scholarly journals Peri-Implant Crestal Bone Loss: A Putative Mechanism

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Yuko Ujiie ◽  
Reynaldo Todescan ◽  
John E. Davies
Keyword(s):  
Bone Loss ◽  
Stromal Cells ◽  
Cell Types ◽  
Osteoclast Formation ◽  
Rt Pcr ◽  
Crestal Bone Loss ◽  
Bacterial Endotoxins ◽  
Immunological Mechanisms ◽  
Study Support ◽  
Putative Mechanism

Purpose. The immunological mechanisms of peri-implant crestal bone loss have, hitherto, not been elucidated. We hypothesized that bacterial products from the microgap cause upregulation of cytokines in otherwise healthy peri-implant cells, which results in osteoclast formation and, ultimately, in bone resorption.Materials and Methods. We used RT-PCR and ELISA to assay mediators of osteoclastogenesis in rat and human macrophages (r-and hMO); bone marrow derived stromal cells (r-and hBMCs); and human gingival fibroblasts (hGF)—with or without stimulation by LPS. TRAP positive multinucleate cells were assessed for their resorptive ability.Results. We show that IL-1α, IL-1β, and IL-6 were expressed by all examined cell types, and TNF-αwas upregulated in hGF. Secretion of IL-1αand IL-1βproteins was stimulated in hMO by LPS, and IL-6 protein secretion was highly stimulated in hBMCs and hGF. Both LPS and RANKL stimulated macrophages to form osteoclast-like TRAP positive cells, which resorbed calcium phosphate substrates.Conclusion. Taken together, the results of our study support the hypothesis that bacterial endotoxins upregulate enhanced mediators of osteoclastogenesis in resident cells found in the healthy peri-implant compartment and that the local synergistic action of cytokines secreted by such cells results in the genesis of resorptively active osteoclasts.

scholarly journals An Essential Role of Cytosolic Phospholipase A2α in Prostaglandin E2–mediated Bone Resorption Associated with Inflammation

2003 ◽  
Vol 197 (10) ◽  
pp. 1303-1310 ◽  
Author(s):  
Chisato Miyaura ◽  
Masaki Inada ◽  
Chiho Matsumoto ◽  
Tomoyasu Ohshiba ◽  
Naonori Uozumi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Resorption ◽  
Bone Loss ◽  
Stromal Cells ◽  
Osteoclast Formation ◽  
Wild Type ◽  
Cytosolic Phospholipase ◽  
Cytosolic Phospholipase A2α ◽  
Cox 2

Prostaglandin E (PGE)2 produced by osteoblasts acts as a potent stimulator of bone resorption. Inflammatory bone loss is accompanied by osteoclast formation induced by bone-resorbing cytokines, but the mechanism of PGE2 production and bone resorption in vivo is not fully understood. Using cytosolic phospholipase A2α (cPLA2α)-null mice, we examined the role of cPLA2α in PGE2 synthesis and bone resorption. In bone marrow cultures, interleukin (IL)-1 markedly stimulated PGE2 production and osteoclast formation in wild-type mice, but not in cPLA2α-null mice. Osteoblastic bone marrow stromal cells induced the expression of cyclooxygenase (COX)-2 and membrane-bound PGE2 synthase (mPGES) in response to IL-1 and lipopolysaccharide (LPS) to produce PGE2. Osteoblastic stromal cells collected from cPLA2α-null mice also induced the expression of COX-2 and mPGES by IL-1 and LPS, but could not produce PGE2 due to the lack of arachidonic acid release. LPS administration to wild-type mice reduced femoral bone mineral density by increased bone resorption. In cPLA2α-null mice, however, LPS-induced bone loss could not be observed at all. Here, we show that cPLA2α plays a key role in PGE production by osteoblasts and in osteoclastic bone resorption, and suggest a new approach to inflammatory bone disease by inhibiting cPLA2α.

scholarly journals Transcript Profiling of the Androgen Signal in Normal Prostate, Benign Prostatic Hyperplasia, and Prostate Cancer

Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5806-5816 ◽  
Author(s):  
David R. Bauman ◽  
Stephan Steckelbroeck ◽  
Donna M. Peehl ◽  
Trevor M. Penning
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Stromal Cells ◽  
Cell Types ◽  
Prostatic Hyperplasia ◽  
Human Prostate ◽  
Rt Pcr ◽  
Retinol Dehydrogenase ◽  
Normal Prostate ◽  
Androgen Ablation

Human prostate adenocarcinoma (CaP) and benign prostatic hyperplasia (BPH) have epithelial and stromal cell origins, respectively. To determine whether the androgen signal is processed differently in these cell types the expression of transcripts for enzymes that control ligand access to the androgen receptor (AR) were measured. Transcripts for type 2 5α-reductase, ketosteroid reductases [aldo-keto reductase (AKR)1C1-AKR1C4], the major oxidative 3α-hydroxysteroid dehydrogenase (HSD) retinol dehydrogenase (RODH)-like 3α-HSD (RL-HSD) and nuclear receptors [AR, estrogen receptor (ER)α, and ERβ] were determined in whole human prostate and in cultures of primary epithelial cells (PEC) and primary stromal cells (PSC) from normal prostate, CaP and BPH by real-time RT-PCR. Normal PEC (n = 14) had higher levels of AKR1C1 (10-fold, P < 0.001), AKR1C2 (115-fold, P < 0.001) and AKR1C3 (6-fold, P < 0.001) than normal PSC (n = 15), suggesting that reductive androgen metabolism occurs. By contrast, normal PSC had higher levels of AR (8-fold, P < 0.001) and RL-HSD (21-fold, P < 0.001) than normal PEC, suggesting that 3α-androstanediol is converted to 5α-dihydrotestosterone to activate AR. In CaP PEC (n = 14), no significant changes in transcript levels vs. normal PEC were observed. In BPH PSC (n = 21) transcripts for AR (2-fold, P < 0.001), AKR1C1 (4-fold, P < 0.001), AKR1C2 (10-fold P < 0.001), AKR1C3 (4-fold, P < 0.001) and RL-HSD (3-fold, P < 0.003) were elevated to increase androgen response. Differences in the AR:ERβ transcript ratios (eight in normal PEC vs. 280 in normal PSC) were maintained in PEC and PSC in diseased prostate. These data suggest that CaP may be more responsive to an ERβ agonist and BPH may be more responsive to androgen ablation.

Survival of Short and Ultra-Short Locking-Taper Implants Supporting Single Crowns in the Posterior Mandible: A 3-Year Retrospective Study

2020 ◽  
Vol 46 (4) ◽  
pp. 396-406 ◽  
Author(s):  
Giorgio Lombardo ◽  
Annarita Signoriello ◽  
Miguel Simancas-Pallares ◽  
Mauro Marincola ◽  
Pier Francesco Nocini
Keyword(s):  
Retrospective Study ◽  
Bone Loss ◽  
Contact Point ◽  
Implant Survival ◽  
Point Position ◽  
Crestal Bone Loss ◽  
Short Implants ◽  
Single Crown ◽  
Bone To Implant Contact ◽  
Single Crowns

The purpose of this retrospective study was to determine survival and peri-implant marginal bone loss of short and ultra-short implants placed in the posterior mandible. A total of 98 patients received 201 locking-taper implants between January 2014 and January 2015. Implants were placed with a 2-stage approach and restored with single crowns. Clinical and radiographic examinations were performed at 3-year recall appointments. At that time, the proportion of implant survival by length, and variations of crestal bone levels (mean crestal bone loss and mean apical shift of the “first bone-to-implant contact point” position) were assessed. Significance level was set at 0.05. The total number of implants examined 36 months after loading included: 71 implants, 8.0 mm in length; 82 implants, 6.0 mm in length; and 48 implants, 5.0 mm in length. Five implants failed. The overall proportion of survival was 97.51%, with 98.59% for the 8.0-mm implants, 97.56% for the 6.0-mm implants, and 95.83% for the 5.0-mm implants. No statistically significant differences were found among the groups regarding implant survival (P = .73), mean crestal bone loss (P = .31), or mean apical shift of the “first bone-to-implant contact point” position (P = .36). Single-crown short and ultra-short implants may offer predictable outcomes in the atrophic posterior mandibular regions, though further investigations with longer follow-up evaluations are necessary to validate our results.

