Awareness and management of peri-implantitis and peri-mucositis among private dental Practitioners in Hyderabad - A cross-sectional study.

BACKGROUND: Implant therapy, in India, has flourished in recent years and is being practiced widely by many dental practitioners today. Along with the increasing number of implants being placed today, there has also been a constant rise in the number of complications associated with it. OBJECTIVES: The aim of this study is to evaluate the knowledge and awareness of implant placement and management of peri-implant diseases among dental professionals. MATERIALS AND METHODS: A total of 568 dental practitioners were approached with a questionnaire for collecting data related to demographic details, experience, and knowledge about implant placement and management of its complications. Of these, only 262 were included as part of the statistical analysis. This data collected were compiled and analyzed using descriptive statistics. RESULTS: Results showed that most dentists who participated in this study have adequate knowledge about etiological factors and its management. Those who acquired implant skills through sources that are not in accordance with accepted standards had unsatisfactory knowledge and practice behavior. CONCLUSION: The awareness and knowledge regarding the implant procedures and their complications such as peri-implant mucositis and peri-implantitis were higher in self-trained dentists and by dentists who are practicing for >10 years and calls for updating of knowledge.

Efficacy of Natural and Allopathic Antimicrobial Agents Incorporated onto Guided Tissue Regeneration Membrane Against Periodontal Pathogens: An in vitro Study.

INTRODUCTION: Periodontal disease is one of the most prevalent afflictions worldwide. It is an infection of the periodontium as a result of subgingival colonization of the specific microbiota, leading to loss of attachment, which requires optimal care for regeneration to its pre-disease state. Guided Tissue Regeneration (GTR) is one of the successful treatment modalities in Periodontal Regenerative Therapy, but is vulnerable to bacterial colonization. The conflict between usage of classical antibiotics and plant origin antimicrobial agents has recently been in the limelight. AIM: The aim of this study was to assess the in vitro antimicrobial activity of amoxicillin, metronidazole and green coffee extract loaded onto GTR membrane against periodonto-pathogens. MATERIALS AND METHODS: Pure form of amoxicillin, metronidazole and green coffee extract were obtained. One percent concentration of each antimicrobial agent was prepared by appropriate dilution with distilled water. GTR membrane was cut into a size of 1x0.5 cm under sterile conditions and was coated with the antimicrobial agents respectively and with distilled water as the negative control. Antimicrobial activity was checked against Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) and Porphyromonas gingivalis (P. gingivalis) using agar disc diffusion method. The statistical analysis was done using Kruskal Wallis ANOVA and Mann-Whitney U test. RESULTS: One percent amoxicillin showed level of significance (p>0.05) against both A. actinomycetemcomitans and P. gingivalis. Green coffee extract showed no zone of inhibition against both the bacterial species. CONCLUSION: Loading of commercially available antimicrobial agents onto GTR membrane can prevent its bacterial colonization leading to better treatment outcomes for periodontal regeneration.

A rare case of temporal arteritis with rheumatoid arthritis and interstitial lung disease mimicking pulpo-periodontal pathology.

A 75-year-old male patient was planned for dental treatment due to pain of suspected pulpo-periodontal origin in relation to right maxillary first molar. Careful evaluation revealed the pain to be non-odontogenic in nature and led to the diagnosis of temporal arteritis with rheumatoid arthritis along with interstitial lung disease (ILD). Characteristic findings of temporal arteritis include headache, jaw claudication, visual loss, and constitutional symptoms (malaise, fever, weight loss, loss of appetite). Temporal artery biopsy (TAB) remains the gold standard for diagnosis. Additional diagnostic tests include blood tests (ESR, CRP). This article reports and discusses how the orofacial manifestations can lead to misdiagnosis of temporal arteritis. Hence, temporal arteritis should be included in the differential diagnosis of orofacial pain in the elderly especially to prevent complications like vision loss.

