scholarly journals PCNA and p53 expression in oral leukoplakia with different degrees of keratinization

2006 ◽  
Vol 14 (4) ◽  
pp. 276-280 ◽  
Author(s):  
Melaine de Almeida Lawall ◽  
Marcelo Macedo Crivelini

Leukoplakias are oral lesions that may have many clinical and histological aspects and they are usually associated with malignancy when dysplastic alterations are shown. However, these transformations may occur in non-dysplastic lesions that show harmless clinical aspect. For this reason, the proposal was to study the p53 and PCNA immunohistochemical expression in non-dysplastic leukoplakias, trying to correlate the results only with the epithelial keratinization degree. For this, 24 leukoplakias degrees I, II and III of Grinspan were used, all of them located in oral mucosa. Most of the leukoplakias showed p53 and PCNA expression in their different keratinization degrees. The p53 marking was confined to the basal and parabasal layers, while the PCNA marking occurred in practically all epithelial layers. The expression pattern of these markers was histologically and statistically similar between the lesions with these keratinization variations. It was evident that non-dysplastic epithelium of leukoplakias showed submicroscopical signs of alterations that lead to malignant transformation, and that the keratinization degree did not correlate to a greater risk of this event.

2013 ◽  
Vol 7 (1) ◽  
pp. 169-174 ◽  
Author(s):  
Montebugnoli Lucio ◽  
Gabusi Andrea ◽  
Gissi Davide Bartolomeo ◽  
Cervellati Fabio ◽  
Servidio Dora

Objective: The present study assessed patients with multiple oral lesions to evaluate the mis-estimation rate in terms of diagnosis and risk of malignant transformation when only one biopsy is performed. Study Design: Thirty-five patients presenting at least two white and/or red lesions in different oral mucosa sites with a final diagnosis of leuko/erythroplakias or lichenoid lesions were included, for a total of 70 biopsies. Results: Nineteen patients (54%) had at least one between-lesion discrepancy considering the presence/absence of dysplasia (10 patients), normal/high cell turnover (13 patients) or diagnosis (5 patients). Discrepancies were not related to clinical aspect or within-patient similarity of lesions. Conclusions: Multiple oral lesions in the same patient can significantly differ in terms of dysplasia, high cell turnover and, even diagnosis. Multiple biopsies are imperative and diagnosis as well as risk of malignant transformation should be formulated for each single lesion rather than for each individual patient.


2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Amita Negi ◽  
Abhiney Puri ◽  
Rakhi Gupta ◽  
Rajat Nangia ◽  
Alisha Sachdeva ◽  
...  

Background. Oral squamous cell carcinoma is the sixth most frequent malignant tumor worldwide and the third most common cancers in developing countries. Oral leukoplakia is the best-known precursor lesion of oral squamous cell carcinoma. The aim of the present study was to compare immunohistochemical expression of antiapoptotic protein survivin in normal oral mucosa, oral leukoplakia, and oral squamous cell carcinoma. Method. Total 45 specimens of formalin fixed paraffin embedded tissue blocks, 15 in each of the following: normal oral mucosa, leukoplakia, and oral squamous cell carcinoma were used for the study. Immunohistochemical reaction for survivin protein was performed for the 4 µm thick histological sections taken on positively charged slides. Results. 20% normal mucosa cases, 53.33% cases of leukoplakia, and 80% of oral squamous cell carcinoma were found out to be survivin positive. One way ANOVA test indicated statistically significant difference of survivin expression between the three different groups p<0.001. Conclusion. A high incidence of survivin protein expression in oral epithelial dysplasia and squamous cell carcinoma samples indicate that survivin protein expression may be an early event in initiation and progression of oral squamous cell carcinoma.


2020 ◽  
Vol 33 (6) ◽  
pp. 1033-1040 ◽  
Author(s):  
Leon J. Wils ◽  
Jos B. Poell ◽  
Ilkay Evren ◽  
Marit S. Koopman ◽  
Elisabeth R. E. A. Brouns ◽  
...  

