Oral mucosal dendritic cells and periodontitis: many sides of the same coin with new twists

Cutler, Christopher W.; Teng, Y.-T.A.

doi:10.1111/j.1600-0757.2007.00222.x

Cited by 53 publications

(64 citation statements)

References 156 publications

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“…Osteoclasts are formed by fusion of precursor cells of the monocyte/macrophage lineage, 60 and CD11c ϩ DCs contribute to the pool of osteoclasts. 44,61 Beyond the direct effects of myeloid cell products on osteoprogenitors, Th17 cells have also been incriminated in the dynamics of bone resorption. 33,59 Potentially relevant is the up-regulation of IL-7R expression in macrophages and DCs by P. gingivalis in light of recent evidence that IL-7 enhances osteoclastogenesis and directly sensitizes T cells to release pro-osteoclastogenic factors including TNF-␣ and RANKL.…”

Section: Discussionmentioning

confidence: 99%

“…Most dramatic chemokine expression was a feature of DCs, likely the first line of defense in the oral epithelium and arbiters of mucosal immunity and tolerance. 44 Oral lymphoid-like follicles containing CD4 ϩ , CD45RA ϩ , and CD45RO ϩ T cells in close proximity to immobilized mature CD83 ϩ DCs and B-cells situated within the gingival lamina 10 may represent an overzealous DC-dependent T-cell response. In particular, elevated levels of CCL20, observed in P. gingivalis LPSstimulated myeloid cells and in inflamed periodontal tissues, 45 through its ability to attract CCR6 ϩ memory T cells, especially Th17 populations 46 and immature DCs, may continue to refuel the inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

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Rapid Myeloid Cell Transcriptional and Proteomic Responses to Periodontopathogenic Porphyromonas gingivalis

Nares

Moutsopoulos

Angelov

et al. 2009

The American Journal of Pathology

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Long-lived monocytes, macrophages, and dendritic cells (DCs) are Toll-like receptor-expressing, antigenpresenting cells derived from a common myeloid lineage that play key roles in innate and adaptive immune responses. Based on immunohistochemical and molecular analyses of inflamed tissues from patients with chronic destructive periodontal disease, these cells, found in the inflammatory infiltrate, may drive the progressive periodontal pathogenesis. To investigate early transcriptional signatures and subsequent proteomic responses to the periodontal pathogen, Porphyromonas gingivalis, donor-matched human blood monocytes, differentiated DCs, and macrophages were exposed to P. gingivalis lipopolysaccharide (LPS) and gene expression levels were measured by oligonucleotide microarrays. In addition to striking differences in constitutive transcriptional profiles between these myeloid populations, we identify a P. gingivalis LPS-inducible convergent, transcriptional core response of more than 400 annotated genes/ESTs among these populations, reflected by a shared, but quantitatively distinct, proteomic response. Nonetheless, clear differences emerged between the monocytes, DCs, and macrophages. The finding that long-lived myeloid inflammatory cells, particularly DCs, rapidly and aggressively respond to P. gingivalis LPS by generating chemokines, proteases, and cytokines capable of driving T-helper cell lineage polarization without evidence of corresponding immunosuppressive pathways highlights their prominent role in host defense and progressive tissue pathogenesis. The shared, unique, and/or complementary transcriptional and proteomic profiles may frame the context of the host response to P. gingivalis, contributing to the destructive nature of periodontal inflammation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Rapid Myeloid Cell Transcriptional and Proteomic Responses to Periodontopathogenic Porphyromonas gingivalis

Nares

Moutsopoulos

Angelov

et al. 2009

The American Journal of Pathology

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“…DCs play an essential role in resistance to infection by their ability to present bacterial antigen to lymphocytes, initiating the adaptive immune response (Cutler and Teng 2007;Hovav 2014). The interactions between DCs and other cells of the innate and adaptive immune responses are thought to be important in the pathogenesis of periodontal disease (Arizon et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Effect of Aging on Periodontal Inflammation, Microbial Colonization, and Disease Susceptibility

Dong

Xiao

et al. 2016

J Dent Res

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Periodontitis is a chronic inflammatory disease induced by a biofilm that forms on the tooth surface. Increased periodontal disease is associated with aging. We investigated the effect of aging on challenge by oral pathogens, examining the host response, colonization, and osteoclast numbers in aged versus young mice. We also compared the results with mice with lineage-specific deletion of the transcription factor FOXO1, which reduces dendritic cell (DC) function. Periodontitis was induced by oral inoculation of Porphyromonas gingivalis and Fusobacterium nucleatum in young (4 to 5 mo) and aged (14 to 15 mo) mice. Aged mice as well as mice with reduced DC function had decreased numbers of DCs in lymph nodes, indicative of a diminished host response. In vitro studies suggest that reduced DC numbers in lymph nodes of aged mice may involve the effect of advanced glycation end products on DC migration. Surprisingly, aged mice but not mice with genetically altered DC function had greater production of antibody to P. gingivalis, greater IL-12 expression, and more plasma cells in lymph nodes following oral inoculation as compared with young mice. The greater adaptive immune response in aged versus young mice was linked to enhanced levels of P. gingivalis and reduced bacterial diversity. Thus, reduced bacterial diversity in aged mice may contribute to increased P. gingivalis colonization following inoculation and increased periodontal disease susceptibility, reflected by higher TNF levels and osteoclast numbers in the periodontium of aged versus young mice.

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“…DCs are known for their role of antigen presenting cells (APCs) and do not appear to play a role in bone homeostasis in non-pathological conditions, but some data suggest that DC could act as OC precursors in an inflammatory milieu, transforming into DC-derived-OC according to phenotypic and functional characterization studies. Moreover, DCs modulate T cell activity through RANK/RANKL pathway and other cytokines associated with osteoclastogenesis [50][51][52] . There is a lack of definitive evidence about the physiological relevance of this phenomenon in vivo but DCs could act as an osteo-immune interface, contributing to bone loss in inflammatory diseases.…”

Section: Inflammation and Bone Lossmentioning

confidence: 99%

Interactions between the immune system and bone

Fornelli¹,

Roato²,

Isaia³

2011

WJO

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Oral mucosal dendritic cells and periodontitis: many sides of the same coin with new twists

Cited by 53 publications

References 156 publications

Rapid Myeloid Cell Transcriptional and Proteomic Responses to Periodontopathogenic Porphyromonas gingivalis

Rapid Myeloid Cell Transcriptional and Proteomic Responses to Periodontopathogenic Porphyromonas gingivalis

Effect of Aging on Periodontal Inflammation, Microbial Colonization, and Disease Susceptibility

Interactions between the immune system and bone

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