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PubMed2002

Comparison of Diaket and MTA when used as root-end filling materials to support regeneration of the periradicular tissues.

AIM: The objective of this study was to evaluate on a comparative basis the potential for mineral trioxide aggregate (MTA) and Diaket to promote periradicular tissue regeneration when used as surgical root-end filling materials. METHODOLOGY: Seven dogs weighing between 15 and 25 kg were anesthetized prior to having the root canals of their mandibular premolars accessed, cleaned, shaped and obturated. Coronal access cavities were restored with IRM. Surgical access to the root ends was established and the root ends were resected and prepared with ultrasonic tips. Root-end fillings of either MTA or thickly mixed Diaket were randomly assigned to the preparations. Reflected tissues were repositioned and sutured with 4-0 vicryl sutures. Sixty days postsurgery, the animals were killed, perfused with 10% neutral buffered formalin and the third and fourth premolars removed in block sections. The specimens were demineralized and sectioned at 6-microm intervals for histological assessment. Sections were stained with either haematoxylin and eosin or Gomori's one step trichrome stain and examined under the light microscope. All evaluations were made by two calibrated examiners and gradings were scored based on established criteria. The raw data was evaluated statistically using anova after adjusting for the animal block effect. RESULTS: Statistical evaluation indicated that there were no statistical differences between the observed regenerative responses of the tissues to the two root-end filling materials. CONCLUSIONS: Both Diaket and MTA can support almost complete regeneration of the periradicular periodontium when used as root-end filling materials in periradicular surgery on noninfected teeth.

Aluminum Compounds↗
PubMed2002

Intracellular Ca2+ signals evoked by stimulation of nicotinic acetylcholine receptors in SH-SY5Y cells: contribution of voltage-operated Ca2+ channels and Ca2+ stores.

Neuronal nicotinic acetylcholine receptors (nAChR) can regulate several neuronal processes through Ca2+-dependent mechanisms. The versatility of nAChR-mediated responses presumably reflects the spatial and temporal characteristics of local changes in intracellular Ca2+ arising from a variety of sources. The aim of this study was to analyse the components of nicotine-evoked Ca2+ signals in SH-SY5Y cells, by monitoring fluorescence changes in cells loaded with fluo-3 AM. Nicotine (30 microm) generated a rapid elevation in cytoplasmic Ca2+ that was partially and additively inhibited (40%) by alpha7 and alpha3beta2* nAChR subtype selective antagonists; alpha3beta4* nAChR probably account for the remaining response (60%). A substantial blockade (80%) by CdCl2 (100 microm) indicates that voltage-operated Ca2+ channels (VOCC) mediate most of the nicotine-evoked response, although the alpha7 selective antagonist alpha-bungarotoxin (40 nm) further decreased the CdCl2- resistant component. The elevation of intracellular Ca2+ levels provoked by nicotine was sustained for at least 10 min and required the persistent activation of nAChR throughout the response. Intracellular Ca2+ stores were implicated in both the initial and sustained nicotine-evoked Ca2+ responses, by the blockade observed after ryanodine (30 microm) and the inositoltriphosphate (IP3)-receptor antagonist, xestospongin-c (10 microm). Thus, nAChR subtypes are differentially coupled to specific sources of Ca2+: activation of nAChR induces a sustained elevation of intracellular Ca2+ levels which is highly dependent on the activation of VOCC, and also involves Ca2+ release from ryanodine and IP3-dependent intracellular stores. Moreover, the alpha7, but not alpha3beta2* nAChR, are responsible for a fraction of the VOCC-independent nicotine-evoked Ca2+ increase that appears to be functionally coupled to ryanodine sensitive Ca2+ stores.

Aniline Compounds↗
PubMed2003

Effects of root-end filling materials on fibroblasts and macrophages in vitro.

