Abnormalities of leukocyte chemotaxis in patients with various forms of periodontitis

Abstract

Prior studies have documented that a majority of patients with juvenile periodontitis have suppressed polymorphonuclear leukocyte (PMN) chemotaxis. However, in other forms of earlyonset periodontitis, PMN migration has been studied only to a limited extent or not at all, and monocyte (MN) chemotaxis has not been extensively studied in patients with any of the forms of periodontitis. Accordingly, PMN and MN chemotaxis was studied in 7 patients with prepubertal, 37 with juvenile, and 35 with rapidly progressive periodontitis. In addition, PMN chemotaxis was studied in 8 patients with adult periodontitis. In the prepubertal group, 5 patients had abnormal PMN chemotaxis, 5 had depressed MN chemotaxis, and one had reduced serum chemotactic activity. All patients in this group had at least one form of leukocyte chemotaxis abnormality. In the juvenile periodontitis group, 17 patients had abnormal PMN responses, 16 of these were depressed while 1 was enhanced. MN chemotaxis was depressed in 4 of these patients and elevated in 2. Five patients had reduced serum chemotactic activity and one manifested a serum chemotactic inhibitor. In total, 65% of juvenile patients had some form of abnormality. In the rapidly progressive group, 15 had abnormal PMN chemotaxis, 7 had aberrant MN chemotaxis, 4 had reduced serum chemotactic activity, and 8 had a serum inhibitor of chemotaxis. No abnormalities were found in the PMNs or sera of patients with adult periodontitis. Overall, 66% of the early‐onset patients manifested some form of cell or serum‐related leukocyte chemotactic abnormality. Thus, abnormalities of leukocyte chemotaxis were present in all patients with prepubertal periodontitis and in a majority of those with juvenile and rapidly progressive disease, while no abnormalities were found in 8 patients with adult periodontitis.

Local Versus Systemic Adjunctive Antibiotic Therapy in 28 Patients With Generalized Aggressive Periodontitis

“…GAgP was diagnosed according to clinical and radiographic criteria by one experienced examiner of the Department of Periodontology. 16,17 The inclusion criteria included at least 20 teeth and no antibiotics in the last 3 months. Prior to scaling and root planing, patients were randomly assigned to 1 of the 2 treatment groups: the local tetracycline fiber group (SRP ؉ TCF) or the amoxicillin/clavulanic acid group (SRP ؉ AUG).…”

Gingival crevicular fluid monocyte chemoattractant protein‐1 and RANTES levels in patients with generalized aggressive periodontitis

“…Increasing literature have implicated that AgP are caused by multiple potential risk factors. Previous studies have shown that the presence of pathogenic oral biofilm (Albandar et al 1997), alteration in host defense cell functions (Altman et al 1985, Emingil et al 2001a, Takahashi et al 2001), disregulated cytokine and inflammatory mediator levels (Shapira et al 1994, Emingil et al 2001b, c), and the presence of specific genetic risk factors (Hart 1996, Parkhill et al 2000) could attribute to the pathogenesis of the aggressive form of periodontal disease. However, the immunopathogenic mechanisms involved in AgP are not completely elucidated.…”

Neutrophil chemotactic behaviour in patients with early‐onset forms of periodontitis

“…The possibility of a PMN chemotactic defect in JP patients was indicated in an early report from Cianciola and colleagues (1977), who found depressed PMN chemotaxis in all 9 patients they studied. In fact, based on the data of Altman et al (1985) there is almost an equal chance or better of PMNs from JP and RPP patients displaying enhanced chemotaciic ability. Enhanced PMN chemotaxis, in contrast, was found in 54% and 57% of patients from each group.…”