Response to Comment on “The B Cell–Stimulatory Cytokines BLyS and APRIL Are Elevated in Human Periodontitis and Are Required for B Cell–Dependent Bone Loss in Experimental Murine Periodontitis”

Hajishengallis, George; Korostoff, Jonathan

doi:10.4049/jimmunol.1502066

Cited by 2 publications

(1 citation statement)

References 10 publications

(2 reference statements)

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“…Our data here show that treatment with RvD2 prevented bone loss around infected implants. This finding could be explained by its ability to reduce the accumulation of neutrophils and B cells, both of which are known to have an important role in the pathogenesis of periodontitis (Hajishengallis & Korostoff, 2015 ; Hajishengallis et al, 2016 ). Furthermore, RvD2 treatment reduced the frequency of gingival lymphocytes, RANKL‐expressing CD4 + cells, pDCs, and migratory DC in the LNs and decreased the basal secretion of IFN‐γ from splenocytes.…”

Section: Discussionmentioning

confidence: 99%

Excessive inflammatory response to infection in experimental peri‐implantitis: Resolution by Resolvin D2

Heyman

Horev

Mizraji

et al. 2022

J Clinic Periodontology

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Aim The aetiology and pathogenesis of peri‐implantitis are currently under active research. This study aimed to dissect the pathogenesis of murine experimental peri‐implantitis and assess Resolvin D2 (RvD2) as a new treatment modality. Materials and Methods Four weeks following titanium implant insertion, mice were infected with Porphyromonas gingivalis using single or multiple oral lavages. RvD2 was administrated following infection, and tissues were analysed using flow cytometry, quantitative RT‐PCR, taxonomic profiling, and micro‐computed tomography. Results Repeated infections with Pg resulted in microbial dysbiosis and a higher influx of innate and adaptive leukocytes to the peri‐implant mucosa (PIM) than to gingiva surrounding the teeth. This was accompanied by increased expression levels of IFN‐α, IL‐1β, and RANKL\OPG ratio. Interestingly, whereas repetitive infections resulted in bone loss around implants and teeth, a single infection induced bone loss only around implants, suggesting a higher susceptibility of the implants to infection. Treatment with RvD2 prevented Pg‐driven bone loss and reduced leukocyte infiltration to the PIM. Conclusions Murine dental implants are associated with dysregulated local immunity and increase susceptibility to pathogen‐induced peri‐implantitis. However, the disease can be prevented by RvD2 treatment, highlighting the promising therapeutic potential of this treatment modality.

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Section: Discussionmentioning

confidence: 99%

Excessive inflammatory response to infection in experimental peri‐implantitis: Resolution by Resolvin D2

Heyman

Horev

Mizraji

et al. 2022

J Clinic Periodontology

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The emerging roles of B cells as partners and targets in periodontitis

Zouali

2016

Autoimmunity

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Initial studies of periodontal disease suggested that T cell-mediated immunity against oral Gram-negative microorganisms is a key player in the pathogenesis of this inflammatory disease. Recent investigations, however, revealed that B cells are also engaged. Given their chief role in innate-like and adaptive immune responses, B cells could exert protective functions in periodontitis. However, the periodontal bacteria-specific antibody response is generally unable to halt disease progression in affected subjects, suggesting that the antibodies produced could exhibit low anti-bacterial blocking functions or opsonophagocytic potential, and/or unfavorable effects. Moreover, although microbial antigens are involved in the induction of the inflammatory responses in human adult periodontitis, endogenous antigens also may contribute to the chronicity of this common disease. Not only antibodies to self-antigens, such as collagen, are locally produced, but the autoreactivities observed in aggressive periodontitis are more severe and diverse than those observed in chronic periodontitis, suggesting that autoimmune reactivity could play a role in the tissue destruction of periodontal disease. Further support for a pathological role of B cells in periodontitis comes from the finding that B cell-deficient mice are protected from bacterial infection-induced alveolar bone loss. Studies in patients indicate that B cells and plasma cells, together with osteoclastogenic factors (RANKL and osteoprotegerin) and specific cytokines involved in their growth and differentiation (BAFF and APRIL) participate in the induction of the pathological bone loss in periodontitis. This novel insight suggests that selective targeting of B cells could represent a future therapeutic avenue for severe periodontal disease.

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Response to Comment on “The B Cell–Stimulatory Cytokines BLyS and APRIL Are Elevated in Human Periodontitis and Are Required for B Cell–Dependent Bone Loss in Experimental Murine Periodontitis”

Cited by 2 publications

References 10 publications

Excessive inflammatory response to infection in experimental peri‐implantitis: Resolution by Resolvin D2

Excessive inflammatory response to infection in experimental peri‐implantitis: Resolution by Resolvin D2

The emerging roles of B cells as partners and targets in periodontitis

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