Bergen Open Research Archive

Pathological mechanisms in oral lichen planus : a atudy of apoptosis - regulatory proteins and risk markers for malignant transformation

Bergen Open Research Archive

Show simple item record Neppelberg, Evelyn eng 2007-06-26T09:08:49Z 2007-06-26T09:08:49Z 2007-05-04 eng
dc.identifier.isbn 978-82-308-0356-1 (print version) eng
dc.description.abstract Oral lichen planus (OLP) is a chronic mucocutaneous disease characterized by basal cell destruction and a subepithelial band-like mononuclear inflammatory cell infiltrate predominated by T cells. Molecular biological changes in the basal cell compartment and keratinocyte cell death have been a matter of particular interest in later OLP research. The majority of OLP lesions run a benign course. However, OLP have been associated with an increased risk of malignant transformation. The aims of this study were to investigate apoptotic cell death and putative regulatory proteins in keratinocytes (Papers I-III), as well as potential risk markers for malignant transformation in OLP (Paper III). Biopsies from clinically and histologically verified OLP were investigated (Papers I-II), as well as a biopsy material from OLP patients where a certain amount of them had developed epithelial dysplasia and oral squamous cell carcinoma (OSCC) (Paper III). Tissues were evaluated by histomorphometry, imunnohistochemistry (Papers I-III), TUNEL method (Paper I), mRNA in situ hybridization (Paper II) and image cytometry for measurement of DNA content (Paper III). Our data show that apoptosis is increased within the epithelium of OLP compared with normal oral mucosa (OM), and that both Fas receptor (FasR) and Fas-ligand (FasL) apoptosis regulatory proteins are expressed within the epithelium and subepithelial cell infiltrate of OLP (Paper I). In actively diseased OLP lesions, basal keratinocytes are CD40 negative and epithelial (E)-cadherin negative in focal areas (Papers II-III). Cyclooxygenase-2 (Cox-2) is up-regulated within the epithelium of OLP lesions, compared with normal OM (Paper III). According to DNA content measurements, all biopsies were classified as diploid including OLP, epithelial dysplasia and OSCC, except for one biopsy from an OLP lesion with epithelial dysplasia which was tetraploid (Paper III). Based on these findings we conclude that basal keratinocytes in OLP die by apoptosis and regulation of apoptosis appears to involve following mechanisms; (1) dysfunction in FasR/FasL system; (2) by down-regulating CD40 in diseased areas, basal keratinocytes may escape CD40-CD40L mediated apoptosis; (3) an up-regulation of Cox-2 , which may inhibit apoptosis; (4) loss of E-cadherin in basal keratinocytes may promote apoptosis and contribute to reduced basal cell structural integrity in OLP, allowing T cells to enter the epithelial compartment. Our biopsy material indicates that neither DNA content, nor expression of Cox-2 and E-cadherin are reliable as prognostic markers to select the OLP patients at risk for development of OSCC. en
dc.language.iso eng eng
dc.publisher The University of Bergen eng
dc.subject Oral lichen planus eng
dc.subject Apoptosis eng
dc.subject FasR eng
dc.subject FasL eng
dc.subject CD40 eng
dc.subject CD40L eng
dc.subject E-cadherin eng
dc.subject Cox-2 eng
dc.subject DNA content eng
dc.subject Epithelial dysplasia eng
dc.subject Oral squamous cell carcinoma eng
dc.title Pathological mechanisms in oral lichen planus : a atudy of apoptosis - regulatory proteins and risk markers for malignant transformation eng
dc.type Doctoral thesis eng
dc.subject.nsi VDP::Medisinske Fag: 700::Klinisk odontologiske fag: 830::Oral medisin: 835 nob

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