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Hyper‐reactive PMNs in Fc γ RIIa 131 H/H genotype periodontitis patients
Author(s) -
Nicu E. A.,
Van der Velden U.,
Everts V.,
Van Winkelhoff A. J.,
Roos D.,
Loos B. G.
Publication year - 2007
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.2007.01136.x
Subject(s) - phagocytosis , periodontitis , genotype , immunology , opsonin , aggressive periodontitis , respiratory burst , elastase , granulocyte , actinobacillus , antibody opsonization , biology , microbiology and biotechnology , medicine , gene , enzyme , genetics , biochemistry
Background: Receptors for the Fc part of IgG (Fc γ RIIa) on polymorphonuclear leukocytes (PMN) mediate phagocytosis and cell activation. Previous results show that one of the genetic variants of the Fc γ RIIa, the 131 H/H, is associated with more periodontal breakdown than the R/R. This may be due to hyper‐reactivity of the H/H‐PMNs upon interaction with bacteria. Aim: To study whether the Fc γ RIIa genotype modifies the PMN reactivity in periodontitis patients. Material and Methods: A cohort of 98 periodontitis patients was genotyped. From these, 10 H/H and 10 R/R consented to participate. PMNs were incubated with immune serum‐opsonized Actinobacillus actinomycetemcomitans ( A.a .). Phagocytosis, degranulation (CD63 and CD66b expression), respiratory burst and elastase release were assessed. Results: Patients of the H/H genotype showed more bone loss than those with the H/R or R/R genotype ( p =0.038). H/H‐PMNs phagocytosed more opsonized A.a . than did R/R‐PMNs ( p =0.019). The H/H‐PMNs also expressed more CD63 and CD66b than did the R/R‐PMNs ( p =0.004 and 0.002, respectively) and released more elastase ( p =0.001). Conclusions: The genotyping results confirm previous reports that more periodontal destruction occurs in the H/H genotype than in the H/R or R/R genotype. The functional studies indicate a hyper‐reactivity of the H/H‐PMN in response to bacteria, which may be one of several pathways leading to more periodontal breakdown.