scholarly journals Histopathological Verification of Osteoimmunological Mediators in Peri-Implantitis and Correlation to Bone Loss and Implant Functional Period

2016 ◽  
Vol 42 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Anna Konermann ◽  
Werner Götz ◽  
Michael Le ◽  
Cornelius Dirk ◽  
Stefan Lossdörfer ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Retention Time ◽  
Correlation Coefficients ◽  
Inflammatory Cells ◽  
Smoking History ◽  
Tnf Α ◽  
Implant Retention ◽  
Higher Rank ◽  
Inflammatory Infiltrates

Peri-implantitis (PI) is characterized by inflammation and bone resorption eventually leading to implant failure, but the characteristic pathologic determinants are undefined to date. This study aims to elucidate the parameters involved in PI pathogenesis, including intraoral implant retention time, extent of bone loss, smoking history, and identification of osteoimmunological markers for inflammation and bone loss. Peri-implant tissues (n = 21) displaying clinically diagnosed PI from patients with vertical bone loss ranging from 0–12 mm and implant function period between 1 and 60 months were evaluated by histochemistry and immunohistochemistry for TRAP, CD3, RANK, RANKL, OPG, and TNF-α. Statistical analyses were performed with the Welch test and correlation coefficients were calculated. Most bone resorption occurred during the first 12 months of implant function and correlated with the extent of inflammation, although histological signs of inflammation strongly varied between samples from minimal appearance of inflammatory cells to extended infiltrates. Implant function period and smoking history did not significantly affect the degree of inflammation. Higher RANK levels emerged in the first 12 months of implant function compared to longer retention times and were negatively correlated to the occurrence of RANKL. Additionally, histological signs of inflammation were about two-fold higher in specimens with bone resorption up from 5 mm compared to under 5 mm. CD3+ cells were more prevalent in extensive inflammatory infiltrates and samples derived from smokers. Our analyses proved that PI-induced bone loss is differentially influenced by the parameters evaluated in this study, but a distinct interconnection between disease severity and implant retention time can be established.

scholarly journals Metformin Hydrochloride-Loaded PLGA Nanoparticle in Periodontal Disease Experimental Model Using Diabetic Rats

2018 ◽  
Vol 19 (11) ◽  
pp. 3488 ◽  
Author(s):  
Aline Pereira ◽  
Gerly Brito ◽  
Maria Lima ◽  
Arnóbio Silva Júnior ◽  
Emanuell Silva ◽  
...  
Keyword(s):  
Bone Loss ◽  
Cathepsin K ◽  
Immunohistochemical Analysis ◽  
Entrapment Efficiency ◽  
Inflammatory Cells ◽  
Plga Nanoparticles ◽  
Diabetic Rats ◽  
Metformin Hydrochloride ◽  
Tnf Α ◽  
Mean Diameter

Evidence shows that metformin is an antidiabetic drug, which can exert favorable anti-inflammatory effects and decreased bone loss. The development of nanoparticles for metformin might be useful for increased therapeutic efficacy. The aim of this study was to evaluate the effect of metformin hydrochloride-loaded Poly (d,l-Lactide-co-glycolide) (PLGA)/(MET-loaded PLGA) on a ligature-induced periodontitis model in diabetic rats. MET-loaded PLGA were characterized by mean diameter, particle size, polydispensity index, and entrapment efficiency. Maxillae were scanned using Microcomputed Tomography (µCT) and histopathological and immunohistochemical analysis. IL-1β and TNF-α levels were analyzed by ELISA immunoassay. Quantitative RT-PCR was used (AMPK, NF-κB p65, HMGB1, and TAK-1). The mean diameter of MET-loaded PLGA nanoparticles was in a range of 457.1 ± 48.9 nm (p < 0.05) with a polydispersity index of 0.285 (p < 0.05), Z potential of 8.16 ± 1.1 mV (p < 0.01), and entrapment efficiency (EE) of 66.7 ± 3.73. Treatment with MET-loaded PLGA 10 mg/kg showed low inflammatory cells, weak staining by RANKL, cathepsin K, OPG, and osteocalcin, and levels of IL-1β and TNF-α (p < 0.05), increased AMPK expression gene (p < 0.05) and decreased NF-κB p65, HMGB1, and TAK-1 (p < 0.05). It is concluded that MET-loaded PLGA decreased inflammation and bone loss in periodontitis in diabetic rats.

scholarly journals Blood-induced bone loss in murine hemophilic arthropathy is prevented by blocking the iRhom2/ADAM17/TNF-α pathway

