NCT07323277

Effect of Smoking on Macrophage Polarization in Periodontitis

The Effect of Smoking on Macrophage Polarization in the Pathogenesis of Periodontitis

• Status: Completed
• Phase: —
• Study type: Observational
• Enrollment: 80 (actual)
• Sponsor: Suleyman Demirel University · Academic / Other
• Sex: All
• Age: 18 Years – 65 Years
• Healthy volunteers: —

Summary

This observational case-control study investigates the effect of smoking on macrophage polarization in the pathogenesis of periodontitis. Adult participants who were either systemically healthy smokers or non-smokers, and who met the clinical criteria for periodontal health or periodontitis, were included. Gingival tissue samples were collected during periodontal procedures performed after completion of Phase I periodontal therapy, and the expression levels of macrophage polarization markers (iNOS and Arginase-1) were analyzed using ELISA. In addition, comprehensive clinical periodontal measurements-including probing pocket depth, clinical attachment level, bleeding on probing, Plaque Index, and Gingival Index-were recorded to evaluate the relationship between smoking status, inflammatory burden, and macrophage phenotype. The study aims to clarify how smoking modulates the balance between M1 and M2 macrophage responses in periodontal tissues.

Detailed description

Periodontitis is a chronic inflammatory disease in which macrophage polarization plays a key regulatory role in the host immune response. Smoking is a well-established risk factor that alters inflammatory pathways and immune cell behavior. This study was designed to examine how smoking influences macrophage polarization-specifically the balance between M1 (iNOS-mediated) and M2 (Arginase-1-mediated) phenotypes-in periodontal tissues. Systemically healthy adult participants were recruited and categorized into four groups based on smoking status and periodontal condition: (1) healthy non-smokers, (2) periodontitis non-smokers, (3) healthy smokers, and (4) periodontitis smokers. Gingival tissue samples (approximately 2×2 mm) were collected during periodontal surgical procedures performed after completion of Phase I periodontal therapy, immediately stored at -80 °C, and processed for biochemical analysis. Comprehensive clinical periodontal measurements-including probing pocket depth (PPD), clinical attachment level (CAL), bleeding on probing (BOP), Plaque Index (PI), and Gingival Index (GI)-were recorded on the same day to evaluate periodontal status and inflammatory burden. ELISA was used to quantify iNOS and Arginase-1 levels in gingival tissues. The primary objective of this study is to determine whether smoking shifts the macrophage phenotype toward a more pro-inflammatory M1 profile or suppresses M2-associated regulatory pathways in the context of periodontitis. The findings are expected to contribute to a better understanding of smoking-related alterations in periodontal immune mechanisms.

Conditions

• Periodontitis

Interventions

Type	Name	Description
OTHER	Smoking Exposure	Exposure to cigarette smoking, defined as smoking ≥10 cigarettes per day. Participants were classified as smokers or non-smokers based on self-reported smoking status.

Timeline

• Start date: 2024-12-01
• Primary completion: 2025-07-15
• Completion: 2025-11-04
• First posted: 2026-01-07
• Last updated: 2026-01-07

Locations

1 site across 1 country: Turkey (Türkiye)