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Basal Cell Layer (basal + cell_layer)
Selected AbstractsApoptosis in oral lichen planusEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 5 2001Evelyn Neppelberg Apoptotic cell death may be a contributory cause of basal cell destruction in oral lichen planus (OLP). Therefore, the purpose of this study was to investigate the rate of apoptosis in OLP and the expression of two proteins (FasR and FasL) regulating this process. Biopsies from 18 patients with histologically diagnosed OLP were investigated, with comparison to normal oral mucosa of healthy persons. For visualisation of DNA fragmentation, the TUNEL method was used. In order to characterise the infiltrating cell population (CD3, CD4, CD8) and expression of FasR and FasL, we used an immunohistochemical technique. The results showed that T cells dominated in the subepithelial cell infiltrate. Within the epithelium the apoptotic cells were confined to the basal cell layer, and more apoptotic cells were seen in areas with basal cell degeneration and atrophic epithelium. There was a prominent expression of FasR/FasL in OLP, with a rather uniform distribution throughout the inflammatory cell infiltrate. In the epithelium, the FasR/FasL expression was more abundant in the basal cell area compared to the suprabasal cell layer. In conclusion, apoptosis within the epithelium is significantly increased in situ in OLP compared to normal oral mucosa, and seems to be related to the epithelial thickness. [source] Lichen planopilaris [cicatricial (scarring) alopecia] in a childINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 7 2001FNASC, FRAS (Lond.), Virendra N. Sehgal MD A mother of a 12-year-old boy, 2 years ago, noticed that he showed patchy loss of hair on the vertex of the scalp. It was asymptomatic and progressive. Subsequently, similar patches appeared elsewhere on the scalp. Some of these patches joined to form a large bald patch. This was accompanied by dusky blue eruptions over the left upper lip and eyebrows. Later, there was localized loss of hair. A family history of a similar ailment was absent. Examination of the scalp revealed plaques of alopecia with mild to moderate erythema. The skin was smooth, shiny, and atrophic (Fig. 1). Atrophy was apparent by the presence of wrinkles in places, and by holding the skin between the thumb and the index finger. The periphery of the lesions was well demarcated and was occupied by erythematous, scaly, follicular papules. Lesions were also located on the patches of alopecia. In addition, flat-topped, dusky blue, papules/plaques were present over the upper lip. Figure 1. Lichen planopilaris: plaques of alopecia showing smooth, shiny, atrophic skin with erythema A study of hematoxylin and eosin-stained microsections prepared from the upper lip and vertex of the scalp was undertaken. The former revealed hyperkeratosis, hypergranulosis, sawtooth irregular acanthosis, and destruction of the basal cell layer which, in turn, was embraced by a lymphohistiocytic infiltrate disposed in a band-like fashion. A few cells were seen invading the epidermis. Pigment-laden histiocytes were found intermingled with the infiltrate. In the scalp skin, on the other hand, atrophy of the epidermis with punctuation of keratin plugs, together with fibrosis of the dermis, was prominent. The walls of the hair follicles were hyperkeratotic, while their lumina were conspicuous by their dilatation and contained keratotic plugs (Fig. 2a,b). Sebaceous and sweat glands were absent. Figure 2. Lichen planopilaris showing atrophy of the epidermis, fibrosis of the dermis, dilatation of the hair follicle lumina containing keratotic plug(s), and hyperkeratosis of the wall of the follicle (hematoxylin and eosin: a , ×,40; b , ×,100) Response to treatment, comprising ultramicronized griseofulvin (Gris O.D.) 375 mg/day (Sehgal VN, Abraham GJS, Malik GB. Griseofulvin therapy in lichen planus ,- a double blind controlled trial. Br J Dermatol 1972; 86: 383,385; Sehgal VN, Bikhchandani R, Koranne RV et al. Histopathological evaluation of griseofulvin therapy in lichen planus. A double blind controlled study. Dermatologica 1980; 161: 22,27) and prednisolone 20 mg/day for 6 months, was excellent (Fig. 3). Topical betamethasone dipropionate (Diprovate) lotion was used as a supplement. Figure 3. Perceptible decline in band-like lymphohistiocytic inflammatory infiltrate (hematoxylin and eosin, a, × 