Blood ◽  
2018 ◽  
Vol 132 (10) ◽  
pp. 1064-1074 ◽  
Author(s):  
Coline Haxaire ◽  
Narine Hakobyan ◽  
Tania Pannellini ◽  
Camila Carballo ◽  
David McIlwain ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Proinflammatory Cytokine ◽  
Hemophilic Arthropathy ◽  
Tnf Α ◽  
Key Points

Key Points Blood and its components activated the iRhom2/ADAM17-dependent release of the proinflammatory cytokine TNF-α from macrophages. The iRhom2/ADAM17/TNF-α pathway emerged as a potential new target to prevent bone resorption following a joint bleed in mice.

scholarly journals The effect of bitter gourd (Momordica charantia) ethanolic extract on inflammatory infiltrates and NF-κB activation in periodontitis

2019 ◽  
Vol 1 (1) ◽  
pp. 6
Author(s):  
Aryudhi Armis ◽  
Tetiana Haniastuti ◽  
Heni Susilowati
Keyword(s):  
Alveolar Bone ◽  
Inflammatory Responses ◽  
Ethanolic Extract ◽  
Inflammatory Cells ◽  
Momordica Charantia ◽  
Bitter Gourd ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Anti Inflammatory ◽  
Inflammatory Infiltrates

Periodontitis is a periodontal disease involving the gingiva, periodontal ligament, cementum, and alveolar bone due to an inflammatory process. Virulence factors of periodontopathogens and inflammatory responses in periodontitis can stimulate nuclear factor-kappa B (NF-κB) activity. Charantoside c and Momordicosides g in bitter gourd prevent NF-κB activation stimulated by TNF-α in HepG2 cells. This study aims to determine the effect of bitter gourd fruit (Momordica charantia) ethanolic extract as an anti-inflammatory substance on the level of inflammatory infiltrates and the number of cells that experience NF-κB activation in the periodontitis model. Eighty male Wistar rats were divided into 5 groups. The mandibular incisors were ligated for 14 days to induce periodontitis. Each group was given Momordica charantia extract of 500 mg/kg BW, 250 mg/kg BW, and 100 mg/kg BW; ibuprofen 100 mg/kg BW; and aquades orally using oral gavage on the day 14. Rat necropsy was carried out on day 1, 3, 5, and 7 after giving the substances. Taking out the lower jaw was done to make tissue preparations followed by staining them with hematoxylin eosin (HE). Immunohistochemicalanalysis was performed to observe cells that were positive for NF-κB activation. The results showed a decrease in the density of inflammatory infiltrates in all groups, except for those given aquades. The number of inflammatory cells ofneutrophils, macrophages, and lymphocytes that experienced NF-κB activation showed the most effective decrease in the group of Momordica charantia 500 mg/kg BW, on the 7th day. The conclusion of this study is that ethanolic extractof Momordica charantia has an anti-inflammatory effect and prevents the activation of NF-kB in rat gingival induced by periodontitis. The highest effect was found at a dose of 500 mg/kg BW on day 7 after giving of extracts.

Inhibitory Effect of Carthamus tinctorius L. Seed Extracts on Bone Resorption Mediated by Tyrosine Kinase, COX-2 (cyclooxygenase) and PG (prostaglandin) E2

2002 ◽  
Vol 30 (01) ◽  
pp. 95-108 ◽  
Author(s):  
Tae Han Yuk ◽  
Joon Hyeog Kang ◽  
San Ryoung Lee ◽  
Sang Won Yuk ◽  
Kwang Gyu Lee ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Tyrosine Kinase ◽  
Kinase Inhibitor ◽  
Carthamus Tinctorius ◽  
Ovariectomized Rats ◽  
Mrna Levels ◽  
Src Tyrosine Kinase ◽  
Tnf Α ◽  
Cox 2

Anti-bone resorption properties of the Korean herbal formulation, Honghwain (HHI; Carthamus tinctorius L. seed) was biochemically investigated. On processing bone metabolism, PGE2 accelerated production of IL-1β in fetal mouse osteoblast and stimulated physiological activation substance, IL-1β. The novel class of Src tyrosine kinase inhibitors, Herbimycin A (HERB) and HHI reduced COX-2 mRNA levels as well as PGE2 production induced by IL-1β, TNF-α and IL-6. HHI inhibited in vitro and in vivo bone resorption by inhibition of phosphorylation of peptide substrates. HHI dose-dependently reduced the hypercalcemia induced in mice by IL-1β and partly prevented bone loss and microarchitectural changes in young ovariectomized rats, showing that the protective effect on bone was exerted via the inhibition of bone resorption. These results indicate that the synergy between IL-β, TNF-α, IL-6 on PGE2 production is due to an enhanced gene expression of COX-2 and that tyrosine kinase (s) are involved in the signal transduction of COX-2 in mouse calvarial osteoblasts. Thus, HHI as a possible Src family kinase inhibitor may be useful for the treatment of diseases associated with elevated bone loss.

