THE EFFECT OF DIHYDROTACHYSTEROL AND FERRIC DEXTRAN ON THE TEETH AND PERIODONTIUM OF THE RAT.
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The ability of alveolar macrophages of dogs to bind and metabolize two antigens was studied. The antigens were ragweed antigen E (AgE) and keyhole limpet haemocyanin (KLH). These antigens were chosen because of the availability of dogs with respiratory hypersensitivity to them and because they are of very different molecular weights. It was shown that: (1) antigen processing was identical using macrophages from hypersensitive as compared with normal dogs; (2) in comparison with AgE, much more of the higher molecular weight antigen, KLH, was bound to macrophages and much less degraded during subsequent incubation, leaving a greater proportion of the antigen bound to the cell membrane; (3) respiratory cells which had taken up AgE at 0 degrees C instead of 37 degrees C and were then incubated at 37 degrees C were much more active in catabolizing bound antigen with consequently less membrane bound antigen remaining; (4) increases in catabolism of bound AgE were also found in cells from relatively recently lavaged animals; (5) there was no evidence that cytophilic antibody contributed to the uptake of AgE.
The first experimental investigation of orthodontic tooth movement was published by Sandstedt in 1904-1905. After 100 years, there is a good understanding of the sequence of events at both tissue and cellular levels and now the current focus of research is at the molecular level. The techniques of reverse transcription-polymerase chain reaction and in situ hybridization to detect mRNAs of interest have revolutionized tooth movement studies and an expanding list of antibodies and enzyme-linked immunosorbent assays directed against human and animal proteins will facilitate their identification in tissue sections and/or culture supernatants. Nevertheless, although this technology has greatly simplified research for the clinical and laboratory investigator, message is not always translated into protein, and the presence of a protein does not necessarily mean it is biologically active. In vivo and in vitro methods have been widely used in tooth movement studies. However, data from in vitro models, in which the mechanical stimulus can be carefully controlled (tension versus compression; intermittent versus continuous), should be correlated with in vivo data from animal models. The current evidence suggests that downstream from the initial mechanotransduction event at focal adhesions which link the extracellular matrix to the cytoskeleton, mechanically induced remodelling is mediated by a complex feedback mechanism involving the synthesis of cytokines such as interleukin-1 (IL-1), IL-6, and receptor activator of nuclear factor k B ligand by cells of the osteoblast and/or fibroblast lineages. These in turn act in an autocrine/paracrine fashion to regulate the expression of transcription factors, cytokines, growth factors, enzymes, and structural molecules involved in the differentiation, proliferation, and function of mesenchymal and other cell types. Contrary to the impression gained from the literature, tooth movement is not confined to events within the periodontal ligament. Orthodontic tooth movement involves two interrelated processes: (1) deflection or bending of the alveolar bone and (2) remodelling of the periodontal tissues.
The aim of the present study was to describe some histopathologic features of tissues collected from root resorption areas of maxillary canines after transalveolar transplantation surgery. In 8 of 101 transplanted canines, complications including cervical root resorption occurred between 6 and 11 years after treatment. The resorptive processes were located at the supra-alveolar portions of the distal and/or mesial aspects of the teeth and were scheduled for treatment involving surgical exploration. The resorption cavities, which extended from the cementoenamel junction to a position immediately below the bone crest, were filled with a granulation tissue. In four of the diagnosed complication cases, this granulation tissue was carefully excised concomitant with the adjacent gingival tissue after flap elevation and placed in a buffered fixative. After proper soft-tissue healing, the cavities were filled with a glass-ionomer material. The collected biopsy specimens were, after fixation and, in one case, decalcification in ethylenediaminetetraacetic acid, dehydrated and embedded in Epon. Sections 3 microns thick were produced, stained in periodic acid-Schiff and toluidine blue, and used for histometric and morphometric analyses. The histologic analysis showed that the dissected tissue harbored well-encapsulated areas of inflammatory infiltrates. The lesions comprised a relatively low volume of collagen and a large number of inflammatory cells, predominantly lymphocytes.
Endotoxin (lipopolysaccharide or LPS) inhalation has been implicated in increased pulmonary edema, most likely due to activation of an inflammatory response. The purpose of this study was to determine the cell types in the lung responsible for binding inhaled lipid A from Enterobacter agglomerans LPS. Five-hour exposures of aerosolized lipid A resulted in measurable pulmonary edema in hamsters, as determined by the accumulation of lung water. Immunocytochemistry was used to localize the inhaled lipid A in the cell types in the lung. Alveolar macrophages had decreased levels of lipid A as compared to unexposed controls, suggesting a possible metabolism by the macrophages. In vitro exposure of macrophages to lipid A resulted in a time-dependent clearance of lipid A which was inversely related to its concentration. Alveolar macrophages thus appear to be responsible for the removal of inhaled lipid A in this model and may initiate the physiological events which bring about pulmonary edema.