AbstractOral leukoplakia is the most common oral potentially malignant disorder with a malignant transformation rate into oral squamous cell carcinoma of 1–3% annually. The presence and grade of World Health Organization defined dysplasia is an important histological marker to assess the risk for malignant transformation, but is not sufficiently accurate to personalize treatment and surveillance. Differentiated dysplasia, known from differentiated vulvar intraepithelial neoplasia, is hitherto not used in oral dysplasia grading. We hypothesized that assessing differentiated dysplasia besides World Health Organization defined (classic) dysplasia will improve risk assessment of malignant transformation of oral leukoplakia. We investigated a retrospective cohort consisting of 84 oral leukoplakia patients. Biopsies were assessed for dysplasia presence and grade, and the expression of keratins 13 (CK13) and 17, known to be dysregulated in dysplastic vulvar mucosa. In dysplastic oral lesions, differentiated dysplasia is as common as classic dysplasia. In 25 out of 84 (30%) patients, squamous cell carcinoma of the upper aerodigestive tract developed during follow-up. Considering only classic dysplasia, 11 out of 56 (20%) patients with nondysplastic lesions progressed. With the incorporation of differentiated dysplasia, only 2 out of 30 (7%) patients with nondysplastic lesions progressed. The risk of progression increased from 3.26 (Hazard ratio, p = 0.002) when only classic dysplasia is considered to 7.43 (Hazard ratio, p = 0.001) when classic and differentiated dysplasia are combined. Loss of CK13, combined with presence of dysplasia, is associated with greater risk of malignant progression (p = 0.006). This study demonstrates that differentiated dysplasia should be recognized as a separate type of dysplasia in the oral mucosa and that its distinction from classic dysplasia is of pathological and clinical significance since it is a strong (co)prognostic histopathological marker for oral malignant transformation. In oral lesions without dysplasia and retained CK13 staining the risk for progression is very low.


2020 ◽  
Vol 8 (12) ◽  
Author(s):  
Vanessa Einsfeld ◽  
Ana Claudia Ramos ◽  
Beatriz Barbosa ◽  
Alberto Zen ◽  
Grasieli de Oliveira Ramos ◽  
...  

