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Article ; Online: Mechanisms of Bone Resorption in Periodontitis.

Hienz, Stefan A / Paliwal, Sweta / Ivanovski, Saso

2015 Volume 2015, Page(s) 615486

Abstract: ... periodontopathic bacteria disturbs the homeostatic balance of bone formation and resorption in favour of bone loss ... 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 ...

Abstract	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 PGE2 also 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.
MeSH term(s)	Alveolar Bone Loss/immunology ; Animals ; Bone Resorption/immunology ; Humans ; Inflammation/immunology ; Osteoclasts/immunology ; Periodontitis/immunology ; RANK Ligand/immunology
Chemical Substances	RANK Ligand
Language	English
Publishing date	2015
Publishing country	Egypt
Document type	Journal Article ; Review
ZDB-ID	2817541-4
ISSN	2314-7156 ; 2314-8861
ISSN (online)	2314-7156
ISSN	2314-8861
DOI	10.1155/2015/615486
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Article: [Effect and mechanism of testosterone level on inflammatory bone resorption in periodontitis with mice].

Wu, Yue-Xia / Si, Shan-Shan / Zhang, Xin / Lian, Ke-Qian

Shanghai kou qiang yi xue = Shanghai journal of stomatology

2020 Volume 29, Issue 4, Page(s) 380–385

Abstract: ... than that of the sham operation group (P<0.05). The alveolar bone resorption area of the castration + testosterone group ... group(P<0.05). The alveolar bone resorption area of the castration group was significantly smaller ... levels were positively correlated with ABL, alveolar bone resorption area, and IL-1β (P<0.05 ...

Abstract	Purpose: To investigate the effect of testosterone level on inflammatory bone resorption in periodontitis with mice. Methods: Forty-eight SD mice were randomly divided into unligated group, sham operation group, castration group, castration + testosterone group, 12 mice in each group. At 6 weeks after ligation, serum testosterone levels were measured, and alveolar bone loss (ABL) and alveolar bone absorption area were compared by hematoxylin - eosin staining and methylene blue staining. The expression of inflammatory cytokine messenger RNA(mRNA) in gingival tissue was measured by real-time fluorescence quantitative PCR. SPSS 20.0 software package was used to analyze the data. Results: Serum testosterone level among four groups was the highest in the unligated group, followed by castration + testosterone group, sham operation group and castration group, with significant difference(P<0.05). The ABL of the castration + testosterone group was significantly larger than that of the unligated group, the sham operation group and the castration group(P<0.05). The ABL of the castration group was significantly smaller than that of the sham operation group (P<0.05). The alveolar bone resorption area of the castration + testosterone group was significantly larger than that of the unligated group, the sham operation group and the castration group(P<0.05). The alveolar bone resorption area of the castration group was significantly smaller than that of the sham operation group (P<0.05). Interleukin-1β (IL-1β) mRNA, interleukin-6(IL-6) mRNA and tumor necrosis factor-α(TNF-α) mRNA levels in gingival tissues of sham operation group, castration group and castration + testosterone group were significantly higher than the unligated group. The levels of interleukin-10(IL-10) mRNA in gingival tissues of sham operation group, castration group and castration + testosterone group were significantly lower than those in unligated group(P<0.05). The level of IL-1β mRNA in gingival tissues among four groups was the the highest in the unligated group, followed by castration + testosterone group, sham operation group and castration group, with significant difference (P<0.05). Serum testosterone levels were positively correlated with ABL, alveolar bone resorption area, and IL-1β (P<0.05). Conclusions: Periodontitis with mice have decreased testosterone levels, and long-term testosterone depletion can reduce inflammatory bone resorption in alveolar bone, which may be achieved by reducing the level of IL-1β, indicating that reduction of the level of testosterone in periodontitis patients may be a new treatment target for alveolar bone resorption.
MeSH term(s)	Alveolar Bone Loss ; Animals ; Cytokines ; Humans ; Mice ; Periodontitis ; Testosterone ; X-Ray Microtomography
Chemical Substances	Cytokines ; Testosterone (3XMK78S47O)
Language	Chinese
Publishing date	2020-09-18
Publishing country	China
Document type	Journal Article
ZDB-ID	2269714-7
ISSN	1006-7248
ISSN	1006-7248
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Article ; Online: Relevant mechanisms of MAIT cells involved in the pathogenesis of periodontitis.

