Materiały źródłowe

• #1 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Oral leukoplakia is a white patch or plaque that develops in the oral cavity. The condition is potentially malignant and is strongly associated with tobacco use. […] Oral leukoplakia is a potentially malignant disorder affecting the oral mucosa. It is defined as essentially an oral mucosal white lesion that cannot be considered as any other definable lesion. […] The etiology of oral leukoplakia is multifactorial, and many causes are idiopathic. The most commonly associated risk factor is the use of tobacco in either smoked or smokeless form. Additionally, the use of areca (betel) nut preparations in many parts of the world (south and southeast Asia) poses a significant risk, as does the use of snuff and other forms of smokeless tobacco. […] When a tissue cell is exposed to any type of carcinogen, it probably tries to adapt to it. An increase in cell proliferation, shrinking the cytosolic capacity, and the allied organelle load could be an effort in adaptation.

• #2 Oral leukoplakia – UpToDate

  https://www.uptodate.com/contents/oral-leukoplakia/print

  Oral leukoplakia is an oral potentially malignant disorder that presents as white patches of the oral mucosa. […] The pathogenesis of oral leukoplakia is largely unknown. It is considered an intermediate stage in oral carcinogenesis, driven by multiple somatic genetic mutations affecting keratinocyte growth, survival, and cycle control. These result in histopathologic (hyperkeratosis, hyperplasia, dysplasia) and clinical (change of color, thickness, and texture) modifications. […] Copy number alterations that originate from gains, amplifications, deletions, and insertions of deoxyribonucleic acid (DNA) sequences involving known oncogenic drivers (eg, CDKN2A, CCND1, EGFR, and MYC) have been found with high frequency in oral leukoplakia. Other common features of oral leukoplakia include DNA ploidy abnormalities; positive telomerase activity; loss of heterozygosity (particularly on 3p, 4q, 9p, and 17p); and gene mutations, the most frequent being those affecting TP53, followed by NOTCH1, FAT1, CDKN2A, KMT2C, and PIK3CA.

• #3 Oral leukoplakia – UpToDate

  https://www.uptodate.com/contents/oral-leukoplakia/print

  Oral leukoplakia is an oral potentially malignant disorder that presents as white patches of the oral mucosa. […] The pathogenesis of oral leukoplakia is largely unknown. It is considered an intermediate stage in oral carcinogenesis, driven by multiple somatic genetic mutations affecting keratinocyte growth, survival, and cycle control. These result in histopathologic (hyperkeratosis, hyperplasia, dysplasia) and clinical (change of color, thickness, and texture) modifications. […] Copy number alterations that originate from gains, amplifications, deletions, and insertions of deoxyribonucleic acid (DNA) sequences involving known oncogenic drivers (eg, CDKN2A, CCND1, EGFR, and MYC) have been found with high frequency in oral leukoplakia. Other common features of oral leukoplakia include DNA ploidy abnormalities; positive telomerase activity; loss of heterozygosity (particularly on 3p, 4q, 9p, and 17p); and gene mutations, the most frequent being those affecting TP53, followed by NOTCH1, FAT1, CDKN2A, KMT2C, and PIK3CA.

• #4 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Oral leukoplakia is a white patch or plaque that develops in the oral cavity. The condition is potentially malignant and is strongly associated with tobacco use. […] Oral leukoplakia is a potentially malignant disorder affecting the oral mucosa. It is defined as essentially an oral mucosal white lesion that cannot be considered as any other definable lesion. […] The etiology of oral leukoplakia is multifactorial, and many causes are idiopathic. The most commonly associated risk factor is the use of tobacco in either smoked or smokeless form. Additionally, the use of areca (betel) nut preparations in many parts of the world (south and southeast Asia) poses a significant risk, as does the use of snuff and other forms of smokeless tobacco. […] When a tissue cell is exposed to any type of carcinogen, it probably tries to adapt to it. An increase in cell proliferation, shrinking the cytosolic capacity, and the allied organelle load could be an effort in adaptation.

• #5 Oral Leukoplakia: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/853864-overview

  The etiology of most cases of OL is unknown (idiopathic). In other cases, the initiation of the condition may depend on extrinsic local factors and/or intrinsic predisposing factors. Factors most frequently blamed for the development of idiopathic leukoplakia include tobacco use, alcohol consumption, chronic irritation, candidiasis, vitamin deficiency, endocrine disturbances, and possibly a virus. […] Follow-up studies suggest that cancer is more likely to occur in individuals with idiopathic leukoplakia than in individuals who do not have this condition. Thus, idiopathic leukoplakia is considered a premalignant lesion. […] A definitive diagnosis of oral leukoplakia is made when any etiologic cause other than tobacco/areca nut use has been excluded and histopathology has not confirmed any other specific disorder.

• #6 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Oral leukoplakia is a white patch or plaque that develops in the oral cavity. The condition is potentially malignant and is strongly associated with tobacco use. […] Oral leukoplakia is a potentially malignant disorder affecting the oral mucosa. It is defined as essentially an oral mucosal white lesion that cannot be considered as any other definable lesion. […] The etiology of oral leukoplakia is multifactorial, and many causes are idiopathic. The most commonly associated risk factor is the use of tobacco in either smoked or smokeless form. Additionally, the use of areca (betel) nut preparations in many parts of the world (south and southeast Asia) poses a significant risk, as does the use of snuff and other forms of smokeless tobacco. […] When a tissue cell is exposed to any type of carcinogen, it probably tries to adapt to it. An increase in cell proliferation, shrinking the cytosolic capacity, and the allied organelle load could be an effort in adaptation.

• #7 Oral Potentially Malignant Disorders: Etiology, Pathogenesis, and Transformation Into Oral Cancer

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9065478/

  In 2005, a new definition of leukoplakia was proposed: A white plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer. […] The definitive cause of leukoplakia is unclear. However, the most common risk factors involve the use of tobacco either in smoke (mainly) or smokeless form together with chronic alcohol consumption. […] An understanding of the molecular pathogenesis of leukoplakia is important to minimize the chances of oncogenic transformation. Various studies have reported the presence of molecular abnormalities associated with both leukoplakia and oral cancer. […] Alterations (insertions/deletions/mutations) in the chromosomal region(s) with tumor suppressor genes or proto-oncogenes increase the carcinogenic potential of OPMDs. Chromosomal deletion in 3p14 and 9p21 region in leukoplakia likely increases the invasive potential of oral cancer.

• #8 Oral Leukoplakia: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/853864-overview

  The etiology of most cases of OL is unknown (idiopathic). In other cases, the initiation of the condition may depend on extrinsic local factors and/or intrinsic predisposing factors. Factors most frequently blamed for the development of idiopathic leukoplakia include tobacco use, alcohol consumption, chronic irritation, candidiasis, vitamin deficiency, endocrine disturbances, and possibly a virus. […] Follow-up studies suggest that cancer is more likely to occur in individuals with idiopathic leukoplakia than in individuals who do not have this condition. Thus, idiopathic leukoplakia is considered a premalignant lesion. […] A definitive diagnosis of oral leukoplakia is made when any etiologic cause other than tobacco/areca nut use has been excluded and histopathology has not confirmed any other specific disorder.

• #9 Oral Leukoplakia: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/853864-overview

  The etiology of most cases of OL is unknown (idiopathic). In other cases, the initiation of the condition may depend on extrinsic local factors and/or intrinsic predisposing factors. Factors most frequently blamed for the development of idiopathic leukoplakia include tobacco use, alcohol consumption, chronic irritation, candidiasis, vitamin deficiency, endocrine disturbances, and possibly a virus. […] Follow-up studies suggest that cancer is more likely to occur in individuals with idiopathic leukoplakia than in individuals who do not have this condition. Thus, idiopathic leukoplakia is considered a premalignant lesion. […] A definitive diagnosis of oral leukoplakia is made when any etiologic cause other than tobacco/areca nut use has been excluded and histopathology has not confirmed any other specific disorder.

• #10

  https://journals.lww.com/jpat/fulltext/2004/08020/oral_leukoplakia__leukokeratosis___compilation_of.4.aspx

  Leukoplakia (white patch) is the most common potentially malignant lesion of the oral mucosa. […] It should be stressed that the diagnosis of leukoplakia denotes mainly, that (a) the mucosa is irritated by either mechanical, chemical or galvanic means and (b) the mucosa is trying to adapt to the noxious stimuli by undergoing hyperkeratinisation of its surface. […] Since leukoplakia is an adaptive response, offered by a viable and healthy oral mucosa against some forms of sustained, low-grade irritant, it is irrational to consider it as a disease entity (hence its assumption of a negative diagnostic state). […] The role of Candida albicans as a possible aetiological factor in leukoplakia and its possible role in malignant transformation is still unclear. […] Epithelial dysplasia is reported to occur four to five times more frequently in candida leukoplakia than in leukoplakia in general.

