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Biomedical subjects

S Lindskog

Publications and source records attributed to S Lindskog.

At least 145 records · Page 8Linked to original sources

Comparative effects of parathyroid hormone on osteoblasts and cementoblasts.

Although bone, dentin and dental cementum are mesenchymal mineralized tissues composed mainly of collagen and hydroxy apatite, they differ markedly in their suceptibility to resorption. Bone undergoes physiological resorption to which the dental tissues appear to be resistant. Recently, the cells covering bone surfaces have been attributed a regulatory role in osteoclastic bone resorption by exposing the bone surface following stimulation with hormones and inflammatory mediators, thereby allowing osteoclasts to colonize the bone surface. In the present study, it was shown that reparative cementum-forming cells covering an experimental cavity in the root surface of replanted monkey incisors were unaffected by parathyroid hormone, a potent mediator of bone resorption. In parallel experiments, endocranial osteoblasts exposed bone surface by widening their inercellular spaces. It was concluded that the layer of cells covering the root surface forms a protective barrier against resorption which serves to preserve the integrity of the dental root.

Animals↗

Cellular colonization of denuded root surfaces in vivo: cell morphology in dentin resorption and cementum repair.

Cellular colonization of denuded root surfaces on replanted teeth was examined with scanning electron microscopy. The dentin surface was rapidly colonized by a few macrophage-like cells which resorbed dentin in limited areas. They had well-developed ruffled borders but no clear zones. The resorptive activity was gradually inhibited by the ingrowth of a monolayer of fibroblast-like cells from the periphery of the denuded area. At the advancing front, the ingrowing fibroblast-like cells were long and slender, with long tail-like projections trailing the nuclear domain. The invading cells behind these were well-spread and tightly packed. They had a granulated surface and showed morphological signs of fibre synthesis. After 6 weeks, the entire cavity was covered by a monolayer of these cells. Removal of the cells with sodium hypochlorite revealed that a cementum-like tissue had been formed under the invading cells, indicating that they were cementoblasts. It was concluded that wound repair on the root surface is dependent upon the differentiation and proliferation of pre-cementoblasts in the periphery of the wound and that cells in the main body of the periodontal membrane are of little significance in the healing process on the root surface.

Animals↗

Evidence for a resorption inhibitor in dentin.

The ability of stimulated and unstimulated peritoneal macrophages to spread in vitro on different inorganic and organic components of dental tissues was studied in order to establish morphologic evidence in favor of a resorption inhibitor in dentin. Macrophages were seeded onto enamel, dentin, predentin, demineralized dentin and collagen-coated coverslips and examined with scanning electron microscopy after varying incubation periods. The cells readily attached and spread on enamel, dentin and collagen-coated coverslips. Cells attached but showed no signs of spreading when incubated on predentin or demineralized dentin. It was concluded that the resistance to resorption of predentin and dentin rests in the organic, non-collagenous component of the tissue, indicating the presence of a resorption inhibitor in dentin.

Animals↗

Resorbing potential of different connective tissue types.

Pieces of dentin were implanted into five different connective tissues in rats and examined with scanning electron microscopy after observation periods of up to 2 weeks. Dentin-oclast-like cells, apparently involved in resorption of the implants, were only seen associated with periosteum and periodontal membrane. These findings indicate that the resorbing potential of connective tissues is related to their ability to induce bone formation.

Animals↗

Galanin: effects on basal and stimulated insulin and glucagon secretion in the mouse.

Galanin was recently demonstrated to be a neuropeptide in intrapancreatic nerves. In this study, the effects of galanin on basal and stimulated insulin and glucagon secretion in the mouse were investigated. Galanin, injected intravenously at dose levels ranging from 0.53 to 8.5 nmol kg-1, markedly lowered basal plasma insulin levels and transiently increased basal plasma glucagon levels. Furthermore, galanin induced hyperglycaemia: plasma glucose levels were 11 +/- 0.2 mmol l-1 2 min after injection of galanin (4.25 nmol kg-1) compared with 9.3 +/- 0.3 mmol-1 in controls (P less than 0.001). Galanin also impaired the plasma insulin response to either glucose or the cholinergic agonist carbachol. Thus, galanin (4.25 nmol kg-1) inhibited the plasma insulin response to glucose by 65% (P less than 0.001), and that to carbachol by 85% (P less than 0.001). Moreover, glucose abolished the galanin-induced plasma glucagon response. Also, galanin and carbachol exerted additive stimulatory effects on glucagon levels. It is concluded from this study in mice that galanin inhibits basal and stimulated insulin secretion, stimulates glucagon secretion, and induces hyperglycaemia. It is suggested that the intrapancreatic neuropeptide galanin is of importance in the regulation of both insulin and glucagon secretion.