scholarly journals Bisleuconothine A protects periodontal tissue via the regulation of RANKL expression and infiltration of inflammatory cells

2020 ◽  
Vol 19 (3) ◽  
pp. 497-503
Author(s):  
Fang Wang ◽  
Ping Sun ◽  
Qiang Sun
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Inflammatory Cells ◽  
Alveolar Bone Loss ◽  
Gingival Tissue ◽  
Enzyme Linked Immunosorbent Assay ◽  
Periodontal Tissue ◽  
Rankl Expression ◽  
Periodontal Tissues ◽  
Tnf Α

Purpose: To investigate the protective effect of bisleuconothine A on periodontal tissue in rats and the mechanism involved. Methods: Adult male Sprague Dawley rats (n = 32) weighing 180 - 200 g (mean weight, 190 ± 10 g) were randomly assigned to four groups of eight rats each: control group, periodontitis group, bisleuconothine A (50 mg/kg) group and bisleuconothine A (100 mg/kg) group. Rats in the treatment groups received bisleuconothine intraperitoneally for two weeks. Periodontitis was induced in the rats using standard procedures. Serum and tissue samples were used for biochemical analysis. Alveolar bone loss was measured in rat maxillae, while the activity of bone alkaline phosphatase (BALP) was determined in serum. Tumor necrosis factor α (TNF-α) interleukin-1β and interleukin-6 (IL-1β and IL-6) were determined in gingival tissue using enzyme-linked immunosorbent assay (ELISA) kit. Gene and protein expressions of receptor activator of nuclear factor kappa-Β ligand (RANKL), osteoprotegerin (OPG), and matrix metallopeptidase-9 (MMP-9) were measured in gingival tissue using real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting, respectively. Results: Bisleuconothine A treatment significantly and dose-dependently reduced alveolar bone loss, as well as serum levels of TNF-α, IL-1β and IL-6, but increased BALP activity in periodontitis rats (p < 0.05). It also significantly and dose-dependently reduced mRNA expressions of RANKL and MMP-9, but significantly increased OPG mRNA expression (p < 0.05). Similarly, treatment with bisleuconothine A significantly and dose-dependently down-regulated RANKL, p-NF-kB, p-IkBα and iNOS proteins in gingival tissue of periodontitis rats (p < 0.05). The results of histopathological examination indicated that bisleuconothine A treatment significantly reversed histological changes in periodontal tissues of periodontitis rats. It also significantly reduced the degree of polymorphonuclear (PMN) cell infiltration in periodontal tissue. Conclusion: The results obtained show that bisleuconothine A protects periodontal tissue via the regulation of RANKL expression and infiltration of inflammatory cells. Keywords: Bisleuconothine A, Expression, Inflammation, Periodontitis, RANKL

Parathyroid Hormone Protects against Periodontitis-associated Bone Loss

2003 ◽  
Vol 82 (10) ◽  
pp. 791-795 ◽  
Author(s):  
S.P. Barros ◽  
M.A.D. Silva ◽  
M.J. Somerman ◽  
F.H. Nociti
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Morphometric Analysis ◽  
Alveolar Bone ◽  
Inflammatory Cells ◽  
Alveolar Bone Loss ◽  
Intermittent Pth ◽  
Major Mediator

Parathyroid hormone (PTH) functions as a major mediator of bone remodeling and as an essential regulator of calcium homeostasis. In addition to the well-established catabolic effects (activation of bone resorption) of PTH, it is now recognized that intermittent PTH administration has anabolic effects (promotion of bone formation). The aim of this study was to investigate whether intermittent administration of PTH in rodents would block the alveolar bone loss observed in rats when a ligature model of periodontitis is used. Morphometric analysis showed that intermittent PTH administration (40 μg/kg) was able to protect the tooth site from periodontitis-induced bone resorption. In addition, there was a significant reduction in the number of inflammatory cells at the marginal gingival area in sections obtained from animals receiving PTH compared with control animals. These findings demonstrated that intermittent PTH administration was able to protect against periodontitis-associated bone loss in a rodent model.

