PubMed Health⌕ Search

Biomedical subjects

F R Denys

Publications and source records attributed to F R Denys.

At least 37 records · Page 2Linked to original sources

Adhesion to enamel and dentin.

The physical and chemical properties of restorative materials and procedures that influence the extent of microleakage at the tooth/restoration interface are discussed. Adhesion to enamel is achieved and microleakage at the enamel/restoration interface has been controlled by acid etching enamel surfaces with orthophosphoric acid. The acid concentration and the duration of etching are reviewed. Adhesion to dentin and microleakage at the restoration/dentin (cementum) interface are more difficult. The development of dentin bonding agents and the tremendous advances made with these restorative systems are reviewed. Particular attention is directed towards the Gluma/Lumifor dentin bonding restorative system and the development of an experimental conditioning solution for both enamel and dentin.

Acid Etching, Dental↗

Tensile bond strengths of orthodontic bonding resins and attachments to etched enamel.

The purpose of this in vitro study was to determine the tensile bond strengths (TBS) of several orthodontic bonding systems and orthodontic brackets to enamel surfaces exposed to different etching procedures. The TBS of four bonding systems were determined by a test method developed by Kemper and Kilian. Twelve test specimens were prepared for each procedure. The test system was modified to determine the TBS of orthodontic brackets bonded to enamel surfaces by six bonding procedures and the TBS were evaluated 15 minutes and 24 hours after specimen preparation. The specimens were loaded to failure in an Instron machine operated at a crosshead speed of 0.02 inch/min. The TBS were expressed in MN.m-2. The TBS of the four bonding systems to etched enamel were not significantly different (P = 0.2528). The TBS of bonded brackets determined 24 hours after specimen preparation were not significantly different than the TBS recorded after 15 minutes except for brackets bonded with Lee Cleanse and Bond I to enamel surfaces etched with 15% H3PO4 for 30 seconds. The TBS of brackets to enamel etched with 15% H3PO4 for 30 seconds were not significantly different from the TBS to enamel surfaces etched with 5% H3PO4 for 15 seconds except for brackets bonded with Lee Cleanse and Bond II and tested 24 hours after bonding.

Acid Etching, Dental↗

The effect of fluoride in phosphoric acid on enamel fluoride uptake and the tensile bond strength of an orthodontic bonding resin.

Decalcification that occurs adjacent to bonded orthodontic brackets is of great concern to orthodontists. Among the many procedures suggested to overcome this problem is the addition of fluoride to the phosphoric acid (H3PO4) etching solution. The purposes of this study were to determine the loss of fluoride from the acidic etching solutions, to evaluate the effect of various fluoride concentrations in H3PO4 on the tensile bond strength of an orthodontic bonding resin, to determine the amount of total and bound fluoride acquired by etched enamel, and to evaluate the effect of these etching solutions on enamel by scanning electron microscopy. Solutions of 50 m/m% H3PO4 containing 0 and approximately 0.01, 0.04, 0.08, 0.2, 0.4 and 0.9% fluoride were prepared. The fluoride concentrations in the etching solutions remained stable up to 3 months after preparation. The tensile bond strengths of the bonding resin to the etched enamel surfaces were not significantly different. Enamel acquired the greatest amount of total fluoride from H3PO4 solutions containing 0.215% fluoride while the bound fluoride acquired by enamel from the fluoride-containing etching solutions was not significantly different. The addition of fluoride to H3PO4 did not impede the etching effect on enamel.

Acid Etching, Dental↗

Pyruvic acid as an etching agent in clinical dentistry.

The objective of this study was to evaluate the use of pyruvic acid as an alternative etching agent to phosphoric acid (H3PO4). Solutions containing 5, 10, 15, 20, 25, and 30 m/m % pyruvic acid and 50% m/m H3PO4 were prepared. The tensile bond strengths of a composite resin to enamel surfaces etched with the respective etching agents were determined. The rates of etching of enamel surfaces by each of the etching solutions were evaluated. Unground and polished enamel surfaces were etched with the respective etching solutions and the surfaces examined by scanning electron microscopy. The tensile bond strengths of the resin to enamel surfaces etched with 10-30% pyruvic acid exceeded those obtained on enamel surfaces etched with 50% H3PO4. The rates of etching of all the pyruvic acid solutions were significantly less than of H3PO4. Well-defined etching patterns were observed on the enamel surfaces etched with all the etching solutions. The results of this laboratory study suggest that pyruvic acid may be a suitable alternative to phosphoric acid as an etching agent in clinical dentistry.

