Association between plaque accumulation and Langerhans cell numbers in the oral epithelium of attached gingiva

Newcomb, G. M.; Seymour, G. J.; Powell, R. N.

doi:10.1111/j.1600-051x.1982.tb02096.x

Cited by 61 publications

(51 citation statements)

References 28 publications

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“…S8) and, thus, might directly interact with RANKL-expressing CD4 + T cells. Although the impact of infiltrating CD4 + T cells on gingival LCs is unknown, the welldocumented reduction in LC numbers during human periodontitis could be a result of an imbalance in CD40L/RANKL expression by local CD4 + T cells (45)(46)(47). Gingival DCs might also regulate the function of T cells accumulating in the tissue.…”

Section: Discussionmentioning

confidence: 99%

Langerhans cells down-regulate inflammation-driven alveolar bone loss

Arizon

Nudel

Segev

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Excessive bone resorption is frequently associated with chronic infections and inflammatory diseases. Whereas T cells were demonstrated to facilitate osteoclastogenesis in such diseases, the role of dendritic cells, the most potent activators of naive T cells, remains unclear. Using a model involving inflammation-driven alveolar bone loss attributable to infection, we showed that in vivo ablation of Langerhans cells (LCs) resulted in enhanced bone loss. An increased infiltration of B and T lymphocytes into the tissue surrounding the bone was observed in LC-ablated mice, including receptor activator of NF-κB ligand (RANKL)-expressing CD4 + T cells with known capabilities of altering bone homeostasis. In addition, the absence of LCs significantly reduced the numbers of CD4 + Foxp3 + T-regulatory cells in the tissue. Further investigation revealed that LCs were not directly involved in presenting antigens to T cells. Nevertheless, despite their low numbers in the tissue, the absence of LCs resulted in an elevated activation of CD4 + but not CD8 + T cells. This activation involved elevated production of IFN-γ but not IL-17 or IL-10 cytokines. Our data, thus, reveal a protective immunoregulatory role for LCs in inflammation-induced alveolar bone resorption, by inhibiting IFN-γ secretion and excessive activation of RANKL + CD4 + T cells with a capability of promoting osteoclastogenesis.

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Section: Discussionmentioning

confidence: 99%

Langerhans cells down-regulate inflammation-driven alveolar bone loss

Arizon

Nudel

Segev

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…We acknowledge that the term "follicle" might imply a proliferating B cell lymphoid organ and hence may be misleading, but nonetheless propose this terminology. We propose that the development of OLF is initiated in gingivitis by LCs homing to the gingival epithelium in response to bacteria/Ags in the oral biofilm (39), as well as a source of the earliest signals for lymphoid/ myeloid trafficking, i.e., epithelium/keratinocytes (40). That the CD1a ϩ cells enumerated in this study were in fact LCs was confirmed by scanning laser confocal microscopy and double immunofluorescence with CD1a and the LC-specific marker of Birbeck granules, LAG (41), as well as single immunoenzyme staining with langerin (Ref.…”

Section: Discussionmentioning

confidence: 99%

Mature Dendritic Cells Infiltrate the T Cell-Rich Region of Oral Mucosa in Chronic Periodontitis: In Situ, In Vivo, and In Vitro Studies

Jotwani

Palucka

Al-Quotub

et al. 2001

The Journal of Immunology

183

239

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Previous studies have analyzed the lymphoid and myeloid foci within the gingival mucosa in health and chronic periodontitis (CP); however, the principal APCs responsible for the formation and organizational structure of these foci in CP have not been defined. We show that in human CP tissues, CD1a+ immature Langerhans cells predominantly infiltrate the gingival epithelium, whereas CD83+ mature dendritic cells (DCs) specifically infiltrate the CD4+ lymphoid-rich lamina propria. In vivo evidence shows that exacerbation of CP results in increased levels of proinflammatory cytokines that mediate DC activation/maturation, but also of counterregulatory cytokines that may prevent a Th-polarized response. Consistently, in vitro-generated monocyte-derived DCs pulsed with Porphyromonas gingivalis strain 381 or its LPS undergo maturation, up-regulate accessory molecules, and release proinflammatory (IL-1β, PGE2) and Th (IL-10, IL-12) cytokines. Interestingly, the IL-10:IL-12 ratio elicited from P. gingivalis-pulsed DCs was 3-fold higher than that from Escherichia coli-pulsed DCs. This may account for the significantly (p < 0.05) lower proliferation of autologous CD4+ T cells and reduced release of IFN-γ elicited by P. gingivalis-pulsed DCs. Taken together, these findings suggest a previously unreported mechanism for the pathophysiology of CP, involving the activation and in situ maturation of DCs by the oral pathogen P. gingivalis, leading to release of counterregulatory cytokines and the formation of T cell-DC foci.

