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At least 19 recordsLinked to original sources
PubMed2001

Accumulative increase of loss of heterozygosity from leukoplakia to foci of early cancerization in leukoplakia of the oral cavity.

BACKGROUND: Oral leukoplakia is a premalignant lesion, but the genetic changes in the foci of early cancerization in leukoplakia have not been studied. METHODS: Loss of heterozygosity (LOH) was successively investigated in 13 cases in the leukoplakia and foci of early cancerization in the same leukoplakia. The authors microdissected both lesions, and 33 microsatellite markers at 14 chromosomal loci were examined by a polymerase chain reaction-based microsatellite assay. RESULTS: Loss of heterozygosity detected in the leukoplakia was identically observed in the foci of early cancerization in leukoplakia in 11 of 13 cases, and in 2 cases allelic divergence was observed. Loss of heterozygosity occurred even in the leukoplakia with high frequency at 9p21 (66.7%), 3p14-25 (61.5%), 4q31-32 (45.5%), and 17p12-14 (44.4%). The foci of early cancerization in leukoplakia showed accumulative increase of LOH at these and other loci. Loss of heterozygosity at 5q21-23 was found to have significant difference between the leukoplakia and the foci of early cancerization in leukoplakia (P = 0.0137, Fisher exact test). Microsatellite instability was observed at low level in three cases. The mean value of fractional allelic loss in the leukoplakia differed significantly from that in the foci of early cancerization in leukoplakia (0.02 < P < 0.05, Student t test). CONCLUSIONS: The high incidence of LOH in the leukoplakia indicated premalignant potentiality of this lesion and that accumulative increase of LOH from leukoplakia to foci of early cancerization in leukoplakia might play a significant role in the cancerization of leukoplakia. Comparison of LOH between the leukoplakia and the foci of early cancerization in leukoplakia suggested that these two lesions were derived from a common clone.

Aged↗
PubMed1975

Leukoplakia revisited. A clinicopathologic study 3256 oral leukoplakias.

During a 13-year period, 3256 specimens clinically diagnosed as leukoplakia (('keratosis," "white patch") were submitted to the oral pathology laboratories of Indiana University School of Dentistry and Emory University School of Dentistry. These comprised 6.2% of the tissue specimens processed by these laboratories. The cases were analyzed as to age of occurrence, site of involvement, and pathologic findings. It was found that: leukoplakia occurs chiefly in the 5th, 6th, and 7th decades; about half of the lesions involved the mandibular mucosa, mandibular sulcus, and buccal mucosa; leukoplakia was slightly more common in men (54.2%). Microscopic study showed that 80.1% of the leukoplakias were varying combinations of hyperorthokeratosis, hyperparakeratosis, and acanthosis without evidence of epithelial dysplasia. Mild to moderate epithelial dysplasia was noted in 12.2% of specimens, and severe epithelial dysplasia or carcinoma in situ was found in 4.5%. Infiltrating squamous cell carcinoma was diagnosed in 3.1% of specimens submitted with a clinical diagnosis of leukoplakia. The risk of epithelial dysplasia, carcinoma in situ, or carcinoma varied between the anatomical locations of leukoplakia. The incidence of epithelial alteration, ranging from dysplasia to carcinoma, was 42.9% for lesions of the floor of the mouth, 24.2% for tongue lesions, and 24.0% for lip leukoplakias. The incidence of similar epithelial alterations in other sites varied from 18.8% for palatal lesions to 11.7% for leukoplakias of the retromolar area. The data suggest that there are regional differences in the incidence and character of leukoplakia in the United States. The Emory material, obtained almost exclusively from patients residing in the Southeastern United States, showed a proportionately higher total incidence, a lower male/female ratio, and a greater frequency of epithelial dysplasia, particularly in females, than the Indiana material, which came almost entirely from residents in the Northcentral United States.

Adolescent↗
PubMed2000

Risk factors for leukoplakia and malignant transformation to oral carcinoma: a leukoplakia cohort in Taiwan.

The effects of betel nut chewing, smoking and alcohol on the occurrence of leukoplakia and its malignant transformation to oral carcinoma were quantified in a leukoplakia cohort (n = 435) from one medical centre between 1988 and 1998 in Taiwan. Sixty oral carcinomas were ascertained in this cohort. A case-control study within the leukoplakia cohort was used to study, risk factors. Using the Weibull survival model, the incidence of malignant transformation of leukoplakia was shown to increase with follow-up years. After adjustment for other relevant risk factors, betel nut chewing (adjusted odds ratio (OR) = 4.59; 95% confidence interval (CI) 1.25-16.86) remained a significant risk factor for malignant transformation. Results from the case-control study showed that the adjusted odds ratios for betel nut chewing and smoking on the occurrence of leukoplakia were 17.43 (95% CI 1.94-156.27) and 3.22 (95% CI 1.06-9.78), respectively. Similar findings were observed when daily frequency and duration were taken into account. This implies that cessation of smoking may reduce by 36% leukoplakia cases, while elimination of betel nuts may prevent 62% of leukoplakia and 26% of malignant transformation to oral carcinoma in the underlying population.