Acid Etching, Dental↗

The effect of topical fluoride treatment on enamel fluoride uptake and the tensile bond strength of an orthodontic bonding resin.

Enamel demineralization occurring adjacent to directly bonded orthodontic attachments is of great concern to orthodontists. The topical application of fluorides to enamel surfaces before acid etching and the bonding of the attachments is not recommended by many investigators. The objective of this study was to determine the enamel fluoride acquired from various topical fluoride agents and to determine the effect of the acquired fluoride on the tensile bond strength of an orthodontic bonding system. Fifty extracted maxillary central incisors were mounted in cups and the facial surfaces of the crowns were polished on 600-grit silicon carbide paper. Enamel microbiopsies were performed just off the midpoint of each tooth. Ten teeth served as controls and received no topical fluoride treatment, while a similar number were treated with either APF, SnF2, Duraphat, or Fluor Protector. The teeth were suspended in synthetic saliva 4 minutes after fluoride application. The topical fluoride agents were removed after 24 hours and the teeth were again suspended in synthetic saliva at 37 degrees C for 7 days. Enamel biopsies were again performed just off the midpoint of each tooth on the side not previously biopsied. The enamel surfaces were etched for 1 minute and the tensile bond strength of Concise orthodontic bonding system to the etched enamel surfaces was determined. The enamel surfaces acquired significantly different amounts of fluoride from the topical fluoride agents, but the bond strengths to these surfaces were not significantly different. The results of this in vitro study suggest that the application of topical fluoride agents to enamel surfaces 7 days before the bonding of orthodontic attachments will not have an adverse effect on bond strength.

Acid Etching, Dental↗

Ultrastructural cytochemistry of proteoglycans associated with calcification of shark cartilage.

Proteoglycans (PGs) as well as sulfated glycosaminoglycans (GAGs) are closely associated with cartilage calcification. An inner zone of endoskeletal tesserae of sharks is composed of a unique calcified hyaline cartilage. Initial calcification can be seen in the cartilage close to the inner zone. We have ultrastructurally examined shark, Triakis scyllia, noncalcifying, calcifying, and calcified cartilage using the tannic acid-ferric chloride (TA-Fe), the high iron diamine (HID), and the HID-thiocarbohydrazide-silver proteinate (HID-TCH-SP) methods for localization of sulfated complex carbohydrates. In noncalcifying cartilage, TA-Fe and HID strongly stained matrix granules which were round, ovoid, elongated, or irregularly shaped and presumably represented PG monomers. The size and staining intensity of the reactive matrix granules progressively decreased in calcifying cartilage toward the calcification front of the calcified cartilage. Similarly, a progressive decrease in the size of the HID-TCH-SP stain deposits in the matrix granules was observed in the calcifying cartilage close to the calcification front and was interpreted as a decrease in length of sulfate containing GAG chains. In the calcified cartilage, the highly calcified areas were often localized in the calcification front and contained few or no small HID-TCH-SP stain deposits, whereas the weakly calcified regions contained more stain deposits. These results indicate that partial and complete degradation of sulfated GAGs and/or PGs may be a requisite for calcification of shark cartilage.

Animals↗

Ultrastructural localization of glycosaminoglycans in human term placenta.

Sulfated glycoconjugates were stained in normal human term placentas using Spicer's high-iron diamine (HID) method with thiocarbohydrazide and silver proteinate (TCH-SP) enhancement. Specific identification of glycosaminoglycans (GAG) was accomplished by digestion of the stained material with chondroitinase ABC or AC for removal of chondroitin sulfates and nitrous acid for removal of N-sulfated GAGs. The syncytiotrophoblast apical surface demonstrated moderate to intense staining with HID-TCH-SP, which was removed by prior digestion with the chondroitinases, but not by nitrous acid. The syncytiotrophoblast basal surface and endothelial cell surfaces lacked sulfate staining. A few cytoplasmic granules in syncytiotrophoblast cells demonstrated staining similar to the apical surface. Three layers of the basal lamina were identified in these preparations. The lamina lucida immediately beneath the syncytiotrophoblast and the majority of the lamina densa stained weakly or not at all, whereas the underlying lamina diffusa and stroma demonstrated moderate to intense staining. The majority of lamina diffusa staining was removed by chondroitinase ABC or AC; the remaining material was removed by nitrous acid digestion. Thus the syncytiotrophoblast surface contains a chondroitin sulfate and the basal lamina contains a mixture of intensely stained chondroitin sulfate and a weakly stained N-sulfated GAG.

