L Ren

Advanced glycation end products inhibit the expression of collagens type I and III by human gingival fibroblasts.

BACKGROUND It is evident that diabetes and periodontal disease are closely interrelated. Accumulation of advanced glycation end products (AGEs), coupled with exaggerated host responses to bacterial infection, may account for the increased periodontal destruction observed in patients with uncontrolled diabetes. The present study investigated the effects of AGEs on the viability of human gingival fibroblasts (HGFs) and the expression of types I and III collagen in HGFs. METHODS The cell viability of HGFs was examined by methylthiazolet-etrazolium assay, whereas the expression of types I and III collagen message and protein was detected by real-time quantitative reverse transcription-polymerase chain reaction and sandwich enzyme-linked immunosorbent assay, respectively. RESULTS AGEs significantly suppressed the cell viability of HGFs from 24 to 72 hours (P <0.01). A high concentration of glucose (25 mmol/l) in the culture media exaggerated the inhibition of the survival rate of HGFs (P <0.01). The expression of collagen types I and III messages and proteins was significantly downregulated at 72 hours by AGEs in a concentration-dependent manner (P <0.05). Moreover, the synthesis of intracellular types I and III collagen protein was markedly inhibited by AGEs (P <0.05). CONCLUSIONS AGEs may suppress the cell viability of HGFs and downregulate the expression of types I and III collagen by the cells. Further investigations are warranted to clarify the molecular mechanisms of AGEs in the regulation of cell function and collagen metabolism in patients with diabetes and periodontitis.

The interplay of lipopolysaccharide‐binding protein and cytokines in periodontal health and disease

AIM Periodontal pathogenesis is characterized by Gram-negative bacteria activation of series of pro- and anti-inflammatory cytokines from host cells through the pathway of lipopolysaccharide (LPS), LPS-binding protein (LBP) and CD14. The present study investigated the expression profiles of interleukin (IL)-1beta and IL-10 in periodontal health and disease, and examined the effects of Escherichia coli LPS and LBP interaction on the expression of IL-1beta and IL-10 by human gingival fibroblasts (HGF). MATERIAL AND METHODS Gingival biopsies were collected from 44 subjects with chronic periodontitis and 15 periodontally healthy subjects. The expression of IL-1beta and IL-10 was detected by immunohistochemistry. The mRNA expression of IL-1beta and IL-10 in HGF was detected by RT-PCR with or without recombinant human LBP (rhLBP), while the peptides were analysed by an enzyme-linked immunosorbent assay. RESULTS IL-1beta was detected in both oral sulcular epithelia of healthy controls and periodontal pocket epithelia of patients. IL-10 was mainly expressed in the intercellular spaces of connective tissues. IL-1beta displayed a reverse pattern of expression levels with reference to IL-10, and a negative correlation existed between LBP and the ratio of IL-1beta/IL-10. rhLBP suppressed E. coli LPS-induced IL-1beta expression by HGF. CONCLUSION An appropriate interplay of LBP and cytokines may have a beneficial effect on innate host defence, thereby contributing to periodontal homeostasis.