Alcohol Drinking↗
PubMed1988

[Epstein-Barr virus detection in oral hairy leukoplakia in AIDS patients, in leukoplakias and on normal tongue epithelia in HIV-1-negative patients].

In 3 patients seropositive for HIV 1 (2 homosexual men and 1 female drug addict), we found "oral hairy leukoplakia" on the lateral margin of their tongues. DNA of Epstein-Barr virus (EBV) and Human Papillomavirus (HPV) were identified in cellular DNA by molecular-virological means using Southern blot hybridization and/or DNA/DNA filter hybridization on epithelial cells taken by swabs from the epithelium of the tongue. The results were compared with those obtained from the identical anatomical sites of 2 HIV-1-seropositive patients without "oral hairy leukoplakia", 3 clinically healthy HIV-1-seronegative patients, and 2 HIV-1-negative patients suffering from oral leukoplakia on their lateral tongues. In all 3 cases investigated, EBV DNA was detected in cells taken from "oral hairy leukoplakia" by filter in situ hybridization. In addition, EBV DNA was found in cells taken from clinically normal epithelia of the tongue as well as in those taken from the 2 leukoplakias mentioned. EBV DNA was regularly detected on the lateral margin of the tongue, but only in one case on the pharyngeal mucosa. Electronmicroscopy on ultrathin sections revealed particles of herpes virus (EBV), particles of HPV, in one case particles of retrovirus, and in another coronavirus and diplococci.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Candida biotypes in patients with oral leukoplakia and lichen planus. Candida biotypes in leukoplakia and lichen planus.

Prevalence of yeasts in 35 leukoplakia and 34 oral lichen planus patients was compared with that observed in persons without oral diseases. Serotype and morphotype were determined on Candida albicans isolates. Yeasts were isolated from the oral cavity specimens of 43.7% of the patients. C. albicans (serotype A) was the predominant species (76% in leukoplakia, 88.2% in lichen planus and 60.8% in healthy persons). Sixteen morphotypes were encountered on malt extract agar, being 732, 733, 734, 753 and 754 the most frequently found. Morphotypes SP1N and SP1Y were the most common on Sabouraud-trypheniltetrazolium agar (68.4% of the isolates from leukoplakia and 73.3% from lichen planus, but only 46.6% of the isolates from healthy oral mucosa showed SP1N morphotype). Presence of oral lesions was associated with a marked reduction in the yeast species and C. albicans biotypes, suggesting that C. albicans and particularly some of its biotypes, show a high potential of adaptation to the changes associated with the development of oral leukoplakia and lichen planus.

Adult↗
PubMed1994

Prevalence and risk factors associated with leukoplakia, hairy leukoplakia, erythematous candidiasis, and gingival hyperplasia in renal transplant recipients.

The aims of this study were to determine the prevalence of intraoral lesions in renal transplant recipients and to identify possible risk factors. The oral mucosa of 159 renal transplant recipients and 160 control patients was examined. The most common lesion in renal transplant recipients was cyclosporin-induced gingival hyperplasia (prevalence 22%) and patients with gingival hyperplasia were found to be taking significantly more cyclosporin-A than those without (p < 0.001). The prevalence of hairy leukoplakia and leukoplakia in renal transplant recipients was 11.3% and 10.7%, respectively, compared with 0% and 5.6% in the controls. Oral candidiasis was observed in 9.4% of renal transplant recipients compared with 2.5% of the controls; 3.8% of renal transplant recipients exhibited erythematous candidiasis, but this was not seen in the controls. Renal transplant recipients had a significantly increased risk of developing gingival hyperplasia (p < 0.0001), oral candidiasis (p < 0.0005), and two other conditions that have a well-established association with the immune suppression accompanying HIV infection, hairy leukoplakia (p < 0.0001) and erythematous candidiasis (p < 0.01).

Alcohol Drinking↗
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↗
PubMed1967

Studies in oral leukoplakias. Prevalence of leukoplakia among 10,000 persons in Lucknow, India, with special reference to use of tobacco and betel nut.

Oral carcinoma has been shown to be correlated with the use of tobacco in various parts of India. In a large-scale dental survey conducted in Lucknow, Bombay and Bangalore various precancerous conditions were investigated and studied for their possible relation to smoking and chewing habits. This paper reports the prevalence of oral leukoplakia among 10 000 dental-clinic patients in Lucknow and the correlation of the condition with the use of tobacco and betel nut in the study population.The results show that leukoplakia is far more prevalent among users of tobacco, betel nut or both than among non-users. A strikingly high frequency was found among smokers of the local cigarette, the bidi.

Adolescent↗
PubMed1998

Malignant transformation of oral leukoplakia: a follow-up study of a hospital-based population of 166 patients with oral leukoplakia from The Netherlands.