Antibiogram pattern of oral microflora in periodontic children of age group 6 to 12 years: a clinicomicrobiological study.

AIM: The study was carried out to see the diversity of oral microflora and its antibiotic sensitivity test in children of age group 6 to 12 years was carried. MATERIALS AND METHODS: Total 50 patients of age group 6 to 12 years were analyzed for their oral microflora and then checked for the antibiotic susceptibility test. The samples that were collected were incubated at 37°C for 48 hours. Once dispersed samples were taken and Gram staining was done, also they were spread on to a number of freshly prepared agar plates and incubated to allow cells to form microbial colony. RESULTS: The result showed microflora common in all types, Gram-positive facultative anaerobic rods and cocci. In normal children Gram-positive facultative anaerobic and fermenting cocci were predominant where as in children with caries growth of microbiota that were Gram-negative and positive, capnophilic, motile and anaerobic rods and cocci belonging to members of genera S. mutans and A. actinomycetemcomitans was seen. CONCLUSION: By the present study it has been concluded that the number of bacteria determined by microscopic counts was twice as high in caries patients as in healthy sites, and also recommended that amoxicillin, ampicillin and amikacin are the most effective antibacterial drugs for the treatment of dental caries.

Evaluation of gingival inflammation in patients using ovulation induction drugs before and after scaling.

OBJECTIVES: To determine and correlate the effect of clomiphene citrate, Letrozole in women undergoing infertility treatment on the gingival inflammatory status. MATERIALS AND METHODS: The present study is a randomized controlled clinical trial which consisted of 26 women using CC for three menstrual cycles, 26 women using CC for more than three cycles, 26 women using Letrozole. All subjects were clinically examined for plaque levels (Plaque Index), gingival inflammation, bleeding on probing (Gingival Index, Sulcus Bleeding Index). Scaling was done to all patients and all periodontal parameters were reassessed 1 month after scaling. The results were compared with a control group of 26 women matched for age, educational status and professional level, and oral habits and who had never used ovulation drugs. RESULTS: Baseline scores of all the test groups showed higher amount of plaque levels and inflammation compared to control. (p < 0.05). After scaling a significant reduction in inflammation was observed in all the test groups along with the control group (p < 0.0001), but women using the drugs showed persistence of inflammation compared to control (p < 0.01). CONCLUSION: It can be concluded from the present study that the presence of elevated levels of hormones due to the effect of ovulation induction drugs may be the reason for the gingival inflammation in test groups.

Where will the stem cells lead us? Prospects for dentistry in the 21 century.

It is dentists' dream to achieve bone repair with predictability, but without donor site morbidity as well as reconstruction of injured or pathologically damaged complex dental structures, however, this will no longer be a dream as these are being made into a reality using stem cell science. Stem cell science is clearly an intriguing and promising area of science. Stem cells have been isolated from a variety of embryonic and adult tissues. Dental stem cells are multipotent mesenchymal stem cells (MSCs) brought new enthusiasm among the researchers because of their easy accessibility, high quality and they don't pose the same ethical concerns and controversy in comparison with embryonic stem cells. This review article provides brief insights about stem cell basics, the state of art in human dental stem cell research and its possible impact on future dentistry. Even though most of these modalities are still in infancy, it is evident that the 21(st) century dentist is going to play a critical role in the field of medicine. The aim of this article is to bring awareness among the dentists about the huge potential associated with the use of stem cells in a clinical setting, as well as proper understanding of related problems.

Mac-1 and Fas activities are concurrently required for execution of smooth muscle cell death by M-CSF-stimulated macrophages.

