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At least 19 recordsLinked to original sources

PubMed2026

Tissue-based genomic instability markers for predicting malignant transformation in oral leukoplakia and proliferative verrucous leukoplakia: a systematic review.

OBJECTIVES: Although several biomarkers have been described for predicting malignant transformation in oral leukoplakias (OLs) and proliferative verrucous leukoplakias (PVLs), no systematic review has comprehensively evaluated tissue-based genomic instability markers. This review aimed to evaluate the evidence for these markers and their potential role in biomarker panel development. METHODS: A systematic review across PubMed, Embase and Cochrane Library was performed to identify studies evaluating the differences in tissue-based genomic markers between OL and PVL patients with and without malignant transformation. RESULTS: 34 observational studies comprising 3,237 patients were included, and genomic aberrations were categorised into DNA-level, chromosomal, and gene-specific alterations. For studies on OLs, DNA-level and chromosomal markers for which individual studies reported associations with malignant transformation included aneuploidy, impaired DNA repair capacity, loss of heterozygosity, chromosomal instability, and copy number alterations. Multiple gene-specific alterations also showed associations (e.g., TP53, MKI67, FGFR1), but findings varied across studies. The genomic markers of PVLs differed substantially, with fewer consistent predictors found. No meta-analysis was performed as all included studies were observational. CONCLUSIONS: Genomic instability across multiple levels contributes to malignant transformation, and represents a promising biological framework for predicting malignant transformation for OLs. While no single marker reliably demonstrates sufficient predictive performance, the integration of complementary genomic alterations with clinical and histopathological risk factors may provide a basis for the development of robust multi-marker panels. Future prospective studies using standardised detection methods and multivariable prediction models are required before clinical implementation. SYSTEMATIC REVIEW REGISTRATION: identifier CRD42024585830.

carcinoma↗

PubMed1975

Cytological and histological keratinization studies in leukoplakias of the mouth.

A correlative histocytological study for keratinization was done in 446 cases of oral leukoplakia. Cytologically, keratinization could be correctly identified in 91% of leukoplakias exhibiting orthokeratosis, 73% of leukoplakias exhibiting parakeratosis, and 78% of cases showing both types of keratinization. Cytologically, orthokeratosis was present in 83% of individuals with homogeneous leukoplakia and in 69% with ulcerated leukoplakia, while parakeratosis was present in 7% of homogeneous leukoplakias and in 19% of ulcerated leukoplakias. A higher frequency of dysplasia was observed in smears and their corresponding histological sections for those cases which had revealed only parakeratosis in the cytological examination and for both orthokeratosis and parakeratosis as compared to those showing only orthokeratosis. It is suggested that the cytological method is a reliable method for studying oral keratinization and is of value to the clinician in identifying the type of leukoplakias which may need to be biopsied for further surveillance.

Cytoplasmic Granules↗

PubMed1979

[Oral candidiasis in leukoplakia and carcinoma of the oral cavity (author's transl)].

The incidence of Candida albicans and other candida species were examined by mycological culture and histologically in 193 patients with various forms of oral leukoplakia and 14 patients with carcinoma of the oral mucosa, the results being compared with a control group of 137 subjects with a normal mucosa. Comparing the leukoplakia groups one with the other and with the control group revealed definite, usually statistically significant, differences in the incidence of fungi: 46.4% of patients, 29.2% among controls. The incidence of oral fungi was 35.4% among those with noxigenic leukoplakia, 50% in precancerous leukoplakia, 71.5% in mucosal carcinoma, and 49% in nosogenic leukoplakia (mainly lichen planus mucosae). The fungal elements could be demonstrated histologically much less frequently than by culture, but the difference of demonstration was statistically more significant between the different forms of leukoplakia. It is probable that chronic candidiasis in leukoplakia is not carcinogenic as such but is the microbiological and indicator of a local or systemic disorder of the cellular immune system.

Candida↗

PubMed1979

[Scanning electron microscopy of oral leukoplakia].