Jiang, Xinrong / Zhao, Qingtong / Huang, Zhanyu / Ma, Fengyu / Chen, Kexiao / Li, Zejian

Frontiers in cellular and infection microbiology

2023 Volume 13, Page(s) 1104932

Abstract: ... that manifests mainly as inflammation of the gums and resorption of the alveolar bone due to periodontal tissue ... basal lamina and are more inclined to secrete IL-17 when activated. Periodontitis is a group of diseases ... invasion by plaque bacteria on the dental surface. The course of periodontitis is often accompanied by a T ...

Abstract	Mucosal-associated invariant T (MAIT) cells are a group of unconventional T cells that are abundant in the human body, recognize microbial-derived vitamin B metabolites presented by MHC class I-related protein 1 (MR1), and rapidly produce proinflammatory cytokines, which are widely involved in the immune response to various infectious diseases. In the oral mucosa, MAIT cells tend to accumulate near the mucosal basal lamina and are more inclined to secrete IL-17 when activated. Periodontitis is a group of diseases that manifests mainly as inflammation of the gums and resorption of the alveolar bone due to periodontal tissue invasion by plaque bacteria on the dental surface. The course of periodontitis is often accompanied by a T-cell-mediated immune response. This paper discussed the pathogenesis of periodontitis and the potential contribution of MAIT cells to periodontitis.
MeSH term(s)	Humans ; Mucosal-Associated Invariant T Cells/metabolism ; Histocompatibility Antigens Class I ; Communicable Diseases ; Cytokines/metabolism ; Periodontitis/metabolism
Chemical Substances	Histocompatibility Antigens Class I ; Cytokines
Language	English
Publishing date	2023-02-21
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2023.1104932
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Article: Diabetes mellitus promotes susceptibility to periodontitis-novel insight into the molecular mechanisms.

Zhao, Mingcan / Xie, Yuandong / Gao, Wenjia / Li, Chunwang / Ye, Qiang / Li, Yi

Frontiers in endocrinology

2023 Volume 14, Page(s) 1192625

Abstract: ... the alveolar bone resorption damage and the epigenetic changes in periodontal tissue induced by diabetes ... mechanisms remain unclear. Diabetes can increase the pathogenicity of the periodontal microbiota and ... Diabetes mellitus is a main risk factor for periodontitis, but until now, the underlying molecular ...

Abstract	Diabetes mellitus is a main risk factor for periodontitis, but until now, the underlying molecular mechanisms remain unclear. Diabetes can increase the pathogenicity of the periodontal microbiota and the inflammatory/host immune response of the periodontium. Hyperglycemia induces reactive oxygen species (ROS) production and enhances oxidative stress (OS), exacerbating periodontal tissue destruction. Furthermore, the alveolar bone resorption damage and the epigenetic changes in periodontal tissue induced by diabetes may also contribute to periodontitis. We will review the latest clinical data on the evidence of diabetes promoting the susceptibility of periodontitis from epidemiological, molecular mechanistic, and potential therapeutic targets and discuss the possible molecular mechanistic targets, focusing in particular on novel data on inflammatory/host immune response and OS. Understanding the intertwined pathogenesis of diabetes mellitus and periodontitis can explain the cross-interference between endocrine metabolic and inflammatory diseases better, provide a theoretical basis for new systemic holistic treatment, and promote interprofessional collaboration between endocrine physicians and dentists.
MeSH term(s)	Humans ; Diabetes Mellitus/etiology ; Periodontitis/complications ; Hyperglycemia/complications ; Risk Factors ; Bone Resorption
Language	English
Publishing date	2023-08-16
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1192625
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Article ; Online: Effect of artesunate on cardiovascular complications in periodontitis in a type I diabetes rat model and related mechanisms.

