Salivary Semaphorin 4D level in patients with different severities of periodontitis (observational case–control study)

Abstract

Background: Periodontal diseases are progressive, destructive, and inflammatory conditions of the tissues that support the teeth. An immune response is triggered by microbial dysbiosis in the sub-gingival biofilm. Semaphorin 4D (Sema4D) is a glycoprotein expressed by osteoclasts, T-cells, and activated B-cells involved in both immune response and bone remolding. Objectives: This study attempted to assess the salivary levels of Sema4D in patients with different severities (stages I–IV) of periodontitis in comparison to healthy control. Materials and Methods: A total of 171 participants of both genders were included into this case–control study. From the dental centers in Al-Najaf city and the Department of Periodontics in the College of Dentistry, University of Kufa, five groups were established for them: clinically healthy periodontium control group (19 subjects), Stage I periodontitis group (38 subjects), Stage II periodontitis group (38 subjects), Stage III periodontitis group (38 subjects), and Stage IV periodontitis group (38 subjects). The clinical periodontal parameters were examined after collecting whole unstimulated salivary samples from all individuals. The levels of Sema4D in saliva samples were estimated utilizing the ELISA technique. Statistical analysis used: ANOVA test, Games-Howell test, and Pearson correlation (r) test. Results: The findings revealed that the mean level of salivary Sema4D was the highest in the stage IV periodontitis group (758.11 ± 139.119), followed by stage III periodontitis group (725.815 ± 127.055), stage II periodontitis group (679.169 ± 121.993), stage I periodontitis group (601.742 ± 145.459), and control group (366.515 ± 47.635) respectively with a significant difference (P ≤ 0.01). Conclusions: The periodontitis patients showed higher Sema4D levels in unstimulated saliva as compared to the control. Hence, this molecule may play an essential role in the pathogenesis of periodontitis.