• #11 Oral Leukoplakia: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/853864-overview

  The etiology of most cases of OL is unknown (idiopathic). In other cases, the initiation of the condition may depend on extrinsic local factors and/or intrinsic predisposing factors. Factors most frequently blamed for the development of idiopathic leukoplakia include tobacco use, alcohol consumption, chronic irritation, candidiasis, vitamin deficiency, endocrine disturbances, and possibly a virus. […] Follow-up studies suggest that cancer is more likely to occur in individuals with idiopathic leukoplakia than in individuals who do not have this condition. Thus, idiopathic leukoplakia is considered a premalignant lesion. […] A definitive diagnosis of oral leukoplakia is made when any etiologic cause other than tobacco/areca nut use has been excluded and histopathology has not confirmed any other specific disorder.

• #12 Oral Leukoplakia: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/853864-overview

  The etiology of most cases of OL is unknown (idiopathic). In other cases, the initiation of the condition may depend on extrinsic local factors and/or intrinsic predisposing factors. Factors most frequently blamed for the development of idiopathic leukoplakia include tobacco use, alcohol consumption, chronic irritation, candidiasis, vitamin deficiency, endocrine disturbances, and possibly a virus. […] Follow-up studies suggest that cancer is more likely to occur in individuals with idiopathic leukoplakia than in individuals who do not have this condition. Thus, idiopathic leukoplakia is considered a premalignant lesion. […] A definitive diagnosis of oral leukoplakia is made when any etiologic cause other than tobacco/areca nut use has been excluded and histopathology has not confirmed any other specific disorder.

• #13 Proliferative verrucous leukoplakia: diagnosis, management and current advances | Brazilian Journal of Otorhinolaryngology

  https://www.elsevier.es/en-revista-brazilian-journal-otorhinolaryngology-english-edition–497-articulo-proliferative-verrucous-leukoplakia-diagnosis-management-S1808869417300058

  In recent years, it has been hypothesized that human papillomavirus (HPV) may influence both potentially and already stablished oral malignant lesions. Although the association between oral squamous cell carcinoma (OSCC) and HPV is already mentioned, its influence on PVL cases is not confirmed yet. […] Histopathological findings may show acanthosis and hyperkeratosis with an interface lymphocytic infiltrate within the superficial lamina propria. If the lesions continue to grow horizontally and vertically, there are histopathological changes that increase roughness of surface with verrucous aspect, and hyperplasia with or without dysplasia. Therefore, over time and without treatment, there is an inexorable progression to VC or OSCC. […] Although there are not enough studies to determine PVL etiology and no simplified diagnosis criteria, the most difficult point is PVL treatment. According to the literature reviewed, PVL seems to be resistant to many therapy attempts and often has high propensity for dysplasia and/or malignancy progression. Modalities such as surgery, laser ablation, photodynamic therapy, retinoid, radiation and chemotherapy are not effective in reducing relapses and malignant transformation.

• #14 Laryngeal Leukoplakia: A Focus on Histology | IntechOpen

  https://www.intechopen.com/chapters/82549

  Dysplastic changes encompass crowded immature epithelial cells, loss of cellular polarity, nuclear pleomorphism and hyperchromasia, increased nucleus-to-cytoplasm ratio, and mitoses including atypical forms. […] LD represents the earliest lesion manifesting, at both microscopic and molecular levels, neoplastic features. […] The carcinogenic role of the Human Papilloma Virus (HPV) infection has been advocated as a causative agent in a subset of LD and SCC. […] The carcinogenetic role of HPV infection relies on the viral integration in the host genome and disruption of intracellular control pathways. […] The risk of progression is known to vary in dysplastic LL according to the grading of dysplasia.

• #15 Oral Potentially Malignant Disorders: Etiology, Pathogenesis, and Transformation Into Oral Cancer

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9065478/

  Among oral diseases, oral cancer is a critical health issue due to its life-threatening potential. […] Oral lesions, inherited genetic mutations (dyskeratosis congenital syndrome), and viral infections (HPV) are early signs of oral cancer. Lesions with dysplastic features have been categorized under oral potentially malignant disorders (OPMDs), such as oral leukoplakia, erythroplakia, oral submucous fibrosis (OSMF), and proliferative verrucous leukoplakia, are assumed to have a high risk of malignancy. […] The development of oral cancer from OPMDs is common, especially in South Asian countries like India where tobacco and areca nut consumption is prevalent. […] Currently identified OPMDs that are associated with a high risk of MT include leukoplakia, proliferative verrucous leukoplakia (PVL), erythroplakia, oral lichen planus (OLP), oral submucous fibrosis (OSMF), actinic cheilitis, palatal lesions of reverse cigar smoking, discoid lupus erythematosus, dyskeratosis congenita, oral lichenoid lesions, and oral graft versus host disease.

• #16 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Oral leukoplakia is a white patch or plaque that develops in the oral cavity. The condition is potentially malignant and is strongly associated with tobacco use. […] Oral leukoplakia is a potentially malignant disorder affecting the oral mucosa. It is defined as essentially an oral mucosal white lesion that cannot be considered as any other definable lesion. […] The etiology of oral leukoplakia is multifactorial, and many causes are idiopathic. The most commonly associated risk factor is the use of tobacco in either smoked or smokeless form. Additionally, the use of areca (betel) nut preparations in many parts of the world (south and southeast Asia) poses a significant risk, as does the use of snuff and other forms of smokeless tobacco. […] When a tissue cell is exposed to any type of carcinogen, it probably tries to adapt to it. An increase in cell proliferation, shrinking the cytosolic capacity, and the allied organelle load could be an effort in adaptation.

• #17 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #18 Oral leukoplakia – UpToDate

  https://www.uptodate.com/contents/oral-leukoplakia

  Oral leukoplakia is an oral potentially malignant disorder that presents as white patches of the oral mucosa. […] The pathogenesis of oral leukoplakia is largely unknown. It is considered an intermediate stage in oral carcinogenesis, driven by multiple somatic genetic mutations affecting keratinocyte growth, survival, and cycle control. These result in histopathologic (hyperkeratosis, hyperplasia, dysplasia) and clinical (change of color, thickness, and texture) modifications. […] Genetic and molecular alterations — Copy number alterations that originate from gains, amplifications, deletions, and insertions of deoxyribonucleic acid (DNA) sequences involving known oncogenic drivers (eg, CDKN2A, CCND1, EGFR, and MYC) have been found with high frequency in oral leukoplakia. Other common features of oral leukoplakia include DNA ploidy abnormalities; positive telomerase activity; loss of heterozygosity (particularly on 3p, 4q, 9p, and 17p); and gene mutations, the most frequent being those affecting TP53, followed by NOTCH1, FAT1, CDKN2A, KMT2C, and PIK3CA.

• #19 Oral leukoplakia – UpToDate

  https://www.uptodate.com/contents/oral-leukoplakia

  Oral leukoplakia is an oral potentially malignant disorder that presents as white patches of the oral mucosa. […] The pathogenesis of oral leukoplakia is largely unknown. It is considered an intermediate stage in oral carcinogenesis, driven by multiple somatic genetic mutations affecting keratinocyte growth, survival, and cycle control. These result in histopathologic (hyperkeratosis, hyperplasia, dysplasia) and clinical (change of color, thickness, and texture) modifications. […] Genetic and molecular alterations — Copy number alterations that originate from gains, amplifications, deletions, and insertions of deoxyribonucleic acid (DNA) sequences involving known oncogenic drivers (eg, CDKN2A, CCND1, EGFR, and MYC) have been found with high frequency in oral leukoplakia. Other common features of oral leukoplakia include DNA ploidy abnormalities; positive telomerase activity; loss of heterozygosity (particularly on 3p, 4q, 9p, and 17p); and gene mutations, the most frequent being those affecting TP53, followed by NOTCH1, FAT1, CDKN2A, KMT2C, and PIK3CA.

