Desquamative Gingivitis - A Clinicopathological Review.

This article aims to review the etiology, clinical features and diagnosis of desquamative gingivitis in order to outline all the aspects necessary to increase the efficiency of patient management. Because of the polymorphic etiology, dental practitioners may elude the correct diagnose. Consequently, we find it important to underline all the clinical features that desquamative gingivitis may have as well as the associated oral lesions. Also we shortly review the systemic disorders that frequently associate desquamative gingivitis. It is important to know that the muco-cutaneous disorders frequently involved can have an abrupt onset with lesions sometimes confined to the gingiva. In evolution these diseases can be life threatening and a quick treatment can assure not only a more favorable evolution but also a better life quality. Laboratory analyses are mandatory in order to correctly diagnose the main systemic disorder. Histology and direct immunofluorescence investigations are the most accurate. Remission of the underlining disease brings improvement or even resolution of the oral lesions.

Epidemiological and etiological aspects of burning mouth syndrome.

Burning mouth syndrome (BMS) is defined as a chronic pain condition characterized by a burning sensation in clinically healthy oral mucosa. Incidence BMS diagnosed in the Department of Oral Medicine - Oral Pathology Dental Faculty of Medicine, "Carol Davila" University of Medicine and Pharmacy Bucharest is 16,23%. The etiology of BMS remains far less known. This article makes an overview of the latest theories about possible etiopathogenic factors involved in the occurrence of BMS.

Characterization of oral keratinocyte stem cells and prospects of its differentiation to oral epithelial equivalents.

OBJECTIVE: Although oral keratinocyte stem cells play a key role in tissue homeostasis, wound healing, and neoplasia, they remain difficult to identify and characterize. The specific aim of the present study is to characterize an oral keratinocyte stem-cell population separated using a magnetic technique. MATERIAL AND METHODS: Oral human keratinocytes obtained from keratinized oral mucosa were magnetically separated using a proliferation-related marker, CD71 and α6ß4 integrin. The expression of different stem cell markers: CD44H, Nestin, Nanog, Oct 3÷4, CD117 was checked by immunofluorescence. The ability of α6ß4pos CD71neg fraction to form oral epithelial equivalents was also assayed. RESULTS: Three different oral keratinocyte subpopulations were obtained following magnetic separation: α6ß4pos CD71neg, α6ß4pos CD71pos and α6ß4neg. Our α6ß4pos CD71neg stem cell fraction was positive for Oct 3÷4, CD44H and cytokeratin 19 while Nanog, Nestin and CD117 expression was absent. At the same time, the other two cell fractions α6ß4pos CD71pos and α6ß4neg were negative for all stem cell markers. Also, α6ß4pos CD71neg fraction was able to regenerate a well stratified and organized oral epithelial equivalent. The distribution of cytokeratin 19 and involucrin in the oral epithelial equivalent reflected the in vivo situation in oral gingival epithelium. CONCLUSIONS: The human gingival α6ß4pos CD71neg fraction was strongly positive for a panel of stem cell markers and could form oral epithelial equivalent. It is also suggested that a magnetic system may be an important tool in acquiring oral keratinocyte stem cells for research.

Oxidative stress markers in oral lichen planus.

Oral lichen planus (OLP) is a relatively common disorder whose cause is still unknown. Oral cancer is preceded in most cases by pre malignant lesions-leukoplasia, submucous fibrosis and lichen planus. Free radicals and reactive oxygen species play important roles in both pathogenesis of lichen planus and carcinogenesis. Thus monitoring systemic and saliva compounds important for the antioxidant defence (oxidative balance) could be important for the clinician's treatment strategy. Thorough medical management and early active treatment are necessary to improve symptoms and might also be a relevant prevention strategy from squamous cell carcinoma risk, although data to fully support this statement still need investigation. The principal aim of this study was to determine the systemic uric acid, GGT, and albumin levels as well as the levels of uric acid and albumin in 20 patients diagnosed with lichen planus and 20 controls. Extensive medline search failed to reveal any study of this type. Our results showed a significant decrease of saliva (p < 0.005) uric acid and an increase in serum gamma glutamyl transpherase (GGT) (p < 0.01) as well as in the total antioxidant capacity of saliva in patient group with respect to the control one. The preliminary conclusion of our study is that uric acid, the most important salivary antioxidant and GGT could be considered in the future as useful markers of oxidative stress for elaboration of treatment strategy and monitoring.

[Oral lichen planus and cancer. Apropos of 2 cases]. / Lichen plan buccal et cancer. A propos de deux cas.

Malignant changes in oral lichen planus lesions are still the subject of controversy. Two new cases provide supportive data for this thesis. Case 1: A 64 year old non smoking diabetic woman presented with combined atrophic lichen planus and erythroplasia lesions of the right buccal mucosa and a unique reticular lichen planus lesion of the left buccal mucosa. Both lesions were histologically confirmed. Despite treatment, degeneration of the Bowen's type lesion into an epidermoid carcinoma was noted within 11 months. Case 2: A 47 year old non smoking woman consulted for combined cutaneous and oral lichen planus lesions. Clinical examination showed an "acute" oral lichen planus associated with extensive ulcerative, atrophic and reticular lesions involving almost the total oral mucosa. Histology of a left buccal biopsy confirmed the diagnosis. Systemic and local corticotherapy produced marked improvement in her condition and she was not seen for five years. Follow up examination then detected a proliferative ulcerative type of epidermoid carcinoma on the left buccal mucosa. These findings appear to fulfil the clinical and histologic criteria suggestive of development of epidermoid carcinoma on a lichen planus lesion.

[Buccal manifestations of AIDS]. / Manifestari bucale în SIDA.

The disease determined by HIV, increasingly more frequent, is affecting certain groups of patients (homosexuals, drug addicts, polytransfused subjects). The clinical picture at the onset is not specific. Later on in the course of the disease the immunological capacity of defense of the organism is affected and a series of symptoms including fever, infections with bacteria, lymph-node inflammation, encephalopathies, Kaposi sarcoma will develop. Apparently buccal infections with fungi are the earliest manifestations, and they are followed, by order of frequency, by herpetic lesions, "hairy" leucoplasia, tumours. Transmission through the saliva from the patient to the stomatologist of the HIV infection is theoretically possible due to scratches on the physicians' hands. Prophylactic measures are described for the stomatologists treating AIDS patients, as well as for the sterilization of the instruments.

Autoantibodies against the basal cell layer: an association with chronic hepatitis B.

The presence of antibodies against the basal cells of squamous epithelium (BCL-Ab) was studied by indirect immunofluorescence in Rumanian and Swedish carriers of hepatitis B surface antigen (HBsAg), in patients with acute viral hepatitis (AVH), chronic liver diseases (CLD), and various other diseases, and in apparently healthy subjects. Titers of BCL-Ab greater than or equal to 40 were found in 8% of 320 HBsAg carriers, in 20% of 292 patients with CLD associated with HBsAg, and in 2% of 816 patients with HBsAg-negative CLD. BCL-Ab were not found in 167 patients with AVH, nor in 1389 patients with various nonhepatic conditions, nor in 344 apparently healthy subjects. These data indicate an association of BCL-Ab with CLD predominantly of hepatitis B etiology. Possibly hepatitis B virus may induce a form of liver metaplasia with the expression of an antigen with a specificity in common with the regenerative layer of basal cells in the squamous epithelium.