Background. Several studies have focused on the association between periodontitis and systemic implications; however, the biological mechanisms of the immune responses before and after periodontal therapy involved in this relationship, such as phagocytic functions, remain unclear. Objectives. This study aimed to investigate whether periodontal treatment improves the phagocytic function of blood monocytes in patients with severe periodontitis. Materials and Methods. A nonrandomized sample of 55 participants was enrolled in the study. Two groups were studied: control (n = 27, healthy subjects without periodontal disease) and patients (n = 28, individuals with periodontitis). Treatment of periodontitis (scaling and root planing) was performed until the clinical resolution of periodontal pockets and inflammation. The following clinical periodontal parameters were assessed: probing depth, clinical attachment level, visible plaque index (PI), and gingival bleeding on probing index before and after mechanical periodontal treatment. The phagocytic index (PhI) and nitro blue tetrazolium test (NBT) were assessed before and immediately after the end of treatment. Results. Periodontitis induced impaired phagocytosis by monocytes. Phagocytosis at baseline was significantly lower in periodontitis patients [median, 13.2 (range of 7.1 to 20.8) and 60.7 (40.6 to 88.6)] than in controls [27.4 (15.5 to 40.5)] and 98 (68.2 to 122.9)] for nonsensitized or sensitized samples, respectively. After supportive therapy, patients showed a significant enhancement of phagocytic functions [33.7 (14.6 to 53.2) and 108.5 (99.6 to 159.5)] for nonsensitized and sensitized samples, respectively. Periodontal treatment increased the phagocytic capacity to a level similar to that observed in the control group and improved the capacity of phagocytes to produce superoxide anion. Conclusions. The results suggest that periodontal therapy in patients with severe periodontitis provides a state of homeostasis due to the reestablishment of phagocytic function and increased production of NBT (Regional Registry No. RBR-24T799; Universal Registry No. U1111-1133-5512).