40; b, ×,100) [source] Erythema dyschromicum perstans and hepatitis C virus infectionINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 5 2001George J. Kontochristopoulos MD A 48-year-old woman with a 10-month history of widespread, hyperpigmented, slightly pruritic macules, with a red border, involving the trunk and the proximal limbs (Fig. 1) was referred to our outpatient department. The oral mucosa, palms, soles, scalp, and nails were normal. Figure 1. Multiple hyperpigmented macules with an active border on the trunk Laboratory tests showed elevated liver enzymes [alanine aminotransferase (ALT), 68 IU/L (normal value, <,40 IU/L); aspartate aminotransferase (AST), 41 IU/L (normal value, <,40 IU/L)], the presence of antibodies to hepatitis C virus (anti-HCV) and HCV RNA (Amplicor Roche). In addition, cryoglobulinemia type III (IgM,,,, IgG,,,) was detected with a high cryocrit value, and there was detectable C-reactive protein, rheumatoid factor, and a low titer of antinuclear antibodies (1 : 80). A percutaneous liver biopsy showed changes compatible with mild chronic hepatitis (grade, 6; stage, 0). The possible source of infection was unknown, as the patient had no history of parenteral transmission (e.g. blood transfusions, intravenous illicit drug use). A skin biopsy specimen from the active border of a lesion showed hyperkeratosis, parakeratosis, and hydropic degeneration of the basal cell layer, with the formation of colloid bodies in the epidermis. A moderate perivascular lymphohistiocytic infiltrate with melanophages and free melanin granules was observed in the upper dermis (Fig. 2). Immunostaining of paraffin-embedded tissue sections with the TORDJT-22 IgG1 mouse monoclonal antibody to HCV (Biogenex, Son Ramon, USA), which is specific for the nonstructural region of HCV (NS3-NSH, C100 antigen) using the avidin,biotin,peroxidase complex (ABC) as well as the alkaline phosphatase antialkaline phosphatase (APAAP) methods, failed to detect HCV in the lesion of erythema dyschromicum perstans (EDP) (Nakopoulou L, Manolaki N, Lazaris A et al. Tissue immunodetection of C100 hepatitis C virus antigen in major thalassemic patients. Hepato-Gastroenterol 1999; 46: 2515,2520). Direct immunofluorescence showed IgG, IgM, IgA, and fibrinogen deposits on colloid bodies. EDP was diagnosed on the basis of these clinical and laboratory findings. Figure 2. Hydropic degeneration of the basal cell layer with colloid bodies in the epidermis. Moderate perivascular lymphohistiocytic infiltrate with melanophages and free melanin granules in the upper dermis (hematoxylin and eosin, ×,200) The patient was treated with interferon-,2b (Intron-A, Schering Plough Athens, Greece), 3 MU thrice weekly subcutaneously for 12 months, with additional topical steroid application. There was no response to this treatment with new lesions appearing in previously unaffected areas of the trunk and extremities. HCV RNA remained persistently positive. Thus, a modified regimen with interferon-,2b, 6 MU thrice weekly for 6 months, was tried. At the end of the treatment course, the eruption of EDP had greatly improved. Liver enzymes were normal (ALT, 22 IU/L; AST, 24 IU/L) and HCV RNA had become negative. Four months later, however, cutaneous lesions reappeared and hepatitis C relapsed. At this time point, combination therapy of interferon-,2b, 3 MU thrice weekly, with ribavirin, 1000 mg daily, was given. Six months later, liver enzymes were normal (ALT, 42 IU/L; AST, 39 IU/L), HCV RNA was negative, and the lesions of EDP had resolved. [source] Overexpression of Fos-related antigen-1 in head and neck squamous cell carcinomaINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 4 2005Flavia R. R. Mangone Summary The activating protein-1 (AP-1) family of transcription factors has been implicated in the control of proliferation and differentiation of keratinocytes, but its role in malignant transformation is not clear. The aim of this study is to assess the pattern of mRNA expression of jun-fos AP-1 family members in 45 samples of head and neck squamous cell carcinomas (HNSCC) and matched adjacent mucosa by means of Northern blot analysis. Transcripts of all family members were identified, except for JunB that was detected only by means of reverse transcription polymerase chain reaction. Neither c-Fos nor JunD or FosB mRNA differed between tumours and normal tissues. We observed a strong Fos-related antigen-1 (Fra-1) and Fra-2 expression, but only Fra-1 