Persistent Acute Inflammation at the Implant-Abutment Interface

2003 ◽  
Vol 82 (3) ◽  
pp. 232-237 ◽  
Author(s):  
N. Broggini ◽  
L.M. McManus ◽  
J.S. Hermann ◽  
R.U. Medina ◽  
T.W. Oates ◽  
...  
Keyword(s):  
Bone Loss ◽  
Polymorphonuclear Leukocytes ◽  
Acute Inflammation ◽  
Inflammatory Cell ◽  
Inflammatory Cells ◽  
The Third ◽  
Initial Surgery ◽  
Cell Accumulation ◽  
Implant Abutment ◽  
Neutrophilic Polymorphonuclear Leukocytes

The inflammatory response adjacent to implants has not been well-investigated and may influence peri-implant tissue levels. The purpose of this study was to assess, histomorphometrically, (1) the timing of abutment connection and (2) the influence of a microgap. Three implant designs were placed in the mandibles of dogs. Two-piece implants were placed at the alveolar crest and abutments connected either at initial surgery (non-submerged) or three months later (submerged). The third implant was one-piece. Adjacent interstitial tissues were analyzed. Both two-piece implants resulted in a peak of inflammatory cells approximately 0.50 mm coronal to the microgap and consisted primarily of neutrophilic polymorphonuclear leukocytes. For one-piece implants, no such peak was observed. Also, significantly greater bone loss was observed for both two-piece implants compared with one-piece implants. In summary, the absence of an implant-abutment interface (microgap) at the bone crest was associated with reduced peri-implant inflammatory cell accumulation and minimal bone loss.

Peri-implant Inflammation Defined by the Implant-Abutment Interface

2006 ◽  
Vol 85 (5) ◽  
pp. 473-478 ◽  
Author(s):  
N. Broggini ◽  
L.M. McManus ◽  
J.S. Hermann ◽  
R. Medina ◽  
R.K. Schenk ◽  
...  
Keyword(s):  
Bone Loss ◽  
Polymorphonuclear Leukocytes ◽  
Inflammatory Cell ◽  
Alveolar Bone ◽  
Inflammatory Cells ◽  
Maximum Density ◽  
Interface Position ◽  
Cell Accumulation ◽  
Implant Abutment ◽  
Neutrophilic Polymorphonuclear Leukocytes

An implant-abutment interface at the alveolar bone crest is associated with sustained peri-implant inflammation; however, whether magnitude of inflammation is proportionally dependent upon interface position remains unknown. This study compared the distribution and density of inflammatory cells surrounding implants with a supracrestal, crestal, or subcrestal implant-abutment interface. All implants developed a similar pattern of peri-implant inflammation: neutrophilic polymorphonuclear leukocytes (neutrophils) maximally accumulated at or immediately coronal to the interface. However, peri-implant neutrophil accrual increased progressively as the implant-abutment interface depth increased, i.e., subcrestal interfaces promoted a significantly greater maximum density of neutrophils than did supracrestal interfaces (10,512 ± 691 vs. 2398 ± 1077 neutrophils/mm2). Moreover, inflammatory cell accumulation below the original bone crest was significantly correlated with bone loss. Thus, the implant-abutment interface dictates the intensity and location of peri-implant inflammatory cell accumulation, a potential contributing component in the extent of implant-associated alveolar bone loss.

scholarly journals Elevated Plasma Level of Interferon-λ1 in Chronic Spontaneous Urticaria: Upregulated Expression in CD8+and Epithelial Cells and Induction of Inflammatory Cell Accumulation

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
S. F. Wang ◽  
X. Q. Gao ◽  
Y. N. Xu ◽  
D. N. Li ◽  
H. Y. Wang ◽  
...  
Keyword(s):  
Mast Cells ◽  
Inflammatory Cell ◽  
Inflammatory Cells ◽  
Chronic Spontaneous Urticaria ◽  
Intercellular Adhesion Molecule ◽  
Double Labeling ◽  
Cell Accumulation ◽  
Healthy Control ◽  
Dose Dependent Increase ◽  
Dose Dependent