Chen, Y / Liang, C / Li, J / Ma, L / Wang, B / Yuan, Z / Yang, S / Nong, X

Journal of endocrinological investigation

2023 Volume 46, Issue 10, Page(s) 2031–2053

Abstract: ... effectively alleviated alveolar bone resorption and density reduction. The sequencing results suggested ... the possible underlying mechanisms.: Methods: Sprague‒Dawley rats were randomly divided into the healthy ... flora. Micro-CT was performed to observe changes in alveolar bone. Blood samples were ...

Abstract	Purpose: Both cardiovascular disease and periodontitis are complications of diabetes that have a great impact on human life and health. Our previous research found that artesunate can effectively improve cardiovascular disease in diabetes and has an inhibitory effect on periodontal disease. Therefore, the present study aimed to explore the potential therapeutic possibility of artesunate in the protection against cardiovascular complications in periodontitis with type I diabetes rats and to elucidate the possible underlying mechanisms. Methods: Sprague‒Dawley rats were randomly divided into the healthy, diabetic, periodontitis, diabetic with periodontitis, and artesunate treatment groups (10, 30, and 60 mg/kg, i.g.). After artesunate treatment, oral swabs were collected and used to determine changes in the oral flora. Micro-CT was performed to observe changes in alveolar bone. Blood samples were processed to measure various parameters, while cardiovascular tissues were evaluated by haematoxylin-eosin, Masson, Sirius red, and TUNEL staining to observe fibrosis and apoptosis. The protein and mRNA expression levels in the alveolar bone and cardiovascular tissues were detected using immunohistochemistry and RT‒PCR. Results: Diabetic rats with periodontitis and cardiovascular complications maintained heart and body weight but exhibited reduced blood glucose levels, and they were able to regulate blood lipid indicators at normal levels after artesunate treatment. The staining assays suggested that treatment with 60 mg/kg artesunate has a significant therapeutic effect on myocardial apoptotic fibrosis. The high expression of NF-κB, TLR4, VEGF, ICAM-1, p38 MAPK, TGF-β, Smad2, and MMP9 in the alveolar bone and cardiovascular tissue in the type I diabetes and type I diabetes with periodontitis rat models was reduced after treatment with artesunate in a concentration-dependent manner. Micro-CT showed that treatment with 60 mg/kg artesunate effectively alleviated alveolar bone resorption and density reduction. The sequencing results suggested that each model group of rats had vascular and oral flora dysbiosis, but artesunate treatment could correct the dysbacteriosis. Conclusions: Periodontitis-related pathogenic bacteria cause dysbiosis of the oral and intravascular flora in type I diabetes and aggravate cardiovascular complications. The mechanism by which periodontitis aggravates cardiovascular complications involves the NF-κB pathway, which induces myocardial apoptosis, fibrosis, and vascular inflammation.
MeSH term(s)	Rats ; Humans ; Animals ; Artesunate/therapeutic use ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/drug therapy ; NF-kappa B ; Cardiovascular Diseases/complications ; Dysbiosis ; Rats, Sprague-Dawley ; Periodontitis/complications ; Periodontitis/drug therapy ; Diabetes Mellitus, Type 1/complications ; Alveolar Bone Loss/complications ; Alveolar Bone Loss/drug therapy ; Alveolar Bone Loss/pathology
Chemical Substances	Artesunate (60W3249T9M) ; NF-kappa B
Language	English
Publishing date	2023-03-09
Publishing country	Italy
Document type	Journal Article
ZDB-ID	432272-1
ISSN	1720-8386 ; 0391-4097 ; 1121-1369
ISSN (online)	1720-8386
ISSN	0391-4097 ; 1121-1369
DOI	10.1007/s40618-023-02052-0
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Article: Associations between Periodontitis, COVID-19, and Cardiometabolic Complications: Molecular Mechanisms and Clinical Evidence.

