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Background Paracetamol and ibuprofen are commonly prescribed pain relievers used in dental treatments, but their use can delay wound healing and lead to malunion and weaken the strength of newly formed bones. This randomized controlled clinical trial aimed to evaluate the wound healing (WH) and anti-inflammatory effects of paracetamol and ibuprofen on tooth extraction wounds in patients. Methods This study involved a total of 20 patients who required removal of their fully erupted upper third molar under local anaesthesia at the Oral and Maxillofacial Surgery Clinic, Faculty of Dentistry, Chiang Mai University. The study subjects were divided into two groups of 10 patients each who were prescribed 400 mg of ibuprofen or 500 mg of paracetamol for seven days. Subsequently, WH was evaluated and the resulting proportions were compared using Landry Turnbull and Howley Index (LTHI) scores. Salivary matrix metalloproteinase 9 (MMP-9) and transforming growth factor beta1 (TGF-β1) concentrations were used as proinflammatory indicators. Accordingly, the WH values and the resulting proportions were compared using Fisher’s exact test with a confidence interval (CI) of 95% ( P  < 0.05). The concentrations of MMP-9 and TGF-β1 were measured using ELISA and compared using the Mann‒Whitney U test at 95% CI ( P  < 0.05). The obtained statistical values were then analysed and interpreted accordingly. Results LTHI values on days 3 and 7 after tooth extraction were not significantly different between the two treatment groups. Salivary MMP-9 levels were lower in the paracetamol-treated group than in the ibuprofen-treated group ( P  < 0.01) on day 3 only. The LTHI concentration was also negatively correlated ( r = -0.433) with the MMP-9 concentration ( P  < 0.05) but was positively correlated ( r  = 0.369) with the salivary TGF-β1 concentration ( P  < 0.05). Interestingly, MMP-9 was negatively correlated with TGF-β1 in the ibuprofen treatment group (r 2 = -0.351). Conclusion Ibuprofen can inhibit the inflammatory process and delay healing in the extraction socket. After discontinuation of medication, no differences were observed in the healing effects between the paracetamol and ibuprofen groups. Trial registration The clinical trial was retrospectively registered at the Australian New Zealand Clinical Trial Registry (ANZCTR) NHMRC Clinical Trials Centre, Camperdown, Australia (Registry URL: https://www.anzctr.org.au ) (Registration number: ACTRN12624000595516 Date: 9/5/2024).

Background To evaluate in patients with aggressive periodontitis (AgP) the effect of nonsurgical periodontal treatment in conjunction with either additional administration of systemic antibiotics (AB) or application of photodynamic therapy (PDT) on the gingival crevicular fluid (GCF) concentration of matrix metalloproteinases 8 and 9 (MMP-8 and -9). Methods Thirty-six patients with AgP were included in the study. Patients were randomly assigned to treatment with either scaling and root planing (SRP) followed by systemic administration of AB (e.g. Amoxicillin + Metronidazole) or SRP + PDT. The analysis of MMP-8 and -9 GCF concentrations was performed at baseline and at 3 and 6 months after treatment. Nonparametric U-Mann-Whitney test was used for comparison between groups. Changes from baseline to 3 and 6 months were analyzed with the Friedman’s ANOVA test with Kendall’s index of consistency. Results In the AB group, patients showed a statistically significant ( p = 0.01 ) decrease of MMP-8 GCF level at both 3 and 6 months post treatment. In the PDT group, the change of MMP-8 GCF level was not statistically significant. Both groups showed at 3 and 6 months a decrease in MMP-9 levels. However, this change did not reach statistical significance. Conclusions Within the limits of the present study, it may be suggested that in patients with AgP, nonsurgical periodontal therapy in conjunction with adjunctive systemic administration of amoxicilin and metronidazole is more effective in reducing GCF MMP-8 levels compared to the adjunctive use of PDT.

