The Association Between Thalassemia Major and Periodontal Health

• Aliye Akcalı ^[1] ; Selda Kahraman Çenel ^[3] ; Pınar Gümüş ^[1] ; Nurcan Buduneli ^[1] ; David F. Lappin ^[2] ; Özgün Özçaka ^[1]
  1. [1] Ege University

     Ege University

     Turquía

     
  2. [2] University of Glasgow

     University of Glasgow

     Reino Unido

     
  3. [3] Department of Haematology, School of Medicine, Aydın Government Hospital, Aydın, Turkey.

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• Localización: Journal of periodontology, ISSN 0022-3492, Vol. 86, Nº. 9, 2015, págs. 1047-1057
• Idioma: inglés
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  • Background: The aim of this cross-sectional study is to compare the local and systemic levels of soluble receptor activator of nuclear factor-κB ligand (sRANKL), osteoprotegerin (OPG), a proliferation-inducing ligand (APRIL), B-cell activating factor (BAFF), interleukin (IL)-6, and IL-8 in biofluids of patients with thalassemia major (TM) with or without gingivitis.

    Methods: Seventy-seven patients are included in this study (TM, n = 29; systemically healthy, n = 48). Gingival crevicular fluid (GCF), saliva, and serum levels of IL-6, IL-8, sRANKL, OPG, BAFF, and APRIL were determined by enzyme-linked immunosorbent assay. Data were analyzed by appropriate non-parametric or parametric statistical tests.

    Results: Median GCF, serum, and saliva levels for BAFF (P <0.001) and IL-6 and IL-8 (P <0.005) were higher in TM gingivitis than in systemically healthy gingivitis (P <0.001). GCF, serum, and saliva levels for APRIL, sRANKL, IL-6, and IL-8 were higher in TM than in systemically and periodontally healthy comparison groups (P <0.05). Positive correlations were found between bleeding on probing (BOP), plaque index (PI) scores, and GCF APRIL, serum sRANKL, serum OPG, and sRANKL concentrations in TM groups (P <0.05). Several significant positive correlations were found between BOP, PI scores, and biofluid parameters also in systemically healthy groups.

    Conclusion: TM may have a role in the underlying systemic hematologic condition and potentially affect gingival inflammation via dysregulation of lymphocytes and increased activation of osteoclasts.