Interferon- (IFN-)λ1 is regarded as a potent bio-active molecule in innate immunity. However, little is known about its role in chronic spontaneous urticaria (CSU). We therefore investigated expression of IFN-λ1 in CSU, its cellular location, and its influence on inflammatory cell accumulation by using flow cytometry analysis, skin tissue dispersion, immunohistochemical stain, and a mouse peritoneal inflammation model. The results showed that level of IFN-λ1 was 2.0-fold higher in plasma of the patients with CSU than the level in healthy control (HC) subjects. Among leukocytes examined, only CD8+T cells expressed more IFN-λ1 in CSU blood. Double labeling immunohistochemical staining revealed that IFN-λ1+inflammatory cells such as mast cells, eosinophils, B cells, neutrophils, and macrophages were mainly located in dermis, whereas epidermis tissue highly expressed IFN-λ1. IFN-λ1 induced a dose-dependent increase in number of eosinophils, lymphocytes, mast cells, macrophages, and neutrophils in the peritoneum of mice at 6 h following injection, which was inhibited by pretreatment of the animals with anti-intercellular adhesion molecule- (ICAM-) 1 and/or anti-L-selectin antibodies. In conclusion, IFN-λ1 is likely to play a role in the pathogenesis of CSU. Blocking IFN-λ1 production may help to reduce the accumulation of inflammatory cells in the involved CSU skin.

Steroids and Asthma

PEDIATRICS ◽  
1995 ◽  
Vol 96 (2) ◽  
pp. 347-348 ◽  
Author(s):  
Gail G. Shapiro
Keyword(s):  
Single Dose ◽  
Inflammatory Cell ◽  
Inflammatory Cells ◽  
Forced Expiratory Volume ◽  
Chronic Asthma ◽  
Optimal Management ◽  
Concomitant Increase ◽  
Biopsy Specimens ◽  
Destructive Change ◽  
Cell Accumulation

It is impossible to read about asthma in the 1990s without being informed that it is an inflammatory disease and that all but the mildest cases require anti-inflammatory therapy for optimal management.1 Bronchoalveolar lavage studies document the influx of inflammatory cells and the upregulation of inflammatory cytokines in bronchial washings of patients with chronic asthma.2 Biopsy specimens confirm an inflammatory cell accumulation and the destructive change to the epithelium that one would expect from this insult.3 The pathophysiology of asthma would seem to justify the use of corticosteroids for its management. A single dose of prednisone can be shown to decrease inflammatory leukotrienes while there is a concomitant increase in forced expiratory volume in 1 second.4

Relationship between Synovial Fluid Inflammatory Cells and Grade of Inflammation of Synovium in Patients with Spondylarthropathy

2008 ◽  
Vol 1 ◽  
pp. CMAMD.S478
Author(s):  
Reijo Luukkainen ◽  
Karl-Ove Söderström ◽  
Milja Möttönen ◽  
Pekka Luukkainen
Keyword(s):  
Synovial Fluid ◽  
Needle Biopsy ◽  
Polymorphonuclear Leukocytes ◽  
Inflammatory Process ◽  
Acute Inflammation ◽  
Joint Destruction ◽  
Chronic Phase ◽  
Inflammatory Cells ◽  
Cellular Composition ◽  
Biopsy Specimens

Objective To study whether the analysis of synovial fluid (SF) inflammatory cells can be used for the estimation of the grade of inflammation in the synovium and, therefore, for the prediction of the possible development of joint destruction in spondylarthropathy. Methods Forty-one patients with spondylarthropathy and hydropsy in a knee joint were studied. The cellular composition of SF aspirates was investigated and the grade of inflammation in synovial biopsy samples was evaluated by analyzing histological needle biopsy specimens. Results The count of SF polymorphonuclear leukocytes (PMN) reflected significantly the activity of acute inflammation. None of the SF cells reflected the chronic inflammation in the synovium. Conclusion The number of SF PMNs may reflect the severity of acute inflammatory process in the synovium in patients with spodylarthropathy at a given moment, but the analysis of SF aspirates may not be of use in estimating the activity of chronic phase of inflammation presumably causing the joint destruction.

scholarly journals Host Cellular Immune Response to Pneumococcal Lung Infection in Mice