Introduction The fascia transversalis is accepted as one of the anatomical structures that can prevent hernia formation. Degradation of collagen within the fascia transversalis is one of the known reasons for the development of inguinal hernia. In the present study, we investigated the roles of matrix metalloproteinases (MMPs), specifically MMP-1, MMP-2, and MMP-9 in the etiology of inguinal hernia. Materials and methods This prospective study included 60 inguinal hernia patients: 30 patients had indirect inguinal hernia and 30 patients had direct inguinal hernia. An additional 30 patients operated for reasons other than hernia in the inguinal canal were included as a control group. All patients underwent operations at Istanbul Training and Research Hospital between 1 June 2009 and 1 December 2009. Tissue specimens were taken from the fascia transversalis from patient and control groups during the operation, and MMP-1, MMP-2, MMP-9 values were investigated using immunohistochemical methods. Results Significantly higher values of MMP-1, MMP-2, MMP-9, were found in inguinal hernia cases than in the control group ( P  = 0.0001, P  = 0.007, P  = 0.021, respectively). Conclusion Increased MMP-1, MMP-2, MMP-9 values play a role in the etiology of inguinal hernia. Since weakening may also occur in other tissues in addition to the floor of inguinal canal in inguinal hernia patients, the association of arterial aneurisms and connective tissue diseases should also be investigated in these patients.

As one of the most widely investigated matrix metalloproteinases (MMPs), MMP-9 is a significant protease which plays vital roles in many biological processes. MMP-9 can cleave many extracellular matrix (ECM) proteins to regulate ECM remodeling. It can also cleave many plasma surface proteins to release them from the cell surface. MMP-9 has been widely found to relate to the pathology of cancers, including but not limited to invasion, metastasis and angiogenesis. Some recent research evaluated the value of MMP-9 as biomarkers to various specific cancers. Besides, recent research of MMP-9 biosensors discovered various novel MMP-9 biosensors to detect this enzyme. In this review, some recent advances in exploring MMP-9 as a biomarker in different cancers are summarized, and recent discoveries of novel MMP-9 biosensors are also presented.

Purpose MMP9 is a matricellular protein associated with extracellular matrix (ECM) remodelling, that promotes tumour progression, and modulates the activity of cell adhesion molecules and cytokines. This study aims to assess the prognostic value of MMP9 and its association with cytoskeletal modulators in early-stage invasive breast cancer (BC). Methods MMP9 expression was evaluated by immunohistochemistry using a well-characterised series of primary BC patients with long-term clinical follow-up. Association with clinicopathological factors, patient outcome and ECM remodelling BC-biomarkers were investigated. METABRIC dataset, BC-GenExMiner v4.0 and TCGA were used for the external validation of MMP9 expression. GSEA gene enrichment analyses were used to evaluate MMP9 associated pathways. Results MMP9 immunopositivity was observed in the stroma and cytoplasm of BC cells. Elevated MMP9 protein levels were associated with high tumour grade, high Nottingham Prognostic Index, and hormonal receptor negativity. Elevated MMP9 protein expression correlated significantly with cytokeratin 17 (Ck17), Epidermal Growth Factor Receptor (EGFR), proliferation (Ki67) biomarkers, cell surface adhesion receptor (CD44) and cell division control protein 42 (CDC42). Cytoplasmic MMP9 expression was an independent prognostic factor associated with shorter BC-specific survival. In the external validation cohorts, MMP9 expression was also associated with poor patients’ outcome. Transcriptomic analysis confirmed a positive association between MMP9 and ECM remodelling biomarkers. GSEA analysis supports MMP9 association with ECM and cytoskeletal pathways. Conclusion This study provides evidence for the prognostic value of MMP9 in BC. Further functional studies to decipher the role of MMP9 and its association with cytoskeletal modulators in BC progression are warranted.

