The correlated expression of COX-2 and keratin 15 in radicular cysts

The expression of cyclooxygenase-2 (COX-2) and Keratin-15 (K15) in radicular cysts (RCs) is poorly understood. Identifying the expression of these two markers may modify the current treatment of RC. The objective of this study was to evaluate the express

Prevalence of unculturable bacteria in the periapical abscess: A systematic review and meta-analysis

Objective To assess the prevalence of unculturable bacteria in periapical abscess, radicular cyst, and periapical granuloma. Methods PubMed, Scopus, Science Direct, and Ovid databases were systematically searched from January 1990 to May 2020. All the included studies were cross-sectional design. The risk of bias was assessed using Joanna Briggs Institute check-list. Heterogeneity was described using meta-regression and mixed-effects model for lesion, country, and sequence technique moderators. Funnel plot and unweighted Egger's regression test were used to estimate the publication bias. Microbiome data on diversity, abundance, and frequency of unculturable bacteria in the periapical lesions were reviewed, analysed, and the principal component analysis (PCA) was performed. Results A total of 13 studies out of 14,780, were selected for the final analysis. These studies focused on the prevalence of unculturable bacteria in periapical abscesses and related lesions. Approximately 13% (95% CI: 7-23%) of the cumulative number of bacteria derived from periapical abscesses was unculturable. Country moderator significantly (P = 0.05) affects the diversity summary proportion. While the pooled frequency of unculturable bacteria was 8%; 95% CI: 5, 14%, the estimate of the pooled abundance of unculturable bacteria was 5%; 95% CI: 2, 12% with a significant (P = 0.05) country moderator that affects the abundance summary proportion. Of the 62 unculturable bacteria, 35 were subjected to PCA and Peptostreptococcus sp. oral clone CK035 was the most abundant species in periapical abscesses. Hybridization techniques were found to be the most reliable molecular methods in detecting the abundance and frequency of unculturable bacteria. Conclusion The significant prevalence of unculturable bacteria in the periapical abscess, suggests that they are likely to play, a yet unknown, critical role in the pathogenesis and progression of the disease. Further research remains to be done to confirm their specific contributions in the virulence and disease progression

Molecular pathogenicity of 1-nonadecene and l-lactic acid, unique metabolites in radicular cysts and periapical granulomas

Recently, 1-nonadecene and l-lactic acid were identified as unique metabolites in radicular cysts and periapical granuloma, respectively. However, the biological roles of these metabolites were unknown. Therefore, we aimed to investigate the inflammatory and mesenchymal-epithelial transition (MET) effects of 1-nonadecene, and the inflammatory and collagen precipitation effects of l-lactic acid on both periodontal ligament fibroblasts (PdLFs) and peripheral blood mononuclear cells (PBMCs). PdLFs and PBMCs were treated with 1-nonadecene and l-lactic acid. Cytokines’ expression was measured using quantitative real-time polymerase chain reaction (qRT-PCR). E-cadherin, N-cadherin, and macrophage polarization markers were measured using flow cytometry. The collagen, matrix metalloproteinase (MMP)-1, and released cytokines were measured using collagen assay, western blot, and Luminex assay, respectively. In PdLFs, 1-nonadecene enhances inflammation through the upregulation of some inflammatory cytokines including IL-1β, IL-6, IL-12A, monocyte chemoattractant protein (MCP)-1, and platelet-derived growth factor (PDGF) α. 1-Nonadecene also induced MET through the upregulation of E-cadherin and the downregulation of N-cadherin in PdLFs. 1-Nonadecene polarized macrophages to a pro-inflammatory phenotype and suppressed their cytokines’ release. l-lactic acid exerted a differential impact on the inflammation and proliferation markers. Intriguingly, l-lactic acid induced fibrosis-like effects by enhancing collagen synthesis, while inhibiting MMP-1 release in PdLFs. These results provide a deeper understanding of 1-nonadecene and l-lactic acid’s roles in modulating the microenvironment of the periapical area. Consequently, further clinical investigation can be employed for target therapy