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“…1,22 Moreover, a large number of previous studies compared gingivitis and periodontitis. 2,4,6 In our understanding, this comparison is not correct because they are distinct periodontal diseases, with different inflammatory cells, cytokines, and pathogens. Moreover, in the majority of previous studies 4,23 , scaling and root planing and oral hygiene instructions were given only to the periodontitis patients, before tissue samples were removed, which would change the number of inflammatory cells.…”

Section: -21mentioning

confidence: 99%

“…2,4,6 In our understanding, this comparison is not correct because they are distinct periodontal diseases, with different inflammatory cells, cytokines, and pathogens. Moreover, in the majority of previous studies 4,23 , scaling and root planing and oral hygiene instructions were given only to the periodontitis patients, before tissue samples were removed, which would change the number of inflammatory cells. In this study, all inflammatory mononuclear plasma cells and lymphocytes were counted; thus, we can affirm that no changes in LC density were observed to be correlated with increased inflammation, which is in accordance with previous studies.…”

Section: -21mentioning

confidence: 99%

“…1 Experimental studies have shown differences in the number of LC among patients with gingivitis, periodontitis, and clinically healthy gingiva. 2,3 Although a larger number of cells was observed with increased inflammation, 4,5 a low quantitative difference was observed between gingivitis and periodontitis. 6 HIV infection is a modifier factor for periodontal disease, responsible for the depletion of CD4+ T lymphocytes, macrophages and LC.…”

Section: Introductionmentioning

confidence: 99%

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Langerhans cells in periodontal disease of HIV- and HIV+ patients undergoing highly active antiretroviral therapy

et al. 2011

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The aim of this study was to assess and compare quantitatively the presence of S100+ Langerhans cells (LC) by immunochemistry techniques in HIV+ and HIV- gingivitis and periodontitis subjects. Additionally, it aimed to evaluate the correlation among densities of these cells with CD4+ and CD8+ T cells, and viral load levels in HIV+ subjects, all using Highly Active Antiretroviral Therapy (HAART). The samples were allocated into four groups: 1) 15 subjects with moderate chronic periodontitis (MCP), HIV+; 2) 15 subjects with MCP, HIV-; 3) 10 subjects with gingivitis (G), HIV+; and 4) 10 subjects with G, HIV-. The S100+ cells were assessed in the pocket epithelium, gingival epithelium, and lamina propria. A statistically significant increase of total S100+ cells in HIV+ periodontitis subjects was observed in relation to HIV- periodontitis subjects. No increase of S100+ cells with increased inflammation was observed. No statistically significant correlation among S100+ cells and blood levels of CD4, CD8, and viral load was observed. In conclusion, the use of HAART can aid in achieving viral loads, and it is suggested that it may prevent the destruction of the LC

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Association between plaque accumulation and Langerhans cell numbers in the oral epithelium of attached gingiva

Cited by 61 publications

References 28 publications

Langerhans cells down-regulate inflammation-driven alveolar bone loss

Langerhans cells down-regulate inflammation-driven alveolar bone loss

Mature Dendritic Cells Infiltrate the T Cell-Rich Region of Oral Mucosa in Chronic Periodontitis: In Situ, In Vivo, and In Vitro Studies

Langerhans cells in periodontal disease of HIV- and HIV+ patients undergoing highly active antiretroviral therapy

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