Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.650394
Title: The role of B cells in periodontitis
Author: Oliver-Bell, Jessica
ISNI:       0000 0004 5356 7131
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 2015
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Abstract:
Introduction: Varying degrees of periodontal disease affect the majority of the population. Severe forms of periodontitis have a considerable impact on oral health and quality of life. Periodontitis results from imbalances in the oral microbiome and the host immune response. The mainstay of periodontal treatment – removal of dental plaque – is only partially successful. B cells infiltrate the gingiva of periodontitis patients, but their role in pathology has not been well characterised. The overarching aim of this research was to better characterise the role of B cells in periodontitis. Periodontitis shares similarities in risk factors and aspects of immunopathology with rheumatoid arthritis. Epidemiological evidence suggests patients with rheumatoid arthritis are more likely to have periodontitis, which cannot be completely explained by shared risk factors. This has led to the hypothesis that the two diseases are immunologically linked, and that periodontitis may precede, and cause, rheumatoid arthritis. A further objective of this research was to investigate whether the autoimmunity characteristic of rheumatoid arthritis emerges in periodontitis. Results: B cell infiltrate in the gingiva of periodontitis patients was confirmed. Periodontitis patients were found to have elevated serum titers of anti-citrullinated peptide antibodies which were generally below the diagnostic threshold for rheumatoid arthritis, and were reduced following non-surgical periodontal treatment. In a murine model of periodontitis, subtle changes to B cell phenotype were observed in tissues regional to the oral cavity in mice with periodontitis, at an early stage of disease. Such changes included increased B cell expression of receptor activator of NfκB ligand in the gingiva, and increased proportions of GC B cells in the draining lymph nodes. Some of these trends were enhanced in mice with periodontitis exacerbated by interleukin-33 treatment. B cell-deficient mice were protected from the alveolar bone loss normally induced in the model of periodontitis. Conclusion: B cells form a substantial proportion of the inflammatory infiltrate in the gingiva of periodontitis patients. Treatment of periodontitis can reduce titers of anti-citrullinated peptide antibodies in patients, potentially reducing their risk of developing rheumatoid arthritis. Evidence from B cell-deficient mice suggests that B cells contribute to pathological alveolar bone loss. Therefore, B cells may be worthy of targeting therapeutically in periodontitis.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.650394  DOI: Not available
Keywords: Q Science (General) ; QR Microbiology ; QR180 Immunology
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