Ultrastructure of the Dermal-epidermal Junction in Experimentally Induced Tumors and Human Oral Lesions**From the Electron Microscopy Unit, Imperial Cancer Research Fund, London, WC2.

Woods, D. A.; Smith, C.J.

doi:10.1038/jid.1969.40

Cited by 62 publications

(18 citation statements)

References 10 publications

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“…Lamination of the basal latnina was observed around sotne of the cytoplasmic islands of invasive carcinomas in the present study. Similar lamination was reported in the studies of experimental or human oral squamous eell earcinomas (Tarin 1967, Woods & Smith 1969, Frithiof 1972a, Okada 1975, McKinney & Singh 1977, Chen & Harwick 1977. McKinney & Singh (1977) stated that tnultilayered duplication of the basal lamina probably represented a response to the dysplastie ehanges oeeurring in the epithelium.…”

Section: Discussionsupporting

confidence: 77%

“…Ultrastructural studies on oral eareinogenesis revealed that the basal lamina of the oral epithelium became indistinct or discontinuous when the epithelial cells transformed into the neoplastic eells (Woods & Smith 1969, Woods & Smith 1970, Kaizuka 1975, MeKinney & Singh 1977. Similar findings were reported in the studies on skin carcinogenesis (Frei 1962, Tarin 1967.…”

Section: Discussionmentioning

confidence: 99%

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Ultrastructural changes of epithelium‐connective tissue junction in experimental lingual tumors

Ôtsubo

Kameyama

1982

J Oral Pathology Medicine

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In this study, plaque‐like lesions, epithelial hyperplasias, and papillary invasive carcinomas were produced in the tongues of hamsters by the application of DMBA combined with trauma for 16 weeks. The junction between the neoplastic epithelial cells and the connective tissue was studied ultrastructurally. In plaque‐like lesions, the basal lamina was partially decreased in both thickness and density or partially discontinuous. In epithelial hyperplasias, cytoplasmic projections were observed in the portion of the basal cell near the intercellular space, and the basal lamina was absent around these cytoplasmic projections. In papillary invasive carcinomas, however, numerous cytoplasmic projections extended from various portions of the basal surface of the basal cells into the underlying connective tissue. The basal lamina was also absent around these projections. In epithelial hyperplasias and papillary invasive carcinomas, some of the cytoplasmic projections appeared almost empty, some contained a small number of tonofilaments and ribosomes, and others were filled with a large number of ribosomes but did not contain the tonofilaments. The collagen fibrils were markedly reduced in number in the area around cytoplasmic projections. The cytoplasm of some fibroblasts in that area contained many intracellular collagen fibrils.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Ultrastructural changes of epithelium‐connective tissue junction in experimental lingual tumors

Ôtsubo

Kameyama

1982

J Oral Pathology Medicine

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“…Similar observations on the basal lamina configuration have been made following treatment with several teratogens (Mato et al, 1975a,b;Shah and Travill, 1976b;Morgan, 1976;Ferguson, 1978;Shah, , 1984Shah et al, 1984). In pathological circumstances, the fragmentation and loss of basal lamina has been related either to its destruction by enzymes or to failure of epithelial cells to form it (Woods and Smith, 1969;Tarin, 1972;Yamanishi et al, 1972;Takarada et al, 1974;Martinez-Hernandez et al, 1976;Frei, 1978;White and Gohari, 1981). Although the present study lacks evidence to support either view, the latter seems more plausible.…”

Section: Discussionsupporting

confidence: 57%

Gross and cellular analysis of 6‐mercaptopurine‐induced cleft palate in hamster

Burdett

Shah

1988

Am. J. Anat.