Buccal mucosa of six patients with leukoplakia and normal controls was examined by scanning electron microscopy. Findings have shown that: 1. there is a difference between the surface epithelial cells of the normal mucosa and those of the mucosa with leukoplakia; 2. according to the various clinical forms of the leukoplakia there are differences between the epithelial cells: in leukoplakia verrucosa presence of keratinized epithelial cells, in leukoplakia erosiva absence of the cell-connecting structures seems to be a characteristic feature; 3. in leukoplakia erosiva with dysplasia atypical arrangement of the cytoplasmic processes of surface epithelial cells can be observed; 4. the most striking difference was revealed between the cells of the normal mucosa and those of leukoplakia erosiva.

Adult↗

PubMed1977

[Morphological classification of oral leukoplakia (author's transl)].

656 cases of oral leukoplakia were analysed according to macroscopic aspects, microscopic growth patterns and histologicalcytological differentiation, and the relationship to cancer of the oral cavity was studied. Homogeneous and speckled leukoplakia can be distinguished macroscopically, while flat (70%), papillary-endophytic (22%) and papillomatous-exophytic (8%) types can be distinguished by their growth pattern. Histological-cytological characteristics consist of epithelial hyperplasia (hyperkeratosis with ortho- or parakeratosis; akanthosis) and epithelial dysplasia (dyskeratosis, basal-cell hyperplasia, loss of polar arrangement of the basal cells, cell polymorphism, increased mitosis rate). No or little dysplasia was demonstrated in 74% of leukoplakias, moderate in 17% and marked in 6%. Carcinoma-in-situ, defined as high-grade dysplasia with additional loss of epithelial layering, was found in 3%. Precancerous leukoplakia (in almost 10% of cases, counting high-grade dysplasias and carcinoma-in-situ) must be delineated as a special group. Numerous correlations were found between dysplastic leukoplakias and oral cavity cancer as regards localisation, age and sex distribution. In the various leukoplakia forms there was an increased incidence of marked stroma reactions and of Candida colonisation with increased degrees of dysplasia.

Adolescent↗

PubMed1975

Investigation of DNA-content of leukoplakia cells or oral mucosa.

DNA-histograms of smears of 11 plain leukoplakias, one of a precancerous leukoplakia, three of leukoplakia carcinoma in early stage, and one of a keratotic seqamous cell carcinoma of the floor of the mouth were prepared. The cell nuclei of the plain leukoplakia are mostly diploid, a small proportion has a DNA-content of 4 C. Intermediate values or polyploid nuclei are absent. In precancerous leukoplakia, intermediate values were noticed; in the cases of carcinoma in early stage, intermediate and polyploid nuclei were present, and in one case only polyploid nuclei. Only 2C and 4C nuclei occurred in a case of keratotic squamous cell carcinoma, which in comparison to earlier examined cases must be termed DNA negative.

Adult↗

PubMed1975

Evaluation, surveillance and treatment of panoral leukoplakia.

Leukoplakia is well-recognised as a premalignant condition of the oral mucosa. Despite many attempts to produce definitive laboratory tests for the prediction of those cases of premalignant leukoplakia which may undergo malignant transformation, there is as yet no fool-proof method of clinical and laboratory assessment. The problem is nowhere more manifest than in the management of panoral leukoplakia, especially in frail, elderly and apprehensive patients. In such cases the selection of sites for biopsy and treatment is often more empirical than logical. The introduction of cryosurgical techniques for the treatment of leukoplakia has enabled the surgeon to eradicate panoral white patches in a more conservative fashion. The application of a diagnostic nuclear staining test using toluidine blue dye, coupled with local exfoliative cytology, has provided a system for evaluation and surveillance of panoral leukoplakia which is clinically simple and at least as reliable as any predictive test previously described.

Aged↗

PubMed1977

Follow-up studies in oral leukoplakia.