Animals↗

Rapid-scan stopped-flow studies of the pH dependence of the reaction between mercuric reductase and NADPH.

The reaction of NADPH with the flavoenzyme mercuric reductase has been studied by rapid-scan stopped-flow spectrophotometry at 5 degrees C in the pH range 5.1-9.5. An intermediate formed within the dead time of the apparatus, and proposed to be an NADPH complex of oxidized enzyme, has an almost pH-independent spectrum. At pH 5.1 the formation of this species is followed by a rapid bleaching (k = 145 s-1) of the main flavin absorption band at 455 nm concomitantly with an absorbance increase around 395 nm. This process, which has a kinetic hydrogen isotope effect of 2.4, becomes less prominent at higher pH values and is not detectable above pH 7. It is suggested that this process includes the formation of a covalent thiol-flavin C-4a derivative stabilized by protonation of the active site. In the presence of an excess of NADPH, the final product of the reaction is probably an NADPH complex of two-electron-reduced enzyme, but below pH 6 the final spectrum becomes less intense suggesting a partial formation of four-electron-reduced enzyme. The spectral changes observed above pH 7 are nearly independent of pH. The first measurable step (k = 48 s-1 at pH 9.5) is thought to include the formation of an NADP+ complex of two-electron-reduced enzyme, while the final step (k = 6.3 s-1 at pH 9.5) results in the above-mentioned NADPH complex with two-electron-reduced enzyme. A minimal kinetic scheme rationalizing the observed pH dependence of the reaction and the observed isotope effects is presented.

Anaerobiosis↗

Activation of bovine muscle carbonic anhydrase by modification of thiol groups.

Two of the five cysteine residues in bovine muscle carbonic anhydrase (isoenzyme III) react rapidly and stoichiometrically with Ellman's reagent without effect on the CO2 hydration activity. These residues, which can be alkylated with iodoacetamide, have been identified as Cys-183 and Cys-188. Treatment of the enzyme with a large excess of Ellman's reagent results in additional derivatization of thiol groups and a 180% increase of the CO2 hydration activity. The cysteine residues associated with this activation are Cys-66 as well as Cys-203 and/or Cys-206. Activation has also been achieved with 2,2'-dithiodipyridine (120%) and with methyl methanethiosulfonate (approx. 400%), whereas no activation could be obtained with iodoacetamide, iodoacetate or N-ethylmaleimide.

Alkylation↗

Evidence for capping of Fc gamma receptors on osteoclasts.

Fc receptors, cell surface structures which bind the Fc portion of immunoglobulins, facilitate endocytosis and mediate triggered enzyme release in the phagocytic cells of the mononuclear phagocyte system (MPS). The osteoclast and the macrophage share many similarities, and it has been suggested that they are both derived from a common MPS precursor cell. Nevertheless, Fc gamma receptors, found on both primitive and well-differentiated cells of the mononuclear phagocyte system, have yet to be demonstrated on the osteoclast cell membrane. The aim of the present study was first, to study the distribution of rat endogenous IgG around resorbing bone using immunohistochemistry and the avidin-biotin-peroxidase (ABC) technique; and second, to determine if rat osteoclasts express Fc gamma receptors, using a recently described technique based on the ABC method. Observations that endogenous IgG accumulated at osteoclast/bone interfaces, and that Fc gamma receptors, expressed by osteoclasts, "capped" in the same area, have important implications regarding the origin of this cell and its mechanisms of bone attachment and resorption.

Animals↗

Immunoglobulin G in cystic lesions of rat enamel organ following fluoride intoxication.

