Expression of human β‐defensins‐1 and ‐2 peptides in unresolved chronic periodontitis
- 25 March 2004
- journal article
- Published by Wiley in Journal of Periodontal Research
- Vol. 39 (4) , 221-227
- https://doi.org/10.1111/j.1600-0765.2004.00727.x
Abstract
Background: Human β-defensins (hBDs) are antimicrobial peptides which contribute to host innate immunity by disrupting the membrane integrity of a broad spectrum of microorganisms. Objectives: This study aimed to determine the expression profiles of hBD-1 and -2 peptides in gingiva and to assess the possible relations of these antimicrobial peptides with periodontal health and disease. Methods: Seven periodontally healthy subjects and 22 patients with unresolved chronic periodontitis were recruited and the gingival biopsies collected consisted of healthy tissues from the healthy subjects (HT-C); periodontal pocket tissues (PoT) and inflamed connective tissues (ICT) from the base of pocket, i.e. granulation tissues, as well as clinically healthy tissues (HT-P) from the adjacent clinically healthy sites from the patients. The expression of hBD-1 and -2 peptides was detected by immunohistochemistry and quantitatively analyzed with a computerized image processing system. Results: Both hBD-1 and -2 peptides were detected in all periodontally healthy subjects, while hBD-1 was detected in all patients and hBD-2 was found in most of the patients. Their expression was mainly confined to the granular and spinous layers of gingival epithelium, in which hBD-1 was detected in both intercellular spaces and cytoplasm, whereas hBD-2 was mainly observed in the cytoplasm. HT-C expressed significantly higher levels of hBD-2 than HT-P (p < 0.05). Within the patients, both defensins were up-regulated significantly in PoT as compared with the adjacent HT-P (p < 0.05). Conclusions: The present study showed that hBD-1 and -2 were frequently expressed in the granular and spinous layers of gingival epithelia and their expression may be associated with periodontal health and disease. © Blackwell Munksgaard, 2004.link_to_subscribed_fulltexKeywords
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