• #20 Oral Potentially Malignant Disorders: Etiology, Pathogenesis, and Transformation Into Oral Cancer

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9065478/

  The DNA ploidy level serves as an important determinant of genetic stability and alteration in genomic sequence. A considerable ploidy level has been observed in OPMDs and subsequently in oral cancer. […] Thus, it is evident that genomic content changes drastically during MT of leukoplakia, and monitoring these changes can provide important information for diagnosis and potential stratification of patients. […] The existence of an immunosuppressive tumor microenvironment, inhibiting the action of infiltrating immune cells, and the presence of immune checkpoints, including PD1/PD-L1 (programmed death/programmed deathligand 1), all together contribute to cancer immune escape and aid cancer progression. […] Although genomic- and protein-based markers have been identified in leukoplakia, further investigation are necessary to determine the diagnostic and prognostic value of the markers.

• #21 Oral leukoplakia – UpToDate

  https://www.uptodate.com/contents/oral-leukoplakia

  Oral leukoplakia is an oral potentially malignant disorder that presents as white patches of the oral mucosa. […] The pathogenesis of oral leukoplakia is largely unknown. It is considered an intermediate stage in oral carcinogenesis, driven by multiple somatic genetic mutations affecting keratinocyte growth, survival, and cycle control. These result in histopathologic (hyperkeratosis, hyperplasia, dysplasia) and clinical (change of color, thickness, and texture) modifications. […] Genetic and molecular alterations — Copy number alterations that originate from gains, amplifications, deletions, and insertions of deoxyribonucleic acid (DNA) sequences involving known oncogenic drivers (eg, CDKN2A, CCND1, EGFR, and MYC) have been found with high frequency in oral leukoplakia. Other common features of oral leukoplakia include DNA ploidy abnormalities; positive telomerase activity; loss of heterozygosity (particularly on 3p, 4q, 9p, and 17p); and gene mutations, the most frequent being those affecting TP53, followed by NOTCH1, FAT1, CDKN2A, KMT2C, and PIK3CA.

• #22 Oral leukoplakia – UpToDate

  https://www.uptodate.com/contents/oral-leukoplakia

  Oral leukoplakia is an oral potentially malignant disorder that presents as white patches of the oral mucosa. […] The pathogenesis of oral leukoplakia is largely unknown. It is considered an intermediate stage in oral carcinogenesis, driven by multiple somatic genetic mutations affecting keratinocyte growth, survival, and cycle control. These result in histopathologic (hyperkeratosis, hyperplasia, dysplasia) and clinical (change of color, thickness, and texture) modifications. […] Genetic and molecular alterations — Copy number alterations that originate from gains, amplifications, deletions, and insertions of deoxyribonucleic acid (DNA) sequences involving known oncogenic drivers (eg, CDKN2A, CCND1, EGFR, and MYC) have been found with high frequency in oral leukoplakia. Other common features of oral leukoplakia include DNA ploidy abnormalities; positive telomerase activity; loss of heterozygosity (particularly on 3p, 4q, 9p, and 17p); and gene mutations, the most frequent being those affecting TP53, followed by NOTCH1, FAT1, CDKN2A, KMT2C, and PIK3CA.

• #23 Oral Potentially Malignant Disorders: Etiology, Pathogenesis, and Transformation Into Oral Cancer

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9065478/

  In 2005, a new definition of leukoplakia was proposed: A white plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer. […] The definitive cause of leukoplakia is unclear. However, the most common risk factors involve the use of tobacco either in smoke (mainly) or smokeless form together with chronic alcohol consumption. […] An understanding of the molecular pathogenesis of leukoplakia is important to minimize the chances of oncogenic transformation. Various studies have reported the presence of molecular abnormalities associated with both leukoplakia and oral cancer. […] Alterations (insertions/deletions/mutations) in the chromosomal region(s) with tumor suppressor genes or proto-oncogenes increase the carcinogenic potential of OPMDs. Chromosomal deletion in 3p14 and 9p21 region in leukoplakia likely increases the invasive potential of oral cancer.

• #24 Leukoplakia | PPT

  https://www.slideshare.net/slideshow/leukoplakia-76138648/76138648

  Leukoplakia PATHOPHYSIOLOGY Tumor suppressor genes are genes involved in the regulation of normal cell turnover and apoptosis (programmed cell death). One of the most studied tumor suppressor genes is p53, which is found on the short arm of chromosome 17. Mutation of p53 can disrupt its regulatory function and lead to uncontrolled cell growth. Mutations of p53 have been demonstrated in the cells from areas of some leukoplakias, especially those with dysplasia and in individuals who smoke and drink heavily. […] TREATMENT Most patches improve on their own and dont require any treatment. Its important to avoid any trigger that may have caused your leukoplakia, such as tobacco use. If its related to irritation from a dental problem, dentist may be able to address this. If a biopsy comes back positive for oral cancer, the patch must be removed immediately. This can help prevent the spread of the cancer. Small patches can be removed by a more extensive biopsy using laser therapy or a scalpel. Large leukoplakia patches require oral surgery. Hairy leukoplakia may not require removal. dentist or doctor might prescribe antiviral medications to help stop the patches from growing. Topical ointments containing retinoic acid can also be used to reduce patch size.

• #25 Oral Leukoplakia/ Pathology of Gastrointestinal tract.pptx

  https://www.slideshare.net/slideshow/oral-leukoplakia-pathology-of-gastrointestinal-tract-pptx/272530591

  Leukoplakia is a predominantly white lesion of the oral mucosa characterized by thickened white patches that cannot be wiped away. […] The condition has various clinical forms, ranging from flat and uniform to raised or irregular patches, and is primarily linked to tobacco use, with smoking being the most common cause. […] Diagnosis is usually made through an oral exam, and if patches appear suspicious, a biopsy is performed to examine the tissue for signs of dysplasia or oral cancer. […] While most leukoplakia is harmless, some may develop into cancer over time, necessitating treatment that can range from monitoring to surgical removal if cancer is detected. […] Tumor suppressor genes are genes involved in the regulation of normal cell turnover and apoptosis (programmed cell death). One of the most studied tumor suppressor genes is p53, which is found on the short arm of chromosome 17. Mutation of p53 can disrupt its regulatory function and lead to uncontrolled cell growth. Mutations of p53 have been demonstrated in the cells from areas of some leukoplakias, especially those with dysplasia and in individuals who smoke and drink heavily.

• #26 Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and M2 polarization of macrophage | International Journal of Oral Science

  https://www.nature.com/articles/s41368-021-00128-2

  Oral immunosuppression caused by smoking creates a microenvironment to promote the occurrence and development of oral mucosa precancerous lesions. This study aimed to investigate the role of metabolism and macrophage polarization in cigarette-promoting oral leukoplakia. […] The results also showed that the supernatant of Raw cells stimulated by CSE could induce excessive proliferation of Leuk-1 and inhibit apoptosis. Glutamine abundance can facilitate this process. Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and macrophage M2 polarization. […] However, the mechanism by which smoking promotes OLK pathogenesis is unclear. […] It incorporates the activation of M1 innate response at a low dose but suppresses the M1 innate response at high-dose particle exposures.

• #27 Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and M2 polarization of macrophage | International Journal of Oral Science

  https://www.nature.com/articles/s41368-021-00128-2

  It was noted that innate response was indeed activated with low initial exposures to either cigarette smoke or diesel exhaust particulate, but that at high doses, the innate response was suppressed. […] Two main macrophage activation programs are called M1 and M2 polarization. […] Long-term smoking reprograms the steady-state macrophage polarization to M1 inactivated, and partially M2-activated macrophages, which enhances the ability of tissue remodeling but reduces the gene expression related to inflammation and immunity. […] The results of this research show M2 polarization is increased with exposure to smoke, while the dose is the important consideration as mentioned in Pappas review. […] The results showed that F4/80+CD206+ cells were significantly increased after CSE stimulation and glutamate abundance.

• #28 Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and M2 polarization of macrophage | International Journal of Oral Science

  https://www.nature.com/articles/s41368-021-00128-2

  It was noted that innate response was indeed activated with low initial exposures to either cigarette smoke or diesel exhaust particulate, but that at high doses, the innate response was suppressed. […] Two main macrophage activation programs are called M1 and M2 polarization. […] Long-term smoking reprograms the steady-state macrophage polarization to M1 inactivated, and partially M2-activated macrophages, which enhances the ability of tissue remodeling but reduces the gene expression related to inflammation and immunity. […] The results of this research show M2 polarization is increased with exposure to smoke, while the dose is the important consideration as mentioned in Pappas review. […] The results showed that F4/80+CD206+ cells were significantly increased after CSE stimulation and glutamate abundance.

