Variations of structure and appearance of the oral mucosa.

Among the most important factors in a thorough clinical examination is the dentist's ability to recognize and make distinctions among normal oral structures, variations of normal structures, and pathologic entities. The practitioner's diagnostic acumen is essential to this process and is a skill gained and refined by clinical experience and continuing education. In this introductory article, the authors describe normal entities, anomalies, and benign soft tissue lesions of interest to the clinician. For presentation, these structures are organized according to their location within the oral cavity.

Leukoedema: a review of the literature.

Leukoedema, a grayish-white lesion of the oral mucosa in humans, was once thought to be a probable precursor to leukoplakia. Clinical examination differentiates leukoedema from leukoplakia, lichen planus, white sponge nevus, and pathomimia morsicatio buccarum. Prevalence rates vary greatly in different countries and in different ethnic groups. For many years, leukoedema was alleged to occur only in adult populations until Martin and Crump found this lesion in children and youth. There is a definite predilection for this lesion in black Americans. Although the etiology is unknown, it has been suggested that leukoedema develops in areas of local irritation. This article reviews the literature related to the prevalence of leukoedema and correlates the independent findings, which might pertain to its etiology.

Clinical signs for the early recognition of cancer of the oral cavity.

The dentist bears a particularly great responsibility with regard to the early detection of cancer of the oral cavity, since only early detection provides the greatest prospect of a cure. A description is therefore given of the features of the oral mucous membrane on which the differential diagnosis of 'carcinoma of the oral cavity' must in particular be made. The author then sets out an examination procedure which every dentist should follow before any treatment is given; this will also make it possible to detect those carcinomas of which the patient himself is not yet aware.

Lesions of the oral mucosa: an epidemiological study of 23785 Mexican patients.

This study is a cross-sectional report of oral mucosal lesions in 23785 patients more than 15 years of age who requested elective dental care in a dental school. Among the patients examined, the general lesion rate was 356.60 lesions per 1000 patients. Sixty-eight entities were identified, the lesions being more common among males. White, red, and ulcerated lesions were seen to predominate, associated mostly with chronic irritative causative factors. The prevalence rates of individual oral mucosal lesions ranged from 0.55 to 105.36 per 1000 patients examined. Age and sex assessment showed some differences in the type and presentation rates of the lesions. These and other epidemiological aspects are discussed.

Oral Candida species and betel quid-associated oral lesions in Padaung women of Northern Thailand.

Purpose of the present investigation was to study the association between the betel quid chewing (BQC) habits, the oral yeast flora and oral lesions in female Padaung of northern Thailand. Oral swabs were taken from the tongue and palate of 50 Padaung women with and 50 control individuals without BQC habit. The spectrum of oral Candida species in both groups was determined microbiologically. In addition, oral mucosal lesions were registered in both groups. Mean age of BQ chewers was 35.4 years, of non-chewers was 19.2 years. Candida parapsilosis was the most common Candida spp. isolated both in BQ chewers (46%) and non-chewers (44%). Candida albicans was revealed in 24% of BQ chewers and 18% of non-chewers. There was no significant difference in carriage of Candida spp. isolated between both groups. Forty-four per cent of BQ chewers revealed betel chewers mucosa, 10% showed leukoedema. Isolated populations such as the Padaung may reveal different patterns of candidal flora, in this case a predominance of Candida parapsilosis.

Abnormal keratohyalin-like forms in leukoedema.

Electron microscopic, histochemical and light-microscopic studies were carried out on biopsy specimens of 12 cases of leukoedema and on the desquamated epithelial cells of a further 50 examples. For comparison, similar observations were made of 4 examples of healthy cheek mucosa and 29 cases of a variety of pathological conditions of the oral mucosa. Only in leukoedema were a series of structures encountered which consisted of an aggregation of ribosomes and electron dense masses, or a network of electron-dense material, or an electron-dense network with a central dense core or a solid body with a few central cavities. Histochemical stains and RNA extraction studies showed that they are probably abnormal forms of keratohyalin granules and that ribosomes is an important component of their composition.

Giant centrifugal miliaria profunda.

A 4-month-old developed rapidly enlarging, white plaques up to several centimeters in diameter in areas where occlusive tape had been applied, almost all on the sites of venous or arterial punctures. Microscopy demonstrated the features of miliaria profunda, with sweat duct occlusion and evidence of extravasation of sweat into the dermis. This clinical entity has not been described previously, and we suggest the name giant centrifugal miliaria profunda.

Leukoedema: ultrastructural and histochemical observations.