Connective Tissue↗

Effect of various root surface treatments on the attachment and growth of human gingival fibroblasts: histologic and scanning electron microscopic evaluation.

Human teeth extracted because of advanced periodontal disease were obtained. The portions of the roots which had been exposed in periodontal pockets were either untreated or were treated with root planing or citric acid, or root planing followed by citric acid. Human gingival fibroblasts were then added to the roots so treated and were allowed to incubate for 72 h. The ability of cells to attach to and grow onto these roots was assessed by means of gross evaluation of staining intensity and by histologic and scanning electron microscopic observation. The results of multiple experiments in each root-treatment category indicated that only roots which had been planed, whether or not citric acid demineralization was used, promoted cell attachment and growth. In addition, there were no discernible morphologic differences in the cells which were plated onto roots which were root planed only, compared to those which were root planed and citric-acid treated. In both situations too, the cells displayed morphology typical of human gingival fibroblasts in culture.

Cell Adhesion↗

Fluoride-treated roots and viability and attachment of human gingival fibroblasts.

Topical fluoride treatment is used to help prevent root caries. It may also be useful in periodontal therapy because of its antimicrobial property. In addition, for therapeutic new attachment to occur, the fibroblasts approximating the treated root surface should remain viable, and should also be able to attach and grow onto the treated root surface. These conditions, at least, are required for fluoride not to interfere with new attachment. This study was designed to determine whether treatment of roots with fluoride adversely affects human gingival fibroblasts in culture; and what effect fluoride treatment has on attachment and growth of cells to the root surface. Cells originally obtained from human gingiva were allowed to grow to confluency in multi-well tissue culture petri dishes, and were then incubated for 24 hr in the presence of root sections as follows: (1) no treatment; (2) root-planed only; (3) 2% NaF only; (4) root-planed + 2% NaF; (5) root-planed + citric acid, pH 1 + 2% NaF. In addition, cells were plated onto roots similarly treated and were subsequently allowed to incubate for 72 hr. Viability of cells was determined by exclusion of vital dye and 51Cr retention. Attachment and growth of cells were determined by histology and scanning electron microscopy. Results indicated that, after 24 hours' exposure, there was little or no difference in cell viability between different treatment groups and control cultures. Also, all roots which had been planed accommodated cell attachment, regardless of additional treatment rendered.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid Etching, Dental↗

Ultrastructural distribution of sulfated complex carbohydrates in elastic cartilage of the young rabbit.

Sulfated glycosaminoglycans are an integral component of elastic cartilage. We have investigated the ultrastructural distribution of sulfated complex carbohydrates (CC) in the mature cartilage and the perichondrium of young rabbit auricles using the high iron diamine-thiocarbohydrazide-silver proteinate (HID-TCH-SP) and the tannic acid-ferric chloride (TA-Fe) methods. In the mature cartilage, HID-TCH-SP stained intracellular Golgi saccules of the mature face, secretory granules, and the extracellular matrix granules, but staining was not discernible in collagen fibrils and osmiophilic elastic fibers consisting of only amorphous elastin. The HID and TA-Fe staining were similarly observed in matrix granules, whereas the elastic fibers and collagen fibrils lacked the staining. The pericellular matrix granules had a diameter of 34 +/- 5 nm (mean +/- SD; n = 30). Thiéry's periodate-TCH-SP (PA-TCH-SP) method stained vicinal glycol-containing CC in collagen fibrils but failed to stain matrix granules and elastic fibers. In the perichondrium, HID-TCH-SP staining of the organelles was less intense in the flattened chondrocytes when compared with those in large mature chondrocytes. The extracellular HID and HID-TCH-SP staining were observed in the matrix granules. The diameter of pericellular matrix granules (19 +/- 4 nm, mean +/- SD; n = 30) was significantly smaller when compared to those in the mature cartilage (P less than 0.001). The HID-TCH-SP staining was closely associated with collagen fibrils. However, the staining was not seen in collagen fibrils and osmiophilic elastic fibers consisting of elastin and microfibrils. The PA-TCH-SP method stained collagen fibrils and microfibrils but did not stain the amorphous elastin. Thus these studies demonstrate that sulfated CC are packaged in chondrocyte secretory granules and are released into the extracellular matrix to form matrix granules, but are not incorporated into collagen fibrils and elastic fibers.

