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Biomedical subjects

Z Metzger

Publications and source records attributed to Z Metzger.

At least 37 records · Page 2Linked to original sources
PubMed1995

Specific cementum attachment protein enhances selectively the attachment and migration of periodontal cells to root surfaces.

A specific cementum attachment protein (CAP) was identified in human cementum and found to bind with high affinity to non-demineralized root surfaces, hydroxyapatite and fibronectin. Attempting to elucidate the biological function of this protein and its possible role in cementogenesis the capacity of CAP to promote selective cell migration towards and attachment of various periodontal derived cell populations to root surfaces in vitro was assessed. Human gingival fibroblasts (HGF), periodontal ligament cells (HPC), and alveolar bone cells (HABC) were labeled with [3H]Thymidine during their exponential growth phase. Root slices, 300 microns thick, were incubated with increasing concentrations of CAP. Untreated and fibronectin (FN) treated root slices served as negative and positive controls, respectively. Migration was assessed by placing root slices on confluent layers of labeled cells maintained in serum free medium and determining the number of cells migrated onto the root surface 3 days thereafter. Attachment was assessed by incubating root slices with labeled cell suspensions for 2 h and determining the number of attached cells. CAP promoted both cell migration and attachment dose dependently. HABC responded better than HPC and HGF to CAP treated root slices, and HPC response was higher than that of HGF. Cell attachment was dose dependently inhibited by synthetic RGD peptides. FN did not affect the migration of HGF, barely enhanced that of HABC, and was less potent than CAP at enhancing the migration of HPC. FN was more effective than CAP in promoting the attachment of HGF to root slices, but it was as potent as CAP in supporting the attachment of HPC and HABC.(ABSTRACT TRUNCATED AT 250 WORDS)

Alveolar Process↗
PubMed1991

Epithelial-connective tissue interaction on the tooth surface: an in vitro model.

In the present study, and in vitro system was developed and designed to examine the interaction between gingival fibroblasts (GF) and epithelial cells (EC) on the tooth surface. Porcine roots were cut transversely into 300 microns-thick root slices (RS). Gingival explants were placed on the upper RS surface and cultured in a defined medium permissive for the growth of EC. After 4 or 6 days, RS yielding EC were transferred onto confluent cultures of GF and further co-cultured for either 4 or 8 d. Cultures were then fixed and examined by SEM. The upper RS surfaces and the upper half of their peripheral aspect were covered by EC. The lower half of the peripheral RS surfaces were populated by GF originating from the confluent culture of GF. EC and GF made contact at approximately the middle of the side of the root slice. In cultures of epithelial components grown in defined medium for either 4 or 6 d and harvested 4 d after assembling the system, the EC-GF junction was located 117 +/- 45 and 271 +/- 82 microns, respectively from the upper RS aspect. Extending the co-culture period did not affect the EC-GF junction location. These results indicate that GF-EC contact stops the migration of these cells on root surfaces in vitro. The described system should be valuable for studying cellular events that may affect the formation of a new dentogingival junction following surgical periodontal therapy.

Animals↗
PubMed1990

Mechanism of endotoxin inhibition of human gingival fibroblast attachment to type I collagen.

Bacterial endotoxin inhibits the attachment of human gingival fibroblasts to collagen. The present study attempted to elucidate the possible mechanism of this inhibition. Two mechanisms were considered: direct toxicity to the cells and steric interference. Collagen substrates were prepared by rat type I collagen being air-dried in the wells of 24 multi-well plates. Experimental collagen substrates were treated with 50 micrograms of endotoxin/well, while untreated collagen substrates served as controls. Two mL of cell suspension (10(4) cells/mL) was added to each well, and these were incubated at 37 degrees C for two h. The average cell number/mm2 attached to experimental and control substrates was determined. Cell attachment to endotoxin-treated collagen was inhibited by 78%, compared with that to untreated collagen. The washing of the endotoxin-treated collagen for two h did not affect the inhibition of cell attachment, whereas after 24 h of washing, cell attachment was inhibited by 54%, compared with that to untreated collagen. Pre-incubation of the cells in endotoxin for two h did not affect their attachment to collagen. The addition of fetal calf serum (15%) to the experimental system completely reversed the inhibition of fibroblast attachment to endotoxin-treated collagen. These findings suggest that endotoxin interferes with fibroblast attachment to collagen through a steric phenomenon, possibly by blocking the binding sites on the collagen molecule recognized by the membrane receptor for collagen.