mRNA densitometric values were higher in tumour, compared to normal adjacent mucosa (t -test, P = 0.006). A direct relationship between the positive expression of Fra-1 mRNA, above tumour median, was associated with the presence of compromised lymph nodes (Fischer exact test, P = 0.006). In addition, Fra-1 protein staining was assessed in a collection of 180 tumours and 29 histologically normal samples adjacent to tumours in a tissue array. Weak reactivity, restricted to the basal cell layer, was detected in 79% of tumour adjacent normal tissues, opposed to the intense reactivity of cancer tissues. In the subgroup of oral cancers, we have observed a shift in Fra-1 immunoreactivity, as long as the number of patients in each category, cytoplasmic or nuclear/cytoplasmic staining, was analysed (Fischer exact test, P = 0.0005). Thus, Fra-1 gene induction and accumulation of Fra-1 protein may contribute to the neoplastic phenotype in HNSCC. [source] Immunohistochemical analysis of the biological potential of odontogenic keratocystsJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 2 2006k Kolá Background:, The aim of this study was to analyse the usefulness of detecting important apoptosis and proliferation markers in assessing the biological potential of odontogenic keratocysts (OKC) and thus selecting the optimal diagnostic algorithm for these lesions. Methods:, Indirect immunohistochemistry and relevant statistical methods were used for analysis of formalin-fixed and paraffin-embedded samples from 98 patients. Results:, Nevoid basal cell carcinoma syndrome (NBCCS) keratocysts were characterized by higher expression of Bcl-2, p27Kip1 and c-erbB-2 as well as by lower proliferative activity measured by Ki-67 in basal cell epithelium and by a lower inflammatory response in comparison with sporadic keratocysts. Dentigerous, radicular and non-specified odontogenic cysts differed from both NBCCS and sporadic keratocysts in a wide spectrum of apoptosis and/or cell cycle-related protein expressions, higher proliferation in the basal cell layer, and vice versa, lower proliferation in the suprabasal cell layer. Conclusions:, The NBCCS keratocysts have a different immunophenotype from sporadic keratocysts and both types are distinguishable from dentigerous, radicular and non-specified odontogenic cysts. These findings confirm the separate biological potential of these lesions and the results of the immunohistochemical analysis have diagnostic and prognostic implications. [source] Immunohistochemical study of syndecan-1 down-regulation and the expression of p53 protein or Ki-67 antigen in oral leukoplakia with or without epithelial dysplasiaJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 9 2003Hideo Kurokawa Abstract Background:, Leukoplakia is an oral pre-cancerous lesion that sometimes develops into squamous cell carcinoma. Therefore, leukoplakia with epithelial dysplasia is useful for studying carcinogenesis at the cellular level. The purpose of this study was to evaluate a potential association between the loss of syndecan-1 expression and the expression of p53 protein and Ki-67 antigen, and to identify reliable markers for predicting malignant changes in oral leukoplakia with epithelial dysplasia. Methods:, Changes in the expression of syndecan-1, p53, and Ki-67 were examined immunohistochemically in 43 cases of oral leukoplakia with or without epithelial dysplasia. The subjects were categorized as: none, 13 cases; mild dysplasia, 5 cases; moderate dysplasia, 17 cases; and severe dysplasia, 8 cases. The expression of these molecules in normal oral epithelia (22 cases) was also investigated. Results:, Strong syndecan-1 expression was observed on the surface of keratinocytes in normal epithelium. Immunopositivity was lost gradually as the extent of epithelial dysplasia increased. In normal epithelium, p53 and Ki-67 appeared mainly in the basal cell layer, while they were more widely distributed in leukoplakia. Specifically, significant changes were observed in the labeling index of p53 and Ki-67 in leukoplakia as epithelial dysplasia progressed from mild to moderate or severe. Conclusion:, Our results reveal that overexpression of p53 protein and Ki-67 antigen, and down-regulation of syndecan-1 expression in the lower part of the epithelium, are associated with dysplastic changes. Therefore, the down-regulation of syndecan-1 expression may be the most important reliable marker for dysplastic