Background. Neutrophils play an important role in maintaining periodontal status in conditions of healthy homeostasis. They achieve their surveillance function by continuously migrating to the gingival sulcus and eradicating periodontal pathogens. In addition, neutrophils are considered an integral element in the pathogenesis of periodontal diseases. Among several neutrophil subsets, low‐density neutrophils (LDN) have recently received attention and are linked with cancer, immunological, inflammatory, and infectious diseases. However, the presence, phenotypes, and potential role of LDN in the pathogenesis of periodontitis have not yet been investigated. Objectives. To investigate the presence, subsets (normal, band, suppressive, and active), and phenotypes via marker expression surface protein known as the cluster of differentiation (CD) (CD16b, CD14, CD15, and CD62L) of LDN in patients with periodontitis. Materials and Methods. The observational case‐control study was conducted to estimate the potential role of LDNs in periodontitis. Venous blood and periodontal indices were obtained from 40 healthy control individuals and 60 periodontitis patients. Subsequently, CD16b, CD62L, CD14, and CD15 expression on the surface of LDN was examined by multicolor flow cytometry, and their subsets were classified as “normal” (CD16brightCD62Lbright), “bands” (CD16dimCD62Lbright), “suppressive” (CD16brightCD62Ldim), and “active” (CD16brightCD62Lnegative). Results. There was a significant difference in the expression of LDN markers for active and suppressive phenotypes, respectively, favoring periodontitis over the control group. In contrast, there were significantly higher levels of CD16b, CD62L, and CD15 (“normal”) in the control group when compared with the periodontitis group. Conclusion. LDN was associated with periodontitis as it was significantly increased in the periodontitis group in comparison with the control group and was positively correlated with all periodontal parameters. Cells from both groups of patients (periodontitis and control) expressed a normal mature phenotype (CD16b + High, CD62L + High, CD15+, and CD14‐). Regarding subsets, the normal LDN (CD16brightCD62Lbright) was the most predominant phenotype in both periodontitis and control groups. However, the active subset increased in periodontitis compared to normal, indicating their destructive role in periodontitis.