Mainas, Giuseppe / Nibali, Luigi / Ide, Mark / Mahmeed, Wael Al / Al-Rasadi, Khalid / Al-Alawi, Kamila / Banach, Maciej / Banerjee, Yajnavalka / Ceriello, Antonio / Cesur, Mustafa / Cosentino, Francesco / Firenze, Alberto / Galia, Massimo / Goh, Su-Yen / Janež, Andrej / Kalra, Sanjay / Kapoor, Nitin / Kempler, Peter / Lessan, Nader /

Lotufo, Paulo / Papanas, Nikolaos / Rizvi, Ali A / Sahebkar, Amirhossein / Santos, Raul D / Stoian, Anca P / Toth, Peter P / Viswanathan, Vijay / Rizzo, Manfredi

Metabolites

2022 Volume 13, Issue 1

Abstract: ... to loss of periodontal attachment and resorption of bone. It is associated with the elevation of systemic inflammatory markers and ... Periodontitis is a microbially driven, host-mediated disease that leads ... several investigations demonstrating the possible relationship between periodontitis and COVID-19 have been reported ...

Abstract	Periodontitis is a microbially driven, host-mediated disease that leads to loss of periodontal attachment and resorption of bone. It is associated with the elevation of systemic inflammatory markers and with the presence of systemic comorbidities. Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although the majority of patients have mild symptoms, others experience important complications that can lead to death. After the spread of the COVID-19 pandemic, several investigations demonstrating the possible relationship between periodontitis and COVID-19 have been reported. In addition, both periodontal disease and COVID-19 seem to provoke and/or impair several cardiometabolic complications such as cardiovascular disease, type 2 diabetes, metabolic syndrome, dyslipidemia, insulin resistance, obesity, non-alcoholic fatty liver disease, and neurological and neuropsychiatric complications. Therefore, due to the increasing number of investigations focusing on the periodontitis-COVID-19 relationship and considering the severe complications that such an association might cause, this review aims to summarize all existing emerging evidence regarding the link between the periodontitis-COVID-19 axis and consequent cardiometabolic impairments.
Language	English
Publishing date	2022-12-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo13010040
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Article ; Online: Epigenetic regulation of inflammation in periodontitis: cellular mechanisms and therapeutic potential.

Jurdziński, Krzysztof T / Potempa, Jan / Grabiec, Aleksander M

Clinical epigenetics

2020 Volume 12, Issue 1, Page(s) 186

Abstract: ... proteins ameliorate inflammation, osteoclastogenesis, and alveolar bone resorption in animal models ... Epigenetic mechanisms, namely DNA and histone modifications, are critical regulators of immunity ... The prevalence and significant morbidity of periodontitis, in combination with accumulating evidence that genetic ...

Abstract	Epigenetic mechanisms, namely DNA and histone modifications, are critical regulators of immunity and inflammation which have emerged as potential targets for immunomodulating therapies. The prevalence and significant morbidity of periodontitis, in combination with accumulating evidence that genetic, environmental and lifestyle factors cannot fully explain the susceptibility of individuals to disease development, have driven interest in epigenetic regulation as an important factor in periodontitis pathogenesis. Aberrant promoter methylation profiles of genes involved in inflammatory activation, including TLR2, PTGS2, IFNG, IL6, IL8, and TNF, have been observed in the gingival tissue, peripheral blood or buccal mucosa from patients with periodontitis, correlating with changes in expression and disease severity. The expression of enzymes that regulate histone acetylation, in particular histone deacetylases (HDACs), is also dysregulated in periodontitis-affected gingival tissue. Infection of gingival epithelial cells, gingival fibroblasts and periodontal ligament cells with the oral pathogens Porphyromonas gingivalis or Treponema denticola induces alterations in expression and activity of chromatin-modifying enzymes, as well as site-specific and global changes in DNA methylation profiles and in histone acetylation and methylation marks. These epigenetic changes are associated with excessive production of inflammatory cytokines, chemokines, and matrix-degrading enzymes that can be suppressed by small molecule inhibitors of HDACs (HDACi) or DNA methyltransferases. HDACi and inhibitors of bromodomain-containing BET proteins ameliorate inflammation, osteoclastogenesis, and alveolar bone resorption in animal models of periodontitis, suggesting their clinical potential as host modulation therapeutic agents. However, broader application of epigenomic methods will be required to create a comprehensive map of epigenetic changes in periodontitis. The integration of functional studies with global analyses of the epigenetic landscape will provide critical information on the therapeutic and diagnostic potential of epigenetics in periodontal disease.
MeSH term(s)	Animals ; Case-Control Studies ; CpG Islands ; Cytokines/metabolism ; DNA Methylation ; Epigenomics/methods ; Epithelial Cells/metabolism ; Epithelial Cells/microbiology ; Fibroblasts/metabolism ; Histone Code/genetics ; Histone Deacetylases/genetics ; Humans ; Inflammation/genetics ; Mice ; Models, Animal ; Periodontitis/epidemiology ; Periodontitis/genetics ; Periodontitis/pathology ; Periodontitis/therapy ; Porphyromonas gingivalis/genetics ; Porphyromonas gingivalis/isolation & purification ; Prevalence ; Promoter Regions, Genetic/genetics ; Proteins/antagonists & inhibitors ; Proteins/metabolism ; Rats ; Severity of Illness Index ; Treponema denticola/genetics ; Treponema denticola/isolation & purification
Chemical Substances	Cytokines ; Proteins ; bromodomain and extra-terminal domain protein, human ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2020-11-30
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2553921-8
ISSN	1868-7083 ; 1868-7075
ISSN (online)	1868-7083
ISSN	1868-7075
DOI	10.1186/s13148-020-00982-7
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Article: Physalis angulata reduces the progression of chronic experimental periodontitis by immunomodulatory mechanisms

