Disease relevance of Mouth Mucosa

• Fifteen of 33 (45%) squamous cell carcinomas of the head and neck expressed p53, but none of four normal control patients (cancer-free nonsmokers) expressed detectable p53 in oral mucosa specimens [1].
• These findings suggest that supplementation with the flavonoids diosmin and hesperidin, individually and in combination, is effective in inhibiting the development of oral neoplasms induced by 4-NQO, and such inhibition might be related to suppression of increased cell proliferation caused by 4-NQO in the oral mucosa [2].
• Topical application of transforming growth factor beta 3 to the oral mucosa of the Syrian golden hamster prior to chemotherapy significantly reduced the incidence, severity, and duration of oral mucositis, reduced chemotherapy-associated weight loss, and increased survival [3].
• Expression of EF along with hyperplasia was also observed in other squamous epithelia such as buccal mucosa, tongue and oesophagus [4].
• The results showed that vascularity, measured by the MVV method using antibodies to either vWF or CD31, increased significantly (P < 0.0001) with disease progression from normal oral mucosa, through mild, moderate, and severe dysplasia to early and late carcinoma (76 paraffin-embedded tissues examined) [5].

Psychiatry related information on Mouth Mucosa

• In this study, sensory and pain thresholds were compared to argon-, copper vapour-, Nd:YAG-, and CO2 laser stimulation on hairy skin and on oral mucosa [6].
• AIMS: Although nicotine replacement therapy (NRT) has been used to aid smoking cessation for the last 20 years, little information exists on the effect of nicotine products on the oral mucosa, particularly with regard to the direct effect at the site of application [7].
• The most common site of occurrence of SCC was the buccal mucosa (263/703 patients; 37.4%), both overall and in patients who chewed betel quid alone or in combination with cigarette smoking and/or alcohol consumption; the tongue was the most common site among patients without any oral habits (18/48 patients; 37.5%) [8].

High impact information on Mouth Mucosa

• Chemical injury of the oral mucosa from verapamil [9].
• Bioactivity of instant glucose. Failure of absorption through oral mucosa [10].
• RESULTS: One of 160 individuals had monoallelic MLH1 hypermethylation in peripheral blood, hair follicles, and buccal mucosa, indicative of a soma-wide alteration [11].
• Introducing a null mutation in the mouse K6alpha and K6beta genes reveals their essential structural role in the oral mucosa [12].
• p63 is a recently identified homolog of p53 that is found in the basal layer of several stratified epithelial tissues such as the epidermis, oral mucosa, prostate, and urogenital tract [13].

Chemical compound and disease context of Mouth Mucosa

• Autoantibody in mucous membrane pemphigoid binds to an intracellular epitope on human beta4 integrin and causes basement membrane zone separation in oral mucosa in an organ culture model [14].
• Upregulation of immunoregulatory Src homology 2 molecule containing inositol phosphatase and mononuclear cell hyporesponsiveness in oral mucosa during chronic periodontitis [15].
• These findings show that LPS, IL-1beta, and TNF-alpha induce lowering of P(if) in the rat oral mucosa and contribute to edema formation in LPS-induced gingivitis [16].
• Reduction in oral mucosa micronuclei frequency following alpha-tocopherol treatment of oral leukoplakia [17].
• The vitamin-A-deficient group also showed a high incidence of squamous papilloma in the tongue, buccal mucosa, and forestomach [18].

Biological context of Mouth Mucosa

• In addition to reverse transcriptase-polymerase chain reaction and Western blot, the ETS/Nic-dependent alterations in gene expression were also detected by semiquantitative immunofluorescence assay directly in KCs comprising murine oral mucosa [19].
• In concurrent oral mucosa biopsies, thymidylate synthase enzyme activity, a marker for DNA synthesis, had a circadian variation with peak activity in early afternoon, coinciding with the timing of S phase in our previous study on cell-cycle timing in human oral mucosa [20].
• The constitutive expression of pBD-1 in airway and oral mucosa, which is consistent with a lack of consensus binding sites for nuclear factor-kappaB or NF-IL-6 in its promoter region, suggests that it may play a surveillance role in maintaining the steady state of microflora on mucosal surfaces [21].
• PP and intestinal mucosa, but not tonsils or oral mucosa, express mucosal addressin cell adhesion molecule-1 (MAdCAM-1) [22].
• At the maximum tolerated dose, accumulation of prelamin A in buccal mucosa cells of patients was evaluated as a marker of farnesyl transferase inhibition by R115777 [23].

