4.1 Article

Memory B Cell as an Indicator of Peri-implantitis Status: A Pilot Study

出版社

QUINTESSENCE PUBLISHING CO INC
DOI: 10.11607/jomi.8641

关键词

B lymphocyte; host response; peri-implantitis

资金

  1. National Natural Science Foundation of China [81970975, 81400550, 81600914, 81901055]
  2. Fundamental Research Funds for the Central Universities [19ykpy81]
  3. Guangdong Provincial Natural Science Foundation [2017A030310207]
  4. Guangdong Financial Fund for High-Caliber Hospital Construction [174-2018-XMZC-000103-0125/D-10]
  5. Guangdong Basic and Applied Basic Research Foundation [2019A1515110854]

向作者/读者索取更多资源

Memory B cells were significantly activated in peri-implantitis and responded to the suprastructure removal treatment. The lack of gingiva-resident memory B cells in the clinically healed implants serves as a hint for the weakness of peri-implant tissue against bacterial plaque.
Purpose: Gingiva-resident memory B cells found recently in healthy periodontal tissue may play important roles in maintaining homeostasis against bacterial plaque. Whether resident memory B cells exist in healthy peri-implant tissue and how they respond in peri-implantitis lesions are of interest. The aim of this study was to preliminarily investigate whether memory B cell activities are related to inflamed or healthy peri-implant status. Materials and Methods: Patients with peri-implantitis or healed implants were recruited. The gingiva samples were collected and divided into inflamed (n = 4), treated (n = 4), and healed (n = 3) groups, followed by a flow cytometry analysis staining with CD3, CD19, CD27, CD38, and RANKL. The biopsy samples were also cryo-embedded for immunofluorescent double staining of CD19 and CD27. Results: CD27(+) CD38(+) ASC comprised 83.3% +/- 3.3% of the total B cells in the inflamed group, and this proportion in the treated group was reduced to 44.5% +/- 13.4%. The proportion of CD27(+) CD3(+) T cells was found to be unchanged between the inflamed and treated groups. Immunofluorescent staining indicated that CD19(+) CD27(+) population infiltrated peri-implant connective tissue. RANKL was expressed by almost all B cells and a portion of T cells in the inflamed group, while the proportions of RANKL(+) B and T cells were significantly reduced in the treated group. Barely any memory B cells were detected in the healed group. Conclusion: Memory B cells were markedly activated in peri-implantitis and responded to the suprastructure removal treatment. The lack of gingiva-resident memory B cells in the clinically healed implants serves as a hint for the weakness of peri-implant tissue against bacterial plaque.

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