Introdução: Quando estamos frente às lesões potencialmente malignas, torna-se imprescindível o acompanhamento rigoroso dessas lesões, pois são lesões frequentes e com risco de transformação maligna consideravelmente relevante, a leucoplasia e a queilite actínica, são as lesões mais comuns encontradas na cavidade bucal. Objetivo: relatar um caso de lesão potencialmente maligna em mucosa labial. Relato de caso: Paciente sexo masculino compareceu à clínica de Diagnóstico VI da Universidade do Oeste de Santa Catarina, com a presença de lesão branca em lábio inferior, o mesmo já se encontrava em acompanhamento há seis anos, com diagnóstico prévio de queilite actínica sem atipia celular (duas biópsias prévias). Aposentado, trabalhava anteriormente como agricultor, ex-fumante e ex-etilista. Clinicamente observava-se lesão esbranquiçada, com aspecto verruciforme, localizada em lábio inferior, medindo 2 cm no maior diâmetro. Além disso, o lábio encontrava-se endurecido, com aspecto roliço. Duas hipóteses de diagnóstico foram levantadas: queilite actínica associada a leucoplasia e carcinoma verrucoso. O paciente foi submetido à nova biópsia incisional. No laudo constatou-se tratar de queilite actínica com displasia epitelial leve e o tratamento proposto foi o uso de protetor labial FPS30, além de acompanhamento clínico semestral. Conclusão: O acompanhamento desse caso clínico foi possível observar alteração no perfil citológico, onde nas primeiras biópsias não era possível observar atipia celular e na biópsia mais recente foi observado uma displasia epitelial leve, portanto o acompanhamento das lesões potencialmente malignas é fundamental para prevenir sua transformação maligna, e uma nova biópsia deve ser realizada sempre que for observada alteração no aspecto clínico da lesão.Descritores: Leucoplasia; Queilite; Biópsia; Lábio.ReferênciasPindborg JJ, Reichart PA, Smith CJ, Van der Waal I. World Health Organization International histological classification of tumours. Histological typing of câncer and precancer of the oral mucosa. Berlin: Springer; 1997.Marley JJ, Linden GJ, Cowan CG, Lamey PJ, Warnakulasuriya KAAS, Scully C. Management of potentially malignant oral mucosa lesions by consultant UK oral and maxillofacial surgeons.  Br J Oral Maxillofac Surg. 1996;34(1):28-36.Neville BW, Dam DD, Allen CM, Chi AC . Patologia oral e maxilofacial. 3. ed. Rio de Janeiro; 2016.Warnakulasuriya S, Johnson NW, van der Waal I. Nomenclature and classification of potentially malignant disorders of the oral mucosa. J Oral Pathol Med. 2007;36(10):575-80.Gupta PC, Murti PR, Bhonsle RB, Mehta FS, Pindborg JJ. Effect of cessation of tobacco use on the incidence of oral mucosal lesions in a 10-yr follow-up study of 12.212 users. Oral Dis. 1995;1(1):54-8.Maito FDM. Avaliação da expressão do PCNA no epitélio lingual de camundongos submetidos à ingestão e aplicação tópica de álcool a 40 GL [dissertação]. Porto Alegre: Faculdade de Odontologia – UFRGS;2001.Markopoulos A, Albanidou-Farmaki E, Kayavis I. Actinic cheilitis: clinical and pathologic characteristics in 65 cases. Oral Dis. 2004;10(4):212-16.Cintra JS, Torres SCM, Silva MBF, Manhães Júnior LRC, Silva Filho JP, Junqueira JLC. Queilite Actínica: estudo epidemiológico entre trabalhadores rurais no município de Paracaia– SP. Ver Assoc Paul Cir Dent. 2013;67(2):118-21.Greespan D, Jordan RCK. The white lesions that kills – aneuploide dysplastic oral leukoplakia. N Engl J Med. 2004;350(14):1382-84.Bánóczy J. Follow-up studies in oral leukoplakia. J Maxillofac Surg. 1977;5(1):69-75.Huber MA. White oral lesions, actinic cheilitis, and leukoplakia: confusions in terminology and definition: facts and controversies. Clin Dermatol. 2010;28(3):262-68.Reibel J. Prognosis of oral pre-malignant lesions: significance of clinical, histopathological and molecular biological characateristics. Crit Rev Oral Biol Med. 2003;14(1):47-62.Scheifele C, Reichart PA, Oral leukoplakia in manifest squamous epithelial carcinoma. A clinical prospective study of 101 patients, Mund Kiefer Gesichtschir. 1998;2(6):326-30.Schepman K, der Meij E, Smeele L, der Waal I. Concomitant leukoplakia in patients with oral squamous cell carcinoma. Oral Dis. 1999;5(3):206-9.Kaugars GE, Pillion T, Svirsky JA, Page DG, Burns JC, Abbey LM. Actinic cheilitis: a review of 152 cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999;88(2):181-86.Abreu MAMA, Silva OMP, Pimentel DRN, Hirata CHW, Weckx LLM, Alchorne MMA et al. Actinic cheilitis adjacent to squamous carcinoma of the lips as an indicator of prognosis. Braz J Otorhinolaryngol. 2006;72(6):767-71.Patrício JFC. Evolução das lesões pré-malignas orais: orientações para os médicos dentistas [dissertação]. Porto: Universidade do Porto; 2011.Shah AY, Doherty SD, Rosen T. Actinic cheilitis: a treatment review. Int J Dermatol. 2010; 49(11):1225-34.Pimenta FJ, Cordeiro GT, Pimenta LGGS, Viana MB, Lopes J, Gomez MV et al.  Molecular alterations in the tumor suppressor gene WWOX in oral Leukoplakias. Oral Oncol. 2008;44(8):753-58Paulo LFB, Rosa RR, Rocha MA, Durighetto Junior AF. Incidência e prevalência das lesões brancas associadas ao tabagismo atendidos no ambulatório da Unidade de Diagnóstico Estomatológico da Universidade Federal de Uberlândia no período de 1997 a 2008. Horizonte Cientifico. 2011;2:1-20.Gandolfo S, Pentenero M, Broccoletti R, Pagano M, Carrozzo M, Scully C. Toluidine blue uptake in potentially malignant oral lesions in vivo: clinical and histological assessment. Oral Oncol. 2006;42(1):89-95.Mashberg A, Samit A. Early diagnosis of asympomatic oral and oropharyngeal squamous cancers. CA Cancer J Clin. 1995;45(6):328-51.Mendes SF, Ramos GO, Rivero ERC, Modolo F, Grando LJ, Meurer MI. Techniques for precancerous lesion diagnosis. J Oncol. 2011. ID 326094.Dib LL, Kowalski LP, Curi MM. Lesões cancerizáveis de boca. In: Kowaski LP, Anelli A, Salvajoli JV, Lopes LF. Manual de condutas diagnosticas e terapêuticas em oncologia. 2.ed. São Paulo: Âmbito Editores; 2002.