The Prevalence of EBV and KSHV in Odontogenic Lesions

Objectives: Odontogenic lesions evolve as a result of altered dental development. This study aimed to evaluate the prevalence and the coinfection of Epstein-Barr virus (EBV) and Kaposi sarcoma–associated herpesvirus (KSHV) in radicular cysts, dentigerous cysts, odontogenic keratocysts, and ameloblastomas. Methods: Polymerase chain reaction (PCR) was used to analyse 66 cases of odontogenic lesions for the presence of EBV-DNA and KSHV-DNA. These lesions were 15 radicular cysts, 16 dentigerous cysts, 18 odontogenic keratocysts, and 17 ameloblastomas. Results: EBV-DNA was detected in 24 (36.4%) of the studied samples as follows: 6 samples (40.0%) of radicular cysts, 4 (25.0%) of dentigerous cysts, 10 (55.6 %) of odontogenic keratocysts, and 4 (23.5%) of ameloblastomas (P = .168). KSHV-DNA was found in 16 (24.2%) of the studied samples as follows: 1 sample (6.7%) of radicular cysts, 6 (37.5%) of dentigerous cysts, 8 (44.4 %) of odontogenic keratocysts, and 1 (5.9%) of ameloblastomas (P = .001). Additionally, EBV and KSHV were positively correlated in all studied samples (P = .002). Conclusions: Both EBV and KSHV are found in odontogenic cysts and ameloblastomas. KSHV and EBV are more prevalent in odontogenic keratocysts than in other studied odontogenic lesions. Further, there is a high prevalence of EBV and KSHV coinfection in odontogenic cysts and ameloblastomas

The response of salivary proinflammatory biomarkers to tooth extraction in individuals with type II diabetes mellitus

Abstract Purpose This study investigated the levels of salivary proinflammatory cytokines in the saliva of patients living with type II diabetes mellitus (DM) compared to those in healthy individuals three times: before tooth extraction and at 2 hours and 2 days after tooth extraction. Methods The study included 27 participants. Among them, 20 (n = 20; 74%) had type II DM, and seven (n = 7; 26%) were healthy control subjects. Saliva samples were collected at three time intervals: before tooth extraction and 2 hours and 2 days after tooth extraction. The salivary biomarkers were investigated using a Luminex multiplex assay. These salivary biomarkers included tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), interleukin 1-beta (IL-1β), and interferon-gamma (IFN-γ). Results At baseline, patients with type II DM had significantly lower levels of IL-1β (P = 0.016). Moreover, 2 hours after extraction, patients with type II DM had significantly lower levels of IL-1β and TNF-α than did healthy control subjects (P = 0.046 and P = 0.020, respectively). In addition, 2 days after tooth extraction, the DM group had significantly greater IL-6 levels (P = 0.010) than the control group. Conclusions In patients with type II DM, salivary proinflammatory biomarker levels are generally comparable or lower than those in healthy control subjects. Proinflammatory cytokines manifest differently in patients with type II DM after tooth extraction than in normal healthy individuals. There is generally a delayed early response of salivary proinflammatory markers in patients living with type II DM who undergo tooth extraction

Molecular pathogenicity of 1-nonadecene and l-lactic acid, unique metabolites in radicular cysts and periapical granulomas

Abstract Recently, 1-nonadecene and l-lactic acid were identified as unique metabolites in radicular cysts and periapical granuloma, respectively. However, the biological roles of these metabolites were unknown. Therefore, we aimed to investigate the inflammatory and mesenchymal-epithelial transition (MET) effects of 1-nonadecene, and the inflammatory and collagen precipitation effects of l-lactic acid on both periodontal ligament fibroblasts (PdLFs) and peripheral blood mononuclear cells (PBMCs). PdLFs and PBMCs were treated with 1-nonadecene and l-lactic acid. Cytokines’ expression was measured using quantitative real-time polymerase chain reaction (qRT-PCR). E-cadherin, N-cadherin, and macrophage polarization markers were measured using flow cytometry. The collagen, matrix metalloproteinase (MMP)-1, and released cytokines were measured using collagen assay, western blot, and Luminex assay, respectively. In PdLFs, 1-nonadecene enhances inflammation through the upregulation of some inflammatory cytokines including IL-1β, IL-6, IL-12A, monocyte chemoattractant protein (MCP)-1, and platelet-derived growth factor (PDGF) α. 1-Nonadecene also induced MET through the upregulation of E-cadherin and the downregulation of N-cadherin in PdLFs. 1-Nonadecene polarized macrophages to a pro-inflammatory phenotype and suppressed their cytokines’ release. l-lactic acid exerted a differential impact on the inflammation and proliferation markers. Intriguingly, l-lactic acid induced fibrosis-like effects by enhancing collagen synthesis, while inhibiting MMP-1 release in PdLFs. These results provide a deeper understanding of 1-nonadecene and l-lactic acid’s roles in modulating the microenvironment of the periapical area. Consequently, further clinical investigation can be employed for target therapy