Synergistic enhancement of collagenous protein synthesis by human gingival fibroblasts exposed to nifedipine and interleukin‐1‐beta <i>in vitro</i>

Johnson, Roger B.; Zebrowski, E.J.; Dai, Xuemei

doi:10.1034/j.1600-0714.2000.290102.x

Cited by 22 publications

(23 citation statements)

References 30 publications

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“…23 Interleukin-6 has been shown to target connective tissue cells, such as fibroblasts, both by enhancing their proliferation and by increasing collagen production and glycosaminoglycan synthesis. 24 This highlights the role of the bacterial biofilm in inducing gingival inflammation, production of cytokines and gingival enlargement.…”

Section: Role Of Matrix Metalloproteinasesmentioning

confidence: 99%

Calcium channel blocker-induced gingival enlargement

Livada

Shiloah

2013

J Hum Hypertens

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Despite the popularity and wide acceptance of the calcium channel blockers (CCBs) by the medical community, their oral impact is rarely recognized or discussed. CCBs, as a group, have been frequently implicated as an etiologic factor for a common oral condition seen among patients seeking dental care: drug-induced gingival enlargement or overgrowth. This enlargement can be localized or generalized, and can range from mild to extremely severe, affecting patient's appearance and function. Treatment options for these patients include cessation of the offending drug and substitution with another class of antihypertensive medication to prevent recurrence of the lesions. In addition, depending on the severity of the gingival overgrowth, nonsurgical and surgical periodontal therapy may be required. The overall objective of this article is to review the etiology and known risk factors of these lesions, their clinical manifestations and periodontal management.

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Section: Role Of Matrix Metalloproteinasesmentioning

confidence: 99%

Calcium channel blocker-induced gingival enlargement

Livada

Shiloah

2013

J Hum Hypertens

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“…It has been hypothesized that vulnerability or resistance to drug induced gingival enlargement may be caused by the existence of variable proportions of fibroblast subsets in each individual thus eliciting a fibrogenic response. [34] As far as the role of inflammatory cytokines is concerned, it was proven that when human gingival fibroblasts were simultaneously exposed to nifedipine and pro-inflammatory cytokines (interleukin-1b and IL-6), that are elevated in inflamed gingival tissues, an up regulation of synthesis of collagen was observed. [45] It has also been postulated that matrix metalloproteinases (MMPs) which are implicated in gingival enlargement may interfere with the synthesis and function of collagenases.…”

Section: Introductionmentioning

confidence: 99%

Gene Polymorphism in Amlodipine Induced Gingival Hyperplasia: A Case Report

Charles¹,

Ramesh²,

Babu³

et al. 2012

Journal of Young Pharmacists

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The management of cardiovascular disorders poses a dilemma for the medical fraternity. Calcium channel blockers are one of the most commonly used drugs for the management of this disorder, and it is also a well known fact that they are one of the most common group of drugs responsible for causing gingival over growth as one of their adverse effects. Amlodipine is a new generation hypertensive, which has found wide acceptance and usage due to its duration of action. Even with all its benefits as a potent hypertensive, its effect on gingival tissues is what causes concern to the patient and dental surgeon equally. The objective of this article is to create awareness regarding the adverse oral effects of amlodipine, its underlying mechanism of action in bringing about this adverse reaction, along with providing a brief review of the pharmacologic profile of this drug.

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“…Some hypotheses have suggested the role of factors such as 1) fibroblasts [27–32], 2) inflammatory cytokines [30, 33–36], and 3) matrix metalloproteinase (MMP) synthesis [31]. CsA, nifedipine, and phenytoin promote the modeling of periodontal fibroblasts through the synthesis of gingival fibroblasts or inhibition of the decomposition of gingival fibroblasts [27–31].…”