Analysis of Variance↗
PubMed1988

A gingival guard for crown preparation.

A device for subgingival margin preparation is presented. The gingival guard consists of a clamp attached to the high-speed handpiece supporting a stainless steel shank terminating in a sphere. The guard permits nontraumatic subgingival margin preparation.

Crowns↗
PubMed1988

The effect of retention grooves on gingival marginal leakage in Class II posterior composite resin restorations.

In this laboratory study, the effect of retention grooves in the proximal portion of class II cavities on the marginal microleakage using light-cured composite resin was examined. The retention grooves were placed at the axio-facial and axio-lingual line angles and in the gingival floor of the cavities. The teeth were restored with Herculite composite resin with etching and dentine bonding and polymerized in two different ways: (i) a single mass of restorative material was polymerized all at once; and (ii) incrementally placed amounts of restorative material were each polymerized separately until the cavity was completely filled. Marginal microleakage was evaluated by the degree of dye penetration at the gingival margin of the restorations after suitable thermocycling procedures. It was concluded that marginal microleakage was significantly reduced when the composite resin was placed and polymerized incrementally, and that no advantage was gained from retention grooves with this incremental technique. However, when polymerizing in one single mass of material, retention grooves were found to be necessary in order to reduce marginal microleakage at the gingival wall.

Acid Etching, Dental↗
PubMed1988

Clearance of Serratia marcescens from blood in mice: role of hydrophobic versus mannose-sensitive interactions.

In the present study, we examined the potential roles of cell surface hydrophobicity and mannose-sensitive (MS) interactions in blood clearance of Serratia marcescens in mice. Hydrophobic strain RZ, partially hydrophobic mutant 3162, and nonhydrophobic mutant 3164 were coinoculated into BALB/c male mice, and blood samples were plated out at different time intervals; colonies of the three strains were distinguished by their different morphologies. All three strains were cleared from the blood stream at similar rates, despite their large relative differences in cell surface hydrophobicity. Clearance from blood was subsequently studied by coinoculating two clinical isolates which differ in their abilities to adhere via MS interactions. MS+ strain 1785 was cleared much more rapidly than MS- strain 3255; moreover, in the presence of D-mannose, clearance of strain 1785 was inhibited to a rate similar to that of MS- strain 3255. When D-glucose was substituted for D-mannose, inhibition was not observed. The results suggest that MS, rather than hydrophobic, interactions are primarily responsible for the rapid clearance of S. marcescens from blood observed.

Animals↗
PubMed1987

Cavity design for class II composite restorations.

Preparation design for posterior composite restorations should differ from that for amalgam restorations in the following manner. Occlusal form should be narrower and the depth shallower. The proximal extensions (facial and lingual) should be placed in areas that can be seen, probed, and polished. Internal line angles should be rounded and retenive grooves placed in proximal line angles (axiofacial and axiolingual) and the gingival wall. Beveling is recommended for proximal margins but not for occlusal margins.

Composite Resins↗
PubMed1987

Resistance to horizontal forces of dowel and amalgam-core restorations: a comparative study.

Four designs of amalgam-core anchorage were compared in a laboratory study for the inability to withstand the horizontal component of occlusal force. Amalgam cores were constructed for extracted teeth with either composite resin-cemented Dentatus dowels, or with Para-post or Flexi-post dowels cemented with phosphate cement. All the posts were of comparable length and diameter. These anchorage designs were compared with each other and to a self-threading (TMS) pin-retained amalgam core, by application of horizontal force and recording forces causing failure. Flexi-post-retained amalgam cores failed at a mean force of 36.5 (+/- 8.5) kg while Dentatus-retained and Para-post-retained cores failed at 41.7 (+/- 8.0) kg and 46.6 (+/- 11.4) kg, respectively. TMS-retained cores resisted forces up to a mean force of 53.5 (+/- 4.5) kg. Patterns of failure varied widely among these groups. Composite resin-cemented Dentatus dowels were retained in the tooth in nine out of ten samples, while none of the ten Flexi-post dowels and only one of the ten Para-post dowels did so. Tooth fracture on failure occurred in seven out of ten Flexi-post-retained cores, while only three out of ten of the Para-post-retained cores and none of the Dentatus dowel-retained cores presented this unrepairable type of failure. Possible reasons for these differences are discussed.