scholarly journals SARS-CoV-2 Is Not Detected in the Cerebrospinal Fluid of Encephalopathic COVID-19 Patients

2020 ◽  
Vol 11 ◽  
Author(s):  
Dimitris G. Placantonakis ◽  
Maria Aguero-Rosenfeld ◽  
Abdallah Flaifel ◽  
John Colavito ◽  
Kenneth Inglima ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Viral Entry ◽  
Cell Types ◽  
Host Cells ◽  
Nasopharyngeal Swab ◽  
Rt Pcr ◽  
Neurologic Sequelae ◽  
Show Evidence ◽  
Novel Coronavirus ◽  
Transmembrane Serine Protease

Neurologic manifestations of the novel coronavirus SARS-CoV-2 infection have received wide attention, but the mechanisms remain uncertain. Here, we describe computational data from public domain RNA-seq datasets and cerebrospinal fluid data from adult patients with severe COVID-19 pneumonia that suggest that SARS-CoV-2 infection of the central nervous system is unlikely. We found that the mRNAs encoding the ACE2 receptor and the TMPRSS2 transmembrane serine protease, both of which are required for viral entry into host cells, are minimally expressed in the major cell types of the brain. In addition, CSF samples from 13 adult encephalopathic COVID-19 patients diagnosed with the viral infection via nasopharyngeal swab RT-PCR did not show evidence for the virus. This particular finding is robust for two reasons. First, the RT-PCR diagnostic was validated for CSF studies using stringent criteria; and second, 61% of these patients had CSF testing within 1 week of a positive nasopharyngeal diagnostic test. We propose that neurologic sequelae of COVID-19 are not due to SARS-CoV-2 meningoencephalitis and that other etiologies are more likely mechanisms.

scholarly journals Made to Measure: Patient-Tailored Treatment of Multiple Sclerosis Using Cell-Based Therapies

2021 ◽  
Vol 22 (14) ◽  
pp. 7536
Author(s):  
Inez Wens ◽  
Ibo Janssens ◽  
Judith Derdelinckx ◽  
Megha Meena ◽  
Barbara Willekens ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Autoimmune Diseases ◽  
Stromal Cells ◽  
Mononuclear Cells ◽  
Treatment Options ◽  
Cell Types ◽  
Peripheral Blood Mononuclear ◽  
Tailored Treatment ◽  
Key Issues ◽  
The Central Nervous System

Currently, there is still no cure for multiple sclerosis (MS), which is an autoimmune and neurodegenerative disease of the central nervous system. Treatment options predominantly consist of drugs that affect adaptive immunity and lead to a reduction of the inflammatory disease activity. A broad range of possible cell-based therapeutic options are being explored in the treatment of autoimmune diseases, including MS. This review aims to provide an overview of recent and future advances in the development of cell-based treatment options for the induction of tolerance in MS. Here, we will focus on haematopoietic stem cells, mesenchymal stromal cells, regulatory T cells and dendritic cells. We will also focus on less familiar cell types that are used in cell therapy, including B cells, natural killer cells and peripheral blood mononuclear cells. We will address key issues regarding the depicted therapies and highlight the major challenges that lie ahead to successfully reverse autoimmune diseases, such as MS, while minimising the side effects. Although cell-based therapies are well known and used in the treatment of several cancers, cell-based treatment options hold promise for the future treatment of autoimmune diseases in general, and MS in particular.

scholarly journals AT1 and AT2 Receptor Knockout Changed Osteonectin and Bone Density in Mice in Periodontal Inflammation Experimental Model

