Pregnancy-induced periodontal inflammation: Influence of salivary cytokines and antimicrobial proteins

• Published in: The Saudi dental journal Vol. 30; no. 4; pp. 306 - 311
• Main Authors: Lasisi, Taye J., Abdus-salam, Rukiyat A.
• Format: Journal Article
• Language: English
• Published: Saudi Arabia Elsevier B.V 01.10.2018; Elsevier
• Subjects: Antimicrobial proteins; Cytokines; Gingivitis; Original; Pregnancy; Saliva; Pregnancy; Cytokines; Saliva; Gingivitis; Antimicrobial proteins
• ISSN: 1013-9052; 1658-3558
• DOI: 10.1016/j.sdentj.2018.07.001

The aim of this study was to evaluate the association between pregnancy-induced periodontal inflammation and levels of some salivary cytokines and antimicrobial proteins (AMPs). The study was a cohort longitudinal study that included pregnant women attending a secondary health facility. Consented participants had oral examination and saliva sampling during pregnancy and post-partum (three months after pregnancy). Saliva samples were used for the analysis of cytokines (TNF-α, IFN-gamma and IL-1β) and AMPs (Lactoferin, Lysozyme, and β defensin-1) using ELISA. Data are presented as median with interquartile range and compared using related sample Wilcoxon signed rank test. Correlations between levels of the salivary factors and indices of periodontal inflammation were determined using Spearman’s correlation test. Salivary flow rate, pH, levels of salivary IL-1β and IFN-gamma were significantly lower; while gingival index, periodontal index and level of salivary TNF-α were significantly higher during pregnancy compared with postpartum period. However, salivary lactoferin, lysozyme and β defensin-1 did not show significant difference comparing during pregnancy and postpartum period. Level of salivary IFN-gamma showed negative correlation with gingival index while level of salivary TNF-α showed positive correlation with gingival and periodontal indices. Lower levels of salivary IL-1β and IFN-gamma along with higher TNF-α concentration during pregnancy suggest their contributions to the pathophysiology of pregnancy-induced periodontal inflammation.