• #29 Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and M2 polarization of macrophage | International Journal of Oral Science

  https://www.nature.com/articles/s41368-021-00128-2

  It was noted that innate response was indeed activated with low initial exposures to either cigarette smoke or diesel exhaust particulate, but that at high doses, the innate response was suppressed. […] Two main macrophage activation programs are called M1 and M2 polarization. […] Long-term smoking reprograms the steady-state macrophage polarization to M1 inactivated, and partially M2-activated macrophages, which enhances the ability of tissue remodeling but reduces the gene expression related to inflammation and immunity. […] The results of this research show M2 polarization is increased with exposure to smoke, while the dose is the important consideration as mentioned in Pappas review. […] The results showed that F4/80+CD206+ cells were significantly increased after CSE stimulation and glutamate abundance.

• #30 Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and M2 polarization of macrophage | International Journal of Oral Science

  https://www.nature.com/articles/s41368-021-00128-2

  It was noted that innate response was indeed activated with low initial exposures to either cigarette smoke or diesel exhaust particulate, but that at high doses, the innate response was suppressed. […] Two main macrophage activation programs are called M1 and M2 polarization. […] Long-term smoking reprograms the steady-state macrophage polarization to M1 inactivated, and partially M2-activated macrophages, which enhances the ability of tissue remodeling but reduces the gene expression related to inflammation and immunity. […] The results of this research show M2 polarization is increased with exposure to smoke, while the dose is the important consideration as mentioned in Pappas review. […] The results showed that F4/80+CD206+ cells were significantly increased after CSE stimulation and glutamate abundance.

• #31 Single-cell RNA sequencing highlights the immunosuppression of IDO1+ macrophages in the malignant transformation of oral leukoplakia

  https://www.thno.org/v14p4787.htm

  Rationale: Immunosuppressive tumor microenvironment (iTME) plays an important role in carcinogenesis, and some macrophage subsets are associated with iTME generation. However, the sub-population characterization of macrophages in oral carcinogenesis remains largely unclear. Here, we investigated the immunosuppressive status with focus on function of a macrophage subset that expressed indoleamine 2,3 dioxygenase 1 (Macro-IDO1) in oral carcinogenesis. […] The iTME formed at preca-OLK stage, as evidenced by increased exhausted T cells, Tregs and some special subsets of macrophages and fibroblasts. Macro-IDO1 was predominantly enriched in preca-OLK and OSCC, distributed near exhausted T cells and possessed tumor associated macrophage transformation potentials. […] Functional analysis revealed the established immunosuppressive role of Macro-IDO1 in preca-OLK and OSCC: enriching the immunosuppression related genes; having an established level of immune checkpoint score; exerting strong immunosuppressive interaction with T cells; positively correlating with the CD8-exhausted.

• #32 Single-cell RNA sequencing highlights the immunosuppression of IDO1+ macrophages in the malignant transformation of oral leukoplakia

  https://www.thno.org/v14p4787.htm

  Rationale: Immunosuppressive tumor microenvironment (iTME) plays an important role in carcinogenesis, and some macrophage subsets are associated with iTME generation. However, the sub-population characterization of macrophages in oral carcinogenesis remains largely unclear. Here, we investigated the immunosuppressive status with focus on function of a macrophage subset that expressed indoleamine 2,3 dioxygenase 1 (Macro-IDO1) in oral carcinogenesis. […] The iTME formed at preca-OLK stage, as evidenced by increased exhausted T cells, Tregs and some special subsets of macrophages and fibroblasts. Macro-IDO1 was predominantly enriched in preca-OLK and OSCC, distributed near exhausted T cells and possessed tumor associated macrophage transformation potentials. […] Functional analysis revealed the established immunosuppressive role of Macro-IDO1 in preca-OLK and OSCC: enriching the immunosuppression related genes; having an established level of immune checkpoint score; exerting strong immunosuppressive interaction with T cells; positively correlating with the CD8-exhausted.

• #33 Single-cell RNA sequencing highlights the immunosuppression of IDO1+ macrophages in the malignant transformation of oral leukoplakia

  https://www.thno.org/v14p4787.htm

  The immunosuppression related gene expression of macrophages also increased in preca-OLK/OSCC compared to PCA. […] Mechanistically, IFN–JAK-STAT pathway was associated with IDO1 upregulation in OLK and OSCC. […] These results highlight that Macro-IDO1-enriched in preca-OLK possesses a strong immunosuppressive role and contributes to oral carcinogenesis, providing a potential target for preventing precancerous legions from transformation into OSCC. […] The present study revealed increased abundance of exhausted T cells and immunosuppressive macrophages and fibroblasts subsets at OLK stage verse the normal counterparts, in line with the recent reports, further supporting the notion that immunosuppression plays an important role in transformation of OLK into OSCC. […] More important, we novelly demonstrated the important role of Macro-IDO1 sub-cluster in shift of precancerous OLK to OSCC, providing a potential target for preventing precancerous legions from transformation into OSCC.

• #34 Single-cell RNA sequencing highlights the immunosuppression of IDO1+ macrophages in the malignant transformation of oral leukoplakia

  https://www.thno.org/v14p4787.htm

  The immunosuppression related gene expression of macrophages also increased in preca-OLK/OSCC compared to PCA. […] Mechanistically, IFN–JAK-STAT pathway was associated with IDO1 upregulation in OLK and OSCC. […] These results highlight that Macro-IDO1-enriched in preca-OLK possesses a strong immunosuppressive role and contributes to oral carcinogenesis, providing a potential target for preventing precancerous legions from transformation into OSCC. […] The present study revealed increased abundance of exhausted T cells and immunosuppressive macrophages and fibroblasts subsets at OLK stage verse the normal counterparts, in line with the recent reports, further supporting the notion that immunosuppression plays an important role in transformation of OLK into OSCC. […] More important, we novelly demonstrated the important role of Macro-IDO1 sub-cluster in shift of precancerous OLK to OSCC, providing a potential target for preventing precancerous legions from transformation into OSCC.

• #35

  https://journals.lww.com/jpat/fulltext/2007/11010/mast_cells_are_increased_in_leukoplakia,_oral.7.aspx

  Oral leukoplakia, submucous fibrosis (OSMF), oral lichen planus (OLP) and oral squamous cell carcinoma (OSCC) are the commonly occurring oral diseases, with characteristic clinical and histological features. These diseases at some stage are associated with chronic inflammation in adjacent connective tissue. Mast cells are the local residents of the connective tissue, and are said to be pro-inflammatory, immunoamplifying in action and producing mitogenic cytokines. These functions of mast cells may play a significant role in the pathogenesis of other oral diseases. […] Mast cell hyperplasia in oral leukoplakia, OSMF, OLP, OSCC suggests their probable role in the pathogenesis of these diseases. […] The authors concluded that the biologically and pharmacologically active agents in the mast cells might contribute to inflammatory reaction seen in leukoplakia. These stimulated mast cells may release interleukin-1, which causes increased epithelial proliferation that is seen in leukoplakia.

• #36

  https://journals.lww.com/jpat/fulltext/2007/11010/mast_cells_are_increased_in_leukoplakia,_oral.7.aspx

  Oral leukoplakia, submucous fibrosis (OSMF), oral lichen planus (OLP) and oral squamous cell carcinoma (OSCC) are the commonly occurring oral diseases, with characteristic clinical and histological features. These diseases at some stage are associated with chronic inflammation in adjacent connective tissue. Mast cells are the local residents of the connective tissue, and are said to be pro-inflammatory, immunoamplifying in action and producing mitogenic cytokines. These functions of mast cells may play a significant role in the pathogenesis of other oral diseases. […] Mast cell hyperplasia in oral leukoplakia, OSMF, OLP, OSCC suggests their probable role in the pathogenesis of these diseases. […] The authors concluded that the biologically and pharmacologically active agents in the mast cells might contribute to inflammatory reaction seen in leukoplakia. These stimulated mast cells may release interleukin-1, which causes increased epithelial proliferation that is seen in leukoplakia.

• #37

  https://journals.lww.com/jpat/fulltext/2007/11010/mast_cells_are_increased_in_leukoplakia,_oral.7.aspx

  The effect of chemical mediators can explain the histopathological changes seen in OSMF. Histamine could probably attribute to submucosal edema seen in early stages of oral submucous fibrosis. […] TNF-alpha released from the mast cells causes increased synthesis of matrix metalloproteinases like collagenase, which cause the basement membrane destruction. […] Interleukin-1 leads to epithelial proliferation. […] In this study, mast cell hyperplasia was observed in all the oral diseases considered. The mediators in mast cells are known to vary with the variation in microenvironment in various diseases. Thus it is probable that mast cells play a key role in mediating the cross talks between the external antigenic agent and the local immunologic factors.

