Biomedical subjects
Publications and source records attributed to Y Zilberman.
Thirty-seven autotransplanted canines in thirty-one patients were observed for a period of 2 to 7 years. Transplants with less than 2 years follow-up were not included in this study. Although the surgical root canal, and fixation techniques were identical, the delayed pathophysiologic changes were different.
A four-unit symmetrical premolar extraction case demands meticulous levelling, overjet reduction, space closure, rotating, paralleling and torqueing to justify the gambit of having extracted the teeth at the commencement of treatment. This involves the patient in complex therapy which may, for any of several reasons, be contra-indicated for that particular patient, though a decision based on the plaster casts alone may have upheld such an approach. The purpose of this article is to discourage automatic decisions to extract first premolars in orthodontic extraction cases. The clinician is offered a classification of special cases in which an alternative should be sought, based on careful consideration of the general dental, facial, physical, psychological and economic state of the patient.
The accuracy for predicting mesiodistal widths of unerupted permanent canines and premolars from x-rays and their estimations based on the already erupted permanent teeth were tested in a group of Israeli children. The observed posteruptive widths related more closely to predicted values obtained from x-ray measurements than from tabulated estimations.
Accumulation of dental plaque for 3 and 7 days respectively was determined by calculating the difference between the postcollection and precollection weights of enamel slabs attached to orthodontic bands cemented to the upper first molars of 3 subjects. Pretreatment of the enamel slabs with amine-fluoride or -chloride respectively-at an equivalent amine concentration-prevented plaque deposition on the slabs, whereas pretreatment with sodium monofluorophosphate was less effective. The fluoride concentrations of all fluoride-pretreated enamel slabs were similar. No convincing demonstration of significant differences between the treatments could be predicted in view of the discrepancy in results at the 3- and 7-day test periods.
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Dental casts of 99 Kurdish and 98 Yemenite Jewish children evenly distributed between the sexes, aged 12 years, were measured for mesiodistal and buccolingual tooth dimensions, and arch depth and width. Dental dimensions showed significant differences between the two groups in certain permanent teeth in mesiodistal length, while in the buccolingual diameter the differences did not reach statistical significance. Dental arch form in Kurdish children was more rounded due to significantly bigger arch width, while arch depth was not significantly different from Yemenites. Intragroup sex differences were found in both groups with reference to arch dimensions, while in the dental parameters they were more strongly expressed in Kurdish children.
Two cases of mandibular prognathism have been presented. In both cases expansion of the dental arches was performed prior to surgery for the achievement of good and stable interarch relationships postoperatively. In the first case maxillary arch was expanded with a rapid-expansion technique; in the second, expansion of the mandibular arch was performed with a modified removable Coffine appliance. Results at 15 months and 2 years after retention showed the expansion to be stable.
Four cases of improper use of elastic bands for minor orthodontic treatment are described. For all the patients, the treated teeth were damaged and local surgical intervention was necessary. To prevent complications when elastic bands are being used, the dentist must provide stabilization of the elastic bands by brackets, bands, or bonded attachments, inform the patient about the possibility of losing the rubber elastic band, and mark the elastic rubber by radiopaque material. Every effort must be made to preserve the damaged anterior teeth by fixation and surgical treatment.
