Evaluation of Gelatinases, Tissue Inhibitor of Matrix Metalloproteinase-2, and Myeloperoxidase Protein in Healthy and Inflamed Human Dental Pulp Tissue

Accorsi-Mendonça, Thais; Silva, Emmanuel João Nogueira Leal; Marcaccini, Andrea M.; Gerlach, Raquel Fernanda; Duarte, Keila Maria Roncato; Souza, Ana Paula de; Line, Sérgio Roberto Peres; Zaia, Alexandre Augusto

doi:10.1016/j.joen.2012.11.011

Cited by 30 publications

(25 citation statements)

References 31 publications

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“…, Accorsi‐Mendonça et al . ). Collagen degradation is an important characteristic of apical periodontitis, and MMPs are likely candidates in this process because this extracellular matrix component is a well‐known MMP substrate (Paula‐Silva et al .…”

Section: Discussionmentioning

confidence: 97%

Root canal content from primary endodontic infection and upregulation of gelatinases in fibroblast cells

et al. 2015

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Section: Discussionmentioning

confidence: 97%

Root canal content from primary endodontic infection and upregulation of gelatinases in fibroblast cells

et al. 2015

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“…As a consequence, MPO mass and/or activity is upregulated in rapidly progressing CP, GCFs, saliva and human dental pulp tissues in order to combat pathogenic microbes. 105,[191][192][193][194][195][196][197][198][199][200][201][202][203][204] Miyasaki and Nemirovsky reported that among dental and periodontal bacteria tested, 204 A. actinomycetemcomitans has the highest capacity to promote the release of neutrophilderived MPO. Owing to its ability to form HOCl, MPO is involved in the destruction of periodontal components and can destroy the ECM by directly activating latent MMP-8 and MMP-9, and by enhancing MMP activity via inactivation of TIMP-1.…”

Section: Mpomentioning

confidence: 99%

Neutrophil proteolytic activation cascades: a possible mechanistic link between chronic periodontitis and coronary heart disease

et al. 2015

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Cardiovascular diseases are chronic inflammatory diseases that affect a large segment of society. Coronary heart disease (CHD), the most common cardiovascular disease, progresses over several years and affects millions of people worldwide. Chronic infections may contribute to the systemic inflammation and enhance the risk for CHD. Periodontitis is one of the most common chronic infections that affects up to 50% of the adult population. Under inflammatory conditions the activation of endogenous degradation pathways mediated by immune responses leads to the release of destructive cellular molecules from both resident and immigrant cells. Matrix metalloproteinases (MMPs) and their regulators can activate each other and play an important role in immune response via degrading extracellular matrix components and modulating cytokines and chemokines. The action of MMPs is required for immigrant cell recruitment at the site of inflammation. Stimulated neutrophils represent the major pathogen-fighting immune cells that upregulate expression of several proteinases and oxidative enzymes, which can degrade extracellular matrix components (e.g. MMP-8, MMP-9 and neutrophil elastase). The activity of MMPs is regulated by endogenous inhibitors and/or candidate MMPs (e.g. MMP-7). The balance between MMPs and their inhibitors is thought to mirror the proteolytic burden. Thus, neutrophil-derived biomarkers, including myeloperoxidase, may activate proteolytic destructive cascades that are involved in subsequent immune-pathological events associated with both periodontitis and CHD. Here, we review the existing studies on the contribution of MMPs and their regulators to the infection-related pathology. Also, we discuss the possible proteolytic involvement and role of neutrophil-derived enzymes as an etiological link between chronic periodontitis and CHD.

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“…Unfortunately, it is not possible to normalize the levels of these proteins to total protein in the sample for 2 reasons: first the paper points themselves contain varying amounts of protein , and second, caries itself contains solubilized proteins, which would then obscure the findings. Furthermore, TIMP (tissue inhibitor of metalloproteinase) levels were not regarded in this study, as these correlate with the degree of pulpal inflammation [Accorsi-Mendonca et al, 2013;Mente et al, 2016].…”

Section: Discussionmentioning

confidence: 99%

“…To this end, dentinal fluid was collected below deep and shallow caries from molars and premolars within the same patients aged 18 and older. Absolute MMP-9 levels were contrasted against the levels of MMP-2, an enzyme related to normal tissue turnover, which is consistently present in pulp tissue [Gusman et al, 2002;Accorsi-Mendonca et al, 2013], embedded in healthy dentin [Vidal et al, 2014], and which can be found in the dentinal fluid of healthy teeth .…”

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confidence: 99%

MMP-9 in Dentinal Fluid Correlates with Caries Lesion Depth

et al. 2017

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The analysis of molecular cues in dentinal fluid from an excavated cavity could improve diagnostics in the context of minimally invasive caries treatment. In the current clinical trial we assessed whether the dentinal fluid levels of MMP-9 (matrix metalloproteinase-9; neutrophil gelatinase) would increase with the progression of carious lesions. MMP-9 is associated with neutrophil-related tissue breakdown in the pulp. Absolute MMP-9 levels were contrasted against the levels of MMP-2, an enzyme related to normal tissue turnover. Dentinal fluid was collected below deep and shallow caries from molars and premolars within the same patients aged 18 years and older (n = 30, 1 tooth per group/patient). Experimental teeth were isolated under a rubber dam prior to excavation. Dentinal fluid was collected from the bottom of the cavity using a size 25 paper point. MMP levels were assessed using an enzyme-linked immunosorbent assay. Nonparametric methods were applied to test for differences between groups. Significantly more (p < 0.05, Wilcoxon test) MMP-9 was collected from the deep carious lesions than from the shallow counterparts. Pairwise comparison of MMP-9 values within patients revealed that there was more MMP-9 collected from deep lesions than from shallow counterparts in 27 of the 30 individuals under investigation (pairwise Wilcoxon test, p < 0.001). In contrast, no such difference existed for MMP-2. There was a high correlation between MMP-9 from deep and shallow lesions (Spearman's ρ = 0.72, p < 0.001), indicating that patients with more MMP-9 in the deep carious lesion also tended to have more MMP-9 in the shallow lesion.

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Evaluation of Gelatinases, Tissue Inhibitor of Matrix Metalloproteinase-2, and Myeloperoxidase Protein in Healthy and Inflamed Human Dental Pulp Tissue

Cited by 30 publications

References 31 publications

Root canal content from primary endodontic infection and upregulation of gelatinases in fibroblast cells

Root canal content from primary endodontic infection and upregulation of gelatinases in fibroblast cells

Neutrophil proteolytic activation cascades: a possible mechanistic link between chronic periodontitis and coronary heart disease

MMP-9 in Dentinal Fluid Correlates with Caries Lesion Depth

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