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The present study analyzes the morphological, histochemical, and ultrastructural aspects of the pathogenesis of 6-mercaptopurine (6MP)-induced cleft palate in hamster fetuses. Gross and light microscopic observations indicated that 6MP stunts the growth of vertical palatal shelves and thus induces cleft palate. Ultrastructural analysis showed that, in contrast to controls, 6MP-induced alterations were first seen in the mesenchymal cells 24 hr after drug administration. The initial alterations were characterized by swelling of the nuclear membrane. During the next 12 hr, lysosomes were seen first in the mesenchymal cells and then in the cells of the medial edge epithelium (MEE) of the developing palatal primordia. The appearance of lysosomes was temporally abnormal and was interpreted as a sublethal response to 6MP treatment. Subsequently, the nuclear alterations and the lysosomes diminished; and 48 hr after 6MP administration, they were absent from the palatal tissues. Ninety hours after 6MP administration, unlike the controls (in which the palatal shelves were already fused), changes were seen at the epithelial-mesenchymal interface in the developing cleft palatal shelves. These changes were characterized by breakdown of the basal lamina and epithelial-mesenchymal contacts. Eventually, at term, the MEE of the vertical shelf stratified. It was suggested that 6MP affected cytodifferentiation in the palatal tissues during the critical phase of early vertical shelf development and thereby induced cleft palate.

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“…Basal keratinocyte herniations could easily extend into the dermis through such gaps in the basal lamina. These occurrences have been correlated with human psoriatic activity (31,32); however, basal keratinocyte herniations have been reported in other hyperproliferative skin disease such as pityriasis rubra pilaris and a number of neoplasms (43)(44)(45)(46)(47). The widespread occurrence of gaps in the lamina densa suggests that such changes may be the nonspecific sequelae of the inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

“…The widespread occurrence of gaps in the lamina densa suggests that such changes may be the nonspecific sequelae of the inflammatory process. Proteolytic enzymes released from macrophages, neutrophils, and endothelial cells are capable of causing basement membrane dissolution and may be responsible for focal dissolutions in the basal lamina (46,47). In addition,chymotrypsin-like enzymes released from the epidermis and damaged mast cells in the dermis may result in the edematous changes observed on the epidermal side of the basal lamina of the fsn/fsn skin (31,48).…”

Section: Discussionmentioning

confidence: 99%

Cutaneous Ultrastructural Features of the Flaky Skin (fsn) Mouse Mutation

Morita

Hogan

Nanney³

et al. 1995

The Journal of Dermatology

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An autosomal recessive genetic disease with clinical and histopathological skin features resembling human psoriasis vulgaris occurs naturally in flaky skin mice (fsn/fsn). Affected mice are normal at birth, except for a hypochromic anemia. Subsequently, they develop hyperkeratotic plaques and acanthosis with elongation of rete ridges. Scanning electron microscopic examination revealed a greatly thickened epidermis, a sparsity of hairs and scale accumulations on the epidermal surface. Hair shafts had conspicuous pits, striations, and exophytic protrusions. Nails were bent at a 90 degrees angle with surface irregularities and accumulations of scale at the nail base. Transmission electron microscopic examination showed increased epidermal thickness, mitochondrial aberrations, and intraepidermal invasion by neutrophils. Keratohyalin abnormalities were detected using immunocytochemical staining for profilaggrin. At the dermal-epidermal junction, numerous macrophages and mast cells were seen in close proximity to focal dissolutions of the basement membrane. A high density of collagen fibers and cellular infiltrates were evident in the papillary dermis. This constellation of ultrastructural aberrations is typically found in psoriasis vulgaris and supports the theory that the flaky skin mouse mutation is a naturally occurring analog to one variety of human psoriasis vulgaris.

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Ultrastructure of the Dermal-epidermal Junction in Experimentally Induced Tumors and Human Oral Lesions**From the Electron Microscopy Unit, Imperial Cancer Research Fund, London, WC2.

Cited by 62 publications

References 10 publications

Ultrastructural changes of epithelium‐connective tissue junction in experimental lingual tumors

Ultrastructural changes of epithelium‐connective tissue junction in experimental lingual tumors

Gross and cellular analysis of 6‐mercaptopurine‐induced cleft palate in hamster

Cutaneous Ultrastructural Features of the Flaky Skin (fsn) Mouse Mutation

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