Section: Discussionmentioning

confidence: 99%

“…CsA, nifedipine, and phenytoin promote the modeling of periodontal fibroblasts through the synthesis of gingival fibroblasts or inhibition of the decomposition of gingival fibroblasts [27–31]. Phenytoin may increase the level of translatable collagen mRNA in human gingival fibroblast [32], while CsA, nifedipine, and phenytoin enhance the synthesis of collagenous proteins in vitro [30, 33–36]. In the case of human gingival fibroblasts simultaneously exposed to nifedipine and interleukin-1β [33], an enhancement of collagenous protein synthesis was observed [33].…”

Section: Discussionmentioning

confidence: 99%

“…Phenytoin may increase the level of translatable collagen mRNA in human gingival fibroblast [32], while CsA, nifedipine, and phenytoin enhance the synthesis of collagenous proteins in vitro [30, 33–36]. In the case of human gingival fibroblasts simultaneously exposed to nifedipine and interleukin-1β [33], an enhancement of collagenous protein synthesis was observed [33]. CsA may cause a decline in the secretion of MMP-1 and an accumulation of collagenous proteins [31].…”

Section: Discussionmentioning

confidence: 99%

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Drug-induced gingival hyperplasia: a retrospective study using spontaneous reporting system databases

Hatahira

Abe

Hane

et al. 2017

J Pharm Health Care Sci

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BackgroundDrug-induced gingival hyperplasia (DIGH) causes problems with chewing, aesthetics, and pronunciation, and leads to the deterioration of the patient’s quality of life (QOL). Thus, the aim of this study was to evaluate the incidence of DIGH using spontaneous reporting system (SRS) databases.MethodsWe analyzed reports of DIGH from SRS databases and calculated the reporting odds ratios (RORs) of suspected drugs (immunosuppressants, calcium channel blockers, and anticonvulsants). The SRS databases used were the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) and the Japanese Adverse Drug Event Report (JADER) database. With the data, we evaluated the time-to-onset profile and the hazard type using the Weibull shape parameter (WSP). Furthermore, we used the association rule mining technique to discover undetected relationships such as possible risk factors.ResultsThe FAERS contained 5,821,716 reports. The RORs (95% confidence interval: CI) for cyclosporine, everolimus, sirolimus, mycophenolate mofetil, amlodipine, nifedipine, carbamazepine, clobazam, levetiracetam, phenobarbital, phenytoin, primidone, topiramate, and valproic acid, were 39.4 (95% CI: 30.3–51.2), 4.2 (1.7–10.0), 6.6 (2.5–17.7), 13.1 (7.2–23.2), 94.8 (80.0–112.9), 57.9 (35.7–94.0), 15.1 (10.3–22.3), 65.4 (33.8–126.7), 6.5 (3.6–11.8), 19.7 (8.8–44.0), 65.4 (52.4–82.9), 56.5 (21.1–151.7), 2.9 (1.1–7.7), and 17.5 (12.6–24.4), respectively. The JADER database contained 430,587 reports. The median time-to-onset of gingival hyperplasia values for immunosuppressants, calcium channel blockers, and anticonvulsants use were 71, 262, and 37 days, respectively. Furthermore, the 95% CI of the WSP β for anticonvulsants was over and excluded 1, which meant that they were wear-out failure type.ConclusionsOur results suggest that DIGH monitoring of patients administered immunosuppressants, calcium channel blockers, or anticonvulsants is important. We demonstrated the potential risk of DIGH following the long-term use of calcium channel blocker over approximately 260 days. Based on the results of the association rule mining approach, patients with intellectual disability who are administered phenytoin should be monitored carefully. We recommend that patients who experience symptoms related to DIGH should be closely monitored.

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Synergistic enhancement of collagenous protein synthesis by human gingival fibroblasts exposed to nifedipine and interleukin‐1‐beta in vitro

Cited by 22 publications

References 30 publications

Calcium channel blocker-induced gingival enlargement

Calcium channel blocker-induced gingival enlargement

Gene Polymorphism in Amlodipine Induced Gingival Hyperplasia: A Case Report

Drug-induced gingival hyperplasia: a retrospective study using spontaneous reporting system databases

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