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1 in D/VDR signaling induces miR-27a/b in oral lichen planus.
2 , 2011, of patients with a diagnosis of otic lichen planus.
3 t that LS does not affect the vagina, unlike lichen planus.
4 sentation, diagnosis, and management of otic lichen planus.
5 prototypic skin disease in this category is lichen planus.
6 onsible for the prototypic LTR/IFD disorder, lichen planus.
7 2-induced apoptosis of keratinocytes in oral lichen planus.
8 s had oral lesions that clinically resembled lichen planus.
9 y show persistent signs and symptoms of oral lichen planus.
10 cts or in subjects with atopic dermatitis or lichen planus.
11 jects with psoriasis, atopic dermatitis, and lichen planus.
12 rythematosus, alopecia areata, vitiligo, and lichen planus.
13 (P = .04) and oral mucosal disorders such as lichen planus.
14 throplakia, oral submucous fibrosis, or oral lichen planus.
15 efficacy and safety profile in treating nail lichen planus.
16 be a therapeutic approach for treating nail lichen planus.
18 al different disease processes, particularly lichen planus and benign mucous membrane pemphigoid.
19 n and immune response in common between Oral Lichen Planus and early and advanced Oral Squamous Cell
20 presentation pathways in common between Oral Lichen Planus and early Oral Squamous Cell Carcinoma.
21 va were collected from 25 patients with oral lichen planus and from 25 age- and sex-matched controls.
23 lyzed the gene expression signatures of Oral Lichen Planus and Oral Squamous Cell Carcinoma in early
24 ate similarities in the gene profile of Oral Lichen Planus and Oral Squamous Cell Carcinoma that may
25 ucosal inflammatory diseases, including oral lichen planus and recurrent aphthous stomatitis, are pai
26 s do not support an association between oral lichen planus and salivary dysfunction in otherwise heal
27 patients with OSCC-R, and patients with oral lichen planus and served as a characteristic biomarker o
28 ases were associated with biopsy-proven oral lichen planus, and all five patients had oral lesions th
31 CC in remission (OSCC-R), patients with oral lichen planus, and healthy controls (HCs)-using a genome
32 eous inflammatory conditions, including oral lichen planus, are common, but development of new treatm
33 o, cutaneous lupus erythematosus, psoriasis, lichen planus, autoimmune bullous diseases, systemic scl
35 an increasingly prevalent form of follicular lichen planus, causing irreversible hair loss predominan
36 flammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls).
39 orrheic dermatitis," "alopecia areata," and "lichen planus." Diverse study populations were defined a
40 tudies have reported new-onset psoriasis and lichen planus following TNFalpha antagonist therapy.
41 unity in GS was uncommon, consisting of oral lichen planus, graft-vs-host disease-like colitis, and p
42 ature to support the position that true oral lichen planus has no inherent predisposition to become m
44 udy was undertaken to determine whether oral lichen planus in otherwise healthy patients is associate
47 rrounding the premalignant potential of oral lichen planus is provided with evidence, rationale, and
48 hroplakia, oral submucous fibrosis, and oral lichen planus-is crucial for early detection and improve
49 R, 0.703; 95% CI, 0.497-0.994; P = .045) and lichen planus/lichenoid dermatitis (HR, 0.511; 95% CI, 0
52 were squamous cell carcinoma, 39 (8.5%) were lichen planus-like keratosis, 21 (4.6%) were melanomas,
53 lanocytic lesions (eg, seborrheic keratosis, lichen planus-like keratosis, basal cell carcinomas) mis
54 ding solar lentigo, seborrheic keratosis and lichen planus-like keratosis; dermatofibroma; melanoma;
55 se report we describe the occurrence of oral lichen planus-like lesions as the first manifestation of
56 phigus vulgaris, mucous membrane pemphigoid, lichen planus, linear immunoglobulin A disease, and chro
60 ognition of the nonspecific symptoms of otic lichen planus may lead to prompt treatment and avoidance
64 the origin and development mechanism of oral lichen planus (OLP) with limited attention to the role o
66 naling has been shown in the context of oral lichen planus (OLP), the molecular basis of its regulato
67 al specimens of patients suffering with oral lichen planus (OLP), the molecular mechanism of miR-27b
69 as benign mucous membrane pemphigoid, 10 as lichen planus or lichenoid mucositis (LP), and one as pe
70 is study, 30 cases were diagnosed as erosive lichen planus or lichenoid mucositis; 29 cases were diag
74 al diagnoses not optimally supported on DIF: lichen planus, porphyria, and connective tissue disease.
75 d at relieving symptoms and controlling oral lichen planus progression is hampered by the lack of exp
76 ds alopecia areata, acne, atopic dermatitis, lichen planus, psoriasis, seborrheic dermatitis, and vit
77 porphyria cutanea tarda [PCT], vitiligo, and lichen planus); renal (membranous glomerulonephritis [GN
78 inflammatory diseases, including psoriasis, lichen planus, rheumatoid arthritis, and inflammatory bo
79 main outcome was posttreatment clinical nail lichen planus severity index, which was scored as clear,
81 l disease, type 2 diabetes, B-cell lymphoma, lichen planus, Sjogren's syndrome, porphyria cutanea tar
83 t association between HCV infection and PCT, lichen planus, vitiligo, cryoglobulinemia, membranoproli
86 hroplakia, oral submucous fibrosis, and oral lichen planus were identified using International Statis
88 tes 7 adult patients with biopsy-proven nail lichen planus who were treated with low-dose naltrexone