Serum and gingival crevicular fluid asprosin levels in obese and normal-weight individuals with and without periodontitis: a cross-sectional study

Obesity and periodontitis are chronic inflammatory conditions linked by shared immunometabolic pathways. Although asprosin has been implicated in metabolic regulation and systemic inflammation, its role in the immunometabolic interaction between obesity and periodontal inflammation remains unclear. This study evaluated local and systemic levels of asprosin, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in obese and normal-weight individuals with and without periodontitis. This cross-sectional study included 60 individuals aged 18–65 years, categorized by body mass index (BMI) as normal weight (18.5–24.9 kg/m²) or obese (≥ 30 kg/m²). Participants were further classified as periodontally healthy or with periodontitis, forming four groups: normal-weight periodontally healthy (NH), obese periodontally healthy (OH), normal-weight periodontitis (NP), and obese periodontitis (OP) (n = 15 each). Plaque index, gingival index, probing pocket depth, clinical attachment level, and bleeding on probing were recorded. Gingival crevicular fluid (GCF) and serum samples were analyzed for asprosin, TNF-α, and IL-6 using an enzyme-linked immunosorbent assay. Intergroup comparisons were performed using a rank-based general linear model adjusted for age and sex. Serum asprosin levels were lower in the NH group than in the NP (p = 0.025), OH (p < 0.001), and OP (p < 0.001) groups and were also lower in the NP group than in the OH (p = 0.006) and OP (p = 0.021) groups. GCF asprosin levels were lower in the NH group compared with the OH (p < 0.001) and OP (p = 0.017) groups, and were also lower in the NP group than in the OH (p = 0.042) and OP (p = 0.022) groups. IL-6 levels were higher in the OH group than in the NH group (p = 0.050), whereas serum TNF-α did not differ significantly among groups (p = 0.078). Although overall group differences were observed for GCF IL-6 (p = 0.014) and TNF-α (p = 0.008), overlap in interquartile ranges limited consistent pairwise comparisons. GCF and serum asprosin levels were higher in obese individuals than in normal-weight participants, while serum asprosin levels were higher in normal-weight individuals with periodontitis than in normal-weight periodontally healthy individuals. These findings are consistent with an association between asprosin levels, obesity, and periodontal status, indicating that obesity status should be considered when interpreting asprosin levels in periodontal conditions. The study was retrospectively registered on ClinicalTrials.gov on March 17, 2025 (Identifier: NCT06879951).

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Journal
BMC Oral Health
Published
2026-04-06
DOI
https://doi.org/10.1186/s12903-026-08249-y
Primary Topic
Adipokines, Inflammation, and Metabolic Diseases
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article
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article

Serum and gingival crevicular fluid asprosin levels in obese and normal-weight individuals with and without periodontitis: a cross-sectional study

Hulya Nur Sodan, Ayşen Bodur, Buse Naz Buyukakcali Altay, FÜSUN BALOŞ TÖRÜNER et al.
BMC Oral Health
Adipokines, Inflammation, and Metabolic Diseases
article

Serum and gingival crevicular fluid asprosin levels in obese and normal-weight individuals with and without periodontitis: a cross-sectional study

Hulya Nur Sodan, Ayşen Bodur, Buse Naz Buyukakcali Altay, FÜSUN BALOŞ TÖRÜNER, Emin Umit Bagriacik, Nihan Oruklu
article en

Abstract

Obesity and periodontitis are chronic inflammatory conditions linked by shared immunometabolic pathways. Although asprosin has been implicated in metabolic regulation and systemic inflammation, its role in the immunometabolic interaction between obesity and periodontal inflammation remains unclear. This study evaluated local and systemic levels of asprosin, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in obese and normal-weight individuals with and without periodontitis. This cross-sectional study included 60 individuals aged 18–65 years, categorized by body mass index (BMI) as normal weight (18.5–24.9 kg/m²) or obese (≥ 30 kg/m²). Participants were further classified as periodontally healthy or with periodontitis, forming four groups: normal-weight periodontally healthy (NH), obese periodontally healthy (OH), normal-weight periodontitis (NP), and obese periodontitis (OP) (n = 15 each). Plaque index, gingival index, probing pocket depth, clinical attachment level, and bleeding on probing were recorded. Gingival crevicular fluid (GCF) and serum samples were analyzed for asprosin, TNF-α, and IL-6 using an enzyme-linked immunosorbent assay. Intergroup comparisons were performed using a rank-based general linear model adjusted for age and sex. Serum asprosin levels were lower in the NH group than in the NP (p = 0.025), OH (p < 0.001), and OP (p < 0.001) groups and were also lower in the NP group than in the OH (p = 0.006) and OP (p = 0.021) groups. GCF asprosin levels were lower in the NH group compared with the OH (p < 0.001) and OP (p = 0.017) groups, and were also lower in the NP group than in the OH (p = 0.042) and OP (p = 0.022) groups. IL-6 levels were higher in the OH group than in the NH group (p = 0.050), whereas serum TNF-α did not differ significantly among groups (p = 0.078). Although overall group differences were observed for GCF IL-6 (p = 0.014) and TNF-α (p = 0.008), overlap in interquartile ranges limited consistent pairwise comparisons. GCF and serum asprosin levels were higher in obese individuals than in normal-weight participants, while serum asprosin levels were higher in normal-weight individuals with periodontitis than in normal-weight periodontally healthy individuals. These findings are consistent with an association between asprosin levels, obesity, and periodontal status, indicating that obesity status should be considered when interpreting asprosin levels in periodontal conditions. The study was retrospectively registered on ClinicalTrials.gov on March 17, 2025 (Identifier: NCT06879951).

BMC Oral Health
Gazi University (TR)
Good health and well-being
Openalex Percentile: Top 20%
Adipokines, Inflammation, and Metabolic Diseases
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