Influence of moderate cigarette-smoking on the peri-implant clinicoradiographic inflammatory parameters around cement- and screw-retained dental implants

2020 ◽  
Author(s):  
Mana Alqahtani
Keyword(s):  
Cigarette Smoking ◽  
Dental Implants ◽  
Smoking History ◽  
Inflammatory Parameters ◽  
Significant Difference ◽  
Implant Retention ◽  
Level Of Significance ◽  
Soft Tissue Inflammation ◽  
Post Hoc ◽  
Adjustment Test

The aim was to assess the influence of moderate cigarette-smoking on the clinical (bleeding on probing [BoP] and probing depth [PD]) and radiographic (crestal bone resorption [CBR]) around cement- and screw-retained dental implants at 5 years’ follow-up. A questionnaire was used to collect information about age, gender, smoking history, duration of implants in function, jaw location of the implant, and daily toothbrushing and flossing. Peri-implant BoP, PD and CBR were measured in all groups. Group comparisons were performed using one-way analysis of variance and for multiple comparisons, the Bonferroni Post hoc adjustment test was performed. Level of significance was set at P&lt;0.05. Forty-eight patients (25 smokers and 23 non-smokers) had cement-retained dental implants; and 48 (24 smokers and 24 non-smokers) had screw-retained dental implants. Among patients with cement and screw-retained dental implants, PD (P&lt;0.05) and CBR (P&lt;0.05) were significantly higher among smokers than non-smokers. The peri-implant sites that demonstrated BoP were statistically significantly higher among non-smokers (P&lt;0.05) than smokers among patients with cement- and screw-retained dental implants. There was no statistically significant difference in peri-implant PD and CBR among smokers with cement- and screw-retained dental implants. Among non-smokers with cement and screw-retained dental implants, there was no statistically significant difference in BoP, PD and CBR. Cigarette-smoking is associated with an increased PD and CBR around cement- and screw-retained dental implants. Cigarette-smoking increases peri-implant soft tissue inflammation as well as loss of crestal bone and this relationship is independent of the type of implant retention protocol used.The author recommends that cement- and screw-retained dental implants are suitable for prosthesis restoration in non-smokers. Further studies on dual-smokers (individuals smoking cigarettes and other forms of tobacco products) are needed related to the clinicoradiographic inflammatory parameters around cement- and screw-retained dental implants

scholarly journals Decitabine Inhibits Bone Resorption in Periodontitis by Upregulating Anti-Inflammatory Cytokines and Suppressing Osteoclastogenesis

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 199
Author(s):  
Urara Tanaka ◽  
Shunichi Kajioka ◽  
Livia S. Finoti ◽  
Daniela B. Palioto ◽  
Denis F. Kinane ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Bone Resorption ◽  
Bone Loss ◽  
Inflammatory Cytokines ◽  
Osteoclast Differentiation ◽  
Tartrate Resistant Acid Phosphatase ◽  
Dependent Manner ◽  
Bone Homeostasis ◽  
Osteoblastic Cell Line ◽  
Anti Inflammatory

DNA methylation controls several inflammatory genes affecting bone homeostasis. Hitherto, inhibition of DNA methylation in vivo in the context of periodontitis and osteoclastogenesis has not been attempted. Ligature-induced periodontitis in C57BL/6J mice was induced by placing ligature for five days with Decitabine (5-aza-2′-deoxycytidine) (1 mg/kg/day) or vehicle treatment. We evaluated bone resorption, osteoclast differentiation by tartrate-resistant acid phosphatase (TRAP) and mRNA expression of anti-inflammatory molecules using cluster differentiation 14 positive (CD14+) monocytes from human peripheral blood. Our data showed that decitabine inhibited bone loss and osteoclast differentiation experimental periodontitis, and suppressed osteoclast CD14+ human monocytes; and conversely, that it increased bone mineralization in osteoblastic cell line MC3T3-E1 in a concentration-dependent manner. In addition to increasing IL10 (interleukin-10), TGFB (transforming growth factor beta-1) in CD14+ monocytes, decitabine upregulated KLF2 (Krüppel-like factor-2) expression. Overexpression of KLF2 protein enhanced the transcription of IL10 and TGFB. On the contrary, site-directed mutagenesis of KLF2 binding site in IL10 and TFGB abrogated luciferase activity in HEK293T cells. Decitabine reduces bone loss in a mouse model of periodontitis by inhibiting osteoclastogenesis through the upregulation of anti-inflammatory cytokines via KLF2 dependent mechanisms. DNA methyltransferase inhibitors merit further investigation as a possible novel therapy for periodontitis.

scholarly journals Estrogen Decreases Cytoskeletal Organization by Forming an ERα/SHP2/c-Src Complex in Osteoclasts to Protect against Ovariectomy-Induced Bone Loss in Mice

