Disruption of Monocyte and Macrophage Homeostasis in Periodontitis

Al-Mubarak, Abdullah I. A.; Kkk, Tanagala; Papapanou, Panos N.; Lalla, Evanthia; Momen-Heravi, Fatemeh

doi:10.3389/fimmu.2020.00330

Cited by 101 publications

(81 citation statements)

References 48 publications

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“…Macrophages play a critical role in mediating periodontal inflammation. 13,43 The balance between proinflammatory and antiinflammatory macrophages is critical in the resolution of tissue inflammation. 13,48 A high ratio of proinflammatory macrophages to anti-inflammatory macrophages leads to aberrant repair of the periodontium.…”

Section: Discussionmentioning

confidence: 99%

“…Bindarit administration alleviates periodontal inflammation in DP mice Persistently elevated inflammation contributes to the progression of DP. 11,13 Therefore, we investigated the impact of bindarit on proinflammatory cytokine and chemokine expression in the periodontal tissues of DP mice. The results of LEGENDplex TM bead-based immunoassays showed that the levels of IL-23, IL-1α, TNF-α, IL-12, IL-1β, IL-17, and GM-CSF were reduced, whereas that of the antiinflammatory cytokine IL-10 was increased in periodontal tissues of DP mice after bindarit administration.…”

Section: Ccl2 Levels Are Persistently Elevated In Dp Micementioning

confidence: 99%

“…11,12 Monocytes are an important source of proinflammatory cytokines in the periodontitisaffected periodontium. 13,14 Diabetes can lead to prolonged monocyte infiltration into inflamed sites by activating precursors in the bone marrow. 13,15 Excessive monocyte infiltration contributes to persistent tissue inflammation and increases the severity of diabetic complications due to the release of inflammatory mediators such as TNF-α, IL-1β, and IL-6 by these cells.…”

Section: Introductionmentioning

confidence: 99%

“…13,14 Diabetes can lead to prolonged monocyte infiltration into inflamed sites by activating precursors in the bone marrow. 13,15 Excessive monocyte infiltration contributes to persistent tissue inflammation and increases the severity of diabetic complications due to the release of inflammatory mediators such as TNF-α, IL-1β, and IL-6 by these cells. 16,17 Monocytes also release matrix metalloproteinases (MMPs), which cause tissue destruction by degrading the extracellular matrix.…”

Section: Introductionmentioning

confidence: 99%

“…28,29 CCL2 derived from inflamed gingiva could be involved in the recruitment of monocytes from the peripheral circulation into periodontal tissues, leading to persistent periodontal inflammation. 13,30 Additionally, CCL2 has been reported to enhance osteoclastogenesis by inducing the expression of receptor activator of NF-κB (RANK) by osteoclast progenitors. 31 RANK ligand (RANKL) further promotes the differentiation of osteoclast progenitors into functional osteoclasts, which could aggravate DP by causing alveolar bone resorption.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of CCL2 by bindarit alleviates diabetes-associated periodontitis by suppressing inflammatory monocyte infiltration and altering macrophage properties

et al. 2020

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Diabetes-associated periodontitis (DP) aggravates diabetic complications and increases mortality from diabetes. DP is caused by diabetes-enhanced host immune-inflammatory responses to bacterial insult. In this study, we found that persistently elevated CCL2 levels in combination with proinflammatory monocyte infiltration of periodontal tissues were closely related to DP. Moreover, inhibition of CCL2 by oral administration of bindarit reduced alveolar bone loss and increased periodontal epithelial thickness by suppressing periodontal inflammation. Furthermore, bindarit suppressed the infiltration of proinflammatory monocytes and altered the inflammatory properties of macrophages in the diabetic periodontium. This finding provides a basis for the development of an effective therapeutic approach for treating DP.

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Section: Discussionmentioning

confidence: 99%

Section: Ccl2 Levels Are Persistently Elevated In Dp Micementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Inhibition of CCL2 by bindarit alleviates diabetes-associated periodontitis by suppressing inflammatory monocyte infiltration and altering macrophage properties

et al. 2020

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Periodic Lamellae‐Based Nanofibers for Precise Immunomodulation to Treat Inflammatory Bone Loss in Periodontitis

He,

Liu,

Zheng

et al. 2024

Adv Healthcare Materials

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Periodontitis is a common oral disease accompanied by inflammatory bone loss. The pathological characteristics of periodontitis usually accompany an imbalance in the periodontal immune microenvironment, leading to difficulty in bone regeneration. Therefore, effective treatment strategies are needed to modulate the immune environment in order to treat periodontitis. Here, we developed a highly‐oriented periodic lamellae poly(ε‐caprolactone) electrospun nanofibers (PLN) by surface‐directed epitaxial crystallization. Our in vitro results showed that the PLN could precisely modulate macrophage polarization toward the M2 phenotype. Macrophages polarized by PLN significantly enhanced the migration and osteogenic differentiation of BMSCs. Notably, results suggested that the topographical cues presented by PLN can modulate macrophage polarization by activating YAP, which reciprocally inhibits the NF‐κB signaling pathway. The in vivo results indicated that PLN can inhibit inflammatory bone loss and facilitate bone regeneration in periodontitis. Our findings suggest that topographical nanofibers with periodic lamellae is a promising strategy for modulating immune environment to treat inflammatory bone loss in periodontitis.This article is protected by copyright. All rights reserved

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Human leukocyte antigens are associated with salivary level of active MMP‐8

Mauramo

Sorsa

et al. 2021

Clinical & Exp Dental Res

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Objectives: This case control study examined the associations of HLA antigens and periodontitis with the salivary level of active .Materials and Methods: A total of 202 subjects, registered as Swiss bone marrow donors, participated in the study. HLA-A, -B, and -C types were determined by serology or PCR. Saliva samples were collected from subjects, followed by a periodontal examination. The salivary level of aMMP-8 was determined with immunofluorometric assay. Results:The mean salivary level of aMMP-8 was directly comparable to the grade of periodontitis and increased from healthy to mild/moderate to severe (125.0 ± 132.1, 200.6 ± 170.2, 290.1 ± 202.3 ng/ml; p < 0.001 between each group, respectively).The only association between the HLA types and the salivary level of aMMP-8 was observed in subjects with HLA-A11. Subjects with healthy periodontium and HLA-A11 had a lower level of aMMP-8 (49.2 ± 32.5 ng/ml) compared with subjects without HLA-A11 (123.6 ± 119.2; p = 0.048). Among subjects with periodontitis, a higher level of aMMP-8 (394.2 ± 255.6 ng/ml) was observed in subjects with HLA-A11 compared with subjects without HLA-A11 (201.1 ± 146.1 ng/ml; p < 0.002). This finding was statistically significant also after adjusting for sex, age, smoking, tooth brushing and the number of medications (p < 0.05).Conclusions: HLA-A11 is associated with the salivary level of aMMP-8 which contributes to the subject's immune and inflammatory response in periodontium.

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Disruption of Monocyte and Macrophage Homeostasis in Periodontitis

Cited by 101 publications

References 48 publications

Inhibition of CCL2 by bindarit alleviates diabetes-associated periodontitis by suppressing inflammatory monocyte infiltration and altering macrophage properties

Inhibition of CCL2 by bindarit alleviates diabetes-associated periodontitis by suppressing inflammatory monocyte infiltration and altering macrophage properties

Periodic Lamellae‐Based Nanofibers for Precise Immunomodulation to Treat Inflammatory Bone Loss in Periodontitis

Human leukocyte antigens are associated with salivary level of active MMP‐8

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