Extraction and immediate placement of root analogue zirconia implants: an overview

Dental implants constitute a well-established approach for replacement of lost teeth with titanium being the most favored material for implantation. However, titanium has its limitations in esthetically demanding cases and neither the form nor material of such implants has changed much over the past 40 years. Immediate implantation has been introduced to overcome the disadvantages of conventional implantation which in turn has many disadvantages owing to the incongruence of the implant to the extraction socket. Today, there is scientific evidence that zirconia dental implants osseointegrate well and offer many advantages over titanium implants. The successful use of zirconia ceramics in orthopedic surgery led to a demand for dental zirconium-based implant systems. Because of its excellent biomechanical characteristics, biocompatibility, and bright tooth-like color, zirconia (zirconium dioxide, ZrO2) has the potential to become a substitute for titanium as dental implant material. In addition, there are previous reports on the successful use of Zirconia as root-analogue implants by reproducing the contours of the extracted tooth. This article presents an overview of the technique of using root analogue zirconia dental implants as an immediate implantation material which are replicas of the extracted tooth and therefore truly anatomical and socket friendly

Stress Activated P38 Mapk Regulates Cell Cycle via AP-1 Factors in Areca Extract Exposed Human Lung Epithelial Cells

Areca nut chewing habits are associated with several oral manifestations like leukoplakia, submucous fibrosis and oral squamous cell carcinoma. Although numerous evidence on areca toxicity is known but the mechanistic pathway of disease causation is to be studied. Aqueous areca nut extract treated A549 cells showed reduced cell viability by 48 h with IC50 value of 0.50%. The toxic nature of areca nut induced the production of reactive oxygen species with decreased anti-oxidant glutathione S transferase levels lead to altered redox homeostasis. PCR studies showed decreased mRNA levels of Jun and Fos AP-1 subunits on extract treatment by 48 h. The protein levels of PCNA, CDK4, RB, p53, c-Jun and c-Fos were found to be downregulated with upregulated CDK inhibitor p21 on extract treatment as compared to control. Results of FACS analysis further confirm G1/S phase cell cycle arrest on areca nut extract exposure. The regulation of downstream AP-1 subunits by MAPKs was studied by using specific inhibitors of ERK, JNK and p38 along with areca nut extract. Results showed the redox activation of MAP kinases down regulated the mRNA levels of AP-1 subunits in aqueous areca nut extract treated cells. Hence the present study aids in elucidating the role of MAP kinases in regulating the AP-1 subunits and their implications on target genes that are involved regulation of various cellular processes. Further, it would help in understanding the mechanistic aspects of the diseased state which may facilitate in designing of new therapeutic modalities that could help in cancer management

Institutionalization of quality assurance within district health management: Experiences from Maharashtra and Karnataka

The Population Council, with financial support from UNFPA, provided technical assistance to the states of Maharashtra and Karnataka, India in implementing a quality assurance (QA) program and helped its institutionalization in the district level of health management. An analysis of all the facilities covered as of December 2007 revealed substantial gaps in the infrastructure and human resources available to provide good-quality services, as well as adherence to standards for providing the services. To build the capacity to undertake QA visits, the Population Council and state authorities organized a series of events to orient and train state and district officials, facility-level workers, and members of the District Quality Assurance Group. The district health officers of both districts have subsequently established a mechanism to monitor and assess the extent to which the facilities have taken initiatives to address the gaps identified during QA visits. There are indications that the QA process is being institutionalized in the overall National Rural Health Mission/Reproductive and Child Health program

Apigenin inhibits PMA-induced expression of pro-inflammatory cytokines and AP-1 factors in A549 cells

Acute and chronic alveolar or bronchial inflammation is thought to be central to the pathogenesis of many respiratory disorders. Cytokines and granulocyte macrophage colony-stimulating factors (GM-CSF) play an important role in chronic inflammation. Activator protein-1 (AP-1) the superfamily of transcription factors is involved in proliferation, differentiation, apoptosis, and transformation including inflammation. Understanding the function and regulation of proinflammatory factors involved in inflammation may provide the novel therapeutic strategies in the treatment of inflammatory diseases. Our aim of the present study is to investigate the pro-inflammatory cytokines and pattern of AP-1 factors expressed during activation of lung adenocarcinoma A549 cells by Phorbol-12-myristate-13-acetate (PMA) and to understand the anti-inflammatory effect of apigenin. A549 cells were treated with and without PMA or apigenin, and the cell viability was assessed by MTT assay. Expressions of inflammatory mediators and different AP-1 factors were analyzed by semi-quantitative RT-PCR. IL-6 protein secreted was analyzed by ELISA, and expressions of IL-1β, c-Jun, and c-Fos proteins were analyzed by Western blotting. Activation of A549 cells by PMA, induced the expression of pro-inflammatory cytokine (IL-1β, IL-2, IL-6, IL-8, and TNF-α) mRNAs and secretion of IL-6 and the expression of specific AP-1 factors (c-Jun, c-Fos, and Fra-1). Treatment of cells with apigenin, significantly inhibited PMA-stimulated mRNA expression of above pro-inflammatory cytokines, AP-1 factors, cyclooxygenase-2, and secretion of IL-6 protein. Results suggested that the AP-1 factors may be involved in inflammation and apigenin has anti-inflammatory effect, which may be useful for therapeutic management of lung inflammatory diseases. © 2015, Springer Science+Business Media New York

