Mast cells – a role in periodontal diseases?

Steinsvoll, Svein; Helgeland, Kristen; Schenck, Karl

doi:10.1111/j.1600-051x.2004.00516.x

Cited by 57 publications

(62 citation statements)

References 65 publications

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“…We found mast cells to be more numerous in regions of active inflammation as seen in other studies done by Rodini DOC et al (2004), 17 Montes LC et al (2004), 8 Smith et al (1989), 13 Steinsvoll S et al (2004), 10 Günhan M et al (1991) 18 and…”

Section: Evaluation Of Association Of Mast Cells With Lymphocytes Andsupporting

confidence: 75%

“…8,13,20 Mast cell derived tryptase can activate matrix metalloproteinases which help in extracellular matrix degradation and bone resorption. 8,10 These findings suggest that one of the main activities of the mast cells in periapical lesions is related to bone destruction for enlargement of the lesions. The hydrostatic pressure of the luminal fluid is important in cyst enlargement and mast cell activity might contribute to this by increasing the osmotic pressure in at least three ways:…”

Section: Role Of Mast Cells In Degradation Of Extracellular Matrix Anmentioning

confidence: 75%

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A Quantitative Analysis of Mast Cells in Inflammatory Periapical and Gingival Lesions

Sheethal¹,

Uma²,

Rao

et al. 2014

The Journal of Contemporary Dental Practice

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Aim:The aim of the study was to quantify the presence of mast cells in various inflammatory lesions like periapical granuloma, periapical cyst, inflammatory gingival hyperplasia and pyogenic granuloma. Mast cell degranulation and association with lymphocytes were also recorded in an attempt to understand the role of mast cells in the pathogenesis of these inflammatory lesions. Materials and methods:The quantification of mast cells was done on toluidine blue stained sections of all the four groups of lesions, using the image analyzer software, Image-Pro-Express (Media Cybernetics, USA).Results: An increased number of mast cells in various inflammatory lesions with a significant difference between the four groups were noted. Mast cell number tended to be greater in the lesions present in the anterior region of the mouth than in the posterior region of the oral cavity. The mean mast cell number decreased with the increasing age which was directly correlated with the age of the patients. Mast cell site, distribution, degranulation and its association with fibroblasts, lymphocytes and blood vessels were noted. Conclusion:The location of mast cells in different areas, their association with lymphocytes, fibroblasts, endothelial cells, and the phenomenon of degranulation helps to appreciate the release of various mediators and multiple interactions among these cells, leading to increased vascular permeability, angiogenic response, collagen synthesis, regulation of inflammation, bone resorption, and extracellular matrix destruction, thus contributing to the pathogenesis of these inflammatory lesions.

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Section: Evaluation Of Association Of Mast Cells With Lymphocytes Andsupporting

confidence: 75%

Section: Role Of Mast Cells In Degradation Of Extracellular Matrix Anmentioning

confidence: 75%

A Quantitative Analysis of Mast Cells in Inflammatory Periapical and Gingival Lesions

Sheethal¹,

Uma²,

Rao

et al. 2014

The Journal of Contemporary Dental Practice

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“…Periodontal diseases are initiated by bacterial plaque on tooth surfaces, inducing inflammation in gingival and periodontal tissues. An increase in T suppressor cells has been reported in the gingival tissues during periodontitis, and a direct correlation between the histamine level in gingival tissue and the degree of periodontal disease has been demonstrated (36). It has also been hypothesized that increased immune function is produced by blocking the effects of histamine on H2 receptors and that H2 receptor antagonists may reduce inflammation by inhibiting the formation of reactive oxygen inflammatory products.…”