2017 ◽  
Vol 6 (1) ◽  
pp. 1444
Author(s):  
Tsvetan Borisov Tsvetanov

Oral leukoplakia is defined as a predominantly white lesion of the oral mucosa that cannot be characterized as any other definable lesion; however, the lesion must be confirmed histopathologically by biopsy in order to discuss malignant transformation of oral leukoplakia. Malignant transformation rates of oral leukoplakia range from 0.13 to 17.5%, while the rates of five-year cumulative malignant transformation range from 1.2 to 14.5%. In this review were described some datas about the frequency, etiology and pathogenesis of oral leukoplakia. Clinical symptoms and treatment methods were described. The basic information sources were up to date articles. The author's results were retrospectively analysed.


Author(s):  
Makadia Krishna ◽  
Ronakgiri V. Gosai ◽  
Virpariya Jignesh ◽  
Chabhadiya Nilesh ◽  
Katrodiya Jayesh ◽  
...  

Oral leukoplakia (OL) is a premalignant lesion described as “a predominant white lesion of the oral mucosa which cannot be defined as any other known lesion”. OL located on the floor of the mouth, soft palate and tongue are considered as high-risk lesions, while, in other areas, they may be considered as of low malignancy risk. A Forty five years old male patient had complaints of white lesion on left lat. Surface of tongue, along with burning sensation since 4-5 months. He was diagnosed with Leukoplakia and he had taken allopathic medicine for 4 to 5 times, but it was inversely relapsed, so he was treated with Pratisarana of Bibhitaka Churna and Rasayana Churna, Yastimadhu Ghanavati as lozenges along with Rasayana tablets orally for a period of 6 months. After 6 month therapy, white lesion became disappear and no burning sensation. Thus this patient was successfully treated with above therapy with no recurrence or any complications till date.


Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 194
Author(s):  
Jutta Ries ◽  
Abbas Agaimy ◽  
Falk Wehrhan ◽  
Christoph Baran ◽  
Stella Bolze ◽  
...  

Background: The programmed cell death ligand 1/programmed cell death receptor 1 (PD-L1/PD-1) Immune Checkpoint is an important modulator of the immune response. Overexpression of the receptor and its ligands is involved in immunosuppression and the failure of an immune response against tumor cells. PD-1/PD-L1 overexpression in oral squamous cell carcinoma (OSCC) compared to healthy oral mucosa (NOM) has already been demonstrated. However, little is known about its expression in oral precancerous lesions like oral leukoplakia (OLP). The aim of the study was to investigate whether an increased expression of PD-1/PD-L1 already exists in OLP and whether it is associated with malignant transformation. Material and Methods: PD-1 and PD-L1 expression was immunohistologically analyzed separately in the epithelium (E) and the subepithelium (S) of OLP that had undergone malignant transformation within 5 years (T-OLP), in OLP without malignant transformation (N-OLP), in corresponding OSCC and in NOM. Additionally, RT-qPCR analysis for PD-L1 expression was done in the entire tissues. Additionally, the association between overexpression and malignant transformation, dysplasia and inflammation were examined. Results: Compared to N-OLP, there were increased levels of PD-1 protein in the epithelial and subepithelial layers of T-OLP (pE = 0.001; pS = 0.005). There was no significant difference in PD-L1 mRNA expression between T-OLP and N-OLP (p = 0.128), but the fold-change increase between these groups was significant (Relative Quantification (RQ) = 3.1). In contrast to N-OLP, the PD-L1 protein levels were significantly increased in the epithelial layers of T-OLP (p = 0.007), but not in its subepithelial layers (p = 0.25). Importantly, increased PD-L1 levels were significantly associated to malignant transformation within 5 years. Conclusion: Increased levels of PD-1 and PD-L1 are related to malignant transformation in OLP and may represent a promising prognostic indicator to determine the risk of malignant progression of OLP. Increased PD-L1 levels might establish an immunosuppressive microenvironment, which could favor immune escape and thereby contribute to malignant transformation. Hence, checkpoint inhibitors could counteract tumor development in OLP and may serve as efficient therapeutic strategy in patients with high-risk precancerous lesions.


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