Altered expression of MZB1 in periodontitis: A possible link to disease pathogenesis.

BACKGROUND: Our previous study explored the molecular signatures of generalized aggressive periodontitis (GAgP) using gingival tissues through omics-based-whole-genome transcriptomic analysis. This continuation study aimed to investigate the whole protein profiling of these gingival samples through liquid chromatography-mass spectroscopy/mass spectroscopy (LC-MS/MS) analysis and to validate the identified proteins through immunohistochemistry to provide further evidence for the quality of the results. METHODS: In previous study, gene expression patterns were identified in gingival tissues from 23 GAgP and 25 control individuals. In the current study, comparative proteomic analysis was performed on isolated proteins from the same study groups using LC-MS/MS analysis. The data from the transcriptomics study published before and the proteomics data were integrated to reveal any common genes and proteins. Additionally, immunohistochemical analysis was conducted to further investigate the findings. RESULTS: The most upregulated proteins in patients compared to controls were ITGAM, AZU1, MMP9, BPI, UGGG1, MZB1, TRFL, PDIA6, PRDX4, and PLG. The top six pathways associated with these proteins were involved in innate immune system, post-translational protein phosphorylation, interleukin-4 and -13 signaling, toll-like receptors cascades, and extracellular matrix organization. Based on the integration and validation analysis of transcriptomics and proteomics data, as well as immunohistochemical analysis, MZB1 was identified as a shared gene and protein that were upregulated in the patients. CONCLUSIONS: MZB1 is a protein that is involved in the development of B cells and the production of antibodies. Its upregulation in periodontitis suggests that there may be a dysregulation of the immune response in this condition, and MZB1 may be a potent biomarker for periodontitis.

The effects of smoking on genotoxic and histopathologic damage in exfoliated oral epithelial cells and the periodontium: A cross-sectional study.

Smoking negatively affects the prognosis of periodontal disease by impairing tissue healing. While micronucleus is the most popular parameter for demonstrating DNA damage, inflammatory cell and vascular densities are the most evaluated parameters for determining histopathologic changes in the periodontium. This study aimed to study the effects of periodontitis and cigarette smoking on genotoxic changes in exfoliated oral epithelial cells and histopathologic changes in periodontal tissue. A cross-sectional study was conducted between November 2018 and July 2019 at a dental university hospital in Turkey, and registered as NCT05484765. Eighty systemically healthy subjects were divided into four groups according to periodontal status and smoking habits: 20 smokers with generalized periodontitis (SGP), 20 nonsmokers with generalized periodontitis (NGP), 20 smokers with healthy periodontium (SHP), and 20 nonsmokers with healthy periodontium (NHP). For each study participant, full-mouth clinical periodontal parameters (CPPs) were measured, smear samples were taken from buccal and gingival mucosa, and periodontal tissue was biopsied from the maxillary molars. Cytogenetic and histopathologic assays (primary and secondary outcomes) were conducted using Feulgen reaction and hematoxylin-eosin staining, respectively. The mean CPPs of healthy periodontium groups were lower than generalized periodontitis groups. No significant differences were found between other groups regarding CPPs. Buccal micronuclei counts in groups decreased with the highest to lowest counts occurring in the order SGP > SHP > NGP > NHP. Gingival micronuclei counts in groups decreased from SGP > SHP > NGP = NHP. The most intense inflammatory cell and vascular densities occurred in SGP and NGP groups, respectively; and the mildest values were in healthy periodontium groups. Histopathological damage score decreased significantly by group in order SGP > NGP > SHP > NHP. The synergy arising from the combination of smoking and periodontitis exposures exacerbates genotoxic and histopathologic damage in oral cells and the periodontium.

Evaluation of adipokine levels in obese women with periodontitis: A cohort study.

PURPOSE: To evaluate the inflammation-related adipokine levels in the body fluids of obese female participants with and without periodontitis using healthy participants as a control group. METHODS: A cohort design study was carried out at Kocaeli University between December 2014 and June 2015. The study sample comprised 25 obese female participants with periodontitis (Group 1), 31 obese female participants without periodontitis (Group 2), and 15 lean female participants with healthy periodontium (Group 3), from whom body mass index, clinical periodontal parameters were measured, and serum, saliva, and gingival crevicular fluid (GCF) samples were collected. The three groups' periodontal parameters and adipokine levels were evaluated and compared, and the primary outcome was the difference in local and systemic adipokine levels between the study groups. RESULTS: In the participants' serum samples, tumor necrosis factor-α (TNF-α) and leptin levels were lower, whereas adiponectin levels were significantly higher in Group 3 than in the obese groups (P< 0.05). In the participants' saliva samples, interleukin-1ß, TNF-α, and resistin levels were lowest in Group 3, but adiponectin was lowest in Group 2 (P< 0.05). In the participants' GCF samples, interleukin-1ß, resistin, and adiponectin levels were higher in Group 1 (P< 0.05). This study showed that the amounts of the adipokines could differ in serum, saliva, and GCF samples from obese female participants with and without periodontitis and from lean female participants with healthy periodontium. CLINICAL SIGNIFICANCE: Periodontal diseases in different severities can affect overall health by altering the amounts of adipokines (IL-1ß, TNF-α, leptin, resistin, and adiponectin) in serum, saliva, and GCF of obese female patients. Clinicians should be aware that periodontal disease can alter inflammatory adipokine levels and may affect other treatment outcomes in obese female patients.

Molecular signatures of chronic periodontitis in gingiva: A genomic and proteomic analysis.

BACKGROUND: To elucidate molecular signatures of chronic periodontitis (CP) using gingival tissue samples through omics-based whole-genome transcriptomic and whole protein profiling. METHODS: Gingival tissues from 18 CP and 25 controls were analyzed using gene expression microarrays to identify gene expression patterns and the proteins isolated from these samples were subjected to comparative proteomic analysis by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The data from transcriptomics and proteomics were integrated to reveal common shared genes and proteins. RESULTS: The most upregulated genes in CP compared with controls were found as MZB1, BMS1P20, IGLL1/IGLL5, TNFRSF17, ALDH1A1, KIAA0125, MMP7, PRL, MGC16025, ADAM11, and the most upregulated proteins in CP compared with controls were BPI, ITGAM, CAP37, PCM1, MMP-9, MZB1, UGTT1, PLG, RAB1B, HSP90B1. Functions of the identified genes were involved cell death/survival, DNA replication, recombination/repair, gene expression, organismal development, cell-to-cell signaling/interaction, cellular development, cellular growth/proliferation, cellular assembly/organization, cellular function/maintenance, cellular movement, B-cell development, and identified proteins were involved in protein folding, response to stress, single-organism catabolic process, regulation of peptidase activity, and negative regulation of cell death. The integration and validation analysis of the transcriptomics and proteomics data revealed two common shared genes and proteins, MZB1 and ECH1. CONCLUSION: Integrative data from transcriptomics and proteomics revealed MZB1 as a potent candidate for chronic periodontitis.