OBJECTIVE: We have previously shown that macrophage colony stimulating factor (M-CSF), a potent survival and mitogenic factor for monocytes/macrophages (MM), enables MM to induce vascular smooth muscle cell (VSMC) apoptosis. The killing requires the binding of MM to VSMC via Mac-1 (CD11b/CD18) on MM and intracellular adhesion molecule-1 (ICAM-1) on VSMC. We hypothesized that, in addition to Mac-1 binding, the killing process requires the activation of the Fas-death receptor pathway, which can be blocked at the level of Fas-Fas ligand interaction. METHODS AND RESULTS: Human peripheral blood monocytes and VSMC were isolated and cultured as previously described. Soluble Fas (sFas) was overexpressed in VSMC by transduction using adenovirus specifying soluble Fas (Ad3hsFas). M-CSF markedly increased the expression of ICAM-1 in VSMC, resulting in enhanced clustering of MM on the surface of VSMC (>/=3 MM per VSMC). MM, but not VSMC, expressed Fas-ligand (FasL), and VSMC apoptosis was inhibited by secretion of sFas by VSMC upon Ad3sFas transduction. CONCLUSIONS: MM and M-CSF-induced VSMC killing requires MM binding to VSMC mediated by Mac-1 and ICAM-1, and Fas-FasL interaction.

Thrombospondin 2 regulates cell proliferation induced by Rac1 redox-dependent signaling.

Thrombospondin 2 (TSP2) is a matricellular protein controlling the apoptosis-proliferation balance in endothelial cells. Little is known about its transcriptional regulation compared with that of TSP1. We found that overexpression of a constitutively active mutant of Rac (Rac(V12)) specifically increases TSP2 mRNA levels without affecting TSP1 in human aortic endothelial cells (HAEC). Moreover, TSP2 induction by Rac(V12) is dependent upon reactive oxygen species (ROS) production, as gp91ds-tat peptide, an inhibitor of NADPH oxidase, and the flavoprotein inhibitor diphenylene iodinium (DPI) block TSP2 synthesis. Furthermore, we found that increasing Rac(V12) expression results in a biphasic proliferative curve, with proliferation initially increasing as Rac(V12) expression increases and then returning to levels less than that of control cells at higher expression. This growth inhibition is mediated by TSP2, as either DPI treatment, which blocks TSP2 synthesis, or pan-TSP blocking antibodies restore the proliferative ability of HAEC with high expression. Mechanistically, we show that the effect of TSP2 on cell proliferation is independent of the antiangiogenic TSP2 Hep1 sequence, which is capable of altering actin cytoskeletal reorganization but not proliferation in our experimental conditions. Finally, we show in vivo that Rac-induced TSP2 expression is observed in the aorta of transgenic mice selectively expressing Rac(V12) in smooth muscle cells. These results identify Rac-induced ROS as a new pathway involved in the regulation of TSP2 expression.

Rac-dependent monocyte chemoattractant protein-1 production is induced by nutrient deprivation.

Under ischemic conditions, the vessel wall recruits inflammatory cells. Human aortic endothelial cells (HAECs) exposed to hypoxia followed by reoxygenation produce monocyte chemoattractant protein-1 (MCP-1); however, most experiments have been performed in the presence of nutrient deprivation (ND). We hypothesized that ND rather than hypoxia mediates endothelial MCP-1 production during ischemia, and that the small GTP-binding protein Rac1 and reactive oxygen species (ROS) are involved in this process. ND was generated by shifting HAECs from 10% to 1% FBS. Superoxide production by HAECs was increased 6 to 24 hours after ND, peaking at 18 hours. MCP-1 production was increased over a similar time frame, but peaked later at 24 hours. These effects were blocked by treatment with antioxidants such as superoxide dismutase mimetic and N-acetylcysteine (NAC), or NADPH oxidase inhibitors, DPI and gp91ds-tat. Superoxide and MCP-1 production were enhanced by RacV12 (constitutively active) in the absence of ND, and were inhibited by RacN17 (dominant-negative) adenoviral transduction under ND, suggesting that the small G-protein Rac1 is required. In conclusion, ND, an important component of ischemia, is sufficient to induce MCP-1 production by HAECs, and such production requires a functional Rac1, redox-dependent pathway.

