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    Serum, saliva, and gingival tissue human beta-defensin levels in relation to retinoic acid use
    (Wiley, 2023) Atalay, Nur; Balcı, Nur; Uslu Toygar, Hilal; Yardımcı, Gürkan; Gürsoy, Ulvi Kahraman
    BackgroundRetinoic acid is an active derivative of vitamin A and regulates the differentiation, proliferation, and antimicrobial peptide expression profiles of human cells. The aim of the present study was to analyze the effect of systemic retinoic acid use on serum, saliva, and gingival tissue levels of human beta-defensin (hBD)-1, hBD-2, and hBD-3. MethodsA total of 69 participants (34 systemic retinoic acid users and 35 healthy controls) were enrolled in this study. Plaque index, probing pocket depth, bleeding on probing (BOP), and clinical attachment loss were measured. Saliva and serum hBD-1, hBD-2, and hBD-3 levels were quantified by enzyme-linked immunosorbent assay. Gingival tissue hBD-1, hBD-2, and hBD-3 levels were determined by immunohistochemistry. A univariate general linear model was used in adjusted comparisons of hBD1, hBD-2, and hBD-3. P values of < 0.05 were considered statistically significant. ResultsReduced salivary levels of hBD-2 (P = 0.042), but not hBD-1 or hBD-3, were detected in systemic retinoic acid users compared to non-user controls. There was a significant difference in the adjusted (for BOP%) salivary hBD-2 concentrations between retinoic acid and control groups (P = 0.031). No difference was observed in serum or tissue levels of hBD-1, hBD-2, or hBD-3 between the two study groups. ConclusionSystemic retinoic acid use was associated with suppressed salivary hBD-2 level, which was independent of gingival inflammation.
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    Systemic factors affecting human beta-defensins in oral cavity
    (Multidisciplinary Digital Publishing Institute (MDPI), 2024) Atalay, Nur; Balcı, Nur; Gürsoy, Mervi; Gürsoy, Ulvi Kahraman
    Human beta-defensins are host defense peptides with broad antimicrobial and inflammatory functions. In the oral cavity, these peptides are produced mainly by the keratinocytes of the epithelium; however, fibroblasts, monocytes, and macrophages also contribute to oral human beta-defensin expressions. The resident and immune cells of the oral cavity come into contact with various microbe-associated molecular patterns continuously and simultaneously. The overall antimicrobial cellular response is highly influenced by local and environmental factors. Recent studies have produced evidence showing that not only systemic chronic diseases but also systemic factors like hyperglycemia, pregnancy, the long-term use of certain vitamins, and aging can modulate oral cellular antimicrobial responses against microbial challenges. Therefore, the aim of this narrative review is to discuss the role of systemic factors on oral human beta-defensin expressions.

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