Anti‐cardiolipin from periodontitis patients induces MCP‐1 production by human umbilical vein endothelial cells

Abstract

Aim Periodontal diseases are associated with a variety of systemic diseases, including cardiovascular disease and stroke, and patients with periodontitis demonstrate elevated levels of anticardiolipin antibodies. We sought to determine if anticardiolipin antibodies from periodontitis patients induced monocyte chemotactic protein-1 production by human vascular endothelial cells. Materials and Methods IgG was purified from sera from 53 subjects, including chronic and aggressive periodontitis patients and periodontally healthy controls, with elevated or normal IgG anticardiolipin levels. In addition, anticardiolipin antibodies were specifically removed from some sera by immunoabsorption. Results We found that, irrespective of diagnostic category, IgG from subjects with elevated anticardiolipin induced significantly greater monocyte chemotactic protein-1 production by human vascular endothelial cells than IgG from those subjects with normal anticardiolipin titers. Removal of anticardiolipin from IgG preparations from periodontitis patients significantly reduced their ability to induce monocyte chemotactic protein-1. Conclusions Since elevated titers of anticardiolipin are found in a significantly greater proportion of patients with periodontitis than in periodontally healthy individuals, and these antibodies activate endothelial cells to produce monocyte chemotactic protein-1, they may explain some of the associations noted between periodontal infections and systemic conditions.

Serum Anticardiolipin Concentrations in Patients With Chronic Periodontitis Following Scaling and Root Planing

“…The previous data indicate that IgG antiCl in sera from patients with CP is biologically active 10 . Isolated IgG from these sera were shown to activate human endothelial cells, stimulating production of MCP‐1 at levels that directly varied with the antiCl titer 10 .…”

“…14 The previous data indicate that IgG antiCl in sera from patients with CP is biologically active. 10 Isolated IgG from these sera were shown to activate human endothelial cells, stimulating production of MCP-1 at levels that directly varied with the antiCl titer. 10 In addition, removal of antiCl from these immunoglobulin preparations reduced production of MCP-1 from endothelial cells.…”

“…It has been observed that periodontal pathogens, including Porphyromonas gingivalis , Actinobacillus actinomycetemcomitans , and Treponema denticola , have antigens bearing peptide sequences of sufficient similarity to key sequences in β2GPI to induce these antibodies 8,9 . Furthermore, the antiCl found in sera of patients with periodontitis are biologically functional, as they are capable of activating endothelial cells to produce the key cytokine monocyte chemotactic protein (MCP)‐1 10 . Additionally, the observation that immunization of mice with P. gingivalis results in production of antibodies reactive with β2GPI, and that passive immunization of pregnant mice with these antibodies results in increased fetal loss 11 …”

“…8,9 Furthermore, the antiCl found in sera of patients with periodontitis are biologically functional, as they are capable of activating endothelial cells to produce the key cytokine monocyte chemotactic protein (MCP)-1. 10 Additionally, the observation that immunization of mice with P. gingivalis results in production of antibodies reactive with b2GPI, and that passive immunization of pregnant mice with these antibodies results in increased fetal loss. 11 It was therefore hypothesized that the source of antiCl in periodontitis is the oral microflora.…”

β2‐Glycoprotein I‐Dependent Anti‐Cardiolipin Antibodies Associated With Periodontitis in Patients With Systemic Lupus Erythematosus

“…MCP‐1 may induce osteoclast differentiation and osteoclastogenesis and relate to bone resorption 46,47 . A recent study published by Schenkein et al 48 also concluded that anti‐CL antibodies may activate endothelial cells to produce MCP‐1, which may result in the association between periodontitis and other systemic conditions. The present study is in line with the previous findings.…”