted the reprogramming of macrophages to the proinflammatory M1 type, but not the anti-inflammatory M2 type, and enhanced the ability of macrophages for migration. Conversely, knockdown of RGS12 in macrophages inhibited the production of inflammatory cytokines and migration of macrophages in response to lipopolysaccharide stimulation. Our results demonstrate for the first time that inhibition of RGS12 in macrophages is a promising therapeutic target for the treatment of periodontitis.
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Crotti, Tania N., Anak A. S. S. K. Dharmapatni, Ekram Alias, and David R. Haynes. "Osteoimmunology: Major and Costimulatory Pathway Expression Associated with Chronic Inflammatory Induced Bone Loss." Journal of Immunology Research 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/281287.
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The field of osteoimmunology has emerged in response to the range of evidences demonstrating the close interrelationship between the immune system and bone metabolism. This is pertinent to immune-mediated diseases, such as rheumatoid arthritis and periodontal disease, where there are chronic inflammation and local bone erosion. Periprosthetic osteolysis is another example of chronic inflammation with associated osteolysis. This may also involve immune mediation when occurring in a patient with rheumatoid arthritis (RA). Similarities in the regulation and mechanisms of bone loss are likely to be related to the inflammatory cytokines expressed in these diseases. This review highlights the role of immune-related factors influencing bone loss particularly in diseases of chronic inflammation where there is associated localized bone loss. The importance of the balance of the RANKL-RANK-OPG axis is discussed as well as the more recently appreciated role that receptors and adaptor proteins involved in the immunoreceptor tyrosine-based activation motif (ITAM) signaling pathway play. Although animal models are briefly discussed, the focus of this review is on the expression of ITAM associated molecules in relation to inflammation induced localized bone loss in RA, chronic periodontitis, and periprosthetic osteolysis, with an emphasis on the soluble and membrane bound factor osteoclast-associated receptor (OSCAR).
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Mazur, I. P., V. A. Habal, M. S. Drohomyretska, and K. M. Lykhota. "Oral cavity status in menopausal and postmenopausal women." REPRODUCTIVE ENDOCRINOLOGY, no. 62 (December 29, 2021): 80–84. http://dx.doi.org/10.18370/2309-4117.2021.62.80-84.
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The purpose of this review was to analyze and summarize the available literature data on changes of oral tissues in menopausal/postmenopausal women. We searched for the relevant references in Pubmed database using appropriate key words. We had revealed about 3,500 references on these topics and analyzed the most relevant. Postmenopausal women have an increased risk of the decrease of bone mineral density due to estrogen deficiency. Estrogens induce osteoclast apoptosis and intensity of this protective mechanism decreases after the cessation of menstruation. Most cross-sectional radiographic studies have confirmed an association between age-related osteoporosis and decreased alveolar bone height. It has been established that postmenopausal women with generalized chronic periodontitis are characterized by severe destruction of the periodontium, which progresses in parallel to a decrease in bone mineral density. Sex hormones maintaining bone integrity and strength, involved in regulating the proliferation, differentiation, and growth of keratinocytes and fibroblasts of the gums. The effect of low estrogen levels on keratinization of the gum epithelium and decreased salivation can lead to menopausal gingivostomatitis. Estrogen deficiency also adversely affects the microenvironment of gingival sulcus, including the composition and circulation of crevicular fluid. Postmenopausal women have lower salivary pH and lower salivation, which is associated with deterioration of periodontal tissues. In addition, the postmenopausal period is characterized by the changes in the microbial composition of the oral cavity, IgG decreases in the crevicular fluid and prooxidant changes of saliva. Conclusions. The oral cavity status in menopausal and postmenopausal women undergoes significant changes: a decrease in bone mineral density, dryness of mucous membranes, microbiome changes, and activation of oxidative and immune processes. These changes necessitate regular examinations, timely treatment and application of all measures of preventive dentistry. There is also a need for randomized clinical trials and create standardized guidelines for the management of postmenopausal patients with periodontal disease.
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Messer, Jonathan G., Stephanie La, Deborah E. Kipp, Evelyn J. Castillo, Joshua F. Yarrow, Marda Jorgensen, Russell D. Wnek, Donald B. Kimmel, and José Ignacio Aguirre. "Diet-induced Generalized Periodontitis in Lewis Rats." Comparative Medicine 69, no. 5 (October 1, 2019): 384–400. http://dx.doi.org/10.30802/aalas-cm-18-000113.
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Periodontitis is an important public health concern worldwide. Because rodents from the genus Rattus are resistant to spontaneous periodontitis, experimental periodontitis must be initiated by mechanical procedures and interventions. Due to their exacerbated Th1 response and imbalanced Th17 regulatory T-cell responses, Lewis rats are highly susceptible to inducible inflammatory and autoimmune diseases. We hypothesized that feeding Lewis rats a diet high in sucrose and casein (HSC) would alter the oral microenvironment and induce inflammation and the development of periodontitis lesions without mechanical intervention. A baseline group (BSL, n = 8) was euthanized at age 6 wk. Beginning at 6 wk of age, 2 groups of Lewis rats were fed standard (STD, n = 12) or HSC (n = 20) chow and euthanized at 29 wk of age. We evaluated the degree of periodontitis through histology and μCT of maxillae and mandibles. The HSC-induced inflammatory response of periodontal tissues was assessed by using immunohistochemistry. Gene expression analysis of inflammatory cytokines associated with Th1 and Th17 responses, innate immunity cytokines, and tissue damage in response to bacteria were assessed also. The potential systemic effects of HSC diet were evaluated by assessing body composition and bone densitometry endpoints; serum leptin and insulin concentrations; and gene expression of inflammatory cytokines in the liver. Placing Lewis rats on HSC diet for 24 wk induced a host Th1-immune response in periodontal tissues and mild to moderate, generalized periodontitis characterized by inflammatory cell infiltration (predominantly T cells and macrophages), osteoclast resorption of alveolar bone, and hyperplasia and migration of the gingival epithelium. HSC-fed Lewis rats developed periodontitis without mechanical intervention in the oral cavity and in the absence of any noteworthy metabolic abnormalities. Consequently, the rat model we described here may be a promising approach for modeling mild to moderate periodontitis that is similar in presentation to the human disease.