Background. In cystic fibrosis (CF) the upper (UAW) and lower airways (LAW) are reservoirs for pathogens like Pseudomonas aeruginosa. The consecutive hosts’ release of proteolytic enzymes contributes to inflammation and progressive pulmonary destruction. Objectives were to assess dynamics of protease : antiprotease ratios and pathogens in CF-UAW and LAW sampled by nasal lavage (NL) and sputum before and after intravenous- (IV-) antibiotic therapy. Methods. From 19 IV-antibiotic courses of 17 CF patients NL (10 mL/nostril) and sputum were collected before and after treatment. Microbiological colonization and concentrations of NE/SLPI/CTSS (ELISA) and MMP-9/TIMP-1 (multiplex bead array) were determined. Additionally, changes of sinonasal symptoms were assessed (SNOT-20). Results. IV-antibiotic treatment had more pronounced effects on inflammatory markers in LAW, whereas trends to decrease were also found in UAW. Ratios of MMP-9/TIMP-1 were higher in sputum, and ratios of NE/SLPI were higher in NL. Remarkably, NE/SLPI ratio was 10-fold higher in NL compared to healthy controls. SNOT-20 scores decreased significantly during therapy ( P = 0.001 ) . Conclusion. For the first time, changes in microbiological patterns in UAW and LAW after IV-antibiotic treatments were assessed, together with changes of protease/antiprotease imbalances. Delayed responses of proteases and antiproteases to IV-antibiotic therapy were found in UAW compared to LAW.

Background The role of tumor-associated macrophages (TAMs) in the cancer immune landscape and their potential as treatment targets or modulators of response to treatment are gaining increasing interest. TAMs display high molecular and functional complexity. Therefore their objective assessment as breast cancer biomarkers is critical. The aims of this study were to objectively determine the in situ expression and significance of TAM biomarkers (CD68, CD163, and MMP-9) in breast cancer and to identify subclasses of patients who could benefit from TAM-targeting therapies. Methods We measured CD68, CD163, and MMP-9 protein expression in formalin-fixed paraffin-embedded tissues of breast carcinomas represented in tissue microarray format using multiplexed quantitative immunofluorescence (QIF) in two independent Yale cohorts: cohort A— n = 398, estrogen receptor–positive (ER + ) and ER − cases—and the triple-negative breast cancer (TNBC)-only cohort B ( n = 160). Associations between macrophage markers, ER status, and survival were assessed. Protein expression measured by QIF was compared with mRNA expression data from the METABRIC study. Results All three macrophage markers were co-expressed, displaying higher expression in ER − cancers. High pan-macrophage marker CD68 correlated with poorer overall survival (OS) only in ER − cases of cohort A ( P = 0.02). High expression of CD163 protein in TAMs was associated with improved OS in ER − cases (cohort A, P = 0.03 and TNBC cohort B, P = 0.04, respectively) but not in ER + cancers. MMP-9 protein was not individually associated with OS. High expression of MMP-9 in the CD68 + /CD163 + TAMs was associated with worse OS in ER + tumors ( P <0.001) but not in ER − cancers. In the METABRIC dataset, mRNA levels followed the co-expression pattern observed in QIF but did not always show the same trend regarding OS. Conclusions Macrophage activity markers correlate with survival differently in ER + and ER − cancers. The association between high co-expression and co-localization of MMP-9/CD163/CD68 and poor survival in ER + cancers suggests that these cancers may be candidates for macrophage-targeted therapies.

Objective: Matrix metalloproteinases are inflammatory biomarkers involved in carotid plaque instability. Our objective was to analyze the inflammatory activity of plasma and carotid plaque MMP-8 and MMP-9 after intravenous administration of hydrocortisone. Methods: The study included 22 patients with stenosis ? 70% in the carotid artery (11 symptomatic and 11 asymptomatic) who underwent carotid endarterectomy. The patients were divided into two groups: Control Group - hydrocortisone was not administered, and Group 1 - 500 mg intravenous hydrocortisone was administered during anesthetic induction. Plasma levels of MMP-8 and MMP-9 were measured preoperatively (24 hours before carotid endarterectomy) and at 1 hour, 6 hours and 24 hours after carotid endarterectomy. In carotid plaque, tissue levels of MMP-8 and MMP-9 were measured. Results: Group 1 showed increased serum levels of MMP- 8 (994.28 pg/ml and 408.54 pg/ml, respectively; P=0.045) and MMP-9 (106,656.34 and 42,807.69 respectively; P=0.014) at 1 hour after carotid endarterectomy compared to the control group. Symptomatic patients in Group 1 exhibited lower tissue concentration of MMP-8 in comparison to the control group (143.89 pg/ml and 1317.36 respectively; P=0.003). There was a correlation between preoperative MMP-9 levels and tissue concentrations of MMP-8 (P=0.042) and MMP-9 (P=0.019) between symptomatic patients in the control group. Conclusion: Hydrocortisone reduces the concentration of MMP- 8 in carotid plaque, especially in symptomatic patients. There was an association between systemic and tissue inflammation.

