Immune Response in Gingival Disease: Role of Macrophage Migration Inhibitory Factor (original) (raw)
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MIF induces osteoclast differentiation and contributes to progression of periodontal disease in mice
Microbes and Infection
Periodontal disease (PD) is a chronic inflammatory and alveolar bone destructive disease triggered by microorganisms from the oral biofilm. Oral inoculation of mice with the periodontopathogen Aggregatibacter actinomycetemcomitans (Aa) induces marked alveolar bone loss and local production of inflammatory mediators, including Macrophage Migration Inhibitory Factor (MIF). The role of MIF for alveolar bone resorption during PD is not known. In the present study, experimental PD was induced in BALB/c wild-type mice (WT) and MIF knockout mice (MIF À/À ) through oral inoculation of Aa. Despite enhanced number of bacteria, MIF À/À mice had reduced infiltration of TRAP-positive cells and reduced alveolar bone loss. This was associated with decreased neutrophil accumulation and increased levels of IL-10 in periodontal tissues. TNFa production was similar in both groups. In vitro, LPS from Aa enhanced osteoclastic activity in a MIF-dependent manner. In conclusion, MIF has role in controlling bacterial growth in the context of PD but contributes more significantly to the progression of bone loss during PD by directly affecting differentiation and activity of osteoclasts.
Objective: The present study was designed to investigate the role of macrophage migration inhibitory factor (MIF) in the exacerbation of pregestational periodontal disease (PGPD). Background: Periodontitis (PT) is a severe stage of periodontal disease characterized by inflammation of the supporting tissues of the teeth, which usually worsens during pregnancy. MIF is a proinflammatory cytokine that is significantly elevated in periodontitis, both at the beginning and at the end of pregnancy. Although periodontitis usually presents with greater severity during pregnancy, the participation of MIF in the evolution of periodontitis has not been established. Methods: To analyze the relevance of MIF in the exacerbation of PGPD, we employed a model of PGPD in WT and Mif-/-mice, both with a BALB/c genetic background. PT was induced with nylon suture ligatures placed supramarginally around the second upper right molar. For PGPD, PT was induced 2 weeks before mating. We evaluated histological changes and performed histometric analysis of the clinical attachment loss, relative expression of MMP-2 and MMP-13 by immunofluorescence, and relative expression of the cytokines mif, tnf-α, ifn-γ, and il-17 by quantitative real-time polymerase chain reaction (qRT-PCR).
https://www.ijhsr.org/IJHSR\_Vol.8\_Issue.7\_July2018/IJHSR\_Abstract.010.html, 2018
Background: Periodontal diseases including gingivitis and periodontitis are among the most frequent oral diseases affecting all age groups, which can critically impact the general health. Since periodontal disease is both preventable and curable, early intervention will minimize the subsequent destruction of periodontal tissues. Objective: Is to assess the gingival crevicular fluid level of Macrophage Chemotactic Protein-1/CCL2 and Interleukin-12 in plaque induced gingivitis patients compared to chronic periodontitis patients. Methods: This was a cross-sectional study with a sample of 32 healthy female patients obtained from the Dental Teaching Hospital, College of Dentistry, Umm Al-Qura University. GCF samples were collected using PerioPaper Strips. Results: Chronic periodontitis patients showed statistically significant higher mean PD (5.50mm) than patients with plaque induced gingivitis (3.06mm). Patients with chronic periodontitis revealed greater levels of MCP-1 (0.094pg/ml) in GCF compared to patients with plaque induced gingivitis (0.079pg/ml). Moreover, chronic periodontitis patients showed higher levels of IL-12 (0.11pg/ml) than plaque induced gingivitis patients (0.101pg/ml). Conclusion: In conclusion, within the limits of the present study, IL-12 and MCP-1 may be regarded as a reliable biochemical marker for periodontal tissue destruction in CP. Further longitudinal studies with larger sample size are recommended to further elucidate the role of these biomarkers in alveolar bone resorption in periodontal disease.
Journal of Dental …, 2011
Background/purpose: This study investigated the relationship between gingival osmotic pressure (GOP) and periodontal disease by correlating GOP with alveolar bone loss (ABL) and gingival proinflammatory cytokine production during periodontitis. Materials and Methods: Experimental periodontitis was induced on the right maxillary molar region of 12 rats by injecting an endotoxin þ saline solution (test group), and the opposite region of the same jaw received a single saline injection in each animal (control group). The linear alveolar bone level was measured to verify periodontitis creation and to quantify ABL. Interleukin (Il)-1b and tumor necrosis factor (TNF)-a levels were determined to assess the gingival proinflammatory cytokine production. The cytokines were measured by enzymelinked immunosorbent assay in gingival supernatants obtained from the groups. GOP was measured in the same supernatants with a digital osmometer. Results: Increased ABL, cytokine, and GOP levels were evident in the test group compared with the control group (P < 0.01). Positive correlations were found between the increase in GOP and ABL, and between the increases in GOP and cytokines in the test group (P < 0.01) (r Z 0.88 for ABL; r Z 0.76 for Il-1b; r Z 0.81 for TNF-a). Conclusions: The results reveal that an increase in the GOP may be correlated with ABL and proinflammatory cytokine production in periodontitis, and it can be possibly used as a marker of the diseased nature of the periodontium.
