Disease relevance of Gingiva

• Metabolism of phenytoin by the gingiva of normal humans: the possible role of reactive metabolites of phenytoin in the initiation of gingival hyperplasia [1].
• The biosynthesis of radioactive prostaglandin E2 (PGE2) and F2 alpha from (1-14C) arachidonic acid has been demonstrated in the microsomal fraction of gingiva of patients with chronic periodontitis in vitro [2].
• Gingival fibromatosis (GINGF) is an oral disorder characterized by enlargement of the gingiva [3].
• Prostaglandin E1 or E2 solutions injected in gingiva lying near the upper first molar caused the appearance of osteoclasts and bone resorption [4].
• To investigate this question, we have studied whether TGF-beta1 may differentially regulate the expression of urokinase at the protein level in primary cultures of fibroblasts derived from healthy gingiva, granulation tissue from gingival wounds, and chronic periodontal disease [5].

High impact information on Gingiva

• Incubation of tissue sections with this antibody and fluorescein isothiocyanate-conjugated secondary antibody revealed that it immunostains cementum but not dentin, gingiva, or periodontal ligament [6].
• No significant K2e expression in nonkeratinized or keratinized oral epithelia, including buccal mucosa, lateral border of tongue and gingiva was detected [7].
• Epithelial cells from inflamed gingiva expressed HLA-DR, CD1a, CD1c, and heat shock protein 60 on the cell surface [8].
• RESULTS: P-gp is expressed in the endothelial layers of blood vessels obtained from healthy or inflamed gingiva [9].
• CXCR4 expression in metastatic cancer tissue was significantly higher than that in nonmetastatic cancer tissue or normal gingiva [10].

Chemical compound and disease context of Gingiva

• In the cases presented in this report, Kaposi's sarcoma developed in the gingiva of two patients with cyclosporine-induced gingival hyperplasia [11].
• Tumor necrosis factor-alpha and its receptors, p55 and p75, in gingiva of adult periodontitis [12].
• Mononuclear cells isolated from gingiva of AP patients did not contain cells producing antibody to antigens such as Escherichia coli K235 LPS, cholera toxin or the hapten dinitrophenyl coupled to bovine serum albumin [13].
• Using bovine gingiva lysate as substrate in an immunoblot assay, autoantibodies to human bullous pemphigoid antigens (BPAg1 and BPAg2), human beta4 integrin, and laminin 5 were measured [14].
• Mannosidosis: isolation and comparison of mannose-containing oligosaccharides from gingiva and urine [15].

Biological context of Gingiva

• Thus we have shown that when cells from the three areas of the gingiva were grown in culture they revert to one phenotype, at least with respect to their keratin expression [16].
• It is suggested that p53 expression associated with DNA damage is a prevalent phenomenon in chronically inflamed human gingiva, and that apoptosis may be a relevant process for the maintenance of local immune homeostasis at sites of chronic bacterial challenge in vivo [17].
• Differences between tooth stimulation and capsaicin-induced neurogenic vasodilatation in human gingiva [18].
• Confirmation that neither phenotype nor hydroxylation of collagen is altered in overgrown gingiva from diphenylhydantoin-treated patients [19].
• CONCLUSIONS: These results are consistent with a significant role for estrogen during primate pregnancy in the regulation of cellular proliferation and differentiation within the gingiva [20].

Anatomical context of Gingiva

• We found that microsomes obtained from the gingiva show significant phenytoin hydroxylase activity as determined by the production of 5-(4'-hydroxyphenyl)-5-phenylhydantoin (HPPH) (range, 12.8 pmol HPPH/min.mg microsomal protein to 276.9 pmol HPPH/min.mg microsomal protein; rat control, 133.7 +/- 11.5 pmol HPPH/min.mg microsomal protein) [1].
• An enzyme with similar activity was also identified in media conditioned by fibroblasts from rat periodontal ligament and gingiva, and by rat osteoblastic cells (ROS 17/2.8, 17/2A, 17/2B) [21].
• In AP, protectin was also strongly expressed by endothelial cells, but in the epithelia the expression was granular and weaker than in the healthy gingiva [22].
• The effect of ethanol on testosterone-5 alpha-A-ring reductase activity was studied in the whole homogenate and/or subcellular fractions (microsomes and cytosol) of buccal mucosa, gingiva, liver and prostate from intact ethanol-fed (36% of dietary calories were given as ethanol for up to 360 days) and pair-fed control rats [23].
• The antibody localized to the prickle-cell layer and to granular layer keratinocytes of human gingiva [24].

Associations of Gingiva with chemical compounds

• Specific estrogen receptors in human gingiva [25].
• We believe that these data support our hypothesis that the proliferative inflammation observed with drugs such as phenytoin, nifedipine, and cyclosporine may be initiated by the formation of reactive metabolites and that the formation of these metabolites may be catalyzed by one or more CYPs found in the gingiva [1].
• Specific 5 alpha-dihydrotestosterone receptors in human gingiva [26].
• The cytoplasm of normal human male and female gingiva contains a receptor capable of specifically binding 17 beta-estradiol and moxestrol (R-2858) with high affinity (Kd = approximately 3.4 X 10(-10) M) and low capacity (4.5 fmol/mg protein) [25].
• In two sessions, intraoral pain was evoked by topical application of 30microL 5% capsaicin to the gingiva [27].

Gene context of Gingiva

• By RT-PCR, we found CTSC is also expressed in epithelial regions commonly affected by PLS, including the palms, soles, knees, and oral keratinised gingiva [28].
• We have also isolated MNC from patients with CP and those with healthy gingiva and show that MNC from CP subjects have a reduced capacity to upregulate TLR2, TLR4, and interleukin-1beta in response to endotoxin [29].
• Interleukin-1 (IL-1) may play a critical role in immune and inflammatory responses in inflamed gingiva, and it is synthesized by a wide variety of host cells [30].
• Since there was a marked difference of S100A4 expression between PDL and gingiva, we propose that S100A4 could be a useful marker for distinguishing cells from these two tissues [31].
• As human gingival fibroblasts (HGF) can be potential targets for TNF-alpha in inflamed gingiva, we hypothesized that HGF partially modulate the cellular responses to TNF-alpha by regulating their own TNFR [32].

Analytical, diagnostic and therapeutic context of Gingiva

• The most coronal 1 mm of gingiva was removed from maxillary and mandibular right molar quadrants (gingivectomy), and the animals re-inoculated following gingivectomy [33].
• Light and transmission electron microscopy of the intact interfaces between non-submerged titanium-coated epoxy resin implants and bone or gingiva [34].
• The distributions of substance P (SP) and the neurokinin-1 receptor (NK1-R), the receptor preferentially activated by SP, were examined in rat gingiva by immunocytochemical methods with light and electron microscopy [35].
• Unilateral surgical sympathectomy or resection of the inferior alveolar nerve failed to affect 5-HT levels in either tissue while dopamine contents in the pulp and gingiva were diminished following sympathectomy [36].
• Laser-Doppler flowmetry was utilized to measure oral tissue vasoconstrictor responses in the maxillary gingiva and from the surface of the tongue [37].

References