Dogukan Yilmaz1, Neslihan Yilmaz2,3, Recep Polat4, Verneri Nissilä3, Elif Gül Aydın2, Jaana Rautava5,6, Mervi Gürsoy3, Ulvi Kahraman Gürsoy3. 1. Department of Periodontology, Faculty of Dentistry, Sakarya University, Sakarya, Turkey. dogukanyilmaz@sakarya.edu.tr. 2. Department of Pediatric Dentistry, Faculty of Dentistry, Sakarya University, Sakarya, Turkey. 3. Department of Periodontology, Institute of Dentistry, University of Turku, Turku, Finland. 4. Department of Pediatric Endocrinology, Faculty of Medicine, Sakarya University, Sakarya, Turkey. 5. Department of Oral and Maxillofacial Diseases, Faculty of Medicine, University of Helsinki and Helsinki University Hospital, ClinicumHelsinki, Finland. 6. Department of Pathology, Faculty of Medicine, University of Helsinki, HUS Diagnostic Center, HUSLAB, Helsinki University Hospital, MedicumHelsinki, Finland.
Abstract
OBJECTIVES: Type 1 diabetes mellitus (T1DM), a chronic autoimmune disease characterized by insulin deficiency, is related to periodontal diseases in children and adolescents. Our aim was to profile salivary human beta-defensin (hBD)-2 and hBD-3 concentrations in relation to periodontal and T1DM status in children and adolescent populations. MATERIAL AND METHODS: Unstimulated saliva samples were collected from 66 participants including periodontally healthy T1DM patients (T1DM + C; n = 18), T1DM patients with gingivitis (T1DM + G; n = 20), systemically and periodontally healthy individuals (SH + C: n = 15), and systemically healthy gingivitis patients (SH + G; n = 13). Full mouth plaque index (PI), bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment level (CAL) were recorded. Salivary hBD-2 and hBD-3 concentrations were evaluated by sandwich ELISA method. A p value of < 0.05 was considered statistically significant. RESULTS: Salivary hBD-3 concentrations were lower in T1DM groups in comparison to systemically healthy counterparts (SH + G vs. T1DM + G; p < 0.001 and SH + C vs. T1DM + C; p < 0.001). Salivary hBD-2 levels did not differ between related groups. The difference in hBD-3 concentrations between T1DM and control groups was still significant (p = 0.008) after being adjusted for PI%, BOP%, and age. CONCLUSION: In the limits of study, T1DM patients were found to have decreased salivary hBD-3 concentrations, regardless of their gingival inflammatory status. CLINICAL RELEVANCE: Altered salivary hBD-3 concentration can partly explain why diabetic children are more prone to periodontal diseases.
OBJECTIVES: Type 1 diabetes mellitus (T1DM), a chronic autoimmune disease characterized by insulin deficiency, is related to periodontal diseases in children and adolescents. Our aim was to profile salivary human beta-defensin (hBD)-2 and hBD-3 concentrations in relation to periodontal and T1DM status in children and adolescent populations. MATERIAL AND METHODS: Unstimulated saliva samples were collected from 66 participants including periodontally healthy T1DM patients (T1DM + C; n = 18), T1DM patients with gingivitis (T1DM + G; n = 20), systemically and periodontally healthy individuals (SH + C: n = 15), and systemically healthy gingivitis patients (SH + G; n = 13). Full mouth plaque index (PI), bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment level (CAL) were recorded. Salivary hBD-2 and hBD-3 concentrations were evaluated by sandwich ELISA method. A p value of < 0.05 was considered statistically significant. RESULTS: Salivary hBD-3 concentrations were lower in T1DM groups in comparison to systemically healthy counterparts (SH + G vs. T1DM + G; p < 0.001 and SH + C vs. T1DM + C; p < 0.001). Salivary hBD-2 levels did not differ between related groups. The difference in hBD-3 concentrations between T1DM and control groups was still significant (p = 0.008) after being adjusted for PI%, BOP%, and age. CONCLUSION: In the limits of study, T1DM patients were found to have decreased salivary hBD-3 concentrations, regardless of their gingival inflammatory status. CLINICAL RELEVANCE: Altered salivary hBD-3 concentration can partly explain why diabetic children are more prone to periodontal diseases.
Authors: Giovanni E Salvi; Lea M Franco; Thomas M Braun; Angie Lee; Gösta Rutger Persson; Niklaus P Lang; William V Giannobile Journal: J Clin Periodontol Date: 2009-12-01 Impact factor: 8.728