Vieceli, Paula Schons / Juiz, Paulo José Lima / Lauria, Pedro Santana Sales / Couto, Ricardo David / Tomassini, Therezinha Coelho Barbosa / Ribeiro, Ivone Maria / Soares, Milena Botelho Pereira / Villarreal, Cristiane Flora

Journal of ethnopharmacology. 2021 June 12, v. 273

2021

Abstract: ... periodontitis suffered alveolar bone loss that was prevented by the treatment with EEPA (50 or 100 mg/kg) or ... as an anti-inflammatory and immunomodulatory agent, and to point out possible mechanisms involved in these effects.EEPA ... by oral route for 14 days. At the end of the experimental period, alveolar bone loss was evaluated along ...

Abstract	Physalis angulata is an herb found in tropical and subtropical regions of the world; it is widely applied in popular medicine due to the therapeutic properties of the whole plant and its parts. Extracts and infusions of this plant have been extensively applied in folk medicine worldwide to treat inflammatory and immune-mediated diseases, including oral inflammatory conditions such as sore throat and gingivitis.The present study was designed to investigate the protective effects of the ethanolic extract of P. angulata (EEPA) in a murine model of chronic periodontitis, aiming to corroborate its traditional use as an anti-inflammatory and immunomodulatory agent, and to point out possible mechanisms involved in these effects.EEPA was obtained from the stems of P. angulata collected in Belém (PA, Brazil). Chronic periodontitis was induced in male C57BL/6 mice by 12 administrations of lipopolysaccharide (LPS; 20 μg/1μL) into the gingival papilla in the course of 28 days. Starting from the 15ᵗʰ day after the first LPS injection, mice were daily treated with EEPA (50 or 100 mg/kg), nimesulide (25 mg/kg, reference drug), or vehicle by oral route for 14 days. At the end of the experimental period, alveolar bone loss was evaluated along with the gingival expression of biomarkers of periodontitis and cytokines by RT-q-PCR and ELISA. Hematological and biochemical parameters suggestive of systemic toxicity were also evaluated. The transcriptional activity of NF-κB was investigated using the luciferase assay in macrophages.Mice with chronic experimental periodontitis suffered alveolar bone loss that was prevented by the treatment with EEPA (50 or 100 mg/kg) or nimesulide (25 mg/kg). EEPA (50 and 100 mg/kg) and nimesulide (25 mg/kg) reduced mRNA levels of MMP-9 mRNA, but not of TIMP-1 in gingival tissue of periodontitis-induced mice. Both treatments also reduced the production of the pro-inflammatory cytokines IL-1β and IL-6. The treatment with EEPA (100 mg/kg) increased the production of the anti-inflammatory cytokine TGF-β. No hematological or biochemical alterations were caused by the daily treatment with EEPA. In vitro luciferase assay suggested that a putative mechanism of EEPA is reducing the transcriptional activity of NF-κB.EEPA exhibited a disease-modifying effect in the chronic experimental periodontitis, along with unidentifiable systemic toxicity. This work corroborates the traditional use of P. angulata in oral inflammatory conditions and provides mechanistic hypotheses to explain its therapeutic effects.
Keywords	Physalis angulata ; animal models ; biomarkers ; bone resorption ; drugs ; gingiva ; interleukin-6 ; lipopolysaccharides ; luciferase ; males ; periodontitis ; pharyngitis ; therapeutics ; toxicity ; traditional medicine ; transcription (genetics) ; Brazil
Language	English
Dates of publication	2021-0612
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2021.113986
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Article ; Online: Protective mechanisms of simvastatin in experimental periodontal disease.