2000 ◽  
Vol 68 (2) ◽  
pp. 492-501 ◽  
Author(s):  
Aras Kadioglu ◽  
Neill A. Gingles ◽  
Kate Grattan ◽  
Alison Kerr ◽  
Tim J. Mitchell ◽  
...  
Keyword(s):  
Inflammatory Cell ◽  
Lung Infection ◽  
Cellular Infiltration ◽  
Wild Type ◽  
Substantial Evidence ◽  
The Third ◽  
Cell Accumulation ◽  
Third Stage ◽  
Important Virulence Factor ◽  
Cellular Immune

ABSTRACT Although there is substantial evidence that pneumolysin is an important virulence factor in pneumococcal pneumonia, relatively little is known about how it influences cellular infiltration into the lungs. We investigated how the inability of mutant pneumococci to produce pneumolysin altered the pattern of inflammation and cellular infiltration into the lungs. The effect on bacterial growth in the lungs also was assessed. There were three phases of growth of wild-type bacteria in the lungs: a decline followed by a rapid increase and then stasis or decline. The absence of pneumolysin was associated with a more rapid early decline and then a much slower increase in numbers. The pattern of inflammatory-cell accumulation also had distinct stages, and the timing of these stages was influenced by the presence of pneumolysin. Neutrophils began to accumulate about 12 to 16 h after infection with wild-type pneumococci. This accumulation occurred after the early decline in pneumococcal numbers but coincided with the period of rapid growth. Following infection with pneumococci unable to make pneumolysin, neutrophil influx was slower and less intense. Coincident with the third stage of pneumococcal growth was an accumulation of T and B lymphocytes at the sites of inflammation, but the accumulation was not associated with an increase in the total number of lymphocytes in the lungs. Lymphocyte accumulation in the absence of pneumolysin occurred but was delayed.

scholarly journals Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model

1997 ◽  
Vol 78 (5) ◽  
pp. 845-855 ◽  
Author(s):  
Joseph Kurantsin-Mills ◽  
Marie M. Cassidy ◽  
Richard E. Stafford ◽  
William B. Weglicki
Keyword(s):  
Inflammatory Cell ◽  
Inflammatory Responses ◽  
Interleukin 1 ◽  
Inflammatory Cells ◽  
Phase Changes ◽  
Prostaglandin E ◽  
The Third ◽  
Inflammatory Phase ◽  
Cell Subpopulations ◽  
Factor Α

Rodents fed on a Mg-deficient (Mg-D) diet develop cardiomyopathic lesions, as well as other types of cardiovascular dysfunction. In the rat, inflammatory cell infiltration of the myocardium begins to occur by week 1, and the lesions develop extensively in the third and fourth weeks on the Mg-D diet. Although the aetiologic mechanisms of Mg-D cardiomyopathy are unknown, we have previously reported that once plasma Mg is markedly reduced, one of the earliest molecular markers of the pathophysiological process is elevation of plasma substance P, calcitonin gene-related peptide and prostaglandin E2, followed by histamine and the inflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-α). In order to evaluate the potential role of specific circulating inflammatory cell subpopulations in the mechanisms underlying pathophysiological changes observed in Mg-deficiency-induced cardiomyopathy, we analysed these cells by flow cytochemistry. Leucocyte subpopulation pools increased progressively in the Mg-D rats. Elevated circulating levels of neutrophils and lymphocytes appeared to contribute to both the acute (week 1–2) and chronic phases (week 3–4) of the inflammatory responses; monocytes, eosinophils, basophils and large unstained cells which are lymphoid in stained smears, on the other hand, increased significantly in the third and fourth weeks and thus contributed to the chronic inflammatory phase. Changes in the circulating leucocyte subpopulations paralleled the chronological progression of the cardiomyopathic lesions, particularly in weeks 3 and 4. Since a pronounced neutrophilia preceded leucocyte infiltration and deposition within the myocardial tissue, modifications of the microvascular barrier may be a prerequisite for cardiomyopathy in this model of neurogenic inflammation.

scholarly journals NF-κB, JNK, and TLR Signaling Pathways in Hepatocarcinogenesis

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Shin Maeda
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathways ◽  
Inflammatory Cell ◽  
Prognostic Markers ◽  
Tumor Promotion ◽  
Neoplastic Cell ◽  
Nuclear Factor ◽  
Tlr Signaling ◽  
The Third

