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1 PTEN's role in the etiology of drug-induced gingival overgrowth.
2 ve a role in the pathogenesis of CsA-induced gingival overgrowth.
3 se and tensin homolog (PTEN) in drug-induced gingival overgrowth.
4 diseases, is overexpressed in the tissue of gingival overgrowth.
5 emory T cells play a key role in CsA-induced gingival overgrowth.
6 iting role of curcumin in the development of gingival overgrowth.
7 ens of eight adult patients with generalized gingival overgrowth.
8 characteristic of all drug-induced forms of gingival overgrowth.
9 nifedipine, and cyclosporine-A often causes gingival overgrowth.
10 hesis that EMT likely occurs in drug-induced gingival overgrowth.
11 CCN2/CTGF expression is elevated in fibrotic gingival overgrowth.
12 ltaneous decrease in apoptosis contribute to gingival overgrowth.
13 poptosis could contribute to the etiology of gingival overgrowth.
14 h are the main complications of drug-induced gingival overgrowth.
15 fibrogenic molecules in gingiva and promote gingival overgrowth.
16 itive effect of those drugs on the degree of gingival overgrowth.
17 e inhibitor and estradiol benzoate developed gingival overgrowth.
18 (HGF) is a rare, autosomal dominant form of gingival overgrowth.
19 trols, cyclosporin A-, or nifedipine-induced gingival overgrowth.
20 ent of fibrotic lesions in phenytoin-induced gingival overgrowth.
21 ted with CsA treatment is the development of gingival overgrowth.
22 tant role in the pathogenesis of CsA-induced gingival overgrowth.
23 requent side effect of CSA administration is gingival overgrowth.
24 rticularly in the oral cavity manifesting as gingival overgrowth.
25 ted with isradipine exhibited an increase in gingival overgrowth.
26 e extent, or prevalence of phenytoin-induced gingival overgrowth.
27 if any, between phenytoin or HPPH levels and gingival overgrowth.
28 ssessed for signs of periodontal disease and gingival overgrowth.
29 n in man, and the prevalence and severity of gingival overgrowth.
30 prevent or attenuate phenytoin-induced human gingival overgrowth, although specific human studies are
31 ues from 20 different individuals with human gingival overgrowth and 15 non-overgrowth samples were e
32 mouse model to mimic human phenytoin-induced gingival overgrowth and assess the ability of a drug to
33 th in mice mimics molecular aspects of human gingival overgrowth and that lovastatin normalizes the t
34 Two-year follow-up revealed that both the gingival overgrowth and the destructive lesions were suc
35 howed severe gingival inflammation with some gingival overgrowth and various degrees of periodontal a
36 patients and PHT-treated patients exhibiting gingival overgrowth as well as patients with severe ging
38 nt of prevention or treatment modalities for gingival overgrowth based on blocking the fibrogenic act
40 ve demonstrated that other drugs which cause gingival overgrowth can upregulate macrophage PDGF-B gen
46 wed that apoptosis decreased in all forms of gingival overgrowth examined (p < 0.05), and inflammatio
49 and periodontal variables were collected and gingival overgrowth (GO) was assessed by visual examinat
52 ing the molecular mechanisms of drug-induced gingival overgrowth have demonstrated that PHT alters th
53 ival overgrowth in children are drug-induced gingival overgrowth, hereditary gingival fibromatosis (H
57 rmine whether the prevalence and severity of gingival overgrowth in renal transplant recipients conco
58 e TGF-beta1 gene influence the expression of gingival overgrowth in renal transplant recipients conco
59 an independent genetic determinant of severe gingival overgrowth in the susceptible subjects studied.
60 characterization of phenytoin-induced human gingival overgrowth in vivo and in vitro characteristics
61 re were significant correlations between the gingival overgrowth index and both the papillary bleedin
66 Thus, estradiol alone prevented the onset of gingival overgrowth induced by estrogen suppression.
67 rat hyperplastic connective tissue and human gingival overgrowth induced by PHT treatment revealed th
76 ecular and cellular characteristics of human gingival overgrowth lesions and highlight how they diffe
79 hogenetic mechanisms underlying drug-induced gingival overgrowth may be enhanced secretion of IL-6 by
80 ular mechanisms responsible for drug-induced gingival overgrowth may involve upregulation of PDGF-B m
81 These findings elucidate the mechanisms for gingival overgrowth mediated by SOS1 gene mutation in hu
83 rst report on direct and indirect effects of gingival overgrowth-related medications on GF IL-6 metab
84 s that epithelial plasticity and EMT promote gingival overgrowth, resulting in compromised basal memb
86 odon 25 had a significantly higher (P= 0.04) gingival overgrowth score than those who were homozygous
87 l proliferation was elevated in all forms of gingival overgrowth tested, independent of inflammation
89 cision is the current treatment modality for gingival overgrowth, the recurrent rate is high despite
91 ly higher CTGF staining in phenytoin-induced gingival overgrowth tissues compared to controls, cyclos
96 and extracellular CTGF content in phenytoin gingival overgrowth tissues was significantly (P<0.05) h
101 atients receiving CSA therapy and exhibiting gingival overgrowth to determine if similar PDGF-B upreg
103 or codon 25 independent predictors of severe gingival overgrowth were the heterozygous arginine/proli
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