Impaired neutrophil chemotaxis in patients with juvenile and rapidly progessing periodontitis

Abstract

Polymorphonuclear leukocyte chemotactic studies were performed in young patients with juvenile periodontitis/periodontosis and adult patients with aggressive periodontitis. In the juvenile periodontitis/periodontosis group, 86% showed modest leukotactic defects, the majority of which were due to intrinsic abnormality of cells. In the older patients with rapidly progressing periodontitis 48% had detectable leukotactic defects; the majority of which were serum associated. The results indicate that some forms of periodontitis are associated with impaired polymorphonuclear leukocyte chemotaxis and suggest that a failure of a major host protective mechanism to dental plaque may increase susceptibility to periodontal disease.

Effect of Ciprofloxacin on Killing ofActinobacillus actinomycetemcomitansby Polymorphonuclear Leukocytes

“…Its virulence factors include a leukotoxin that kills PMNs and macrophages (32,34). In patients with aggressive periodontitis, the defense against A. actinomycetemcomitans may be further compromised by a defect in PMN chemotaxis (12,26). It is unclear whether this defect is inherited or induced by proinflammatory cytokines in the serum (1,27).…”

“…Since A. actinomycetemcomitans is capable of invading the gingival soft tissue (21), systemic antibiotics can be useful in eliminating this pathogen. Patients with aggressive periodontitis frequently express a PMN chemotactic defect that impairs their ability to control subgingival A. actinomycetemcomitans levels (12,26). PMNs play a critical protective role in the host defense against pathogens associated with periodontal diseases (14,16).…”

Neutrophil Receptor Modulation in the Pathogenesis of Periodontal Diseases

“…In the periodontium, neutrophils accumulate at the tissue-plaque interface and below the junctional epithelium to form a "barrier" against microbial invasion. This "barrier" may be intrinsically compromised by dysfunctional neutrophils as in LJP (Cianciola et al, 1977;Clark et al, 1977;Lavine et al, 1979; or may be overwhelmed in some other way. The mechanisms of periodontal breakdown in the healthy host are poorly defined.…”

“…The clearest example of this phenomenon is in patients with localized juvenile periodontitis (LJP). In addition to the characteristically early onset and severe bone loss, 75% of LJP patients exhibit abnormalities in neutrophil functions, including chemotaxis (Cianciola et al, 1977;Clark et al, 1977;Lavine et al, 1979;Van Dyke et al, 1980), phagocytosis, and bactericidal activity (Cianciola et al, 1977;Suzuki et al, 1983). Since periodontal disease is an infectious disease, compromise of the host's first line of defense presumably permits the initiation of the infectious disease process.…”

Interdisciplinary Treatment of Aggressive Periodontitis: Three-Dimensional Cone-Beam X-Ray Computed Tomography Evaluation

“…AgP is defined as a destructive periodontal disease affecting more than 14 teeth in young individuals. Its etiology has been linked to the presence of Aggregatibacter actinomycetemcomitans (Fine et al, 2007;Haraszthy et al, 2000;Di Rienzo et al, 1994), host response defects (Page et al, 1984Lavine et al, 1979), and possibly to genetic inheritance (Hart & Kornman, 1997;Kinane et al, 2000;Boleghman et al, 1992;Beaty et al, 1987;Hart et al, 1992;Melnick et al, 1976;. In contrast, chronic periodontitis is characterized by a lower rate of progression (Schätzle et al, 2009), although like AgP it can reach a severe stage, leading to tooth loss and edentualism.…”