• #38

  https://journals.lww.com/jpat/fulltext/2007/11010/mast_cells_are_increased_in_leukoplakia,_oral.7.aspx

  The effect of chemical mediators can explain the histopathological changes seen in OSMF. Histamine could probably attribute to submucosal edema seen in early stages of oral submucous fibrosis. […] TNF-alpha released from the mast cells causes increased synthesis of matrix metalloproteinases like collagenase, which cause the basement membrane destruction. […] Interleukin-1 leads to epithelial proliferation. […] In this study, mast cell hyperplasia was observed in all the oral diseases considered. The mediators in mast cells are known to vary with the variation in microenvironment in various diseases. Thus it is probable that mast cells play a key role in mediating the cross talks between the external antigenic agent and the local immunologic factors.

• #39 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #40 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #41 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #42 Oral Leukoplakia/ Pathology of Gastrointestinal tract.pptx

  https://www.slideshare.net/slideshow/oral-leukoplakia-pathology-of-gastrointestinal-tract-pptx/272530591

  The degree of hyperkeratosis, epithelial thickness (acanthosis/atrophy), dysplasia and inflammatory cell infiltration in the underlying lamina propria are variable. […] Tissue biopsy is usually indicated to rule out other causes of white patches and also to enable a detailed histologic examination to grade the presence of any epithelial dysplasia. This is an indicator of malignant potential and usually determines the management and recall interval. […] Most patches improve on their own and don’t require any treatment. […] If a biopsy comes back positive for oral cancer, the patch must be removed immediately. […] Many cases of leukoplakia can be prevented with lifestyle changes: Stop smoking or chewing tobacco. Reduce alcohol use. Eat antioxidant-rich foods such as spinach and carrots. Antioxidants may help deactivate irritants that cause patches.

• #43 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #44 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #45 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #46 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #47 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #48 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #49 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #50 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #51 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #52 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #53 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #54 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  As an adaptative response, the hastened pace of cell division noted at the earlier stages of transformation facilitates further genetic damage, thereby forcefully pushing the cells further along the path to malignant transformation. […] Histologically, oral leukoplakias present as either hyperkeratosis, mild dysplasia, moderate dysplasia, severe dysplasia, or carcinoma-in-situ. […] The main histopathological changes seen are: Keratinization of the epithelium (hyper ortho-keratinization or hyper para-keratinization), Increased thickness of the epithelium, Acanthosis, Basement membrane becomes thin, The inflammatory component in connective tissue, Change in the cellular layer, Increased nuclear-cytoplasmic ratio, Hyperchromatic nuclei, Nuclear hyperplasia, Abnormal mitotic figures, Increased mitosis, Pleomorphic nuclei, Basilar hyperplasia, Drop-shaped rete pegs, Loss of polarity.

• #55 Laryngeal Leukoplakia: A Focus on Histology | IntechOpen

  https://www.intechopen.com/chapters/82549

  Dysplastic changes encompass crowded immature epithelial cells, loss of cellular polarity, nuclear pleomorphism and hyperchromasia, increased nucleus-to-cytoplasm ratio, and mitoses including atypical forms. […] LD represents the earliest lesion manifesting, at both microscopic and molecular levels, neoplastic features. […] The carcinogenic role of the Human Papilloma Virus (HPV) infection has been advocated as a causative agent in a subset of LD and SCC. […] The carcinogenetic role of HPV infection relies on the viral integration in the host genome and disruption of intracellular control pathways. […] The risk of progression is known to vary in dysplastic LL according to the grading of dysplasia.

• #56 Oral leukoplakia: an update for dental practitioners | Published in Journal of the Irish Dental Association

  https://jida.scholasticahq.com/article/93880-oral-leukoplakia-an-update-for-dental-practitioners

  Oral leukoplakia (OLK) is a common mucosal pathology frequently encountered in general dental practice which belongs to a group of conditions known as oral potentially malignant disorders (OPMDs). […] The development of oral leukoplakia appears to be multifactorial in nature. However, the definitive cause is unclear. Smoking has been identified as the predominant risk factor, with oral leukoplakia six times more common in smokers. […] The degree of dysplasia is regarded as the most important determinant for progression to invasive carcinoma, with the risk of malignant transformation increasing with increasing degrees of OED. […] The presence of redness or nodularity in an oral leukoplakia is associated with a greater risk of developing carcinoma and these are red flags for GDPs to be aware of, as they require urgent referral.

• #57 Laryngeal Leukoplakia: A Focus on Histology | IntechOpen

  https://www.intechopen.com/chapters/82549

  Dysplastic changes encompass crowded immature epithelial cells, loss of cellular polarity, nuclear pleomorphism and hyperchromasia, increased nucleus-to-cytoplasm ratio, and mitoses including atypical forms. […] LD represents the earliest lesion manifesting, at both microscopic and molecular levels, neoplastic features. […] The carcinogenic role of the Human Papilloma Virus (HPV) infection has been advocated as a causative agent in a subset of LD and SCC. […] The carcinogenetic role of HPV infection relies on the viral integration in the host genome and disruption of intracellular control pathways. […] The risk of progression is known to vary in dysplastic LL according to the grading of dysplasia.

• #58 Laryngeal Leukoplakia: A Focus on Histology | IntechOpen

  https://www.intechopen.com/chapters/82549

  Dysplastic changes encompass crowded immature epithelial cells, loss of cellular polarity, nuclear pleomorphism and hyperchromasia, increased nucleus-to-cytoplasm ratio, and mitoses including atypical forms. […] LD represents the earliest lesion manifesting, at both microscopic and molecular levels, neoplastic features. […] The carcinogenic role of the Human Papilloma Virus (HPV) infection has been advocated as a causative agent in a subset of LD and SCC. […] The carcinogenetic role of HPV infection relies on the viral integration in the host genome and disruption of intracellular control pathways. […] The risk of progression is known to vary in dysplastic LL according to the grading of dysplasia.

• #59 Laryngeal Leukoplakia: A Focus on Histology | IntechOpen

  https://www.intechopen.com/chapters/82549

  Dysplastic changes encompass crowded immature epithelial cells, loss of cellular polarity, nuclear pleomorphism and hyperchromasia, increased nucleus-to-cytoplasm ratio, and mitoses including atypical forms. […] LD represents the earliest lesion manifesting, at both microscopic and molecular levels, neoplastic features. […] The carcinogenic role of the Human Papilloma Virus (HPV) infection has been advocated as a causative agent in a subset of LD and SCC. […] The carcinogenetic role of HPV infection relies on the viral integration in the host genome and disruption of intracellular control pathways. […] The risk of progression is known to vary in dysplastic LL according to the grading of dysplasia.

• #60 Prevalence and determinants of oral potentially malignant disorders in western rajasthan | Scientific Reports

  https://www.nature.com/articles/s41598-025-98096-8

  Oral Potentially Malignant Disorders (OPMDs) were previously referred to as pre-cancerous conditions/lesions and, in the year 2005, redefined by WHO as any abnormality in the oral cavity associated with a higher risk of development into oral cancer. […] The significant risk factors of OPMDs in Western countries include cigarette smoking and alcohol drinking. In contrast, the prominent risk factors in Asian countries include smokeless tobacco consumption, smoking, and betel quid chewing. […] Tobacco consumption exposes the oral mucosal cavity to carcinogens such as polycyclic aromatic hydrocarbons, Tobacco-specific N-nitrosamines, formaldehyde, acetaldehyde, and reactive oxygen species (ROS), leading to oxidative stress, chronic inflammation, and DNA damage. […] Alcohol acts as a solvent that facilitates the penetration of carcinogens into the oral epithelium.

• #61 Prevalence and determinants of oral potentially malignant disorders in western rajasthan | Scientific Reports

  https://www.nature.com/articles/s41598-025-98096-8

  The combined effect of tobacco and alcohol enhances the production of reactive oxygen species, promotes epithelial dysplasia, leading to the development of OPMD, and increases the risk of their malignant transformation. […] Tobacco consumption leads to the abnormal expression of p53, p16, Glucose transporters 1 (GLUT-1), Death-associated protein kinase (DAPK), O6-methylguanine-DNA methyltransferase (MGMT), phosphatidylinositol 3-kinase (P13 K) genes in oral epithelium, which is associated with the occurrence of oral cancer. […] Tobacco consumption causes the inhibition of multiple systemic immune functions and leads to the escape of cancer cells from the immune system thereby leading to the development of OPMD and oral cancer. […] The study identified a high prevalence of OPMDs (14.84%) in Jodhpur, with leukoplakia being the most common OPMD.

