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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Peripheral Blood Mononuclear Phagocytes From Patients With Chronic Periodontitis Are Primed for Osteoclast Formation

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Herrera, Bruno S. [1, 2, 3] ; Bastos, Alliny S. [4, 5] ; Coimbra, Leila S. [1, 2] ; Teixeira, Simone A. [6] ; Rossa, Jr., Carlos [4, 5] ; Van Dyke, Thomas E. [3] ; Muscara, Marcelo N. [6] ; Spolidorio, Luis C. [1, 2]
Total Authors: 8
[1] State Univ Sao Paulo, Araraquara Dent Sch, Dept Physiol, Araraquara - Brazil
[2] State Univ Sao Paulo, Araraquara Dent Sch, Dept Pathol, Araraquara - Brazil
[3] Forsyth Inst, Dept Appl Oral Sci, Cambridge, MA 02142 - USA
[4] State Univ Sao Paulo, Araraquara Dent Sch, Dept Diag, Araraquara - Brazil
[5] State Univ Sao Paulo, Araraquara Dent Sch, Dept Surg, Araraquara - Brazil
[6] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Sao Paulo - Brazil
Total Affiliations: 6
Document type: Journal article
Source: Journal of Periodontology; v. 85, n. 4, p. E72-E81, APR 2014.
Web of Science Citations: 9

Background: During inflammatory periodontal disease, peripheral blood mononuclear cells (PBMCs) are attracted to bone and differentiate into active bone-resorbing osteoclasts (OCs), thus providing evidence that the impact of chronic periodontitis (CP) on the activity of circulating mononuclear cells is of central importance. The authors test the hypothesis that peripheral blood mononuclear phagocytes (PBMPs) from patients with CP are activated and more susceptible to differentiation into OCs, which in turn would lead to more intense bone resorption. Methods: In vitro cytokine production by both unstimulated and lipopolysaccharide-stimulated PBMCs from individuals with (n = 10) or without (n = 12) periodontitis was determined by cytokine array. OC differentiation from CD14(+) PBMCs was induced by receptor activator of nuclear factor-kappa B ligand (RANKL), either alone or in the presence of macrophage colony-stimulating factor (M-CSF). PBMC differentiation to OCs was confirmed by tartrate-resistant acid phosphatase staining; bone resorbing activity was assessed by using an osteologic plate assay (bone resorption pit formation). Results: PBMCs from patients with CP produced tumor necrosis factor-a and higher amounts of interferon-gamma, interleukin (IL)-1 alpha, IL-1 beta, IL-1r alpha, CXC motif chemokine 10, macrophage migration inhibitory factor, macrophage inflammatory protein (MIP)-1 alpha, and MIP-1 beta than the control cells. OC differentiation was induced by RANKL alone in PBMCs from patients with CP, but not in PBMCs from the healthy controls, which required the addition of M-CSF. In addition, PBMC-derived OCs from patients with CP showed significantly higher resorption activity than that observed in the healthy controls. Also, the circulating concentrations of M-CSF were significantly higher in patients with CP than in the control participants. Conclusions: These data indicate that in patients with CP, circulating PBMCs are primed for increased proinflammatory activity and that M-CSF plays a central role in this process by increasing OC formation and the consequent bone resorption activity. (AU)

FAPESP's process: 11/17800-4 - Consequences of the presence of ligature-induced periodontitis on rat blood pressure and in vitro vasomotor response
Grantee:Marcelo Nicolas Muscara
Support Opportunities: Regular Research Grants
FAPESP's process: 08/02893-4 - Set-up and standardization of human osteoblast and osteoclast cell cultures as tools for the study of the mechanisms involved in the alveolar bone loss secondary to periodontitis
Grantee:Bruno Schneider Herrera
Support Opportunities: Scholarships in Brazil - Post-Doctoral