Apoptosis in Chronic Adult Periodontitis Analyzed by <i>In Situ</i> DNA Breaks, Electron Microscopy, and Immunohistochemistry

Gamonal, Jorge; Bascones, A; Acevedo, Agustín; Blanco, E; Silva, A.

doi:10.1902/jop.2001.72.4.517

Cited by 106 publications

(111 citation statements)

References 49 publications

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“…FGFs and fibroblast growth factor receptors (FGFRs) are key players in the processes of fibroblast proliferation and differentiation of gingival tissues [36][37][38]. Bcl family members act as anti-or pro-apoptotic regulators, which are involved in a wide variety of cellular activities [39][40]. RANKL is a critical factor required in the processing of alveolar bone resorption [41].…”

Section: Discussionmentioning

confidence: 99%

Comparison of microRNA profiles of human periodontal diseased and healthy gingival tissues

et al. 2011

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MicroRNAs (miRNAs) have been demonstrated to play an important role in regulation of the immunoinflammatory response; however, the function of miRNAs in periodontal inflammation has not been investigated. The objective of this study was to explore the properties of miRNAs in periodontal inflammation by comparing miRNA profiles of inflamed and healthy gingival tissues. Gingival tissues were obtained from 10 periodontitis patients and 10 healthy subjects. After RNA extraction, miRNA profiles were analyzed by microarray, and expression levels of selected miRNAs were confirmed by real-time quantitative reverse transcription polymerase chain reaction (RT-PCR). Analyses using two computational methods, Targetscan and MicroRNA.org, were combined to identify common targets of these miRNAs. Finally, the individual miRNA expression levels of three toll-like receptor (TLR)-related miRNAs from inflamed and healthy gingival tissues were evaluated by RT-PCR. Ninety-one miRNAs were found to be upregulated and thirty-four downregulated over two-fold in inflamed gingival tissue compared with those in healthy gingival tissue. Twelve selected inflammatory-related miRNAs, hsa-miR-126*, hsa-miR-20a, hsa-miR-142-3p, hsa-miR-19a, hsa-let-7f, hsa-miR-203, hsa-miR-17, hsa-miR-223, hsa-miR-146b, hsa-miR-146a, hsa-miR-155, and hsa-miR-205 showed comparable expression levels by microarray and real-time quantitative RT-PCR analyses. In addition, the putative inflammation targets of these miRNAs were predicted, and three that were tested (hsa-miRNA-146a, hsa-miRNA-146b, and hsa-miRNA-155), showed significant differences between inflamed and healthy gingiva. This remarkable difference in miRNA profiles between periodontal diseased and healthy gingiva implicates a probable close relationship between miRNAs and periodontal inflammation. The data also suggest that the regulation of TLRs in periodontal inflammation may involve miRNA pathways.

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Section: Discussionmentioning

confidence: 99%

Comparison of microRNA profiles of human periodontal diseased and healthy gingival tissues

et al. 2011

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“…The loss of cells through infection-induced apoptosis is widely recognized as contributing to gastritis (21,32). A similar process may be important in periodontal disease, where it has been shown that apoptosis of fibroblasts is enhanced (12,24,26,34,40). It has also recently been reported that apoptosis of fibroblastic cells is associated with loss of attachment (11).…”

Section: Discussionmentioning

confidence: 99%

Immunization Enhances Inflammation and Tissue Destruction in Response toPorphyromonas gingivalis

et al. 2006

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It is well established that host-bacterium interactions play a critical role in the initiation and progression of periodontal diseases. By the use of inhibitors, it has been shown that mediators associated with the innate immune response significantly contribute to the disease process. Less is known regarding the role of the acquired immune response. To investigate mechanisms by which the acquired immune response to Porphyromonas gingivalis could affect connective tissue, we used a well-documented calvarial model to study hostbacterium interactions. Injection of P. gingivalis stimulated gamma interferon, interleukin 6, macrophage inflammatory protein 2, and monocyte chemoattractant protein 1 expression as determined by real-time PCR. Prior immunization against P. gingivalis significantly enhanced the mRNA levels of these cytokines and chemokines. Similarly, immunization significantly increased and prolonged the formation of a polymorphonuclear leukocyte and mononuclear cell infiltrate (P < 0.05). In addition, the area of connective tissue destruction, osteoclastogenesis, bone loss, mRNA expression of proapoptotic genes, and degree of fibroblast apoptosis were increased in immunized mice (P < 0.05). These results indicate that activation of the acquired immunity by P. gingivalis increases the inflammatory and destructive responses which occur in part through up-regulating the innate immune response and enhancing osteoclastogenesis and fibroblast apoptosis.

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“…Furthermore, there is evidence for the presence of apoptotic cells in periodontitis (19,34,51,57). Therefore, understanding the mechanisms of endothelial apoptosis induction in the periodontal pocket by P. gingivalis could provide new therapeutic targets of periodontitis and insights into the relationship between P. gingivalis and cardiovascular disease.…”

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confidence: 99%

Gingipains from Porphyromonas gingivalis W83 Synergistically Disrupt Endothelial Cell Adhesion and Can Induce Caspase-Independent Apoptosis

et al. 2006

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We have shown previously that gingipains from Porphyromonas gingivalis W83 can induce cell detachment, cell adhesion molecule (CAM) cleavage, and apoptosis in endothelial cells; however, the specific roles of the individual gingipains are unclear. Using purified gingipains, we determined that each of the gingipains can cleave CAMs to varying degrees with differing kinetics. Kgp and HRgpA work together to quickly detach endothelial cells. Interestingly, in the absence of active caspases, both gingipain-active W83 extracts and purified HRgpA and RgpB induce apoptotic morphology, suggesting that the gingipains can induce both caspase-dependent and caspase-independent apoptosis. Using z-VAD-FMK to inhibit Kgp activity and leupeptin to inhibit Rgp activity in gingipain-active W83 extracts, we investigated the relative significance of the synergistic role of the gingipains. z-VAD-FMK or leupeptin delayed, but did not inhibit, cell detachment induced by gingipain-active W83 extracts or purified gingipains. There was partial cleavage of N-cadherin and cleavage of VE-cadherin was not inhibited. Degradation of integrin ␤1 was inhibited only in the presence of z-VAD-FMK. These results further clarify the role P. gingivalis plays in tissue destruction occurring in the periodontal pocket.

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Apoptosis in Chronic Adult Periodontitis Analyzed by In Situ DNA Breaks, Electron Microscopy, and Immunohistochemistry

Cited by 106 publications

References 49 publications

Comparison of microRNA profiles of human periodontal diseased and healthy gingival tissues

Comparison of microRNA profiles of human periodontal diseased and healthy gingival tissues

Immunization Enhances Inflammation and Tissue Destruction in Response toPorphyromonas gingivalis

Gingipains from Porphyromonas gingivalis W83 Synergistically Disrupt Endothelial Cell Adhesion and Can Induce Caspase-Independent Apoptosis

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