| ORIGINAL RESEARCH |
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| Year : 2021 | Volume
: 12
| Issue : 1 | Page : 15-21 |
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Possible Protective Role of NLRC4 Inflammasome in Periodontal Diseases: A Preliminary Study
Sneha Parameswaran1, Vanaja Krishna Naik2, Kubra Aral3, Sugirtharaj Gunasekaran4, Devapriya Appukuttan1, Michael R Milward3, Ramya Ramadoss4
1 Department of Periodontics, SRM Dental College, Chennai, India
2 Department of Periodontics, SRM Dental College, Chennai; Department of Periodontics (Restorative Dentistry), School of Dentistry, University of Leeds, Leeds, UK, India
3 School of Dentistry, University of Birmingham, Birmingham, UK
4 Department of Oral Pathology, SRM Dental College, Ramapuram, India
Correspondence Address:
Vanaja Krishna Naik
Department of Restorative Dentistry, Worsley Building, Level 6, School of Dentistry, University of Leeds,LS29LU Leeds, UK
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/denthyp.denthyp_88_20
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Introduction: Inflammasomes are multiprotein complexes, which regulate proinflammatory cytokines, Interleukin-18 (IL-18), and Interleukin-1β (IL-1β) that are associated with periodontal breakdown. This study investigated the expression of NOD-like receptor pyrin domain-containing-3 (NLRP3) and NOD-like receptor family CARD domain-containing protein 4 (NLRC4) inflammasomes in different periodontal diseases in humans and their potential association with IL-18 release in gingival crevicular fluid (GCF). Materials and Methods: A total of 45 participants (21 males and 24 females) divided into four groups; periodontally healthy (H), gingivitis (G), chronic periodontitis (CP), and aggressive periodontitis (AgP) based on periodontal examination. NLRC4 and NLRP3 expression were detected by immunohistochemistry in gingival tissue samples for all groups. Expression percentage (%) and staining intensity distribution score (SID) were calculated for both NLRC4 and NLRP3. IL-18 was measured in GCF via enzyme linked immunosorbent assay (ELISA). Results: Positive immunoreactivity was seen for NLRC4 and NLRP3 across groups. No differences were found for NLRC4 expression %, but SID scores were slightly higher in G and AgP compared to other groups (P > 0.05). Results showed a significant increase of NRLP3 expression % in group CP compared to group H (P < 0.05) without affecting SID scores (P > 0.05). IL-18 levels were significantly higher in AgP and CP groups compared to H and G groups (P < 0.05). IL-18 significantly and positively correlated with clinical attachment levels across groups. Conclusion: Within the limitations of this preliminary study, we suggest that the NLRC4 platform may have a protective role contrary to the NLRP3 platform influencing IL-18 release and associated periodontal tissue breakdown.
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