Quantitative assessment of apoptotic and proliferative gingival keratinocytes in oral and sulcular epithelium in patients with gingivitis and periodontitis

Jarnbring, Fredrik; Somogyi, E; Dalton, John R.; Gustafsson, Anders; Klinge, B.

doi:10.1034/j.1600-051x.2002.291203.x

Cited by 44 publications

(50 citation statements)

References 26 publications

(34 reference statements)

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“…Among other effectors of the apoptotic response, the products of p53 and Bcl-2 proteins have been shown to play fundamental roles (Handfield et al 2005;Mao et al 2007;Tonetti Cortellini and Lang 1998a;Vaux Cory and Adams 1988). Emerging evidence supports the concept that bacterium-modulated apoptosis is a relevant phenomenon in the pathogenesis of periodontal diseases (Arakawa et al 2000;Bantel et al 2005a;Chen and Zychlinsky 1994;Graves Jiang and Genco 2000;Jarnbring et al 2002;Kato et al 1995;Tonetti Cortellini and Lang 1998a;Tonetti Cortellini and Lang 1998b;Vitkov Krautgartner and Hannig 2005;Wang et al 1999).…”

Section: Apoptosismentioning

confidence: 83%

Beyond Good and Evil in the Oral Cavity: Insights into Host-Microbe Relationships Derived from Transcriptional Profiling of Gingival Cells

2008

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In many instances, the encounter between host and microbial cells can be, through a longstanding evolutionary association, a balanced interaction whereby both cell types co-exist and inflict a minimal degree of harm on each other. In the oral cavity, despite the presence of large numbers of diverse organisms, health is the most frequent status. Disease will only ensue when the host-microbe balance is disrupted on a cellular and molecular level. With the advent of microarrays, it is now possible to monitor the responses of host cells to bacterial challenge in a global scale. However, microarray data are known to be inherently noisy, which is caused in part by their great sensitivity. Hence, we will address a number of important general considerations required to maximize the significance of microarray analysis in order to faithfully depict relevant host-microbe interactions. Several advantages and limitations of microarray analysis that may directly impact the significance of array data are highlighted and discussed. Further, this review revisits and contextualizes recent transcriptional profiles that were originally generated to specifically study intricate cellular interactions between gingival cells and four important plaque microorganisms. This is, to our knowledge, the first report that systematically investigates the cellular responses of a cell line to challenge by 4 different microorganisms. Of particular relevance to the oral cavity, the model bacteria span the entire spectrum of documented pathogenic potential from commensal to opportunistic to overtly pathogenic. These studies provide a molecular basis of the complex and dynamic interaction between the oral microflora and its host, which may lead, in the long run, to the development of novel, rational and practical therapeutic, prophylactic and diagnostic applications.

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Section: Apoptosismentioning

confidence: 83%

Beyond Good and Evil in the Oral Cavity: Insights into Host-Microbe Relationships Derived from Transcriptional Profiling of Gingival Cells

2008

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“…Apoptosis is a highly regulated form of programmed cell death, defined by distinct morphological and biochemical features (Vaux and Strasser, 1996;Peter et al, 1997b). Abnormal apoptosis has been implicated in various pathologies, e.g., cancer, AIDS, Alzheimer's disease, rheumatoid arthritis (Thompson, 1995;Peter et al, 1997a;, periodontal diseases (Tonetti et al, 1998;Jarnbring et al, 2002;Bantel et al, 2005), and diabetes (Alikhani et al, 2005a;Graves et al, 2006). Apoptosis can be modulated by mediators of inflammation (Dalgleish and O'Byrne, 2006;Graves et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Apoptosis in Gingival Overgrowth Tissues