OBJECTIVE: The aim of this study was to investigate the effects of 4 root-end filling materials (mineral trioxide aggregate [MTA], intermediate restorative material [IRM], amalgam, and Retroplast) on cell growth, cell morphology, and cytokine (interleukin [IL]1beta and IL-6) production in mouse fibroblasts and macrophages. STUDY DESIGN: Millipore culture plate inserts with freshly mixed or set root-end filling material were placed into 6-well cell culture plates with already attached mouse fibroblasts or macrophages. Cells cultured with only the Millipore culture plate inserts served as a control. After a 3-day incubation, cell morphology was examined, and the total cell number per well was counted and analyzed by using 1-way analysis of variance. For cytokine assay, mouse macrophages were incubated in 24-well flat-bottom plates with set root-end filling material disks in the bottom. Cells cultured without the material disks served as negative controls, and cells cultured with lipopolysaccharides served as positive controls. After 24-hour incubation, culture media were collected for cytokine assay by using enzyme-linked immunosorbent assay. RESULTS: All root-end filling materials inhibited the cell growth of mouse fibroblasts and macrophages. There was no growth in the originally seeded cells in the fresh IRM, the fresh Retroplast, and the set IRM group. There was no difference between MTA and amalgam for cell growth either in the fresh material groups or in the set material groups. The total cell number in the set Retroplast group was significantly less than that in the set MTA group. Morphologically, MTA was characterized by denatured medium proteins and dead cells adjacent to the material, which were observed only in the fresh MTA group. There was no detected cytokine production in any of the tested material groups. CONCLUSION: All root-end filling materials inhibited cell growth, and none induced IL-1beta and IL-6 production.

Aluminum Compounds↗
PubMed2003

Identification of hard tissue after experimental pulp capping using dentin sialoprotein (DSP) as a marker.

The purpose of this study was to identify the hard tissue formed early in experimental pulp exposures capped with mineral trioxide aggregate (MTA) or bone morphogenetic protein (BMP)-7 using dentin sialoprotein (DSP) as a marker. The pulps of 35 maxillary first, second, and third molar teeth from 10 male rats were experimentally exposed. The pulps were capped with MTA alone as a pulp-capping agent and final restoration or with BMP-7 followed by restoration with MTA. Five teeth with class I occlusal preparations, no exposure, and no restoration served as positive controls. Five teeth that received pulp exposures and no restoration served as negative controls. Five untreated third molars served as additional controls. The animals were killed at 2 weeks. The specimens were prepared and evaluated histologically and with immunohistochemistry using polyclonal antibodies raised against rat DSP. Pulps capped with MTA formed hard tissue that demonstrated significantly more immunostaining for DSP compared with BMP-7 (p = 0.0031). MTA-capped pulps also showed significantly more complete bridge formation compared with BMP-7 (p = 0.0008). Pulps capped with BMP-7 demonstrated a hard tissue that was bone-like in appearance and devoid of DSP staining.

Aluminum Compounds↗
PubMed1989

Effect of calcium-channel blockers and salbutamol on the isolated mare uterus--interaction with the calcium agonist Bay K 8644.

The effects of nifedipine, verapamil and diltiazem were investigated in the isolated mare uterus in comparison with salbutamol. All the calcium-channel blockers and salbutamol inhibited the spontaneous, KC1- and electrically induced contractions; nifedipine and salbutamol were the most potent compounds. The calcium agonist Bay K 8644 (10(-8)-10(-6) mol/l) competitively antagonized the inhibitory effect of nifedipine (pA2 value = 8.54 +/- 0.06), whereas it was only slightly or totally ineffective against verapamil, diltiazem and salbutamol. These results indicate that calcium-channel blockers are potent inhibitors of mare uterine motility in vitro and emphasize the importance of Ca2+-related mechanisms in the control of uterine smooth-muscle contractility. Moreover, the validity of Bay K 8644 as a tool to distinguish classes of calcium-channel antagonists is confirmed.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2005

The use of guided tissue regeneration principles in endodontic surgery for induced chronic periodontic-endodontic lesions: a clinical, radiographic, and histologic evaluation.

BACKGROUND: Chronic periodontic-endodontic lesions are not uncommon in clinical practice and their regenerative capacity has long been questioned. However, there are no published studies investigating the application of guided tissue regeneration techniques in combination with endodontic surgery using an induced perio-endo defect model. This study evaluated the clinical, radiographic, and histologic outcomes of three surgical procedures used to treat induced perio-endo lesions. METHODS: Pulpal necrosis was induced in foxhounds along with surgical removal of radicular buccal bone. After 4 weeks, chronic lesions were clinically and radiographically assessed. Treatment surgery consisted of apicoectomy, root canal instrumentation, and retrofilling with mineral trioxide aggregate. Teeth were then assigned to one of the following treatment groups: open flap debridement only (OFD), OFD with bioabsorbable porcine-derived collagen membrane (BG), or OFD with BG and anorganic bovine bone matrix (BO/BG). Clinical parameters and standardized radiographs were assessed at defect creation; treatment surgery; and at 1, 2, 4, and 6 months. Animals were sacrificed at 6 months and specimens prepared for histometric analysis. RESULTS: Clinical and radiographic conditions improved during the study period. Mean epithelial attachment was similar between all groups. Mean connective tissue attachment for groups OFD, BG, and BO/BG was 3.79 mm, 2.63 mm, and 1.75 mm, respectively, and mean radicular bone height was 2.16 mm, 3.24 mm, and 3.45 mm, respectively. Statistically significant increases in the amount of new cementum were observed in groups BG and BO/BG when compared with OFD (P <0.05). CONCLUSIONS: Treatment of combined induced perio-endo lesions using bioabsorbable collagen membranes alone or in combination with anorganic bovine bone matrix resulted in increased amounts of bone, periodontal ligament, and significant increases in the amount of new cementum when compared to open flap debridement in a canine model.

