A histochemical and electron-microscope study of submucous fibrosis of the palate

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Lanthanum staining of cell surface and junctional complexes in normal and malignant human oral mucosa

Biopsies from normal and malignant human oral epithelium were studied electron histochemically using lanthanum nitrate for a selective demonstration of junctional complexes at the plasma membrane of adjacent cells. The heavy metal complex was found to settle irregularly, sometimes in intimate proximity to the epithelial cell, in areas corresponding to the glycocalyx, gap junctions, desmosomes and nonspecific contact areas. Tight junctions were rarely seen. The lack of these morphological adhesive areas, the desmosomal detachment seen between cancer cells and the increased lanthanum-positive cell surface may be possible factors responsible for the dissociation of oral malignant cells

Mast cell response in early and advanced oral submucous fibrosis

The clinical and pathological features of oral submucous fibrosis have been described by a number of workers (Joshi 1953, Lal 1963, Su 1953, Sirsat & Khanolkar 1957,1960, 1962, De Sa 1957, Rao 1962, Pindborg & Singh 1964, Pindborg & Zachariah 1965). Recent reports show the disease is fairly wide spread in all parts of India (Pindborg & Sirsat 1966). A significant correlation between the parallel presence of sub- mucous fibrosis and cancers of various sites in the oral mucosa has also been noted (Paymaster 1957, Pindborg & Zachariah 1965). The aetiology of this condition remains obscure, though the slow irritant action of capsaicin, (the irritant principle of chillies-e-Cupsicum annum) has been assessed on the rat oral mucosa, as a possible causative factor (Sirsat & Khanolkar 1960a, 1960b), The subepithelial response in oral submucous fibrosis (Sirsat & Pindborg 1967) as also in the vesicles which occasionally erupt as an early clinical sign (Pindborg & Singh 1965) suggest a rather complex pathogenesis. Biopsies from patients with this disease are therefore being studied from various aspects towards understanding the basic reactions in it. This paper reports the mast cell response in histologically early and advanced stages of the disease

The vascular response in early and advanced oral submucous fibrosis

Oral submucous fibrosis has been recognised as a distinct clinical and pathological entity (Sirsat & Khanolkar 1962, Pindborg & Sirsat 1966). The etiology and pathogenesis of this disease have not been fully understood as yet. Attempts to do so are being made by studying the basic tissue reactions in this oral disorder. This paper reports the vascular response in early and advanced stages of the disease

The relevance of gap junctions to stage I tumor promotion in mouse epidermis

A previous paper reports that the potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), has a time-dependent effect on mouse epidermal gap junctions. A single topical application of 1.0 μ g TPA results in the absence of gap junctions from mouse interfollicular epidermis between 18 and 30 h post-treatment. This paper describes the dose-dependent effect of TPA on mouse epidermis. Observations indicate that only promoting doses of TPA affect the gap junctions. Similarly, while a low dose of the hyperplasiogenic compound mezerein (1.0 μ g) is ineffective, a higher dose (4.0 μ g) results in a significant reduction in the gap junction number. One and two applications of TPA had identical effects. The potent inhibitor of both stage I and stage II of tumor promotion, Fluocinolone acetonide, used in combination with TPA, completely suppressed the hyperplasiogenic and the gap junction modulating effects of TPA. Retinoic acid, which inhibits only stage II of tumor promotion, did not influence the gap junction eliminating property of TPA. Tosylphenylalanine chloromethyl ketone which is a mild but specific inhibitor of only stage I of tumor promotion counteracted the action of TPA on gap junctions to some extent, which remained present in smaller numbers than in normal tissue at 24 h after the treatment. These results suggest that gap junctions are essential and specifically relevant to stage I tumor promotion

Histological, electron-microscope and enzyme studies of submucous fibrosis of the palate

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Changes in vitamin A conditioned hamster cheek pouch epithelium on exposure to commercial shell lime (calcium hydroxide) and tobacco. I. Optical histopathology

Epidemiologically a high incidence of oral cancer and addiction to tobacco, singly or in combination with other ingredients of the betel quid, are closely correlated. Attempts at the induction of malignancy in laboratory animals on exposure to these ingredients have hitherto failed. Studies are reported on cheek pouch epithelium of 152 Syrian golden hamsters exposed to commercial shell lime (calcium hydroxide) and tobacco, singly and in combination, with parallel conditioning by Vitamin A palmitate. The abnormal changes found especially in lime and lime-plus-tobacco treated epithelia are massive hyperplasia, keratinization anomalies, marked edema and dysplasia. The most significant findings are (1) greater epithelial alteration caused by lime, lime plus vitamin A, tobacco plus vitamin A, lime plus tobacco and lime plus tobacco and vitamin A, than by tobacco alone; (2) increasing epithelial dysplasia in response to longer periods of exposure to the test substances; and (3) enhancement of tissue changes in the presence of vitamin A

Subepithelial changes in oral submucous fibrosis

Submucous fihrosis was reported as a distinct morbid entity of the human oral mucosa by Joshi (1953). He described the symptoms as vesicles on the palate in early cases, gradually increasing oral fibrosis leading to trismus, and a marked inability to eat food spiced with chillies. The identical oral state has been called variously as "Atrophia idiopathica tropica mucosae oris" (Schwarz 1952). "Diffuse oral submucous fibrosis (Lal 1953) ; "idiopathic scleroderma of the mouth" (Su 1954); "Idiopathic palatal fibrosis" (Rao 1962) and "Selcrosing stomatitis (Behl 1962)-the interesting point being that, except for Su's cases, which occurred in the Chinese in Taiwan, this condition has been reported only in lndians. Clinical aspects of the disease, its histopathology, and probable etiology have all been commented upon during the last few years (Sirsat & Khanolkar 1957, 1960, 1960a, 1960b, 1962, l962a, DeSa 1957, George 1958, Sharan 1959, Pindborg et al. 1964). A recent paper reports the epithelial changes that occur in the oral mucosa in submucous fibrosis (Pindborg et al 1965). This paper describes in detail the subepithelial changes that supervene in submucous fibrosis and assays a histologicaI comparison in early and advanced stages of the disease

Sequential ultrastructural alterations in the mouse epidermis after a single subcutaneous injection of 20-methylcholanthrene

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Phorbol ester tumor promoter affects the mouse epidermal gap junctions

Gap junctions are known to mediate cell to cell coupling. This study shows that the potent tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), drastically affects the presence of gap junctions between mouse interfollicular epidermal (IFE) cells. In a time course ultrastructural study after a single application of 1 μ g of TPA the gap junctions between the IFE basal cells begin to decrease by 10 h post-exposure, are totally absent between 18 h and 30 h, and start reappearing at 30 h after TPA application. The potent hyperplasiogen, but very weak tumor promoter, mezerein, produces comparable hyperplasia and wide intercellular spaces but the population of gap junctions remains unchanged