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<p>This study aimed to explore the role of CD11b, CD38, and HLA-DR in saliva, linking rheumatoid arthritis (RA) and periodontitis. We hypothesized that their expression reflects shared immunological pathways and correlates with clinical periodontal variables. An observational case–control study was conducted with RA patients (cases), healthy participants, and individuals with degenerative chronic joint pain (controls). Salivary CD11b, CD38, and HLA-DR levels were measured using flow cytometry for the first time. Periodontal assessments included PPD, in a periodontal lesion severity index (PIRIM), CAL, in a periodontal extension index (Arbes), plaque index (PI) and BOP. Biochemical markers such as anti-citrullinated peptide antibodies (ACPA), rheumatoid factor, and C-reactive protein were measured in the patients’ clinical analyses and included in this pilot study. Thirty-three RA patients and 22 controls were analyzed. CD11b (p = 0.043) and CD38 (p = 0.002) were significantly elevated in RA patients. CD11b correlated positively with BOP (p = 0.047), PI (p = 0.035), and the PIRIM index (p = 0.040). ACPA levels associated with BOP (p = 0.046), and HLA-DR levels positively associated with the number of teeth (p = 0.037). Patients with RA exhibit higher salivary levels of CD11b and CD38 compared to controls. CD11b was associated with all clinical periodontal variables except for the number of teeth. We hypothesize that CD11b acts as a key regulator of osteoclastogenesis, supporting the hypothesis of a bidirectional relationship between RA and periodontitis.</p>

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CD11b as a diagnostic biomarker of rheumatoid arthritis and as a risk factor of periodontitis: a pilot study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月13日

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  • Marco Bonilla,
  • Manuel Bravo,
  • Mahtab Moradi,
  • Natividad Martín-Morales,
  • Enrique Raya-Álvarez,
  • Francisco Mesa

摘要

This study aimed to explore the role of CD11b, CD38, and HLA-DR in saliva, linking rheumatoid arthritis (RA) and periodontitis. We hypothesized that their expression reflects shared immunological pathways and correlates with clinical periodontal variables. An observational case–control study was conducted with RA patients (cases), healthy participants, and individuals with degenerative chronic joint pain (controls). Salivary CD11b, CD38, and HLA-DR levels were measured using flow cytometry for the first time. Periodontal assessments included PPD, in a periodontal lesion severity index (PIRIM), CAL, in a periodontal extension index (Arbes), plaque index (PI) and BOP. Biochemical markers such as anti-citrullinated peptide antibodies (ACPA), rheumatoid factor, and C-reactive protein were measured in the patients’ clinical analyses and included in this pilot study. Thirty-three RA patients and 22 controls were analyzed. CD11b (p = 0.043) and CD38 (p = 0.002) were significantly elevated in RA patients. CD11b correlated positively with BOP (p = 0.047), PI (p = 0.035), and the PIRIM index (p = 0.040). ACPA levels associated with BOP (p = 0.046), and HLA-DR levels positively associated with the number of teeth (p = 0.037). Patients with RA exhibit higher salivary levels of CD11b and CD38 compared to controls. CD11b was associated with all clinical periodontal variables except for the number of teeth. We hypothesize that CD11b acts as a key regulator of osteoclastogenesis, supporting the hypothesis of a bidirectional relationship between RA and periodontitis.