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Alveolar bone reconstruction in growing dog during the retention period following orthodontic tooth movement was studied. Three beagle dogs (8-10 kg body weight, about one-year-old) were used and two of the animals were subjected to histological observation. The upper 2nd and lower 3rd premolars on both sides were extracted prior to the orthodontic treatments. After a healing period of one month, the upper 3rd premolar and the lower 4th premolar on the right side were moved mesially with a conventional orthodontic force for 8 weeks, and then retained in their new position for 4 weeks. The contralateral corresponding premolars were used as control. The alveolar bone was double-labeled with tetracycline (TC) during the movement and calcein (Cal) during the retention period. Alveolar bone structure and labeling patterns were examined by contact microradiography, conventional fluorescence microscopy, and confocal laser scanning microscopy (CLSM). Optimizing the separation of TC and Cal labelings in the alveolar bone was attained by the simultaneous use of ultraviolet (364 nm) and argon (488 nm) laser sources for excitation of TC and Cal, respectively. Cal labeling, indicative of new bone deposition showed two distinct patterns: lamination at the periodontal surface and rings circumscribing the vascular canal. The cementum surface also exhibited active deposition during the experimental period. Bone formation was affected by slight changes in magnitude and direction of orthodontic or occlusal forces. CLSM is valuable in deciphering the process of alveolar bone remodeling.
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Histological study of 40 alveolar wounds of altogether 5 dogs have given evidence to the fact that remains of the periodontal membrane could remain in the apical area of the alveoli in their whole width. In the middle part of the alveoli, remains of it are found in a thin layer. In the marginal area, bone can be found lying open with torn remnants, which are lying free in the coagulum. In these adhering rests of the periodontal membrane plenty of dynamic cells as well as dilated vessels can be observed. All these facts lead to the idea of considering the part that the remains of the periodontal membrane may possibly play in the beginning process of alveolar wound healing.
The development of a standardized method of collecting data from a questionnaire and a simplified, yet relatively complete, occlusal and temporomandibular examination form has been described. The questionnaire and clinical examination form have evolved from earlier forms developed by the author1 which have been used in numerous private offices and institutions for a period of five years. These earlier forms have now been augmented and modified as a result of personal consultation with users of earlier forms and numerous clinical and academic authorites.2-27 The selection of information to be obtained through the use of the questionnaire and clinical examination forms was further influenced by the work of numerous authors.28-63 Part II of this report deals with (1) the development of a companion Data Processing Form and a method of transcribing to this form the data from the Patient Questionnaire and clinical examination forms, as well as (2) key-punch instructions consistent with data processing requirements.
Marginal bone height and bone density were evaluated for 2 years after two-piece dense hydroxyapatite implant (Apaceram) placement using standardized radiography and digital image processing. The chronological changes in marginal bone height were divided into three groups: Group I-level was constant or became higher with time; Group II-bone decreased gradually after superstructure placement; and Group III-bone decreased in height rapidly after abutment placement. Bone density around the successful Apaceram implant, especially in the crestal region, increased clearly. The results suggest that bone resorption/formation around the implant is related to occlusal stress, and that adequate occlusal stress should be exerted on the implant at each phase after the implant placement.
Prosthetic care in cases of severe traumatic maxillary injuries remains topical. Alveolar maxillary processes atrophy make prosthetic treatment more difficult due to insufficient fixation and stabilization. At the stage of surgical treatment some corrective operations for a complete recovery of the disturbed functions and anatomic interrelations are made. Maxillary defects are rather variable in the form and size being dependent upon etiological factor, defect topography, terms of prosthetic treatment and time after operative intervention. Introduction of the method of dental implantation solves many problems of the appliance fixation and its adaptation in the place of the defect. A case is reported of rational prosthetic treatment after reconstructive-restorative operation on the upper jaw followed by 5 dental implants installation.