Anatomical context of Mouth Mucosa

• In organ culture of human oral mucosa, MMP-13 mRNA expression was observed in epithelial cells growing into connective tissue of the specimens [24].
• In contrast, the ADH3 protein is extremely stable, and consequently is retained during the keratinocyte life span in oral mucosa [25].
• We genetically analyzed the CIAS1 gene in various blood cells and the buccal mucosa of the patient [26].
• Two EPLIN isoforms, a 600 amino acid EPLIN-alpha and a 759 amino acid EPLIN-beta, are detected in primary epithelial cells of oral mucosa, prostate and mammary glands [27].
• In noninvolved oral mucosa, cD1 expression differs from that in truly normal epithelium obtained from nontumor patients [28].

Associations of Mouth Mucosa with chemical compounds

• CONCLUSION: In contrast to the prestudy hypothesis that a chlorhexidine mouthwash might provide benefit for patients receiving radiation therapy to the oral mucosa, this study provides strong evidence suggesting that a chlorhexidine mouthwash is detrimental in this clinical situation [29].
• Extracted DNA was 32P-postlabeled using the butanol enhancement method, and DNA adduct levels were quantified to compare the accuracy of adduct detection in buccal mucosa versus oral biopsies [30].
• Results of our metabolism studies showed that curcumin significantly inhibited CYP1A1-mediated benzo(a)pyrene diol bioactivation in both oral SCC cells and intact oral mucosa [31].
• Mechanisms of smokeless tobacco-induced oral mucosa inflammation: role of bradykinin [32].
• Finally, substantial capacity for formaldehyde detoxification is shown from quantitative assessments of alcohol- and aldehyde-oxidizing activities including K:(m) determinations, indicating that ADH3 is the major enzyme involved in formaldehyde oxidation in oral mucosa [25].

Gene context of Mouth Mucosa

• In this study, we investigated the effects of tobacco smoke on the expression of COX-2 in oral mucosa [33].
• Recently, elevated levels of amphiregulin, a ligand of the EGFR, were found in the oral mucosa of smokers [34].
• In sections including normal differentiated oral mucosa, the cells above the basal cell layer were positive for both TGF-alpha and EGF [35].
• Hyperproliferation is also observed in the buccal mucosa and the tongue epithelia of E6/E7 mice, and p53 levels are markedly increased in these epithelia [36].
• Immunoblotting was performed to compare Dsg1 and Dsg3 expression levels in extracts from epidermis and oral mucosa [37].

Analytical, diagnostic and therapeutic context of Mouth Mucosa

• Immunohistochemistry analysis done on oral cancers showed that normal oral mucosa (100%, 12 of 12) and 69.1% (47 of 68) of dysplastic oral epithelia expressed readily detectable hCG2 in the nuclei [38].
• Immunoblotting demonstrated that COX-2 protein was present in six of six cases of HNSCC but was undetectable in normal oral mucosa from healthy subjects [39].
• Localization of filaggrin, a human epithelial structural protein, was investigated by indirect-immunofluorescence microscopy of oral mucosa [40].
• By scraping, extraction, and semiquantitative Western blotting, the concentration of PBD-1 in the dorsal tongue surface and the buccal mucosa was estimated at 20 to 100 micrograms/ml [41].
• Oral mucosal lesions are seen in most cases of pemphigus vulgaris, whereas they are only rarely seen in pemphigus foliaceus; however, both pemphigus vulgaris and pemphigus foliaceus sera show positive immunofluorescence staining on oral mucosa [37].

References