changes. [source] Histopathological varieties of oral carcinoma in situ: Diagnosis aided by immunohistochemistry dealing with the second basal cell layer as the proliferating center of oral mucosal epitheliaPATHOLOGY INTERNATIONAL, Issue 3 2010Takanori Kobayashi To make reproducible diagnoses for oral carcinoma in situ (CIS), combined immunohistochemistry directed at the positioning of squamous cell proliferation (Ki-67) and differentiation (keratin (K) 13 and K19) was used, both of which support histological evaluations by providing biological evidence. Normal/hyperplastic epithelia was defined by K19+ cells only in the first basal layer, K13+ cells in the third basal and upper layers, and sporadic Ki-67+ cells in the second basal layer. These profiles indicated that a proliferating center of the oral epithelium is located in the parabasal cell layer, and K19 and K13 can be regarded as markers for basal and prickle cells, respectively. Epithelial dysplasia was characterized by irregular stratification of Ki-67+ cells and the absence of K19/K13 in proliferating cells. Irregular emerging of K19+ and K13+ cells in proliferating foci with unique stratification of atypical Ki-67+ cells indicated CIS. When the definition was applied, surgical margins in 172 recurrent cases were shown to contain CIS (39.4%) and squamous cell carcinoma (55.8%), indicating that the new diagnostic criteria for CIS reflected clinical behaviors of the cases. The results indicate that oral CIS contain more histological variations, especially those with definite keratinization, than what had been previously defined. [source] Expression of FasL in squamous cell carcinomas of the cervix and cervical intraepithelial neoplasia and its role in tumor escape mechanism,CANCER, Issue 5 2006Ramy Ibrahim M.D. Abstract BACKGROUND To date, several mechanisms have been described by which malignant cells escape from the immune system. One of these is through the expression of FasL. The authors hypothesized that the Fas/FasL interaction enables cervical carcinoma cells to induce apoptosis of the cells of the immune system and thereby escape from them. METHODS The authors tested the expression of FASL on the surface of cervical carcinoma tissues. Next, they stained the same cervical tissues with anti-human leukocyte common antigen and TUNEL to identify apoptotic cells. An in vitro functional assay was then done to test if the FASL expressed on the surface of cervical carcinoma cell lines was or was not responsible for inducing apoptosis in T-cells. Finally, they compared the expression of FASL on normal and dysplastic cervical tissues. RESULTS Ninety-four percent of the cervical carcinoma tissues the authors tested expressed FasL and the majority of the apoptotic cells in the specimens were leukocytes with very few tumor cells. In the in vitro functional assay, only the Fasl expressing cell line and not the Fasl negative cell line was able to induce apoptosis of the Fas-expressing Jurkat cells. On examining the normal cervical tissues, the authors found that the expression of Fasl was confined to the basal cell layer with loss of expression observed in the suprabasal layers, which made it an immune privileged site. Conversely, there was persistent expression of FasL in the dysplastic layers in cervical dysplasia and squamous cell carcinoma specimens. CONCLUSIONS The findings of the current study support the authors' hypothesis that persistent expression of FasL plays a role in the ability of cervical carcinoma cells to escape from the immune system. Cancer 2006. Published 2006 by the American Cancer Society. [source] 2331: Are the Meibomian glands "hair follicles without a hair shaft" ?ACTA OPHTHALMOLOGICA, Issue 2010E KNOP Purpose The Meibomian glands (MG) are atypically large sebaceous glands in the eyelids with numerous generations of secretory acini along an extensive central duct. They share similarities with the ciliary hairs in development, and hyper-keratinisation leading to obstructive MG dysfunction (MGD) represents the typical pathology. It was hence investigated which structural similarities they share with cilia. Methods Conjunctival whole-mounts including the lid margin from ten normal human body donors were embedded in paraffin. Serial sections were stained by H&E, Masson-Goldners stain and by immunohistochemistry (IHC) against cytokeratins and associated proteins. Results The terminal part (excretory duct) of the MG central duct is an ingrowth of epidermis