A follow-up study of a hospital-based population of 166 patients with oral leukoplakia revealed a 2.9% annual malignant transformation rate. The median follow-up period was 29 months. Parameters associated with an increased risk of malignant transformation were female gender (P < 0.025), absence of smoking habits in women (P < 0.05), and a non-homogeneous clinical aspect (P = 0.01). For uniform reporting, a recently proposed classification and staging system has been used. Leukoplakias in stage IV, consisting of lesions with moderate or severe epithelial dysplasia, were associated with an increased risk of malignant transformation (P < 0.01). There were no oral subsites associated with an increased risk. Patients who had any form of intervention did not have a statistically significantly lower chance for malignant transformation than patients who were kept under surveillance without intervention.

Adult↗
PubMed1999

Concomitant leukoplakia in patients with oral squamous cell carcinoma.

OBJECTIVE: There is an ongoing debate on the prevalence of premalignant lesions, in particular leukoplakia, at the time of diagnosis of an oral squamous cell carcinoma (OSCC). The aim of the present study was to determine the presence of concomitant leukoplakia in 100 patients with OSCC, and to evaluate possible differences in clinical and histopathological parameters of the OSCC between those with or without concomitant leukoplakia. PATIENTS AND METHODS: One hundred consecutive patients, 61 men and 39 women, with a histologically proven OSCC were screened on the presence of leukoplakia. Four groups were distinguished: (I) leukoplakia adjacent to the OSCC, (II) combination of leukoplakia adjacent to the OSCC, and leukoplakia at another oral site, (III) leukoplakia present at another oral site, but not adjacent to the OSCC, and (IV) no leukoplakia present. RESULTS: In 47 (47%) patients with OSCC the presence of concomitant leukoplakia was observed. Thirty-six (36%) patients had a leukoplakia adjacent to the OSCC (groups I and II), of which eight (8%) patients (group II) also had a leukoplakia present at another oral site. Eleven (11%) patients (group III) had no leukoplakia adjacent to the OSCC, but a leukoplakia present at another oral site. Fifty-three (53%) patients (group IV) with OSCC had no concomitant leukoplakia present. No differences were noted between men and women, nor was there any preference for an oral subsite with regard to the carcinoma. There were no statistically significant differences in clinical and histopathological presentation of OSCC's between those with or without concomitant leukoplakia. CONCLUSION: Almost 50% of oral squamous cell carcinomas are presumably associated with or preceded by leukoplakia. Early detection and active management of patients with oral leukoplakia may prevent the true development of a number of oral squamous cell carcinomas.

Adult↗
PubMed1983

[Oral leukoplakia: clinical or histologic entity?].

The term leukoplakia was coined by the Hungarian Schwimmer to describe the clinical aspect of white lesions appearing on the mucosae. Unfortunately, the use of leukoplakia for diagnostic purposes in oral pathology has led to so much confusion that diagnosis of leukoplakia has been established, using strict histological criteria, for lesions that did not appear as white patches. Moreover, it is known that what has previously been termed leukoplakia is now shown to consist of several distinct entities. The current clinical concept was established by W.H.O. Leukoplakia: a white patch or plaque that cannot be characterized clinically or pathologically as any other disease. Analysis of histological criteria and classification appearing in the literature and review of the cell and tissue abnormalities reveal that many conditions from hyperkeratosis to epidermoid carcinoma can occur within clinical leukoplakia. Orthokeratosis or hyperorthokeratosis is often found in leukoplakia simplex and leukoplakia verrucosa while parakeratosis or hyperparakeratosis is mainly observed in cases of erosive or speckled leukoplakia. Speckled leukoplakia (nodular white excrescences on an erythematous base) is the clinical type involving the more frequently severe dysplasia and carcinoma. This study demonstrate that the term leukoplakia only describes clinical conditions and does not carry any histological connotation

Diagnosis, Differential↗
PubMed1998

[Oral leukoplakia in manifest squamous epithelial carcinoma. A clinical prospective study of 101 patients].

OBJECTIVE: The Uppsala-definition of leukoplakia has recently redefined oral leukoplakia. Based on this definition, the aim of our study was to reevaluate the prevalence of oral leukoplakia in patients with histologically proven primary oral cancer. DESIGN: A total of 101 in-patients in four tumor centers in Berlin were interviewed and clinically examined just prior to surgery of an oral squamous cell carcinoma (OSCC). RESULTS: The prevalence of leukoplakia immediately adjacent to the carcinoma was 15.8%. Additional leukoplakias without relation to the carcinoma were found in 4% of the patients. There were no significant differences in age- or sex-distribution, history of tobacco habits or diet between patients with or without leukoplakia. T1 carcinomas were found in 62.5% of patients with, and 24.4% of patients without associated leukoplakia, whereas a balanced distribution was found for the pre-operative staging of the tumor. CONCLUSIONS: The prevalence of oral leukoplakia in patients with OSCC was low, compared to retrospective studies. The presence or absence of leukoplakia indicated no influence on the prognosis of the tumor, except of tumor size. The results emphasize that most OSCC develop from healthy appearing oral mucosa.

Adult↗