Background and Objective Proinflammatory cytokines and enzymes responsible for tissue destruction are important in the development of periodontitis. This study compared salivary concentrations of interleukin‐1 beta (IL‐1β), matrix metalloproteinases (MMP‐8), and (MMP‐9) in individuals with and without periodontitis to evaluate their diagnostic utility as potential biomarkers. Materials and Methods A comprehensive search was performed across PubMed, Scopus, ScienceDirect, and Google Scholar, supplemented by manual searches in relevant journals up to January 2024. Eligibility criteria focused on human studies with defined diagnostic criteria for periodontitis and saliva samples analyzed for IL‐1β, MMP‐8, and MMP‐9. Data were extracted to compare salivary levels of these markers between periodontitis patients and healthy controls. The Joanna Briggs Institute tool was used to evaluate the risk of bias and quality of the included studies. Statistical analysis employed a random effects model to calculate standardized mean differences and assess heterogeneity and publication bias. Results The search yielded 122 articles, with 27 meeting the inclusion criteria. Fifteen percent of these studies presented a moderate risk of bias, while the remaining 85% exhibited a low risk of bias. The meta‐analyses indicated significantly higher levels of IL‐1β, MMP‐8, and MMP‐9 in the saliva of subjects with periodontitis compared to healthy individuals: IL‐1β: Standardized Mean Difference (SMD) = 163.29 (95% CI = 104.64–221.95), p < 0.001; MMP‐8: SMD = 282.22 (95% CI = 209.68–354.77), p < 0.001; MMP‐9: SMD = 311.85 (95% CI = 179.64–444.05), p < 0.001. Conclusion Elevated salivary levels of IL‐1β, MMP‐8, and MMP‐9 are linked to periodontitis.

Hypertensive small vessel disease is a major cause of vascular cognitive impairment (VCI). Spontaneously hypertensive/stroke prone rats (SHR/SP) with unilateral carotid artery occlusion (UCAO) and a Japanese permissive diet (JPD) have white-matter (WM) damage similar to that seen in VCI. We hypothesized that WM injury was due to hypoxia-mediated, blood–brain barrier (BBB) disruption. Twelve-week-old SHR/SP had UCAO/JPD and were studied with immunohistochemistry, biochemistry, multimodal magnetic resonance imaging (MRI), and Morris water maze (MWM) testing. One week after UCAO/JPD, WM showed a significant increase in hypoxia inducible factor-1α (HIF-1α), which increased further by 3 weeks. Prolyl hydroxylase-2 (PHD2) expression decreased at 1 and 3 weeks. Infiltrating T cells and neutrophils appeared around endothelial cells from 1 to 3 weeks after UCAO/JPD, and matrix metalloproteinase-9 (MMP-9) colocalized with inflammatory cells. At 3 weeks, WM immunostained for IgG, indicating BBB leakage. Minocycline (50 mg/kg intraperitoeally) was given every other day from weeks 12 to 20. Multimodal MRI showed that treatment with minocycline significantly reduced lesion size and improved cerebral blood flow. Minocycline improved performance in the MWM and prolonged survival. We propose that BBB disruption occurred secondary to hypoxia, which induced an MMP-9-mediated infiltration of leukocytes. Minocycline significantly reduced WM damage, improved behavior, and prolonged life.