• #62 Prevalence and determinants of oral potentially malignant disorders in western rajasthan | Scientific Reports

  https://www.nature.com/articles/s41598-025-98096-8

  The combined effect of tobacco and alcohol enhances the production of reactive oxygen species, promotes epithelial dysplasia, leading to the development of OPMD, and increases the risk of their malignant transformation. […] Tobacco consumption leads to the abnormal expression of p53, p16, Glucose transporters 1 (GLUT-1), Death-associated protein kinase (DAPK), O6-methylguanine-DNA methyltransferase (MGMT), phosphatidylinositol 3-kinase (P13 K) genes in oral epithelium, which is associated with the occurrence of oral cancer. […] Tobacco consumption causes the inhibition of multiple systemic immune functions and leads to the escape of cancer cells from the immune system thereby leading to the development of OPMD and oral cancer. […] The study identified a high prevalence of OPMDs (14.84%) in Jodhpur, with leukoplakia being the most common OPMD.

• #63 Prevalence and determinants of oral potentially malignant disorders in western rajasthan | Scientific Reports

  https://www.nature.com/articles/s41598-025-98096-8

  Oral Potentially Malignant Disorders (OPMDs) were previously referred to as pre-cancerous conditions/lesions and, in the year 2005, redefined by WHO as any abnormality in the oral cavity associated with a higher risk of development into oral cancer. […] The significant risk factors of OPMDs in Western countries include cigarette smoking and alcohol drinking. In contrast, the prominent risk factors in Asian countries include smokeless tobacco consumption, smoking, and betel quid chewing. […] Tobacco consumption exposes the oral mucosal cavity to carcinogens such as polycyclic aromatic hydrocarbons, Tobacco-specific N-nitrosamines, formaldehyde, acetaldehyde, and reactive oxygen species (ROS), leading to oxidative stress, chronic inflammation, and DNA damage. […] Alcohol acts as a solvent that facilitates the penetration of carcinogens into the oral epithelium.

• #64 Prevalence and determinants of oral potentially malignant disorders in western rajasthan | Scientific Reports

  https://www.nature.com/articles/s41598-025-98096-8

  The combined effect of tobacco and alcohol enhances the production of reactive oxygen species, promotes epithelial dysplasia, leading to the development of OPMD, and increases the risk of their malignant transformation. […] Tobacco consumption leads to the abnormal expression of p53, p16, Glucose transporters 1 (GLUT-1), Death-associated protein kinase (DAPK), O6-methylguanine-DNA methyltransferase (MGMT), phosphatidylinositol 3-kinase (P13 K) genes in oral epithelium, which is associated with the occurrence of oral cancer. […] Tobacco consumption causes the inhibition of multiple systemic immune functions and leads to the escape of cancer cells from the immune system thereby leading to the development of OPMD and oral cancer. […] The study identified a high prevalence of OPMDs (14.84%) in Jodhpur, with leukoplakia being the most common OPMD.

• #65

  https://journals.lww.com/jpat/fulltext/2004/08020/oral_leukoplakia__leukokeratosis___compilation_of.4.aspx

  Leukoplakia (white patch) is the most common potentially malignant lesion of the oral mucosa. […] It should be stressed that the diagnosis of leukoplakia denotes mainly, that (a) the mucosa is irritated by either mechanical, chemical or galvanic means and (b) the mucosa is trying to adapt to the noxious stimuli by undergoing hyperkeratinisation of its surface. […] Since leukoplakia is an adaptive response, offered by a viable and healthy oral mucosa against some forms of sustained, low-grade irritant, it is irrational to consider it as a disease entity (hence its assumption of a negative diagnostic state). […] The role of Candida albicans as a possible aetiological factor in leukoplakia and its possible role in malignant transformation is still unclear. […] Epithelial dysplasia is reported to occur four to five times more frequently in candida leukoplakia than in leukoplakia in general.

• #66

  https://journals.lww.com/jpat/fulltext/2004/08020/oral_leukoplakia__leukokeratosis___compilation_of.4.aspx

  Leukoplakia (white patch) is the most common potentially malignant lesion of the oral mucosa. […] It should be stressed that the diagnosis of leukoplakia denotes mainly, that (a) the mucosa is irritated by either mechanical, chemical or galvanic means and (b) the mucosa is trying to adapt to the noxious stimuli by undergoing hyperkeratinisation of its surface. […] Since leukoplakia is an adaptive response, offered by a viable and healthy oral mucosa against some forms of sustained, low-grade irritant, it is irrational to consider it as a disease entity (hence its assumption of a negative diagnostic state). […] The role of Candida albicans as a possible aetiological factor in leukoplakia and its possible role in malignant transformation is still unclear. […] Epithelial dysplasia is reported to occur four to five times more frequently in candida leukoplakia than in leukoplakia in general.

• #67

  https://journals.lww.com/jpat/fulltext/2004/08020/oral_leukoplakia__leukokeratosis___compilation_of.4.aspx

  Various evidence has been presented to justify an aetiologic role for candida in neoplastic transformation, which includes among others the catalytic transformation in-vitro of the carcinogenic nitrasamine, N-nitrosobenzyl-methylamine, by stains of C. albicans demonstrated to be selectively associated with leukoplakia. […] The possible contributory role of viral agents (human papillorna virus strains 16, 18) in the pathogenesis of oral leukoplakia has also been discussed, particularly with regard to exophytic verrucous leukoplakia. […] On the other hand, disappearance of oral leukoplakia has occasionally been reported in patients who continued to smoke. […] It is apparent that in addition to tobacco use, intake of specific nutrients and their deficiency may have a role in the development and progression of oral precancerous lesions.

• #68 Oral Leukoplakia: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/853864-overview

  OL is considered to be potentially malignant, with a transformation rate in various studies and locations that range from 0.6 to 20%. […] A literature review by Paglioni et al indicated that size is one of the factors influencing malignant transformation in potentially malignant oral disorders, with the chance of turning malignant being 4.10-fold greater in leukoplakia lesions more than 200 mm2 in size. […] In addition, the study indicated that non-homogenous oral leukoplakia has a 6.52-fold greater chance of transformation to cancer.

• #69 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Anywhere from 1% to 9% of patients with oral leukoplakia will develop invasive cancer in the lesion or a frank malignancy. Despite the excision of invasive lesions, recurrence is not uncommon. […] The following factors increase the risk for malignant transformation of leukoplakia: Female gender, A long duration of leukoplakia, Leukoplakia in non-smokers (idiopathic leukoplakia), Location on the tongue and/or floor of the mouth, Size greater than 200 mm, Non-homogeneous type, Presence of Candida albicans, Presence of epithelial dysplasia.

• #70 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Anywhere from 1% to 9% of patients with oral leukoplakia will develop invasive cancer in the lesion or a frank malignancy. Despite the excision of invasive lesions, recurrence is not uncommon. […] The following factors increase the risk for malignant transformation of leukoplakia: Female gender, A long duration of leukoplakia, Leukoplakia in non-smokers (idiopathic leukoplakia), Location on the tongue and/or floor of the mouth, Size greater than 200 mm, Non-homogeneous type, Presence of Candida albicans, Presence of epithelial dysplasia.

• #71 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Anywhere from 1% to 9% of patients with oral leukoplakia will develop invasive cancer in the lesion or a frank malignancy. Despite the excision of invasive lesions, recurrence is not uncommon. […] The following factors increase the risk for malignant transformation of leukoplakia: Female gender, A long duration of leukoplakia, Leukoplakia in non-smokers (idiopathic leukoplakia), Location on the tongue and/or floor of the mouth, Size greater than 200 mm, Non-homogeneous type, Presence of Candida albicans, Presence of epithelial dysplasia.

• #72 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Anywhere from 1% to 9% of patients with oral leukoplakia will develop invasive cancer in the lesion or a frank malignancy. Despite the excision of invasive lesions, recurrence is not uncommon. […] The following factors increase the risk for malignant transformation of leukoplakia: Female gender, A long duration of leukoplakia, Leukoplakia in non-smokers (idiopathic leukoplakia), Location on the tongue and/or floor of the mouth, Size greater than 200 mm, Non-homogeneous type, Presence of Candida albicans, Presence of epithelial dysplasia.