Absorbable Implants↗
PubMed1981

Spasmolytic effect of lidamidine on uterine smooth muscle.

1-(2,6-Dimethylphenyl)-3-methylamidinourea hydrochloride (lidamidine hydrochloride) has previously been reported to inhibit intestinal smooth muscle contractile activity in vivo and in vitro. This study showed lidamidine also inhibited contractile activity in the isolated gravid rat uterus preparation and antagonized, the spasmogenic effects of acetylcholine, serotonin, oxytocin, and PGF2 alpha and BaCl2. Increasing Ca2+ concentrations in the bathing medium from 0.9 mmol/l to 7.2 mmol/l effectively antagonized the lidamidine inhibition of responses to BaCl2 and acetylcholine in the gravid rat uterus preparation. These results suggest that the spasmolytic effect of lidamidine may be due to its interference with the availability of Ca2+ necessary for excitation-contraction coupling in smooth muscle.

Acetylcholine↗
PubMed1985

The mode of action of the calcium ionophore A23187 on T cell proliferation. I. The ionophore does not replace lymphokines but acts via induction of IL-2 production on IL-2 responsive cells.

The two compounds, the calcium ionophore A23187 and phorbol myristate acetate (PMA), which are not mitogenic for mouse thymocytes, induce proliferation when added in combination to thymocyte cultures. Short exposure to PMA renders the cells responsive to IL-2, added exogeneously. The cells rendered IL-2-responsive by PMA are enriched in the more mature peanut agglutinin (PNA)-negative population. The ionophore does not render PNA-negative thymocytes IL-2-responsive, but induces proliferation of PMA-pulsed PNA-negative thymocytes. PMA-pulsed PNA-negative thymocytes proliferating in response to either exogeneous IL-2 or ionophore express IL-2 receptors. However, the ionophore does not mimic IL-2 action but acts indirectly by induction of both IL-2 production and of IL-2 receptor expression via IL-2. This view is based on the following findings: 1) IL-2 could be detected in supernatants derived from PMA-preactivated thymocytes incubated with the ionophore; 2) The IL-2-induced proliferation, as well as the ionophore-induced proliferation, was specifically blocked by a monoclonal anti-IL-2-receptor antibody; 3) The proliferation induced by exogeneous IL-2, as well as that induced by the ionophore, could be specifically inhibited by metabolically blocked T lymphoblasts carrying IL-2 receptors competing with the responder cells for the available IL-2 added or produced in the system.

Animals↗
PubMed2002

Crosstalk between ryanodine receptors and IP(3) receptors as a factor shaping spontaneous Ca(2+)-release events in rabbit portal vein myocytes.

