ISSN:
1600-0765
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Objective: This study aimed to investigate the expression patterns of the newly discovered human β-defensin-3 (hBD-3) in human gingiva.Background: Human β-defensins (hBDs) are a group of small, broad-spectrum, cationic antimicrobial peptides. Our recent study showed that the expression levels of hBD-1 and 2 peptides were associated with periodontal conditions.Methods: A total of 49 gingival biopsies were collected, including 33 samples from 21 patients with chronic periodontitis and 16 samples from 16 periodontally healthy subjects. The expression of hBD-3 was detected by immunohistochemistry and in situ hybridization. Double staining was undertaken to identify hBD-3 peptide-positive cells, using CD-1a and cytokeratin 20 as markers for Langerhans cells and Merkel cells, respectively.Results: hBD-3 peptide was detected in 88% of the samples, which was confined to the gingival epithelia. In healthy control subjects, hBD-3 peptide was more frequently detected in the basal layer as compared to the patients (53% vs. 18%, p 〈 0.05). In patients, hBD-3 expression extended from the basal layer to the spinous layers (82%), in which hBD-3 was confined to the basal and deep spinous layers in clinically healthy tissues from patients, whereas it extended to the superficial spinous layers in pocket tissues from patients (0% vs. 50%, p 〈 0.05). In both groups, hBD-3 peptide was expressed not only in gingival keratinocytes, but also in Langerhans cells and Merkel cells. hBD-3 transcripts were detected in 90% of the samples and they were confined to the basal and/or suprabasal layers of gingival epithelia.Conclusions: This study shows that hBD-3 is frequently expressed in gingival epithelia. The appropriate expression of hBD-3 peptide may contribute to the maintenance of periodontal homeostasis, possibly through its antimicrobial effect and promotion of adaptive immune responses.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1600-0765.2005.00827.x
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