et al. 2007

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Variations in the balance between cell proliferation and apoptosis could contribute to the etiology of gingival overgrowth. The aim of this study was to test the hypothesis that, in fibrotic gingival lesions, fibroblast proliferation is stimulated and apoptosis is decreased. Apoptotic index, caspase 3 expression, the proliferative index, FOXO1 expression, and histological inflammation were measured in situ. Analysis of data showed that apoptosis decreased in all forms of gingival overgrowth examined (p < 0.05), and inflammation caused a small but significant increase compared with non-inflamed tissues (p < 0.05). The greatest decrease of apoptosis occurred in the most fibrotic tissues. Cell proliferation was elevated in all forms of gingival overgrowth tested, independent of inflammation (p < 0.05). To identify potential mechanisms of transcriptional regulation of apoptosis, we assessed FOXO1 and caspase 3 expression levels and found them to correlate well with diminished apoptosis. Analysis of data suggests that increased fibroblast proliferation and a simultaneous decrease in apoptosis contribute to gingival overgrowth.

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“…Another contributing factor for periodontal tissue destruction is reported to be the induction of host cell apoptosis by specific subgingival plaque pathogens (5). In gingival biopsies from patients with chronic periodontitis, apoptotic cells have been reported to constitute about 10% of the total cell population and included epithelial and fibroblast cells (31,36). Tonetti et al (86) have reported that exposure of clinically healthy gingival tissues to plaque bacteria induces apoptosis-associated DNA damage and the expression of proapoptotic p53 protein.…”

mentioning

confidence: 99%

“…Tonetti et al (86) have reported that exposure of clinically healthy gingival tissues to plaque bacteria induces apoptosis-associated DNA damage and the expression of proapoptotic p53 protein. Furthermore, in gingival biopsies from patients with periodontitis, epithelial cell apoptosis was reported to be more prevalent in the most apical part of the sulcus closest to the subgingival plaque (31,86). These observations suggest that interactions with certain bacterial products may play an important role in inducing apoptosis in gingival tissue cells.…”

mentioning

confidence: 99%

Porphyromonas gingivalisRgpA-Kgp Proteinase-Adhesin Complexes Penetrate Gingival Tissue and Induce Proinflammatory Cytokines or Apoptosis in a Concentration-Dependent Manner

et al. 2009

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The RgpA-Kgp proteinase-adhesin complexes of Porphyromonas gingivalis were observed, using immunostaining, in human gingival tissue associated with periodontitis but not in healthy tissue. The staining pattern suggested a concentration gradient from the subgingival plaque into the subjacent gingival connective tissue. Intense immunostaining was observed in areas displaying gross disturbance of tissue architecture. P. gingivalis cells and the RgpA-Kgp complexes at low concentrations were shown to stimulate secretory intercellular adhesion molecule 1, interleukin-8 (IL-8), IL-6, and macrophage chemoattractant protein secretion from cultured human epithelial (KB) and fibroblast (MRC-5) cells. However, at high concentrations a reduction in the level of these mediators was observed. In contrast, macrophage inflammatory protein 1␣ and IL-1␣ were stimulated only at high P. gingivalis cell concentrations. P. gingivalis cells and the RgpA-Kgp complexes were shown to induce apoptosis in KB and MRC-5 cells in a time-and dose-dependent manner. These data suggest that the RgpA-Kgp complexes penetrate the gingival connective tissue; at low concentrations distal from the plaque the complexes stimulate the secretion of proinflammatory mediators, while at high concentrations proximal to the plaque they induce apoptosis and attenuate the secretion of proinflammatory mediators.

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Quantitative assessment of apoptotic and proliferative gingival keratinocytes in oral and sulcular epithelium in patients with gingivitis and periodontitis

Cited by 44 publications

References 26 publications

Beyond Good and Evil in the Oral Cavity: Insights into Host-Microbe Relationships Derived from Transcriptional Profiling of Gingival Cells

Beyond Good and Evil in the Oral Cavity: Insights into Host-Microbe Relationships Derived from Transcriptional Profiling of Gingival Cells

Apoptosis in Gingival Overgrowth Tissues

Porphyromonas gingivalisRgpA-Kgp Proteinase-Adhesin Complexes Penetrate Gingival Tissue and Induce Proinflammatory Cytokines or Apoptosis in a Concentration-Dependent Manner

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