Dalcico, Roberta / de Menezes, Adriana M A / Deocleciano, Otacilio B / Oriá, Reinaldo B / Vale, Mariana L / Ribeiro, Ronaldo A / Brito, Gerly A de C

Journal of periodontology

2013 Volume 84, Issue 8, Page(s) 1145–1157

Abstract: ... data suggest that simvastatin prevents inflammatory bone resorption in experimental periodontitis ... a therapeutic impact on bone. This study evaluates the effect of simvastatin on rats subjected to experimental ... kg/day) until sacrifice on day 11. Alveolar bone loss was determined by macroscopic and histologic ...

Abstract	Background: Simvastatin is a cholesterol-lowering drug whose pleiotropic effects may have a therapeutic impact on bone. This study evaluates the effect of simvastatin on rats subjected to experimental periodontal disease. Methods: Periodontitis was induced by ligature placement around the maxillary left second molar of rats for 11 days. Groups of six animals received oral saline or simvastatin (3, 10, and 30 mg/kg/day) until sacrifice on day 11. Alveolar bone loss was determined by macroscopic and histologic examination. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total alkaline phosphatase (TAP) were evaluated. Gingival myeloperoxidase activity and gingival levels of interleukin-1β (IL-1β), tumor necrosis factor-α, IL-10, reduced glutathione, malonaldehyde, and nitrate/nitrite were analyzed to investigate oxidative stress and inflammation. Expression of inducible nitric oxide synthase (iNOS), matrix metalloproteinases 1 and 8 (MMP-1 and -8), bone morphogenetic protein-2 (BMP-2), receptor activator of nuclear factor κB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) were also investigated by immunohistochemistry to assess bone turnover and metabolism. Immunofluorescence microscopy was used to confirm the expression of RANKL in rats' maxillae. Results: Treatment with simvastatin improved alveolar bone loss within all of the parameters studied, thus demonstrating anti-inflammatory and antioxidant activity. Simvastatin reduced expression of iNOS, MMP-1 and -8, RANK, and RANKL and increased BMP-2 and OPG levels in the periodontal tissue. Simvastatin (30 mg/kg) increased TAP activity on day 11 compared with the saline group. No differences were found in the levels of AST and ALT in any of the groups studied. Conclusion: The present data suggest that simvastatin prevents inflammatory bone resorption in experimental periodontitis, which may be mediated by its anti-inflammatory and antioxidant properties.
MeSH term(s)	Alanine Transaminase/drug effects ; Alkaline Phosphatase/drug effects ; Alveolar Bone Loss/prevention & control ; Animals ; Anti-Inflammatory Agents/therapeutic use ; Antioxidants/therapeutic use ; Aspartate Aminotransferases/drug effects ; Bone Morphogenetic Protein 2/drug effects ; Female ; Gingiva/drug effects ; Glutathione/drug effects ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Interleukin-10/analysis ; Interleukin-1beta/drug effects ; Malondialdehyde/analysis ; Matrix Metalloproteinase 1/drug effects ; Matrix Metalloproteinase 8/drug effects ; Nitrates/analysis ; Nitric Oxide Synthase Type II/drug effects ; Nitrites/analysis ; Osteoprotegerin/drug effects ; Oxidative Stress/drug effects ; Periodontitis/prevention & control ; Peroxidase/drug effects ; RANK Ligand/drug effects ; Rats ; Rats, Wistar ; Receptor Activator of Nuclear Factor-kappa B/drug effects ; Simvastatin/therapeutic use ; Tumor Necrosis Factor-alpha/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Antioxidants ; Bmp2 protein, rat ; Bone Morphogenetic Protein 2 ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Interleukin-1beta ; Nitrates ; Nitrites ; Osteoprotegerin ; RANK Ligand ; Receptor Activator of Nuclear Factor-kappa B ; Tnfrsf11b protein, rat ; Tumor Necrosis Factor-alpha ; Interleukin-10 (130068-27-8) ; Malondialdehyde (4Y8F71G49Q) ; Simvastatin (AGG2FN16EV) ; Peroxidase (EC 1.11.1.7) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, rat (EC 1.14.13.39) ; Aspartate Aminotransferases (EC 2.6.1.1) ; Alanine Transaminase (EC 2.6.1.2) ; Alkaline Phosphatase (EC 3.1.3.1) ; Matrix Metalloproteinase 8 (EC 3.4.24.34) ; MMP1 protein, rat (EC 3.4.24.7) ; Matrix Metalloproteinase 1 (EC 3.4.24.7) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2013-08
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	390921-9
ISSN	1943-3670 ; 0022-3492 ; 1049-8885 ; 0095-960X
ISSN (online)	1943-3670
ISSN	0022-3492 ; 1049-8885 ; 0095-960X
DOI	10.1902/jop.2012.120114
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Article: [Mechanisms for bone resorption induced by periodontal pathogens].