Bite Force↗
PubMed1987

Cell surface hydrophobicity of Actinobacillus actinomycetemcomitans Y4.

Oral bacteria colonize the dento-gingival tissues in a selective manner. Hydrophobic reactions have been suggested as one of the major mechanisms of adhesion. Hydrophobicity of Actinobacillus actinomycetemcomitans Y4 (Aa) cells was studied in vitro using adherence to the liquid hydrocarbon, octane. Adherence of Aa cells to octane varied from 60-90%, depending on the medium in which they were grown, age of the culture and the buffer in which the assay was carried out. These data suggest that Aa is a hydrophobic bacterium, the hydrophobicity of which is expressed to a varying degree, and may have a rôle in its adherence to oral tissues.

Actinobacillus↗
PubMed1987

Bacterial endotoxin inhibits migration, attachment, and orientation of human gingival fibroblasts in vitro and delays collagen gel contraction.

The purpose of this study was to assess the effect of endotoxin adsorbed to dental surfaces and to collagen type I on the migration, attachment, and orientation of human gingival fibroblasts (HGF). Transversely cut porcine tooth root slices (RS), 200 micron thick, were prepared. Half of the RS obtained were partially demineralized in EDTA. Half of the demineralized and non-demineralized RS were incubated with 400 micrograms/mL of endotoxin for 24 hr, whereas the other half were maintained in PBS and served as controls. Experimental and control RS were placed on confluent layers of HFG and cultured for six days. Cell migration toward and cell attachment to the periphery of the RS and the formation of oriented cell sheets were assessed by means of photographic techniques. Additionally, six-day-old cultures were fixed and processed for SEM observation. In separate experiments, the effect of endotoxin on cell attachment to collagen type I and on contraction of three-dimensional collagen gels was assessed. It was found that: (i) bacterial endotoxin inhibited migration and attachment of HGF to both demineralized and non-demineralized cementum and interfered with the development of oriented cellular structure: (ii) the inhibitory effect was significantly more pronounced for non-demineralized than for demineralized cementum: (iii) the morphology of HGF attached to endotoxin-treated dental surfaces was altered compared with that of their controls: and (iv) bacterial endotoxin inhibited cell attachment to collagen type I and delayed the contraction of collagen gel.

Animals↗
PubMed1986

Suppression of fibroblast proliferation by activated macrophages: involvement of H2O2 and a non-prostaglandin E product of the cyclooxygenase pathway.

Macrophages are considered promoters of fibroblast proliferation; however, suppression by activated macrophages may outweigh this effect. Activated murine peritoneal macrophages obtained by in vivo exposure to C. parvum or by in vitro LPS-activation of thioglycollate-induced macrophages, were tested for their effect on normal syngeneic dermal fibroblasts. C. parvum-activated macrophages, but not resident peritoneal macrophages suppressed fibroblast proliferation. Similarly, macrophages activated in vitro by LPS, but not those unexposed to LPS, suppressed fibroblast proliferation. Catalase partially protected fibroblasts from suppression by either activated macrophage population, suggesting involvement of H2O2 in the suppression. The effect of cyclooxygenase inhibitors on the suppression was also tested. Indomethacin, acetylsalicyclic acid, or eicosatetraynoic acid, all partially protected the fibroblasts from macrophage-mediated suppression. Prostaglandins E2, E1, and F2 alpha, added exogenously at concentrations as high as 10(-6) M, failed to suppress the proliferation of the fibroblasts. These findings suggest that a non-prostaglandin product of the cyclooxygenase pathway is involved in macrophage-mediated suppression of fibroblast proliferation.

Animals↗