Overexpression of soluble fas attenuates transplant arteriosclerosis in rat aortic allografts.

BACKGROUND: The killing of vascular cells by activated macrophages is an important step in the process of destabilization of the arterial wall. The death receptor Fas is implicated in vascular cell death. Hence, we extended our studies in a rat aortic allograft model, using adenovirus-mediated overexpression of soluble Fas (sFas) to block Fas binding to Fas ligand (Fas-L). The contribution of Fas to vascular cell injury and consequent transplant arteriosclerosis was investigated. METHODS AND RESULTS: Activated monocytes in the presence of macrophage colony-stimulating factor induce endothelial cell apoptosis in vitro, which was significantly inhibited by adenovirus-mediated sFas overexpression. Next, donor rat abdominal aortas were either untreated or transduced with adenoviruses encoding (1) rat soluble Fas (Ad3rsFas), (2) no insert (Ad3Null), and (3) beta-galactosidase (Ad3nBg). A total of 175 aortic grafts were harvested 2 to 90 days after transplantation. Vascular cell apoptosis and CD45+ cell infiltration were significantly reduced in Ad3rsFas-transduced aortas, as compared with control allografts. Moreover, the control allografts developed marked intimal thickening, whereas Ad3rsFas-transduced allografts had significantly less neointima until the 90-day time point. CONCLUSIONS: sFas overexpression protects the integrity of the vessel wall from immune injury and attenuates transplant arteriosclerosis.

Pathophysiology of plaque instability: insights at the genomic level.

Atherosclerosis and plaque rupture represent complex "traits" of unknown cause that involve multiple genes and their variants. Novel genomic technologies provide us with the tools that will allow for the identification of groupings of genes that determine either susceptibility or resistance relative to the development of atherosclerosis and its thromboembolic complications. This information may, in turn, lead to a clearer understanding of the cause and risk for atherosclerosis. Diagnostic tools, as well as preventive and therapeutic strategies, will be derived from such heightened understanding of the disease process. With this chapter, we have presented the current state of knowledge of atherosclerosis genomics.

Activated monocytes induce smooth muscle cell death: role of macrophage colony-stimulating factor and cell contact.

BACKGROUND: Plaque disruption is the inciting event for coronary thrombosis and acute coronary syndromes. Multiple factors influence plaque rupture, including the loss of vascular smooth muscle cells (VSMCs). We hypothesized that monocytes/macrophages (MMs) activated by macrophage colony-stimulating factor (M-CSF) are responsible for VSMC death. METHODS AND RESULTS: VSMC apoptosis was markedly increased in the presence of both M-CSF and MMs (58.8+/-3.3%) compared with VSMCs plus M-CSF without MMs (15.7+/-1.5%, P< or =0.00005), VSMCs plus MMs without M-CSF (22.7+/-3.7%, P< or =0.0001), or control VSMCs alone (13.2+/-2.1%, P< or =0.0001). MM cell contact was required for M-CSF-stimulated killing of VSMCs, and MMs displayed an M-CSF concentration-dependent killing effect. Abciximab binds Mac-1 (CD11b/CD18) on MMs. When added to VSMCs exposed to MMs and M-CSF, abciximab (7 microg/mL) significantly reduced VSMC apoptosis (19.1+/-2.2%, P< or =0.0003). Therapeutic doses of tirofiban (0.35 microg/mL) and eptifibatide (5 microg/mL), which inhibit platelet glycoprotein (GP) IIb/IIIa but not Mac-1, did not block activated MM-induced VSMC apoptosis (65.0+/-3.4% and 51.3+/-2.5%, respectively). A recombinant anti-CD-18 antibody had an effect similar to that of abciximab (16.5+/-0.4%). CONCLUSIONS: These data suggest that monocytes and physiological concentrations of M-CSF trigger VSMC apoptosis. Abciximab and specific inhibitors of the Mac-1 receptor can antagonize this process.