In smooth muscle cells freshly isolated from rabbit portal vein, there was only one site discharging the majority of spontaneous Ca(2+)-release events; the activity of this single site was studied using laser scanning confocal imaging after loading the cells with the fluorescent Ca(2+) indicator fluo-4 acetoxymethyl ester. Localised spontaneous Ca(2+)-release events visualised by line-scan imaging revealed two predominant spatiotemporal patterns: (i) small-amplitude, fast events similar to Ca(2+) sparks in cardiomyocytes and (ii) larger and slower events. The sum of two Gaussian profiles was well fitted to the amplitude histogram (peak frequencies at 1.8 and 3.2 F/F(0)) and spatial spread (full width at half-maximal amplitude) histogram (peak frequencies at 2 and 3.8 microm) for the 230 localised Ca(2+)-release events analysed. The existence of two populations of Ca(2+)-release events was also supported by the histograms of the rise times and half-decay times, which revealed modes at 38 and 65 ms, respectively. Shifting the scan line along the z-axis during imaging from a single discharge site suggested that the appearance of two populations of Ca(2+)-release events is not due to out-of-focus imaging. Both small and large events persisted upon 3-5 min exposure to 1-5 microM nicardipine, but were abolished after 10-15 min exposure to 50-100 microM ryanodine, 0.1 microM thapsigargin or 10 microM cyclopiazonic acid. Only small-amplitude, fast events persisted in the presence of inhibitors of inositol 1,4,5-trisphosphate (IP(3))-induced Ca(2+) release, 10 microM xestospongin C or 30 microM 2-aminoethoxy-diphenylborate (2-APB), or in the presence of 2.5 microM U-73122 (a phospholipase C (PLC) inhibitor). Coupling between neighbouring Ca(2+)-release domains giving rise to spontaneous [Ca(2+)](i) waves was abolished in the presence of 2-APB. Examination of the saltatory propagation of the waves suggested that the critical factor that determines propagation between domains is a time-dependent change in the sensitivity of ryanodine receptors and/or IP(3) receptors to Ca(2+), which can give rise to 'loose coupling' between release sites. These results suggest that activation of IP(3) receptors (due to the tonic activity of PLC and ongoing production of IP(3)) recruits neighbouring domains of ryanodine receptors, leading to larger Ca(2+) releases and saltatory propagation of [Ca(2+)](i) waves in portal vein myocytes.

Animals↗
PubMed2005

Involvement of phospholipase C in Yersinia enterocolitica heat stable enterotoxin (Y-STa) mediated rise in intracellular calcium level in rat intestinal epithelial cells.

In response to Yersinia enterocolitica heat stable enterotoxin (Y-STa) intracellular calcium level was increased with a prolong sustained phase in presence of calcium chloride in extracellular environment in rat intestinal epithelial cells. Chelation of extracellular calcium with EGTA (extracellular calcium chelator) and suspension of cells in calcium free buffer demonstrated a rapid but transient rise in calcium level, which suggested that Y-STa induced rise in intracellular calcium concentration was the combination of both intracellular calcium store depletion and calcium influx from extracellular environment. Moreover, in response to Y-STa phosphoinositide specific phospholipase C activity and inositol tri phosphate (IP3) level was increased and U73122, a phospholipase C inhibitor could completely inhibit Y-STa induced calcium rise. However, treatment of rat enterocytes with dantrolene IP3, a mediated calcium release inhibitor from intracellular store resulted partial inhibition of Y-STa induced rise in intracellular calcium level. Similar observation was noted with IP3 receptor antagonist 2ABP (2-amino-ethoxydiphenylborate). These results suggested that beside phospholipase C IP3 pathway, phospholipase C might have an independent role in Y-STa induced calcium influx. Rise in phospholipase Cgamma isoform activity in response to Y-STa suggested that gamma isoform of phospholipase C might have a role in Y-STa mediated rise in intracellular calcium level.

Animals↗
PubMed1992

Tetraethylammonium blocks muscarinically evoked secretion in the sheep parotid gland by a mechanism additional to its blockade of BK channels.

Since the secretory cells of the sheep parotid gland contain large numbers of high-conductance, voltage- and Ca(2+)-activated K+ channels (BK channels), we have used tetraethylammonium (TEA), a commonly employed blocker of BK channels, to investigate their role in secretion by this gland. In patch-clamp studies we found that 10 mmol/l TEA applied extracellularly inhibits the BK channel but not a 30-pS K+ channel also seen in this gland. We then showed by in-vivo perfusion that muscarinically evoked secretion is inhibited almost completely by 10 mmol/l TEA. We next used microspectrofluorimetry with fura-2 to demonstrate that muscarinic agonists cause the intracellular free Ca2+ concentration to increase. Unexpectedly, however, we found that 0.3-10 mmol/l TEA inhibited the increase in intracellular free Ca2+ induced by 5.0 mumol/l bethanechol or by 0.1 mumol/l acetylcholine. Consequently we conclude that the inhibition of muscarinically evoked secretion by the sheep parotid gland by TEA cannot be attributed solely to blockade of the BK channel--rather it must be attributed, at least in part, to blockade of some step in muscarinic signal transduction, for instance, receptor-agonist binding or Ca2+ release into the cytosol.

Animals↗