Hepatocellular carcinoma (HCC) is the third largest cause of cancer deaths worldwide. The role of molecular changes in HCC have been used to identify prognostic markers and chemopreventive or therapeutic targets. It seems that toll-like receptors (TLRs) as well as the nuclear factor (NF)-κB, and JNK pathways are critical regulators for the production of the cytokines associated with tumor promotion. The cross-talk between an inflammatory cell and a neoplastic cell, which is instigated by the activation of NF-κB and JNKs, is critical for tumor organization. JNKs also regulate cell proliferation and act as oncogenes, making them the main tumor-promoting protein kinases. TLRs play roles in cytokine and hepatomitogen expression mainly in myeloid cells and may promote liver tumorigenesis. A better understanding of these signaling pathways in the liver will help us understand the mechanism of hepatocarcinogenesis and provide a new therapeutic target for HCC.

scholarly journals The Symmetric 3D Organization of Connective Tissue around Implant Abutment: A Key-Issue to Prevent Bone Resorption

Symmetry ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1126
Author(s):  
Giovanna Iezzi ◽  
Francesca Di Lillo ◽  
Michele Furlani ◽  
Marco Degidi ◽  
Adriano Piattelli ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Connective Tissue ◽  
Inflammatory Cell ◽  
Soft Tissues ◽  
Three Dimensional ◽  
Collagen Fibers ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Oral Epithelium ◽  
Implant Abutment

Symmetric and well-organized connective tissues around the longitudinal implant axis were hypothesized to decrease early bone resorption by reducing inflammatory cell infiltration. Previous studies that referred to the connective tissue around implant and abutments were based on two-dimensional investigations; however, only advanced three-dimensional characterizations could evidence the organization of connective tissue microarchitecture in the attempt of finding new strategies to reduce inflammatory cell infiltration. We retrieved three implants with a cone morse implant–abutment connection from patients; they were investigated by high-resolution X-ray phase-contrast microtomography, cross-linking the obtained information with histologic results. We observed transverse and longitudinal orientated collagen bundles intertwining with each other. In the longitudinal planes, it was observed that the closer the fiber bundles were to the implant, the more symmetric and regular their course was. The transverse bundles of collagen fibers were observed as semicircular, intersecting in the lamina propria of the mucosa and ending in the oral epithelium. No collagen fibers were found radial to the implant surface. This intertwining three-dimensional pattern seems to favor the stabilization of the soft tissues around the implants, preventing inflammatory cell apical migration and, consequently, preventing bone resorption and implant failure. This fact, according to the authors’ best knowledge, has never been reported in the literature and might be due to the physical forces acting on fibroblasts and on the collagen produced by the fibroblasts themselves, in areas close to the implant and to the symmetric geometry of the implant itself.

scholarly journals Urokinase Attenuates Pulmonary Thromboembolism in an Animal Model by Inhibition of Inflammatory Response

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ying Shi ◽  
Zhirong Zhang ◽  
Danli Cai ◽  
Jing Kuang ◽  
Shuifang Jin ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Animal Model ◽  
Inflammatory Response ◽  
Inflammatory Cell ◽  
Pulmonary Thromboembolism ◽  
Thrombus Formation ◽  
Inflammatory Cells ◽  
Hemodynamic Instability ◽  
Synergistic Action ◽  
Determining Factor

Inflammatory response is an important determining factor for the mortality of patients with pulmonary thromboembolism. Inflammatory mediators can promote thrombus formation and increase hemodynamic instability. Urokinase is a commonly used drug for the treatment of PTE. The effect of urokinase on inflammatory reaction in PTE is still unclear. Our study was aimed at evaluating the effects of the intervention of urokinase and urokinase combined with aspirin in PTE rats. Results revealed that a large amount of infiltrated inflammatory cells surrounding the bronchus, vessels, and pulmonary mesenchyme, and even pulmonary abscess were observed in the PTE rats. CX3CL1/CX3CR1 coexpression, CX3CL1/NF-κB coexpression, and TXA2 were significantly higher. After treatment with urokinase, pulmonary embolism was partially dissolved and inflammatory cell infiltration was significantly reduced. The expression of TNNI3, BNP, D2D, PASP, PADP, PAMP, and TXA2, as well as CX3CL1/CX3CR1 coexpression and CX3CL1/NF-κB coexpression were significantly lowered. Aspirin showed no synergistic action. Therefore, these findings suggested the occurrence of inflammation during the process of PTE in rats. Urokinase treatment reduced the inflammatory response.

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.

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