• #73 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Anywhere from 1% to 9% of patients with oral leukoplakia will develop invasive cancer in the lesion or a frank malignancy. Despite the excision of invasive lesions, recurrence is not uncommon. […] The following factors increase the risk for malignant transformation of leukoplakia: Female gender, A long duration of leukoplakia, Leukoplakia in non-smokers (idiopathic leukoplakia), Location on the tongue and/or floor of the mouth, Size greater than 200 mm, Non-homogeneous type, Presence of Candida albicans, Presence of epithelial dysplasia.

• #74 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Anywhere from 1% to 9% of patients with oral leukoplakia will develop invasive cancer in the lesion or a frank malignancy. Despite the excision of invasive lesions, recurrence is not uncommon. […] The following factors increase the risk for malignant transformation of leukoplakia: Female gender, A long duration of leukoplakia, Leukoplakia in non-smokers (idiopathic leukoplakia), Location on the tongue and/or floor of the mouth, Size greater than 200 mm, Non-homogeneous type, Presence of Candida albicans, Presence of epithelial dysplasia.

• #75 White Oral Lesions That Need Your Attention

  https://ostrowonline.usc.edu/white-oral-lesions-that-need-your-attention/

  Oral leukoplakia is a term used to describe a white patch or plaque in the oral cavity that cannot be clinically or pathologically categorized as any other specific disease. Studies have shown that leukoplakia can progress into a malignant disorder in the oral cavity. Plaques, erosive and ulcerative sites, especially on the soft palate, lateral, and ventral surface of the tongue or floor of the mouth, show more tendency for harboring dysplasia or carcinoma […] Proliferative verrucous leukoplakia (PVL) is a rare form characterized by progressive and multifocal white patches with a high rate of malignant transformation to either squamous cell cancer or verrucous carcinoma. It exhibits a predilection for women (female-to-male ratio, 2.7: 1 to 4: 1), with a mean age at diagnosis of 67 years. Even with treatment, recurrence rates range from 87% to 100%, and malignant transformation rates are 70%

• #76 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Anywhere from 1% to 9% of patients with oral leukoplakia will develop invasive cancer in the lesion or a frank malignancy. Despite the excision of invasive lesions, recurrence is not uncommon. […] The following factors increase the risk for malignant transformation of leukoplakia: Female gender, A long duration of leukoplakia, Leukoplakia in non-smokers (idiopathic leukoplakia), Location on the tongue and/or floor of the mouth, Size greater than 200 mm, Non-homogeneous type, Presence of Candida albicans, Presence of epithelial dysplasia.

• #77 Oral Leukoplakia: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/853864-overview

  OL is considered to be potentially malignant, with a transformation rate in various studies and locations that range from 0.6 to 20%. […] A literature review by Paglioni et al indicated that size is one of the factors influencing malignant transformation in potentially malignant oral disorders, with the chance of turning malignant being 4.10-fold greater in leukoplakia lesions more than 200 mm2 in size. […] In addition, the study indicated that non-homogenous oral leukoplakia has a 6.52-fold greater chance of transformation to cancer.

• #78 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Anywhere from 1% to 9% of patients with oral leukoplakia will develop invasive cancer in the lesion or a frank malignancy. Despite the excision of invasive lesions, recurrence is not uncommon. […] The following factors increase the risk for malignant transformation of leukoplakia: Female gender, A long duration of leukoplakia, Leukoplakia in non-smokers (idiopathic leukoplakia), Location on the tongue and/or floor of the mouth, Size greater than 200 mm, Non-homogeneous type, Presence of Candida albicans, Presence of epithelial dysplasia.

• #79 Oral Leukoplakia: Practice Essentials, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/853864-overview

  OL is considered to be potentially malignant, with a transformation rate in various studies and locations that range from 0.6 to 20%. […] A literature review by Paglioni et al indicated that size is one of the factors influencing malignant transformation in potentially malignant oral disorders, with the chance of turning malignant being 4.10-fold greater in leukoplakia lesions more than 200 mm2 in size. […] In addition, the study indicated that non-homogenous oral leukoplakia has a 6.52-fold greater chance of transformation to cancer.

• #80 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Anywhere from 1% to 9% of patients with oral leukoplakia will develop invasive cancer in the lesion or a frank malignancy. Despite the excision of invasive lesions, recurrence is not uncommon. […] The following factors increase the risk for malignant transformation of leukoplakia: Female gender, A long duration of leukoplakia, Leukoplakia in non-smokers (idiopathic leukoplakia), Location on the tongue and/or floor of the mouth, Size greater than 200 mm, Non-homogeneous type, Presence of Candida albicans, Presence of epithelial dysplasia.

• #81 Oral Leukoplakia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442013/

  Anywhere from 1% to 9% of patients with oral leukoplakia will develop invasive cancer in the lesion or a frank malignancy. Despite the excision of invasive lesions, recurrence is not uncommon. […] The following factors increase the risk for malignant transformation of leukoplakia: Female gender, A long duration of leukoplakia, Leukoplakia in non-smokers (idiopathic leukoplakia), Location on the tongue and/or floor of the mouth, Size greater than 200 mm, Non-homogeneous type, Presence of Candida albicans, Presence of epithelial dysplasia.

• #82 Oral leukoplakia: an update for dental practitioners | Published in Journal of the Irish Dental Association

  https://jida.scholasticahq.com/article/93880-oral-leukoplakia-an-update-for-dental-practitioners

  Oral leukoplakia (OLK) is a common mucosal pathology frequently encountered in general dental practice which belongs to a group of conditions known as oral potentially malignant disorders (OPMDs). […] The development of oral leukoplakia appears to be multifactorial in nature. However, the definitive cause is unclear. Smoking has been identified as the predominant risk factor, with oral leukoplakia six times more common in smokers. […] The degree of dysplasia is regarded as the most important determinant for progression to invasive carcinoma, with the risk of malignant transformation increasing with increasing degrees of OED. […] The presence of redness or nodularity in an oral leukoplakia is associated with a greater risk of developing carcinoma and these are red flags for GDPs to be aware of, as they require urgent referral.

• #83 Oral Erythroleukoplakia – A Potentially Malignant Diso…

  https://otorhinolaryngologypl.com/seo/article/01.3001.0000.6170/en

  Histologically, leukoplakia can show several epithelial changes. The presence of dysplasia with varying degrees of severity is very common. […] Erythroplakia is another oral lesion considered as a potentially malignant disorder which precedes the development of cancer. […] Erythroplakia, when associated with leukoplakia, has a higher malignant potential and shall be called erythroleukoplakia. […] The histopathological features of erythroleukoplakia include epithelial atrophy with varying degrees of atypia. […] The importance of early diagnosis of erythroleukoplakia follows from a potential for dysplastic changes and progression to frank carcinoma. […] Oral biopsy is mandatory to recognize the presence and the severity of epithelial dysplasia, which is a decisive factor for subsequent treatment planning.

• #84 Recurrence rates after surgical removal of oral leukoplakia—A prospective longitudinal multi-centre study | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0225682

  This study also shows that a non-homogeneous type of OL and the use of snuff predispose the patient to OL recurrence. […] Our results showing that patients with non-homogeneous OL have a higher risk for recurrence after surgery than patients with homogeneous OL is in line with the findings reported in several studies. […] Recurrence probably indicates the emergence of instability of the intracellular cell cycle-regulating mechanisms. […] The concept of field cancerization is widely accepted as an explanation for the recurrence of OSCC after surgery. […] This makes a comparison between patients with solitary OL and multiple OLs of interest. […] However, we observed no difference in recurrence rate between patients with solitary lesions and those with multiple lesions. […] The results from the uni-variable and multi-variable Cox regression analyses revealed that the clinical diagnosis of non-homogeneous OL, showed a tendency to a correlation and the use of snuff remained as a significant risk for recurrence of OL. […] In conclusion, in this study, the cumulative incidence of recurrence of OL is found to be 45% after 4 years and 49% after 5 years. Parameters that predict the recurrence of OL are non-homogeneous clinical type and the use of snuff.