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 619
Author(s):  
Hyun-Jung Park ◽  
Malihatosadat Gholam-Zadeh ◽  
Sun-Young Yoon ◽  
Jae-Hee Suh ◽  
Hye-Seon Choi
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Ring Formation ◽  
Tartrate Resistant Acid Phosphatase ◽  
Actin Ring ◽  
Collagen Crosslinks ◽  
Trap Staining ◽  
Src Activation

Loss of ovarian function is closely related to estrogen (E2) deficiency, which is responsible for increased osteoclast (OC) differentiation and activity. We aimed to investigate the action mechanism of E2 to decrease bone resorption in OCs to protect from ovariectomy (OVX)-induced bone loss in mice. In vivo, tartrate-resistant acid phosphatase (TRAP) staining in femur and serum carboxy-terminal collagen crosslinks-1 (CTX-1) were analyzed upon E2 injection after OVX in mice. In vitro, OCs were analyzed by TRAP staining, actin ring formation, carboxymethylation, determination of reactive oxygen species (ROS) level, and immunoprecipitation coupled with Western blot. In vivo and in vitro, E2 decreased OC size more dramatically than OC number and Methyl-piperidino-pyrazole hydrate dihydrochloride (MPPD), an estrogen receptor alpha (ERα) antagonist, augmented the OC size. ERα was found in plasma membranes and E2/ERα signaling affected receptor activator of nuclear factor κB ligand (RANKL)-induced actin ring formation by rapidly decreasing a proto-oncogene tyrosine-protein kinase, cellular sarcoma (c-Src) (Y416) phosphorylation in OCs. E2 exposure decreased physical interactions between NADPH oxidase 1 (NOX1) and the oxidized form of c-Src homology 2 (SH2)-containing protein tyrosine phosphatase 2 (SHP2), leading to higher levels of reduced SHP2. ERα formed a complex with the reduced form of SHP2 and c-Src to decrease c-Src activation upon E2 exposure, which blocked a signal for actin ring formation by decreased Vav guanine nucleotide exchange factor 3 (Vav3) (p–Y) and Ras-related C3 botulinum toxin substrate 1 (Rac1) (GTP) activation in OCs. E2/ERα signals consistently inhibited bone resorption in vitro. In conclusion, our study suggests that E2-binding to ERα forms a complex with SHP2/c-Src to attenuate c-Src activation that was induced upon RANKL stimulation in a non-genomic manner, resulting in an impaired actin ring formation and reducing bone resorption.

Febuxostat Attenuates the Progression of Periodontitis in Rats

Pharmacology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Naseratun Nessa ◽  
Miyuki Kobara ◽  
Hiroe Toba ◽  
Tetsuya Adachi ◽  
Toshiro Yamamoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Bone Resorption ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Gingival Tissue ◽  
Systemic Effects ◽  
Rt Pcr ◽  
Tnf Α ◽  
And Oxidative Stress

Introduction: Periodontitis is a lifestyle-related disease that is characterized by chronic inflammation in gingival tissue. Febuxostat, a xanthine oxidase inhibitor, exerts anti-inflammatory and antioxidant effects. Objective: The present study investigated the effects of febuxostat on periodontitis in a rat model. Methods: Male Wistar rats were divided into 3 groups: control, periodontitis, and febuxostat-treated periodontitis groups. Periodontitis was induced by placing a ligature wire around the 2nd maxillary molar and the administration of febuxostat (5 mg/kg/day) was then initiated. After 4 weeks, alveolar bone loss was assessed by micro-computed tomography and methylene blue staining. The expression of osteoprotegerin (OPG), a bone resorption inhibitor, was detected by quantitative RT-PCR and immunological staining, and the number of osteoclasts in gingival tissue was assessed by tartrate-resistant acid phosphatase staining. The mRNA and protein expression levels of the proinflammatory cytokines, tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β), in gingival tissue were measured using quantitative RT-PCR and immunological staining. Oxidative stress in gingival tissue was evaluated by the expression of 4-hydroxy-2-nonenal (4-HNE), and 8-hydroxy-2-deoxyguanosine (8-OHdG). To clarify the systemic effects of periodontitis, blood pressure and glucose tolerance were examined. Results: In rats with periodontitis, alveolar bone resorption was associated with reductions in OPG and increases in osteoclast numbers. The gingival expression of TNF-α, IL-1β, 4-HNE, and 8-OHdG was up-regulated in rats with periodontitis. Febuxostat significantly reduced alveolar bone loss, proinflammatory cytokine levels, and oxidative stress. It also attenuated periodontitis-induced glucose intolerance and blood pressure elevations. Conclusion: Febuxostat prevented the progression of periodontitis and associated systemic effects by inhibiting proinflammatory mediators and oxidative stress.

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