Follow-up examinations of 670 patients with oral leukoplakia during a 30-year-period showed cancer development in 40 cases, i.e. 6%. Dysplasia was observed in 24% of the histologically examined leukoplakia cases; 13% of the dysplasia cases subsequently showed development of carcinoma. The age distribution revealed the prevalence of leukoplakia in the age-group 51-60 years; that of carcinoma in the age-group of 61-70 years. The sex distribution showed a male-female ratio of 3.2 : 1 in the leukoplakia-group, and a 1.9 : 1 ratio in the carcinoma-group. The tongue and the lips were the site of predilection for malignant transformation and for dysplasia. Among aetiological factors, Candida albicans infection and the simultaneous existence of several aetiological factors seemed to play a role in malignant transformation. Erosive leukoplakia showed the highest risk, developing in 25.9% of the cases into cancer.

Adult↗

PubMed1976

[Observation of the course of leukoplakia in the Larynx (author's transl)].

During a period of 15 years biopsies of the larynx of 3000 patients were taken out. At 319 patients the first histodiagnosis "Leukoplakia" was made. 10% carcinomas were found out later on grounds of observation of the course and by letter. 7% of these carcinomas occured within 1 year after the first histodiagnosis of "Leukoplakia". The first biopsy of these 7% carcinomas diagnosed as a "Leukoplakia" must be interpreted as a biopsy out of the marginal area of an already existent carcinoma. 3% of the carcinomas developed from the "Leukoplakia" just in the following years.

Biopsy↗

PubMed1977

[Leukoplakias of the larynx (i. clinical and histological classification) (author's transl)].

A clinical and histological classification of leukoplakias of the larynx is described. Basis for this classification is the prognostically important systematical, histologic and cytologic knowledge gained in gynecology. The early clinical diagnosis limited to a macroscopic description of leukoplakias is completed by a prognostic attribute won by cytology and/or histology. Thus the final diagnosis of precancerous lesions of the larynx is classified into leukoplakias with low-graded dysplasias, middle-graded dysplasia, highgraded dysplasia and atypical epithelium. The old nomenclature regards dysplasias as facultative precancerous lesions and the atypical epithelium as an obligatory precancerous lesion.

Diagnosis, Differential↗

PubMed1978

[Ultrastructure of the mouth mucosa in various types of oral leukoplakia].

12 cases of laukoplakia of the oral cavity was studied by electron microscopy. A correlation between the clinical type, histological- and ultrastructure of the leukoplakia was revealed. In types of leukoplakia simplex and verrucosa, where histologically cornification was found, by electron microscopy signs of keratinization (tonifibrils, granules of keratohyalin) were to be observed. In leukoplakias clinically showing erosions, histologically dysplasia, ultrastructural changes were alike those, seen in some carcinomas.

Leukoplakia, Oral↗

PubMed1977

[Oral florid papillomatosis or "speckled" leukoplakia? A discussion with reference to three cases (author's transl)].

Three patients in whom the diagnosis of oral florid papillomatosis or speckled leukoplakia was made are reported. All three patients were elderly men, who had been heavy smokers for years. In two of the treated patients the disease recurred. Histologically pseudohyphae of Candida could be demonstrated of all three cases. The etiology and the differential diagnosis of oral florid papillomatosis and speckled leukoplakia are discussed. In our opinion, there is no essential difference between oral florid papillomatosis and speckled leukoplakia.

Candidiasis↗

PubMed1977

[Comparative histological and autoradiographic investigations on benign oral leukoplakias (author's transl)].

Proliferation was studied in 18 patients with benign oral leukoplakias of the buccal mucosa by in vitro labelling with 3H-TdR. Identical investigations were performed in clinically normal mucosa of the same patients. Significant differences were found between the LI of both groups. On the other hand the total of labelled cells per 100 micron length of the basal membrane was approximately equal in leukoplakias and normal mucosa. In the majority of cases the LI was increased in leukoplakic regions whereas the number of labelled suprabasal cells was lowered compared to normal. These findings are supposed to be a consequence of shifting of epithelial keratinization to the lower stratum spinosum. From that results an increased proliferation in the basal cell layer.

Adult↗

PubMed1975

Histochemistry of the keratohyalin granules in human oral leukoplakia.