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BACKGROUND: Among the approximately 6.5 million fractures suffered in the United States every year, about 15% are difficult to heal. As yet, for most of these difficult cases there is no effective therapy. We have developed a mouse radial segmental defect as a model experimental system for testing the capacity of Genetically Engineered Pluripotent Mesenchymal Cells (GEPMC, C3H10T1/2 clone expressing rhBMP-2), for gene delivery, engraftment, and induction of bone growth in regenerating bone. METHODS: Transfected GEPMC expressing rhBMP-2 were further infected with a vector carrying the lacZ gene, that encodes for beta-galactosidase (beta-gal). In vitro levels of rhBMP-2 expression and function were confirmed by immunohistochemistry, and bioassay. Differentiation was assayed using alkaline phosphatase staining. GEPMC were transplanted in vivo into a radial segmental defect. The main control groups included lacZ clones of WT-C3H10T1/2-LacZ, and CHO-rhBMP-2 cells. New bone formation was measured quantitatively via fluorescent labeling, X-ray analysis and histomorphometry. Engrafted mesenchymal cells were localized in vivo by beta-gal expression, and double immunofluorescence. RESULTS: In vitro, GEPMC expressed rhBMP-2, beta-gal and spontaneously differentiated into osteogenic cells expressing alkaline phosphatase. Detection of transplanted cells revealed engrafted cells that had differentiated into osteoblasts and co-expressed beta-gal and rhBMP-2. Analysis of new bone formation revealed that at four to eight week post-transplantation, GEPMS significantly enhanced segmental defect repair. CONCLUSIONS: Our study shows that cell-mediated gene transfer can be utilized for growth factor delivery to signaling receptors of transplanted cells (autocrine effect) and host mesenchymal cells (paracrine effect) suggesting the ability of GEPMC to engraft, differentiate, and stimulate bone growth. We suggest that our approach should lead to the designing of mesenchymal stem cell based gene therapy strategies for bone lesions as well as other tissues.
BACKGROUND: Human mesenchymal stem cells (hMSCs) are pluripotent cells that can differentiate to various mesenchymal cell types. Recently, a method to isolate hMSCs from bone marrow and expand them in culture was described. Here we report on the use of hMSCs as a platform for gene therapy aimed at bone lesions. METHODS: Bone marrow derived hMSCs were expanded in culture and infected with recombinant adenoviral vector encoding the osteogenic factor, human BMP-2. The osteogenic potential of genetically engineered hMSCs was assessed in vitro and in vivo. RESULTS: Genetically engineered hMSCs displayed enhanced proliferation and osteogenic differentiation in culture. In vivo, transplanted genetically engineered hMSCs were able to engraft and form bone and cartilage in ectopic sites, and regenerate bone defects (non-union fractures) in mice radius bone. Importantly, the same results were obtained with hMSCs isolated from a patient suffering from osteoporosis. CONCLUSIONS: hMSCs represent a novel platform for skeletal gene therapy and the present results suggest that they can be genetically engineered to express desired therapeutic proteins inducing specific differentiation pathways. Moreover, hMSCs obtained from osteoporotic patients can restore their osteogenic activity following human BMP-2 gene transduction, an important finding in the future planning of gene therapy treatment for osteoporosis.
Thymic lymphomas and hybridomas vary in their sensitivity to dexamethasone (DEX). Identical variance has been demonstrated in our laboratory for apoptosis of such cells by primary thymic epithelial cells or a cell line (TEC). We have also shown that apoptosis induced by TEC was partially mediated by TEC-derived glucocorticoids (GC). We studied the responses of various thymic lymphomas and hybridomas to TEC and DEX. Of these cells, PD1.6 and 2B4 were sensitive whereas B10 were relatively resistant to either inducer. In the present study we found that TEC and DEX synergize in inducing B10 cell apoptosis. B10 cells could also undergo apoptosis by TEC, conditional upon the presence of a TEC-sensitive cell (PD1.6 or 2B4). Contact between TEC and B10 was essential for apoptosis to occur. Thus, TEC may provide two signals, one mediated by GC and the other requiring cell to cell contact. We then analyzed the involvement of co-stimulatory or adhesion molecules in the TEC-induced apoptosis of thymic lymphoma cells. Soluble anti-CD44 antibodies but not anti-CD18, CD2 or CD28, inhibited TEC-induced apoptosis of PD1.6. Dimerization of CD44 by immobilized antibodies augmented DEX-induced apoptosis of all the lymphomas tested. CD44 cross-linkage up-regulated expression of the pro-apoptotic protein Bax, and down-regulated the anti-apoptotic protein, Bclx(L), in the presence of DEX. Taken together, the data suggest that CD44 enhances the apoptotic response of T lymphoma cells to DEX, and that CD44 modulates TEC-induced apoptosis of thymic lymphomas.