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Glucose-mediated Alteration of Cellular Function in Human Periodontal Ligament Cells

Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700, Japan

V. Terranova

Laboratory of Tumor Biology and Connective Tissue Research, Columbia University School of Dental and Oral Surgery, 630 W. 168th Street, New York, New York 10032, (current adress) Edward Hines Jr. Hospital, 151 Research Service, Hine, Illinois 60141

H. Foo

Laboratory of Tumor Biology and Connective Tissue Research, Columbia University School of Dental and Oral Surgery, 630 W. 168th Street, New York, New York 10032

M. Kurihara

Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700, Japan

H. Kurihara

Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700, Japan

Y. Murayama

Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700, Japan, to whom correspondence and reprint requests should be addressed

Because diabetic patients are easily led to manifest severe periodontitis, we wanted to determine whether various glucose levels interfere with normal cellular function. Human periodontal ligament (PDL) cells were cultured in glucose-free medium, or in medium containing either 1100 mg/L of glucose (normal-glucose medium) or 4500 mg/L of glucose (high-glucose medium). Cells cultured in glucose-free medium changed their morphology from spindle-shaped to round, and incorporated trypan blue in a time-dependent manner. The incorporation rate was much faster in cells with shorter cell cycles than in those with longer cycles, suggesting the involvement of cell-cycle progression in cell death. However, fragmented DNA, which suggests apoptotic cell death, was not observed in these cells. We reasoned that initial cell rounding and detachment from the culture plate might be due to the conformational changes in cell-surface receptors to fibronectin, a major extracellular matrix for fibroblasts. Western blot analysis revealed that cells cultured in glucose-free medium lost their fibronectin receptor in a time-dependent manner. In addition, fibronectin receptor expression was much higher in cells cultured in high-glucose medium than in cells cultured in normal-glucose medium. Furthermore, the over-expression of the fibronectin receptor resulted in a suppressed chemotactic response of these cells to platelet-derived growth factor. On the basis of these data, it was hypothesized that a high glucose level induced over-expression of these receptors. This might be the mechanism by which a high glucose level compromises wound healing in diabetic patients and, at least in part, might be the reason diabetic patients are subject to severe periodontal destruction.

Key Words: glucose • periodontal ligament cells • cell death • fibronectin receptor • chemotaxis.

Journal of Dental Research, Vol. 75, No. 9, 1664-1671 (1996)
DOI: 10.1177/00220345960750090801


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