Fluoride given as a high single dose to young rats with developing molars has earlier been shown to cause subameloblastic cysts with disorganized ameloblasts in the cystic wall and an irregular mineralization pattern of the underlying enamel. In the present study immunohistochemistry has been employed to determine if an increased permeability of the enamel organ occurred at the areas of cell disturbances. For this purpose 5-day-old rats were injected with 60 mg sodium fluoride per kg body weight. They were decapitated after 24 h, the maxilla prepared histologically and paraffin sections incubated for the demonstration of IgG according to the avidin-biotin-peroxidase complex method. Staining for IgG was present in the cystic lumina and in areas of disorganized ameloblasts. No reaction was observed in areas of unaffected ameloblasts. It was suggested that the fluoride-induced cell injury increased the permeability of the ameloblastic cell layer. Diffusion of IgG and most likely other substances as well, through the ameloblastic layer may have contributed to cyst formation and to the irregular mineral deposits that have been found in the ameloblastic layer and at the enamel surface.

Ameloblasts↗

Scanning electron microscopy of fluoride-induced disturbances on the enamel surface of rat molars.

Rats were given a single high dose of fluoride at the age of 5 days and killed after 24 h, 10 or 15 days. The maxillary first molars were prepared for scanning electron microscopic examination. It was concluded that a single dose of fluoride, preferentially affecting ameloblasts with a high secretory activity, leads to the formation of subameloblastic cysts and enamel hypoplasias covered with granular deposits.

Ameloblasts↗

Macrophage colonization of infected and non-infected dental tissues in vitro.

Attachment and spreading of phagocytes on a mineralized tissue surface is crucial for their proper resorptive function. In other studies, attachment and spreading have been shown to be highly dependent on the nature and composition of the surface. In the present study, peritoneal macrophages were cultured on infected and non-infected mineralized and non-mineralized dental tissues, which were examined with scanning electron microscopy at different observation periods. Although some cells had attached to non-infected predentin, only a few showed signs of spreading, even after long incubation times. This contrasted with the behavior of macrophages cultivated on enamel, mineralized dentin and infected predentin. Most of these cells showed spreading and the characteristics of active, phagocytosing cells. The reluctance of macrophages to spread on non-infected predentin was suggested to be due to the non-mineralized nature of this tissue, although an influence of endogenous resorption inhibitors cannot be excluded.

Animals↗

Immunocytochemical localization of a tartrate-resistant and vanadate-sensitive acid nucleotide tri- and diphosphatase.

Purified rabbit antiserum to a tartrate-resistant and vanadate-sensitive acid phosphatase (nucleotide tri- and diphosphatase) prepared from rat bone was used in immunocytochemical studies. The antigen was localized in sections of fixed, decalcified tissue (head from rat) using the peroxidase-antiperoxidase bridge (PAP) or the avidin-biotin-peroxidase complex (ABC) technique. Both techniques resulted in similar and specific immunostaining in the following cells and tissues: osteoclasts situated in resorption lacunae, epithelium overlying enamel-free areas of tips of cusps of unerupted molars, cilia of respiratory epithelium, and tissue macrophages. This distribution corresponds to the cellular sites of tartrate-resistant acid phosphatase activity, as revealed by enzyme histochemistry. With the ABC method, staining in osteoclasts was obtained with antiserum dilutions of up to 1:10,000. Biochemical studies revealed that vanadate-sensitive acid ATPase activity in liver subcellular fractions was almost exclusively confined to lysosomes. Thus, the immunostaining has revealed the presence of the tartrate-resistant and vanadate-sensitive nucleotide phosphatase in many cells associated with tissue resorption and phagocytosis.

Adenosine Triphosphatases↗

Occurrence and appearance of cementum hypoplasias in localized and generalized juvenile periodontitis.

The occurrence and appearance of cementum hypoplasias have been studied on teeth affected by juvenile periodontitis. Scanning electron microscopy showed the presence of cementum hypoplasias on the root surface of all extracted first molars and one incisor from nine patients with localized juvenile periodontitis and on most extracted teeth from two patients with generalized juvenile periodontitis. No hypoplasias were found on the extracted third molars. The alveolar bone loss in these patients seemed to be correlated to the frequency and extension of the hypoplastic areas in the associated teeth. The distribution of the teeth affected by localized juvenile periodontitis showed a symmetric distribution in the jaws. The patients with generalized juvenile periodontitis showed considerable deposits of dental calculus and wide areas of root resorption. The disturbance of cementum formation may have been caused by hereditary systemic factors, which subside with increasing age of the patient. The clinical appearance of juvenile periodontitis may therefore be influenced by the age at onset, the duration, and the frequency of such systemic factors, giving rise to a localized form and a more generalized form. One such factor may be a varying degree of hypophosphatasia.

Adolescent↗