The ultrastructural features of 12 cases of leukoedema were investigated and compared with clinically normal buccal mucosa. Histochemistry was undertaken to try to resolve some of the observed ultrastructural changes. The characteristic "intracellular edema" of the epithelial cells in leukoedema is due to vacuolation in the cytoplasm of cells. Abnormal mitochondria were observed in these cells. The vacuoles contained a granular material somewhat like clumped glycogen granules, but histochemistry failed to identify this material as glycogen. Towards the surface of the epithelium, the vacuolated cells collapsed into a compact layer of flattened cells. The outer cells of this layer abruptly swelled again to form the characteristic superficial layer of "ballooning" cells of leukoedema. The latter cells were not vacuolated but contained remnants of organelles, membraned vesicles with remnants of organelles, keratohyalin granules and structures apparently related to keratohyalin granules. We propose that the vacuolation represents a limited reversible form of cellular degeneration resulting from cell damage and that impeded mitochondrial function may be the cause of the vacuolation. The superficial "ballooning" cells are degenerated cells. The flattening of the vacuolated cells into a compact layer and the presence of keratohyalin granules and keratohyalin-like structures in the superficial cells are regarded as features of an aborted form of keratinization.

White sponge nevus (leukoedema exfoliativum mucosae oris): ultrastructural observations.

Biopsy specimens from the oral lesions of white sponge nevus (WSN) in thirteen patients were analyzed by electron microscopy. Several marked deviations from the normal ultrastructure were recorded. Similarities and dissimilarities with other hereditary disturbances affecting the epithelium are discussed. Profound disturbance of the tonofilament system, with atypical aggregation of tonofilaments, was observed. Odland bodies, which are numerous in keratinized epithelia and are extruded into the intercellular space prior to the exfoliation of the surface cells, were also abundant in the WSN specimens. Very little material originating from Odland bodies appears, however, in the intercellular space in WSN. Presumably, the Odland bodies fail to properly function enzymatically in WSN.

[Electron microscopic observations in leukoedema exfoliativum mucosae oris (white sponge nevus)]. / Elektronmikroszkópos megfigyelések leukoedema exfoliativum mucosaw oris (white sponge nevus) kórképében

Biopsia taken from 13 cases of leukoderma exfoliativum mucosae oris (white sponge nevus) was investigated by the aid of electron microscope. Significant changes as compaired to the normal ultrastructure were revealed. The disease is a hereditary one manifesting itself in the disturbance of differentiation of epithelial cells mainly of the oral mucosa. Arrangment of the tonofilaments is disturbed, formation of tonofibrills and keratohyaline granules ceases. Odland-bodies occure in a great number but the lack of emptiing their content into the interecellular space is striking. Exfoliation of the epithelial cells diminishes, presumably because of the disturbance of their enzymatic function and the presence of a great number of desmosomes between the cells of the superficial layer. The diminished exfoliation histologically and clinically produces a hyerplasia of the epithelium with an enormous quantitity of superficial epithelial cells.

Pseudo oral hairy leukoplakia in a renal allograft recipient.

Oral hairy leukoplakia (OHL) is a disorder of the tongue associated with Epstein-Barr virus (EBV). OHL is seen mainly in HIV infection but is also rarely seen in the course of iatrogenic immunosuppression, especially in kidney transplantation; OHL is even more rarely seen in immunocompetent hosts. Lesions that clinically and histologically mimicked OHL but were not associated with EBV were recently characterized as pseudo hairy leukoplakia. We present such a case that occurred in a renal allograft recipient; light and electron microscopy, immunohistochemistry, and in situ hybridization were used to examine the patient for the presence of EBV and human papillomavirus. Two independent treatments with topical retinoid and oral amoxicillin resulted in complete remission. Pseudo hairy leukoplakia may correspond, at least in some cases, to the conditions known as leukoedema and white sponge nevus; the distinction of these diseases from OHL is of importance because OHL is a hallmark of severe immunosuppression.

An investigation into the association between leukoedema and smoking.

One thousand, nine-hundred and ninety-six Cape Coloured high school pupils (655 females and 1,341 males, 14-18 years old) were examined to determine the prevalence of leukoedema and to investigate its relationship with smoking. Results were contradictory. Only in some subgroups was it found that the proportion of smokers with leukoedema was significantly larger than non-smokers with leukoedema; that those with leukoedema consumed significantly more tobacco than those without leukoedema, and that there was a corresponding increase in smoking and leukoedema with age. An analysis of the relationship between smoking, the sex, and leukoedema showed a relationship between sex and leukoedema, but that leukoedema was independent of smoking. Also the prevalence of the condition in smokers and ex-smokers was not significantly different. No correlation existed with the type of smoking and between the severity of the lesion and the amount of tobacco consumed. It is concluded that smoking does not cause the lesion but may aggravate it and that its etiology must be multifactorial.