The keratohyalin granules from 25 human oral leukoplakias, showing benign hyperorthokeratosis histologically, were examined employing a series of histochemical techniques. The tissues were fixed in 10% neutral buffered formalin, 80% methanol, or Carnoy's fluid. The keratohyalin granules stained intensely with Pauly's reagent, Congo red and Harris hematoxylin, indicating the presence of proteins. This was confirmed by abolishing the staining reaction by pretreatment with proteolytic enzymes. The keratohyalin granules also reacted with methyl green-pyronin by staining pink at their peripheries; this staining was abolished by pretreatment with ribonuclease, indicating the presence of ribonucleotides. The keratohyalin granules partially stained with toluidine blue and colloidal iron, indicating the presence of acid polysaccharides. The keratohyalin granules did not react with the Feulgen reagent, suggesting the absence of DNA. Our studies indicate that the keratohyalin granules in human oral leukoplakia are primarily protein(s) complexed with polyribonucleotides. The presence of a carbohydrate moiety suggests the possibility of a protein-polysaccharide component in the granules.

Adult↗

PubMed1977

Clinical, histological and ultrastructural features of a possibly virus-induced oral leukoplakia.

Two male patients with oral leukoplakias exhibiting a peculiar type of apparent dysplastic changes have been followed for 4 and 6 years, and a series of biopsies have been examined by light and electron microscopy. The apparent lack of normal epithelial stratification below the keratinized cell layers was mainly caused by the frequent appearance of large ballooned cells and multinuclear giant cells. The centre of the large ballooned cells contained aggregations of chromatin and evenly-dispersed microtubulus surrounded by a thick rim of tonofibril bundles. In the peripheral cytoplasm large numbers of smooth-surfaced endoplasmic reticulum were found, but no Golgi apparatus was observed. In addition, several autophagocytic bodies were recorded. Along the cell membrane only a few desmosomes were present, whereas aggregations of digested desmosomes were found in the cytoplasm. On the basis of the ultrastructural findings, it is suggested that the large ballooned cells represented epithelial cells arrested in early stages of mitotic division. The epithelial cells in interphase exhibited a normal ultrastructure except for large nucleoli with varying degrees of condensation of nucleolonema and vacuolization. Further, atypical dense granular aggregations and strands of fine fibrillar material were recorded in the nuclei. It is suggested that this new type of oral leukoplakia has a viral etiology.

Aged↗

PubMed1976

Cell-mediated immunity to herpes simplex virus types 1 and 2 antigens in leukoplakia and carcinoma in man.

Cell-mediated immune responses to herpes simplex virus 1 and type 2 virion and non-virion antigens were assessed in patients and in controls with oral leukoplakia, carcinoma and recurrent herpes labialis. Enhanced proliferation was found in lymphocytes from patients with recurrent herpes labialis or with leukoplakia showing epithelial atypia, and depressed responses were found in carcinoma. Very significantly positive correlations were shown between the responses to each of the herpes virus antigens. A specific increase in cell-mediated immunity to herpes virus in epithelial atypia was confirmed, but separation of the nonvirion from virion antigen is necessary before specific cell-mediated immune responses to the non-virion antigen can be assessed.

Antigens, Neoplasm↗

PubMed1979

Intraoral leukoplakia, abrasion, periodontal breakdown, and tooth loss in a snuff dipper.

Dentists should be aware that snuff dipping or chewing is increasing in southern states and perhaps in other sections of the United States. These habits can lead to clinical leukoplakia, gingival recession, tooth abrasion, and periodontal bone destruction. The possibility also exists that a malignant transformation of leukoplakia can develop in persons who use snuff and other forms of tobacco.

Adult↗

PubMed1978

[Leukoplakia simplex or metaplastic keratosis of the mouth mucosa?].

Leukoplakia simplex lesions affecting the oral mucous membrane of cheeks and the floor of the mouth were characterized from the clinical, histological, electron-microscopical and stereological point of view. An integration of the various observations suggested that a combination of atrophic and metaplastic processes give rise to this type of leukoplakia-lesion which imitates epidermal structures and, therefore, could be defined as a metaplastic keratosis. Possible pathogenetic mechanisms are formulated which might be responsible for and cause this type of oral mucous membrane lesion.

Adult↗