Interplay of nuclear receptors (ER, PR, and GR) and their steroid hormones in MCF-7 cells

Steroid hormones and their nuclear receptors play a major role in the development and progression of breast cancer. MCF-7 cells are triple-positive breast cancer cells expressing estrogen receptor (ER), progesterone receptor (PR), and glucocorticoid receptor (GR). However, interaction and their role in expression pattern of activator protein (AP-1) transcription factors (TFs) are not completely understood. Hence, in our study, MCF-7 cells were used as an in vitro model system to study the interplay between the receptors and hormones. MCF-7 cells were treated with estradiol-17β (E2), progesterone (P4), and dexamethasone (Dex), alone or in combination, to study the proliferation of cells and expression of AP-1 genes. MTT assay results show that E2 or P4 induced the cell proliferation by more than 35 %, and Dex decreased the proliferation by 26 %. E2 and P4 are found to increase ERα by more than twofold and c-Jun, c-Fos, and Fra-1 AP-1 TFs by more than 1.7-fold, while Dex shows opposite effect of E2- or P4-induced effect as well as effect on the expression of nuclear receptors and AP-1 factors. E2 antagonist Fulvestrant (ICI 182,780) found to reduce proliferation and E2-induced expression of AP1-TFs, while P4 or Dex antagonist Mifepristone (RU486) is found to block GR-mediated expression of NRs and AP-1 mRNAs. Results suggest that E2 and P4 act synergistically, and Dex acts as an antagonist of E2 and P4

Aqueous areca nut extract induces oxidative stress in human lung epithelial A549 cells: Probable role of p21 in inducing cell death

Areca nut a well-known masticator used across globe. Habitual chewing of areca nut is associated with serious oral health effects. However, the role of areca nut in oxidative stress induction and cell death is less understood. Hence, in the present study we aimed to evaluate the toxic mechanism of areca nut extract on human lung epithelial A549 cells. Cells were treated with or without aqueous areca nut extract and cell viability was measured by MTT assay. Cells treated with areca nut extract show reduced viability in a dose dependent manner with the IC50 of 0.5 concentration. Areca nut extract induced the reactive oxygen species (ROS), lipid peroxidation followed by membrane damage with leakage of lactate dehydrogenase (LDH) enzyme. Cells with continuous exposure of areca nut extract depletes the free radical neutralizing anti-oxidant enzymes like superoxide dismutase (SOD), Glutathione peroxidase (GSH-Px) and Glutathione-S-transferase (GST). Further, the analysis of mRNA expression of apoptotic genes and cell cycle regulators show decreased expression of anti-apoptotic gene (Bcl-2), Cyclin E1, Cyclin D1, CDK4, Rb and p53 whereas induced expression of p21 and marginal increase of pro-apoptotic gene (Bax) confirms the toxic nature of areca nut. Thus, cell death due to areca nut exposure may be through different mechanism rather than the conventional apoptotic pathway, where p21 induction might be independent of p53 action, which possibly suggests that there may be a role of p21 in oxidative stress induced cell death. Further FACS analysis confirms cell death in areca nut treated cells. © 2016 Elsevier Inc

Cadmium induces oxidative stress and apoptosis in lung epithelial cells

Cadmium (Cd) is one of the well-known highly toxic environmental and industrial pollutants. Cd first accumulates in the nucleus and later interacts with zinc finger proteins of antiapoptotic genes and inhibit the binding of transcriptional factors and transcription. However, the role of Cd in oxidative stress and apoptosis is less understood. Hence, the present study was undertaken to unveil the mechanism of action. A549 cells were treated with or without Cd and cell viability was measured by MTT assay. Treatment of cells with Cd shows reduced viability in a dose-dependent manner with IC50 of 45 μM concentration. Cd significantly induces the reactive oxygen species (ROS), lipid peroxidation followed by membrane damage with the leakage of lactate dehydrogenase (LDH). Cells with continuous exposure of Cd deplete the antioxidant super oxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzymes. Further, analysis of the expression of genes involved in apoptosis show that both the extrinsic and intrinsic apoptotic pathways were involved. Death receptor marker tumor necrosis factor-α (TNF-α), executor caspase-8 and pro-apoptotic gene (Bax) were induced, while antiapoptotic gene (Bcl-2) was decreased in Cd-treated cells. Fluorescence-activated cell sorting (FACS) analysis further confirms the induction of apoptosis in Cd-treated A549 cells