similar to the hair follicles of the cilia. Characterization of individual cytokeratinis by IHC showed that CK14, a marker for undifferentiated cells, was expressed in the basal cell layer of the skin, MG ducts and the secretory acini. The excretory duct epithelium expressed the skin keratin CK10 and the keratinisation marker involucrin but in proximal direction along the central duct full cornification as well as both markers were gradually lost. Filaggrin, however, a marker for incipient stages of keratinisation located in keratohyalin granules continued in the superficial epithelial layer all along the MG ductal system. Conclusion All parts of the normal human MG ductal system have signs of incipient keratinisation and preserve a commitment to full cornification. This supports the assumption that the MG are basically "hair follicles without a hair shaft" in which the progression to full epithelial cornification is apparently blocked during embryological development but may reoccur under pathological influences. Support DFG KN317/11 [source] Keratinisation status and cytokeratins of the human Meibomian gland epitheliumACTA OPHTHALMOLOGICA, Issue 2009E KNOP Purpose The Meibomian gland (MG) is an indispensable component of the functional anatomy of the ocular surface. Increasing evidence points to a high impact of hyper-keratinisation as a major cause of obstructive MG dysfunction (MGD) and evaporative dry eye. Information of normal keratinisation status and cytokeratin composition of the human MG is limited. Methods Conjunctival whole-mount specimens including the lid margin from ten body donors of older age were embedded in paraffin. Serial sections were stained by H&E and Masson-Goldner stain and by immunohistochemistry with an antibody panel to cytokeratins. Results In conventional stains, the MG shows distinct similarities with the pilo-sebaceous unit of the cilia. The keratinised skin epithelium extended into the terminal part of the MG excretory duct similar to the hair follicle. Preliminary IHC results showed that the epithelium was positive there for the skin keratin CK10. Along the central duct the keratinisation CK10 expression was gradually lost similar to keratinisation marker involucrin. However, filaggrin, a marker for incipient stages of keratinisation and located in keratohyalin granules continued in the superficial layer of the duct epithelium all along the Meibomian central ductal system. CK14 a marker for basal undifferentiated cells showed a homogenous expression all along the basal cell layer of the MG ducts and the acini. Conclusion The MG shares similarities with the cilia in embryology, in structure and in the cytokeratin composition. It can hence be regarded as a "hair without a hair shaft". All parts of the MG ducts have signs of incipient keratinisation and preserve a commitment to keratinisation. Upregulation in MGD explain hyper-keratinisation as a typical event in obstructive MGD. [source] Quantitative evaluation of corneal epithelial oedema by confocal microscopyCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 3 2009Naoyuki Morishige MD PhD Abstract Background:, To develop a novel quantitative index for evaluation of corneal epithelial oedema, the pixel intensity of confocal microscopic images was measured derived from the basal cell layer (BCL) of the corneal epithelium in normal eyes, eyes before and after cataract surgery, and eyes affected by bullous keratopathy. Methods:, Five eyes of five normal volunteers, 14 eyes of 11 cataract patients and 12 eyes of 12 bullous keratopathy patients were examined by confocal microscopy. The cataract patients underwent cataract surgery, and they were examined by confocal microscopy, corneal pachymetry, and anterior fluorometry both before and at various times after surgery. The pixel intensity of BCL images obtained by confocal microscopy was measured and expressed as the BCL index. Results:, The coefficient of variation for repeated (five times) measurement of the BCL index in each of the five normal eyes was 3.4%. The BCL index was 54.8 ± 5.3 (mean ± SD) before surgery, increased significantly to 65.2 ± 10.0 on the day after surgery, and gradually decreased thereafter in the cataract patients. The time-course of the BCL index coincided well with that of corneal thickness and anterior fluorometry value. The BCL index in eyes affected by bullous keratopathy was significantly increased at 95.0 ± 6.4. Conclusion:, The BCL index was