The retrocuspid papilla and factor XIIIa: an epidemiologic and histomorphologic study.

The retrocuspid papilla (RCP) is a poorly recognized entity. In one part of our study, we found 10 cases of lesions clinically compatible with RCP in 1150 consecutively examined patients. In another part of the study, we found 15 cases of RCP in more than 2000 consecutive cases of oral mucosal hyperplasia submitted as surgical biopsies during 1989-92. The lesions were situated in the attached gingiva, lingual to the two mandibular canines, often bilaterally. They were covered by normal pink mucosa with a size and a height each of 2-3 mm. Histologically, the RCP was a broad-based, often downfolded hyperplasia, covered with a parakeratinized epithelium of normal thickness. The rete pegs were often elongated and blunt, frequently bent inward toward the center. The lamina propria was mostly composed of a loosely arranged, delicate, fibrous connective tissue. The lesions could be classified into two groups by the presence or absence of stellate and occasionally multinucleated fibroblasts. Immunohistochemical staining with an FXIIIa antibody disclosed a population of reactive spindle-shaped cells, mainly localized in the connective-tissue papillae. These cells may be of pathogenetic importance.

Plasma-cell gingivitis in children and adults. A clinical and histological description.

Plasma-cell gingivitis (PCG) is a rare, non-symptomatic lesion found in the attached gingiva. In the county of Södermanland 14 cases of PCG were identified during the last 13 years. Clinically, the PCG is a sharply demarcated red area within the attached gingiva. Abundant plasma cells are found in the connective tissue beneath a thin epithelium. Lesions with similar clinical appearance were also found in the genital mucosa of five of the patients with a PCG. An extensive bacterial plaque was frequently found on the gingiva and teeth in the affected areas. Although an improved oral or genital hygiene did not heal the lesions, an allergic reaction to the bacterial plaque may be the cause.

Disappearance of smoker's melanosis after reducing smoking.

Besides genetic factors, tobacco smoking is known to be the main cause of oral melanin pigmentation. The present study compares the frequency of oral melanin pigmentation in a large number of former smokers with that of non-smokers. It also describes in two patients the disappearance of smoker's melanosis in the buccal mucosa following a considerable reduction in smoking.

Melanin depigmentation of the palatal mucosa in reverse smokers: a preliminary study.

The melanin pigmentation in the palate of Indian reverse smokers was histologically studied in 80 biopsies, which were compared with corresponding tissue from 49 nontobacco users. The morphology of epithelium containing melanin in its basal part was normal in smokers and nonsmokers, in contrast to areas with a local melanin depigmentation of the epithelium found in some of the reverse smokers. Here an epithelial thinning, inflammation in the underlying connective tissue, and eventually a cancer was found. The histologic appearance was in accordance with the theory that as long as a smoker's melanosis or a genetic melanin pigmentation is present, melanin functions as a defence against toxic agents penetrating into the oral mucosa.

Smoker's melanosis may explain the lower hearing loss and lower frequency of Parkinson's disease found among tobacco smokers--a new hypothesis.

A new hypothesis is presented explaining the preventive effect of tobacco smoking found on noise induced hearing loss and on the frequency of Parkinson's disease. The hypothesis is based on the finding of a melanocyte stimulation of tobacco smoking in the human oral mucosa, resulting in a higher melanin content in the epithelial cells, and a higher frequency of visible oral melanin pigmentation--smoker's melanosis. The preventive influence of smoking found in the cochlea and substantia nigra may also be due to a higher melanin content and to the ability of melanin to strongly bind specific chemical agents for a long time. Melanin may in this way act as a scavenger against cell toxic factors in these organs.

Oral melanin pigmentation in 467 Thai and Malaysian people with special emphasis on smoker's melanosis.

At the faculties of dentistry in Chiang Mai, Thailand (CM), and Kuala Lumpur, Malaysia (KL), 234 and 233 consecutive out-patients were interviewed concerning tobacco and chewing habits and examined for the presence of oral melanin pigmentation. Tobacco was regularly used by 32% and 28% of the studied populations in CM and KL. Cigarette smoking was the predominant habit, but the chewing of betel and tea leaves (miang) and the smoking of banana leaf cigars (khi yo) was also registered. The genetically acquired pigmentation dominated. Although nearly all non-tobacco users in the Malay and Indian populations had oral melanin pigmentation, it was found that tobacco smokers had significantly more oral surfaces pigmented than non-tobacco users. Among Thais, the percentage of pigmented individuals was significantly higher among tobacco smokers. It was concluded that tobacco smoking stimulates oral melanocytes to a higher melanin production also in dark-skinned ethnic groups.

In vitro activation of amphibian dermal melanocytes by nicotine.

Epidemiologic investigations have shown that nicotine could be a factor causing oral melanin pigmentation in man. Nicotine was therefore tested on amphibian skin melanocytes. Cell reactions were registered by spectrophotometry, in vitro light microscopy, photomicrography and light and electron microscopy. It was found that dermal melanocytes in the toad Bufo bufo and the frog Rana arvalis were activated by nicotine and that this activation was not mediated via beta-adrenergic receptors in melanocytes.

Specimen holder improvements for the study of amphibian skin pigmentation.

A skin specimen holder was constructed permitting nearly identical experimental conditions during in vitro spectrophotometry and photomicrography of amphibian skin melanocytes. The specimen holder was made of non-corrosive steel thread and made to fit a spectrophotometer cuvette and the light microscope stage. The improvements were compared to earlier constructions.

Epidemiologic study of excessive oral melanin pigmentation with special reference to the influence of tobacco habits.

The prevalence of oral melanin pigmentation was studied in a population of 30 118 adult individuals in Sweden. Among these, 9.9% showed melanin pigmentation in the oral mucosa. The anterior labial gingiva in the mandible was the most frequently pigmented location. The presence of melanin pigmentation was positively correlated to tobacco smoking. Among tobacco smokers 21.5% were pigmented as compared to 3.0% among individuals not using tobacco. The smoking-related oral pigmentation, smokers' melanosis, could thus be calculated at a prevalence of 18.5% among smokers and the total frequency of smokers' melanosis was calculated at 6.8%. The prevalence of pigmentation was found to increase prominently during the first year of smoking but also to decrease to the level found among non-tobacco users about 3 years after cessation of smoking. Snuff dipping did not significantly elevate the prevalence of oral melanin pigmentation.

Smokers' melanosis. Occurrence and localization in the attached gingiva.

The aim was to clinically study the frequency and extension of the melanin pigmentation in the attached gingiva and its relation to tobacco smoking. The population examined consisted of patients and dental nurse students at the School of Dentistry in Umeå, Sweden. All of the patients with pigmentation proved to be tobacco smokers. The pigmentation was given to name "smokers' melanosis.". Between 12.9% and 14.9% of those examined and between 25.5% and 31.0% of those who smoked had smokers' melanosis. Patients with smokers' melanosis had a significantly higher tobacco consumption than smokers without pigmentation. In 95.2%, smokers' melanosis was found in the mandible and was most common in the attached gingiva on the labial side of the canines and incisors. Smokers' melanosis is thus condidered to be caused by tobacco smoking and is expected to be found in other parts of the oral mucosa.