Yoshimura, Kentaro / Miyamoto, Yoichi / Kamijo, Ryutaro

Clinical calcium

2012 Volume 22, Issue 11, Page(s) 1685–1692

Abstract: ... of periodontal tissues. Here we review the mechanisms by which periodontal pathogens cause bone resorption. ... progression of this pathological condition is also considered as a major cause of alveolar bone resorption and ... mechanisms causes breakdown of host innate and acquired immune systems, and subsequent destruction ...

Abstract	Periodontitis is the inflammatory disease caused by periodontal pathogens in dental plaque, and progression of this pathological condition is also considered as a major cause of alveolar bone resorption and subsequent tooth depletion. LPS and several kinds of proteinases produced by periodontal pathogens directly destroy periodontal tissues. On the other hand, host defense systems existing in the periodontal tissues exert essential roles in protection of periodontal tissues from bacterial invasion. Immune system divides broadly into 2 categories, innate immune and acquired immune systems. The former is the first defensive barrier against infectious diseases of pathogens, and phagocytic cells including macrophages and neutrophils are involved in this immune system as innate immune function. The latter is the secondary immune system that antigen-presenting cells such as dendritic cells detect smaller pathogens or intracellular pathogens, and antigens which retain as intact proteins on the surfaces of these cells activate T cells and B cells. However, once inflammation becomes persistent with bacteria, these biological defective mechanisms causes breakdown of host innate and acquired immune systems, and subsequent destruction of periodontal tissues. Here we review the mechanisms by which periodontal pathogens cause bone resorption.
MeSH term(s)	Animals ; Bone Resorption/immunology ; Bone Resorption/metabolism ; Dental Plaque/immunology ; Dental Plaque/microbiology ; Humans ; Lipopolysaccharides/immunology ; Periodontitis/immunology ; Periodontitis/microbiology ; Porphyromonas gingivalis/growth & development ; Porphyromonas gingivalis/immunology ; Signal Transduction/immunology
Chemical Substances	Lipopolysaccharides
Language	Japanese
Publishing date	2012-11
Publishing country	Japan
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	2386417-5
ISSN	0917-5857
ISSN	0917-5857
DOI	CliCa121116851692
Database	MEDical Literature Analysis and Retrieval System OnLINE

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