Comparison of Neutrophil Apoptosis α-Defensins and Calprotectin in Children with and without Severe Early Childhood Caries

نویسندگان

  • Alireza Akbarzadeh Baghban Department of Biostatics, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  • Mandana Sattari Department of Immunology, Shahid Beheshti University of Medical Sciences
  • Nazanin Hashemi Department of Pediatric Dentistry, Dental School
  • Nikoo Tadayon Department of Pediatric Dentistry, Dental School
چکیده مقاله:

Background: The infectious nature of severe early-childhood caries (S-ECC) points to the possible participation of immunologic host responses including neutrophils and their antimicrobial products. Objectives: The aim of this study was to determine the neutrophil apoptosis, α-defensins (HNP1-3) and calprotectin levels in the saliva of preschool children and the association with S-ECC. Methods: Oral examinations were performed on 87 children aged 3-5 years and non stimulated whole saliva samples were collected. Thirty of these subjects were considered S-ECC children, 30 with moderate caries (MC) and 27 were caries free (CF). To detect apoptosis, cell staining was done with Annexin-V-Fluos and propidium iodide, and they were analyzed by fluorescent microscopy. The concentration of α-defensins and calprotectin were assessed using ELISA. Results: There were no statistical differences between groups considering the HNP1-3 or calprotectin salivary levels (p=0.06 and p=0.23, respectively). The HNP1-3 and calprotectin levels were negatively correlated and the correlation was significant in MC group (p=0.03). Lower levels of apoptotic neutrophils were obtained from CF subjects as compared with S-ECC children (p=0.03). Conclusions: Our findings establish that apoptotic mechanisms could be implicated in the immunity responses associated with S-ECC. We cannot yet

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comparison of neutrophil apoptosis α-defensins and calprotectin in children with and without severe early childhood caries

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عنوان ژورنال

دوره 8  شماره 1

صفحات  11- 19

تاریخ انتشار 2011-03-01

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