increased after cataract surgery and in eyes affected by bullous keratopathy, conditions associated with corneal epithelial oedema. This quantitative measure obtained by confocal microscopy may prove useful in the clinical evaluation of corneal epithelial oedema. [source] Nerve growth factor ,/pro-nerve growth factor and their receptors in normal human oral mucosaEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 5 2007Katsuhiko Hayashi Nerve growth factor , (NGF- ,) and its precursor proNGF are important for the differentiation and survival of neurons and dermal keratinocytes. The aim of this study was to determine the role that NGF might play in the differentiation and wound healing of oral mucosa. Cultured normal human oral mucosal keratinocytes expressed mRNA for NGF- ,/proNGF and for their receptors TrkA and p75NTR. Lysates from cultured oral mucosal keratinocytes did not contain detectable amounts of mature 14-kDa NGF- , but did contain several NGF proforms with molecular weights between 32 and 114 kDa. Culture medium from oral mucosal keratinocytes contained 75 kDa proNGF. The addition of NGF- , significantly enhanced the proliferation of oral mucosal keratinocyte cultures and in vitro scratch closure. Immunostaining of biopsies from normal oral mucosa showed the presence of proNGF in all epithelial layers. NGF staining was observed in the granular and upper spinous cell layers. TrkA immunoreactivity was detected in basal and parabasal cells, with weak to moderate staining in spinous and granular cell layers. p75NTR staining was seen in basal cell layers. These findings indicate that NGF- ,/proNGF have mitogenic and motogenic effects on oral mucosal keratinocytes and therefore may aid in the healing of oral wounds. Differential expression of NGF and NGF receptors throughout the epithelium suggests a role in epithelial differentiation. [source] Immunohistochemical demonstration of p63 in DMBA-induced hamster buccal pouch squamous cell carcinogenesisORAL DISEASES, Issue 5 2003YK Chen Objectives: Abnormalities in the p53 gene are regarded as the most consistent genetic abnormalities detected in head and neck squamous cell carcinogenesis. Two new members of the p53 gene family, p73 at the 1p36 region and p63 at the 3q27-29 region, have recently been identified. They share considerable sequence homology with p53 in the transactivation, DNA binding, and oligomerization domains, indicating possible involvement in carcinogenesis. To our knowledge, however, p63 expression in experimental oral carcinogenesis has not been studied. Materials and methods: Immunohistochemical analysis of p63 protein expression was performed in 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch squamous cell carcinogenesis. Fifty outbred, young (6 weeks), male, Syrian golden hamsters (Mesocricatus auratus) were randomly divided into three experimental groups (each consisting of 10 3-, 9- and 15-week DMBA treated animals), and two control groups (with 10 animals in each). The pouches of the three experimental groups were painted bilaterally with a 0.5% DMBA solution three times a week. The treatment protocol for animals in one of the control groups was identical with only mineral oil applied, while the other control group remained untreated throughout the experiment. Results: In all of the untreated and mineral oil-treated pouch mucosa, nuclear positivity for p63 was mainly observed in the basal/parabasal cell layers. The p63 nuclear positivity extended from the basal/parabasal layers to the whole epithelial layers in the 3- and 9-week DMBA-treated pouch mucosa. Furthermore, the positive nuclear-stain cells were randomly distributed throughout the entire epithelial layers in the 3- and 9-week DMBA-treated pouch-mucosa specimens. In carcinomas from 15-week DMBA-treated pouch specimens, p63 staining was more uniform and homogeneous for the less-differentiated tumor areas. By contrast, p63 expression was noted mainly in the peripheral cells of tumor nests in the well-differentiated tumor areas. Conclusions: The results of this study are consistent with those from previous analyses of p63 expression in human oral mucosa, suggesting that p63 may be associated with the regulation of epithelial differentiation and proliferation in DMBA-induced hamster buccal pouch squamous cell carcinogenesis. Further study is required to investigate which p63 isoform(s) is/are involved in hamster buccal pouch carcinogenesis. [source] | ||||||||||