Animals↗

Ultrastructural cytochemistry of complex carbohydrates in osteoblasts, osteoid, and bone matrix.

Glycosaminoglycans (GAGs) and glycoproteins are essential components for osteogenesis. We have examined rat osteoblasts, osteoid, transitional zone, and fully calcified bone matrix, utilizing Spicer's high-iron diaminethiocarbohydrazide-silver protein (HID-TCH-SP) method for sulfated glycoconjugates and Thiéry's periodate-TCH-SP (PA-TCH-SP) method for vicinal glycol-containing glycoconjugates. HID-TCH-SP stained cytoplasmic granules of osteoblasts. Stain deposits in the extracellular matrix were observed in decreasing amounts in osteoid, the transitional zone, and fully calcified bone matrix. Enzyme digestion with testicular hyaluronidase removed most HID-TCH-SP stain deposits. PA-TCH-SP staining was observed with increasing intensity in rough endoplasmic reticulum, Golgi saccules, and cytoplasmic granules. Collagen fibrils in osteoid were weakly stained with PA-TCH-SP, and their staining appeared even weaker in fully calcified bone matrix. In contrast, collagen fibrils in calcified cartilage stained intensely with the PA-TCH-SP method. Focal circular profiles (0.1-0.5 mumol in diameter), which lacked collagen fibrils but reacted moderately with PA-TCH-SP, were frequently seen in the transitional zone and fully calcified bone matrix, but were only occasionally present in osteoid. The presence of testicular hyaluronidase-resistant GAG and acid phosphatase in these focal areas suggests that they represent sites of GAG degradation. The eventual loss of HID-TCH-SP staining in the bone matrix suggests that removal of sulfated glycoconjugates may be a requisite for expansion of initial calcification sites and/or complete calcification.

Acid Phosphatase↗

Ultrastructural localization of the transferrin receptor and transferrin on marrow cell surfaces.

The monoclonal antibody OKT9 (a known transferrin receptor antibody) and a monoclonal antibody to transferrin (ATfn) were used to localize the transferrin receptor and transferrin on marrow cells. After incubation of cell suspensions with the antibody, the cells were reacted with an affinity purified Fab fragment of goat anti-mouse IgG conjugated to horseradish peroxidase (GAM-HRP), which was in turn visualized by reaction with 3,3'-diaminobenzidine (DAB). Erythroblast cell surfaces stained intensely with OKT9-GAM-HRP-DAB, weaker staining was observed on reticulocyte surfaces, whereas erythrocyte surfaces lacked staining. Staining was present on surface caveolae, which often contained endogenous ferritin particles. Moderate to strong OKT9 staining was observed on less than 10% of presumed lymphoid cells. Monocytes, macrophages, promyelocytes, granulocytes, megakaryocytes and platelets consistently lacked OKT9 staining. ATfn-GAM-HRP-DAB staining of erythroid cells was similar to that observed with OKT9 staining; however, in contrast to the latter staining, ATfn stained the surfaces of megakaryocytes, platelets, monocytes and most lymphocytes. Promyelocytes stained weakly, whereas late granulocytes lacked staining. These results indicate that the T9 transferrin receptor (1) is largely confined to erythroid cells in marrow, (2) is diffusely distributed on the surface of early erythroid cells, (3) decreases with cell maturation, and (4) is lost when haemoglobin synthesis is completed. Transferrin appears in a similar distribution on erythroid cell surfaces but also appears to bind to some cell surfaces lacking the T9 receptor.

Antibodies, Monoclonal↗