Section: Discussionmentioning

confidence: 94%

Topical H2 Antagonist Prevents Periodontitis in a Rabbit Model

et al. 2006

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Cimetidine is a powerful H2 receptor antagonist that eliminates histamine's effects on chemotaxis, phagocytosis, and superoxide anion production by phagocytes. The purpose of this study was to analyze the clinical and histopathological changes associated with experimental periodontitis in rabbits in response to topically applied cimetidine. Experimental periodontitis was induced in 21 New Zealand White rabbits using Porphyromonas gingivalis (10 9 CFU) topically applied three times a week for a 6-week period to previously ligatured teeth. Topical application of cimetidine in a liposome carrier for the prevention of periodontitis was evaluated in four groups of four animals each: 1, 10, and 100 mg/ml and no treatment (positive control). In addition, there was a vehicle group (n ‫؍‬ 3) that received liposome preparation (carrier) only, and two animals with ligature application alone served as negative controls. Periodontal disease was quantified by direct visualization and radiographical evaluation of bone loss on defleshed skulls and by histological analyses of sections stained with hematoxylin-eosin and tartrate-resistant acid phosphatase. In the no-treatment (positive control) and liposome (vehicle) groups, direct visualization and radiological measurements revealed statistically significant bone loss compared to the negative control. Application of cimetidine at all concentrations tested inhibited inflammation and bone loss by >90%. Histological findings revealed that ligated sites of the positive control and vehicle groups showed significant reduction in bone level (P < 0.05) compared to the three cimetidine groups, with a marked decrease in inflammation. The findings of this study provide morphological and histological evidence that topically active cimetidine is a potent inhibitor of P. gingivalis-elicited periodontal inflammation, arresting and/or preventing tissue destruction and influencing cell populations present in the inflammatory cell infiltrate.

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“…Nonetheless, the basal PGE 2 production of these cells may still contribute to enhanced total PGE 2 production through an additive effect, because an increased number of mast cells has been reported in inflamed gingival tissue, compared with healthy gingival tissue. 64,65 To our knowledge, there are a very limited number of studies investigating the expression of PGE 2 -synthesizing enzymes or PGE 2 production in mast cells; however, COX-2 expression and PGE 2 production are increased by antigen stimulation and by the phospholipase A 2 activator melittin, respectively. 66,67 In addition to the PGE 2 -synthesizing enzymes, the cytokine IL-1␤, apparently localized to CD45 ϩ cells, was positively stained in the gingival tissue biopsies of patients with periodontitis.…”

Section: Discussionmentioning

confidence: 99%

Expression of Prostaglandin E Synthases in Periodontitis

Båge

Kats

Lopez

et al. 2011

The American Journal of Pathology

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The inflammatory mediator prostaglandin E 2 (PGE 2 ) is implicated in the pathogenesis of chronic inflammatory diseases including periodontitis; it is synthesized by cyclooxygenases (COX) and the prostaglandin E synthases mPGES-1, mPGES-2, and cPGES. The distribution of PGES in gingival tissue of patients with periodontitis and the contribution of these enzymes to inflammationinduced PGE 2 synthesis in different cell types was investigated. In gingival biopsies, positive staining for PGES was observed in fibroblasts and endothelial, smooth muscle, epithelial, and immune cells. To further explore the contribution of PGES to inflammation-induced PGE 2 production, in vitro cell culture experiments were performed using fibroblasts and endothelial, smooth muscle, and mast cells. All cell types expressed PGES and COX-2, resulting in basal levels of PGE 2 synthesis. In response to tumor necrosis factor (TNF-␣), IL-1␤, and cocultured lymphocytes, however, mPGES-1 and COX-2 protein expression increased in fibroblasts and smooth muscle cells, accompanied by increased PGE 2 , whereas mPGES-2 and cPGES were unaffected. In endothelial cells, TNF-␣ increased PGE 2 production only via COX-2 expression, whereas in mast cells the cytokines did not affect PGE 2 enzyme expression or PGE 2 production. Furthermore, PGE 2 production was diminished in gingival fibroblasts derived from mPGES-1 knockout mice, compared with wild-type fibroblasts. These results suggest that fibroblasts and smooth muscle cells are important sources of mPGES-1, which may contribute to increased PGE 2 production in the inflammatory condition periodontitis.

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Mast cells – a role in periodontal diseases?

Abstract: We certainly feel that this is a key cell in inflamed periodontal tissue and its role in periodontitis needs to be revisited.

Cited by 57 publications

References 65 publications

A Quantitative Analysis of Mast Cells in Inflammatory Periapical and Gingival Lesions

A Quantitative Analysis of Mast Cells in Inflammatory Periapical and Gingival Lesions

Topical H2 Antagonist Prevents Periodontitis in a Rabbit Model

Expression of Prostaglandin E Synthases in Periodontitis

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