title: Hyper-reactive PMNs in FcgammaRIIa 131 H/H genotype periodontitis patients.
abstract: BACKGROUND
  Receptors for the Fc part of IgG (FcgammaRIIa) on polymorphonuclear leukocytes (PMN) mediate phagocytosis and cell activation. Previous results show that one of the genetic variants of the FcgammaRIIa, 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.
  
  
  OBJECTIVE
  To study whether the FcgammaRIIa genotype modifies the PMN reactivity in periodontitis patients.
  
  
  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.
authors: Department of Periodontology, Academic Center for Dentistry Amsterdam, Universiteit van Amsterdam and Vrije Universiteit, Amsterdam, The Netherlands. E.Comandasu@vumc.nl
authors: E A
authors: EA
authors: Nicu
authors: U
authors: U
authors: Van der Velden
authors: V
authors: V
authors: Everts
authors: A J
authors: AJ
authors: Van Winkelhoff
authors: D
authors: D
authors: Roos
authors: B G
authors: BG
authors: Loos
mesh_terms: D000328:Adult; D016976:Aggregatibacter actinomycetemcomitans; D016301:Alveolar Bone Loss / Q000201:enzymology / Q000235:genetics* / Q000382:microbiology; D015703:Antigens, CD / Q000032:analysis; D015815:Cell Adhesion Molecules / Q000032:analysis; D015550:Cell Degranulation; D005260:Female; D058851:GPI-Linked Proteins; D005838:Genotype; D006801:Humans; D008297:Male; D008336:Mandibular Diseases / Q000201:enzymology / Q000235:genetics / Q000382:microbiology; D008439:Maxillary Diseases / Q000201:enzymology / Q000235:genetics / Q000382:microbiology; D009504:Neutrophils / Q000502:physiology*; D010196:Pancreatic Elastase / Q000032:analysis; D010518:Periodontitis / Q000201:enzymology / Q000235:genetics* / Q000382:microbiology; D010587:Phagocytosis / Q000502:physiology; D010980:Platelet Membrane Glycoproteins / Q000032:analysis; D017452:Receptors, IgG / Q000235:genetics*; D016897:Respiratory Burst / Q000502:physiology; D060149:Tetraspanin 30
chemical_list: D015703:Antigens, CD; C554586:CD63 protein, human; C504120:CEACAM8 protein, human; D015815:Cell Adhesion Molecules; C445323:FCGR2A protein, human; D058851:GPI-Linked Proteins; D010980:Platelet Membrane Glycoproteins; D017452:Receptors, IgG; D060149:Tetraspanin 30; D010196:Pancreatic Elastase