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Biomedical subjects

D Gazit

Publications and source records attributed to D Gazit.

63 records · Page 4Linked to original sources
PubMed1985

Calcification of non-collagenous matrix in human gingiva: a light and electron microscopic study.

Tissue samples obtained from human gingiva with soft tissue calcification were processed for light and transmission electron microscopy. The stroma in these specimens revealed numerous foci of calcification in a matrix that consisted of closely packed branching microfibrils, 12 nm in diameter and a maximum of 2.5 micron in length. Calcospherites, 0.25-1.11 micron in diameter, were present within the matrix. They were constructed of needle-like units shown by high resolution electron microscopy and energy dispersive X-ray microanalysis to be apatite. Larger calcified masses were composed of calcospherites which were fused together. Matrix vesicles or other forms of membraneous material could not be found. The relationship between the mineral and non-collagenous microfibrils may suggest a role for the latter in the onset of calcification in this ectopic site.

Amelogenesis Imperfecta↗
PubMed1984

A study of a sample of oral cancer in Israel.

A review of data on oral cancer in Israel revealed a lower incidence and a later onset age than in other countries. These data are reviewed and consideration is given to the high prevalence of smoking and the low incidence of alcoholism in Israel.

Adolescent↗
PubMed1982

Correlative clinico-pathological evaluation of oral premalignancy.

In 1972, the World Health Organization's "Meeting of Investigators on the Histological Definitions in Precancerous Lesions" defined a precancerous lesion as a "morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counter part" (Pindborg 1980). There are two generally accepted precancerous lesions in the oral cavity, leukoplakia and erythroplakia (Pindborg 1980). Leukoplakia is currently defined as "a white patch or plaque that cannot be characterized clinically or pathologically as any other disease" (WHO 1978). This definition has no histological connotation and is used in a strictly clinical sense (Pindborg 1980, Banoczy 1977). Erythroplakia is defined as a "bright red velvety plaque which cannot be characterized clinically or pathologically as being due to any other condition" (Pindborg 1980).

Diagnosis, Differential↗
PubMedDate not supplied

Engineered pluripotent mesenchymal cells integrate and differentiate in regenerating bone: a novel cell-mediated gene therapy.

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.

Animals↗
PubMedDate not supplied

Engineered human mesenchymal stem cells: a novel platform for skeletal cell mediated gene therapy.

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.

Adenoviridae↗
PubMedDate not supplied

Successful high-dose calcium treatment of aluminum-induced metabolic bone disease in long-term home parenteral nutrition.

A patient who developed severe metabolic bone disease is presented. He had received long-term home parenteral nutrition (HPN) following extensive small bowel resection after mesenteric vein thrombosis. Bone disease caused by aluminum intoxication had components of osteomalacia and low-turnover osteoporosis. Aluminum was detected at the surface of mineralized bone and was elevated in the serum, resulting in a positive deferoxamine infusion test. One year of treatment with high doses of calcium (up to 24 mEq per day) significantly diminished the patient's bone pain, increased the serum levels of calcium, abolished aluminum deposits in the mineralized trabecula, improved bone formation, and increased trabecular bone volume as assessed by repeated histomorphometric analysis.

Aluminum↗