Fibrinogen (FBG), together with its polymerized form fibrin, modulates cellular responses during wound repair and tissue remodeling. Thus, we sought to determine whether A549 lung epithelial type II-like cells would endocytose insoluble, surface-bound FBG as a potential mechanism of alveolar matrix remodeling. Surface-bound FBG was endocytosed into either lysosomes or late endosomes by A549 cells through arg-gly-asp-dependent binding to alphavbeta3 but not alpha5beta1 integrin receptors. Soluble FBG added to confluent monolayers of A549 cells was not endocytosed. Unlike the uptake of the extracellular matrix glycoproteins vitronectin and thrombospondin by other cell types, endocytosis of FBG by A549 cells was neither inhibited by heparin nor dependent on binding to cell-surface heparan sulfate proteoglycans. FBG did not colocalize with endocytosed transferrin, whereas dextran showed partial colocalization with FBG in endocytic vesicles, suggesting nonclathrin-mediated endocytosis. Inhibition of actin filament polymerization blocked endocytosis of both dextran and FBG but not transferrin, providing further support that FBG is endocytosed via a nonclathrin pathway. Disruption of actin polymerization inhibited integrin-mediated cell spreading, which contributed to an overall reduction in FBG clearance that was most likely due to reduced cell migration and associated pericellular proteolysis. Trasylol inhibition of extracellular plasmin activity did not inhibit endocytosis of FBG. The endocytosed FBG was degraded to trichloroacetic acid-soluble fragments that showed an electrophoretic pattern distinctly different from plasmin-degraded FBG. Together, these results suggest that endocytosis of matrix-associated FBG by alveolar epithelial cells may be involved in the processes of alveolar tissue repair and matrix remodeling.
This study was designed to evaluate the potential to reconstruct localized ridge defects with bone by preventing non-osteogenic extraskelatal connective tissue from participating in the process of healing following experimental ridge augmentation treatment procedures. Following the elevation of buccal muco-periosteal flaps, buccal, interproximal, and interradicular bone was removed to the apical level of the second and third premolar teeth and the teeth were extracted to create bucco-lingual ridge defects that averaged 13 mm x 7 mm x 3.5 mm in each quadrant of two adult beagle dogs. The defects were permitted to heal for 90 days. The defects did not fill in with new bone. Subsequently, buccal muco-periosteal flaps were elevated and a membrane was placed over the defect and positioned so that it rested on bone that was exposed adjacent to the defect. In two quadrants test support materials were used to ensure that a space was maintained between the surface of the defect and the membrane. One quadrant was maintained as a sham-operated control site, three sites received membranes and no supporting implants and two sites received supporting implants and no membranes. The surgical schedule was designed to yield sacrifice times of 8 to 12 weeks. In the three quadrants available for study that were covered with membranes, bone and/or non-mineralized connective tissue was found to fill all of the space that had been provided by the membrane. Histologic examination confirmed that the space was filled with young, actively growing bone by 90 days. No new bone formation (bone fill) was observed in the sham-operated control site.
Magnetic resonance imaging is not established in the preoperative diagnosis of mandibular cystic lesions; therefore, no attempts have been made thus far to evaluate the course of the mandibular neurovascular bundle along the process. However, the radiologist can detect the neurovascular bundle along the cystic lesion by high-resolution MR imaging and convey this information to the maxillofacial surgeon. This reduces the risk of intraoperative damage of the nerve. The examination of the neurovascular bundle can easily be integrated in a tumor MRI protocol of the jaw if the slice orientation is adapted to the course of the mandibular canal.
In alveolar type II cells, the release of surfactant is considerably delayed after the formation of exocytotic fusion pores, suggesting that content dispersal may be limited by fusion pore diameter and subject to regulation at a postfusion level. To address this issue, we used confocal FRAP and N-(3-triethylammoniumpropyl)-4-(4-[dibutylamino]styryl) pyridinium dibromide (FM 1-43), a dye yielding intense localized fluorescence of surfactant when entering the vesicle lumen through the fusion pore (Haller, T., J. Ortmayr, F. Friedrich, H. Volkl, and P. Dietl. 1998. Proc. Natl. Acad. Sci. USA. 95:1579-1584). Thus, we have been able to monitor the dynamics of individual fusion pores up to hours in intact cells, and to calculate pore diameters using a diffusion model derived from Fick's law. After formation, fusion pores were arrested in a state impeding the release of vesicle contents, and expanded at irregular times thereafter. The expansion rate of initial pores and the probability of late expansions were increased by elevation of the cytoplasmic Ca2+ concentration. Consistently, content release correlated with the occurrence of Ca2+ oscillations in ATP-treated cells, and expanded fusion pores were detectable by EM. This study supports a new concept in exocytosis, implicating fusion pores in the regulation of content release for extended periods after initial formation.