Localization of TNF-α and Macrophages in the Periodontal Ligament during Orthodontic Tooth Movement
International Journal of Oral-Medical Sciences, 2013
Remodelling of the periodontium after application of mechanical forces constitutes the basis of clinical orthodontics, and various immunoregulatory molecules are involved in this process. The present study focused on the localizations of the tumor necrosis factor-α (TNF-α)and macrophages in periodontal ligament(PDL)during experimental tooth movement in rats. A total of 15 male 6-weeks-old Wistar rats were subjected to an orthodontic force of 10 g to induce a mesially tipping movement of the upper first molars. Experimental tooth movement was accomplished for seven days. We determined the localization of TNF-α and RM-4(an antibody specific for identification of macrophages)in the PDL during orthodontic tooth movement using immunohistochemistry. Immunoreactivity for TNF-α and RM-4 was detected in PDL fibroblasts in the compressive side by the orthodontic force of 10 g. On the first day after tooth movement, the immunoreactivity of TNF-α and RM-4 was weak. On the third and fifth days, more TNF-α and RM-4 positive reactions in some nucleuses of fibroblasts were recognized than on the first day. Furthermore, these positive reactions were decreased after seven days. Therefore, RM-4 (+)cells involved in the expression of TNF-α may play an important role in the initial reaction of the PDL and in the induction of the osteoclastic bone resorption during orthodontic tooth movement.
Cytokines’ Involvement in Periodontal Changes
Cytokines, 2020
The bacterial challenge on the periodontal tissues triggers an inflammatory reaction, driven by pro-inflammatory cytokines, that eventually leads to the periodontal structures' damage. The pathogenic mechanisms of this inflammatory reaction are complex and are influenced by the type of host-immune response and certain local and systemic factors. These factors can influence periodontal inflammation, through the action of the various pro-inflammatory cytokines. Periodontal disease and certain systemic conditions can have a mutual association, as the pathogenic mechanisms of these diseases can involve similar molecular and cellular elements. The concept of 'periodontal medicine' comprises these pathogenic connections, focusing on the key role that periodontal health has on the general homeostasis and well-being.
Macrophage immunomodulation in chronic osteolytic diseases—the case of periodontitis
Journal of Leukocyte Biology, 2018
Periodontitis (PD) is a chronic osteolytic disease that shares pathogenic inflammatory features with other conditions associated with nonresolving inflammation. A hallmark of PD is inflammation-mediated alveolar bone loss. Myeloid cells, in particular polymorphonuclear neutrophils (PMN) and macrophages (Mac), are essential players in PD by control of gingival biofilm pathogenicity, activation of adaptive immunity, as well as nonresolving inflammation and collateral tissue damage. Despite mounting evidence of significant innate immune implications to PD progression and healing after therapy, myeloid cell markers and targets for immune modulation have not been validated for clinical use. The remarkable plasticity of monocytes/Mac in response to local activation factors enables these cells to play central roles in inflammation and restoration of tissue homeostasis and provides opportunities for biomarker and therapeutic target discovery for management of chronic inflammatory conditions, including osteolytic diseases such as PD and arthritis. Along a wide spectrum of activation states ranging from proinflammatory to pro-resolving, Macs respond to environmental changes in a site-specific manner in virtually all tissues. This review summarizes the existing evidence on Mac immunomodulation therapies for osteolytic diseases in the broader context of conditions associated with nonresolving inflammation, and discusses osteoimmune implications of Macs in PD.
Cytokines: The Double Edge Sword for Periodontal Disease
Cytokines play a major role in pathogenesis of periodontal disease. These chemical mediators act as inter and intra-cellular signaling for stimulating various cells to carry out different range of functions. These cytokines also help in mediating inflammatory responses, stimulating development of certain immune cells and also aid in hematopoiesis of immune cells, macrophages and platelets. The intricate mechanism of cellsignaling through cytokines also forms the basis of pathogenesis of periodontal disease. Better understanding of various cytokines, its receptors and function could benefit us in designing therapeutic aids for prevention and management of periodontal disease.