2021 ◽  
Vol 22 (10) ◽  
pp. 5217
Author(s):  
Maria Laura de Souza Lima ◽  
Caroline Addison Carvalho Xavier de Medeiros ◽  
Gerlane Coelho Bernardo Guerra ◽  
Robson Santos ◽  
Michael Bader ◽  
...  
Keyword(s):  
Bone Density ◽  
Bone Loss ◽  
Experimental Model ◽  
At2 Receptor ◽  
Micro Ct ◽  
Rt Pcr ◽  
Osteoblast Cells ◽  
Periodontal Inflammation ◽  
Bone Trabeculae

Background: The aim of this study was to evaluate the role of AT1 and AT2 receptors in a periodontal inflammation experimental model. Methods: Periodontal inflammation was induced by LPS/Porphyromonas gingivalis. Maxillae, femur, and vertebra were scanned using Micro-CT. Maxillae were analyzed histopathologically, immunohistochemically, and by RT-PCR. Results: The vertebra showed decreased BMD in AT1 H compared with WT H (p < 0.05). The femur showed increased Tb.Sp for AT1 H and AT2 H, p < 0.01 and p < 0.05, respectively. The Tb.N was decreased in the vertebra (WT H-AT1 H: p < 0.05; WT H-AT2 H: p < 0.05) and in the femur (WT H-AT1 H: p < 0.01; WT H-AT2 H: p < 0.05). AT1 PD increased linear bone loss (p < 0.05) and decreased osteoblast cells (p < 0.05). RANKL immunostaining was intense for AT1 PD and WT PD (p < 0.001). OPG was intense in the WT H, WT PD, and AT2 PD when compared to AT1 PD (p < 0.001). AT1 PD showed weak immunostaining for osteocalcin compared with WT H, WT PD, and AT2 PD (p < 0.001). AT1 H showed significantly stronger immunostaining for osteonectin in fibroblasts compared to AT2 H (p < 0.01). Conclusion: AT1 receptor knockout changed bone density, the quality and number of bone trabeculae, decreased the number of osteoblast cells, and increased osteonectin in fibroblasts.

scholarly journals Bone marrow stromal cells from MDS and AML patients show increased adipogenic potential with reduced Delta-like-1 expression

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Marie-Theresa Weickert ◽  
Judith S. Hecker ◽  
Michèle C. Buck ◽  
Christina Schreck ◽  
Jennifer Rivière ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Fate ◽  
Stromal Cells ◽  
Adipogenic Differentiation ◽  
Cell Types ◽  
Bone Marrow Niche ◽  
Differentiation Potential ◽  
Hematopoietic Stem ◽  
Bm Niche

AbstractMyelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are clonal hematopoietic stem cell disorders with a poor prognosis, especially for elderly patients. Increasing evidence suggests that alterations in the non-hematopoietic microenvironment (bone marrow niche) can contribute to or initiate malignant transformation and promote disease progression. One of the key components of the bone marrow (BM) niche are BM stromal cells (BMSC) that give rise to osteoblasts and adipocytes. It has been shown that the balance between these two cell types plays an important role in the regulation of hematopoiesis. However, data on the number of BMSC and the regulation of their differentiation balance in the context of hematopoietic malignancies is scarce. We established a stringent flow cytometric protocol for the prospective isolation of a CD73+ CD105+ CD271+ BMSC subpopulation from uncultivated cryopreserved BM of MDS and AML patients as well as age-matched healthy donors. BMSC from MDS and AML patients showed a strongly reduced frequency of CFU-F (colony forming unit-fibroblast). Moreover, we found an altered phenotype and reduced replating efficiency upon passaging of BMSC from MDS and AML samples. Expression analysis of genes involved in adipo- and osteogenic differentiation as well as Wnt- and Notch-signalling pathways showed significantly reduced levels of DLK1, an early adipogenic cell fate inhibitor in MDS and AML BMSC. Matching this observation, functional analysis showed significantly increased in vitro adipogenic differentiation potential in BMSC from MDS and AML patients. Overall, our data show BMSC with a reduced CFU-F capacity, and an altered molecular and functional profile from MDS and AML patients in culture, indicating an increased adipogenic lineage potential that is likely to provide a disease-promoting microenvironment.

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