• #85 Recurrence rates after surgical removal of oral leukoplakia—A prospective longitudinal multi-centre study | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0225682

  This study also shows that a non-homogeneous type of OL and the use of snuff predispose the patient to OL recurrence. […] Our results showing that patients with non-homogeneous OL have a higher risk for recurrence after surgery than patients with homogeneous OL is in line with the findings reported in several studies. […] Recurrence probably indicates the emergence of instability of the intracellular cell cycle-regulating mechanisms. […] The concept of field cancerization is widely accepted as an explanation for the recurrence of OSCC after surgery. […] This makes a comparison between patients with solitary OL and multiple OLs of interest. […] However, we observed no difference in recurrence rate between patients with solitary lesions and those with multiple lesions. […] The results from the uni-variable and multi-variable Cox regression analyses revealed that the clinical diagnosis of non-homogeneous OL, showed a tendency to a correlation and the use of snuff remained as a significant risk for recurrence of OL. […] In conclusion, in this study, the cumulative incidence of recurrence of OL is found to be 45% after 4 years and 49% after 5 years. Parameters that predict the recurrence of OL are non-homogeneous clinical type and the use of snuff.

• #86 Recurrence rates after surgical removal of oral leukoplakia—A prospective longitudinal multi-centre study | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0225682

  This study also shows that a non-homogeneous type of OL and the use of snuff predispose the patient to OL recurrence. […] Our results showing that patients with non-homogeneous OL have a higher risk for recurrence after surgery than patients with homogeneous OL is in line with the findings reported in several studies. […] Recurrence probably indicates the emergence of instability of the intracellular cell cycle-regulating mechanisms. […] The concept of field cancerization is widely accepted as an explanation for the recurrence of OSCC after surgery. […] This makes a comparison between patients with solitary OL and multiple OLs of interest. […] However, we observed no difference in recurrence rate between patients with solitary lesions and those with multiple lesions. […] The results from the uni-variable and multi-variable Cox regression analyses revealed that the clinical diagnosis of non-homogeneous OL, showed a tendency to a correlation and the use of snuff remained as a significant risk for recurrence of OL. […] In conclusion, in this study, the cumulative incidence of recurrence of OL is found to be 45% after 4 years and 49% after 5 years. Parameters that predict the recurrence of OL are non-homogeneous clinical type and the use of snuff.

• #87 Recurrence rates after surgical removal of oral leukoplakia—A prospective longitudinal multi-centre study | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0225682

  This study also shows that a non-homogeneous type of OL and the use of snuff predispose the patient to OL recurrence. […] Our results showing that patients with non-homogeneous OL have a higher risk for recurrence after surgery than patients with homogeneous OL is in line with the findings reported in several studies. […] Recurrence probably indicates the emergence of instability of the intracellular cell cycle-regulating mechanisms. […] The concept of field cancerization is widely accepted as an explanation for the recurrence of OSCC after surgery. […] This makes a comparison between patients with solitary OL and multiple OLs of interest. […] However, we observed no difference in recurrence rate between patients with solitary lesions and those with multiple lesions. […] The results from the uni-variable and multi-variable Cox regression analyses revealed that the clinical diagnosis of non-homogeneous OL, showed a tendency to a correlation and the use of snuff remained as a significant risk for recurrence of OL. […] In conclusion, in this study, the cumulative incidence of recurrence of OL is found to be 45% after 4 years and 49% after 5 years. Parameters that predict the recurrence of OL are non-homogeneous clinical type and the use of snuff.

• #88 Proliferative verrucous leukoplakia: diagnosis, management and current advances | Brazilian Journal of Otorhinolaryngology

  https://www.elsevier.es/en-revista-brazilian-journal-otorhinolaryngology-english-edition–497-articulo-proliferative-verrucous-leukoplakia-diagnosis-management-S1808869417300058

  Proliferative verrucous leukoplakia is a multifocal and progressive lesion of the oral mucosa, with unknown etiology, and commonly resistant to all therapy attempts with frequent recurrences. It is characterized by a high rate of oral squamous cell carcinoma and verrucou carcinoma transformations. […] Proliferative verrucous leukoplakia (PVL) is a very aggressive and rare form of oral leukoplakia (OL) with high morbidity. The first description has been made by Hansen et al. (1985) as a distinct form of OL which develops initially as a white plaque that eventually becomes multifocal slow-growing lesions resistant to all therapeutic procedures, including surgery, with a high recurrence rate and an oral cancer transformation trend. […] Hansen et al. (1985) described PVL as a disease with unclear etiology, but typically associated with tobacco use. However, the role of tobacco in PVL lesions is unknown since these lesions are seen in smokers and nonsmokers.

• #89 Proliferative verrucous leukoplakia: diagnosis, management and current advances | Brazilian Journal of Otorhinolaryngology

  https://www.elsevier.es/en-revista-brazilian-journal-otorhinolaryngology-english-edition–497-articulo-proliferative-verrucous-leukoplakia-diagnosis-management-S1808869417300058

  Proliferative verrucous leukoplakia is a multifocal and progressive lesion of the oral mucosa, with unknown etiology, and commonly resistant to all therapy attempts with frequent recurrences. It is characterized by a high rate of oral squamous cell carcinoma and verrucou carcinoma transformations. […] Proliferative verrucous leukoplakia (PVL) is a very aggressive and rare form of oral leukoplakia (OL) with high morbidity. The first description has been made by Hansen et al. (1985) as a distinct form of OL which develops initially as a white plaque that eventually becomes multifocal slow-growing lesions resistant to all therapeutic procedures, including surgery, with a high recurrence rate and an oral cancer transformation trend. […] Hansen et al. (1985) described PVL as a disease with unclear etiology, but typically associated with tobacco use. However, the role of tobacco in PVL lesions is unknown since these lesions are seen in smokers and nonsmokers.

• #90 Proliferative verrucous leukoplakia: diagnosis, management and current advances | Brazilian Journal of Otorhinolaryngology

  https://www.elsevier.es/en-revista-brazilian-journal-otorhinolaryngology-english-edition–497-articulo-proliferative-verrucous-leukoplakia-diagnosis-management-S1808869417300058

  Proliferative verrucous leukoplakia is a multifocal and progressive lesion of the oral mucosa, with unknown etiology, and commonly resistant to all therapy attempts with frequent recurrences. It is characterized by a high rate of oral squamous cell carcinoma and verrucou carcinoma transformations. […] Proliferative verrucous leukoplakia (PVL) is a very aggressive and rare form of oral leukoplakia (OL) with high morbidity. The first description has been made by Hansen et al. (1985) as a distinct form of OL which develops initially as a white plaque that eventually becomes multifocal slow-growing lesions resistant to all therapeutic procedures, including surgery, with a high recurrence rate and an oral cancer transformation trend. […] Hansen et al. (1985) described PVL as a disease with unclear etiology, but typically associated with tobacco use. However, the role of tobacco in PVL lesions is unknown since these lesions are seen in smokers and nonsmokers.

• #91 Proliferative verrucous leukoplakia: diagnosis, management and current advances | Brazilian Journal of Otorhinolaryngology

  https://www.elsevier.es/en-revista-brazilian-journal-otorhinolaryngology-english-edition–497-articulo-proliferative-verrucous-leukoplakia-diagnosis-management-S1808869417300058

  In recent years, it has been hypothesized that human papillomavirus (HPV) may influence both potentially and already stablished oral malignant lesions. Although the association between oral squamous cell carcinoma (OSCC) and HPV is already mentioned, its influence on PVL cases is not confirmed yet. […] Histopathological findings may show acanthosis and hyperkeratosis with an interface lymphocytic infiltrate within the superficial lamina propria. If the lesions continue to grow horizontally and vertically, there are histopathological changes that increase roughness of surface with verrucous aspect, and hyperplasia with or without dysplasia. Therefore, over time and without treatment, there is an inexorable progression to VC or OSCC. […] Although there are not enough studies to determine PVL etiology and no simplified diagnosis criteria, the most difficult point is PVL treatment. According to the literature reviewed, PVL seems to be resistant to many therapy attempts and often has high propensity for dysplasia and/or malignancy progression. Modalities such as surgery, laser ablation, photodynamic therapy, retinoid, radiation and chemotherapy are not effective in reducing relapses and malignant transformation.

• #92 Proliferative verrucous leukoplakia: diagnosis, management and current advances | Brazilian Journal of Otorhinolaryngology

  https://www.elsevier.es/en-revista-brazilian-journal-otorhinolaryngology-english-edition–497-articulo-proliferative-verrucous-leukoplakia-diagnosis-management-S1808869417300058

  Proliferative verrucous leukoplakia is a multifocal and progressive lesion of the oral mucosa, with unknown etiology, and commonly resistant to all therapy attempts with frequent recurrences. It is characterized by a high rate of oral squamous cell carcinoma and verrucou carcinoma transformations. […] Proliferative verrucous leukoplakia (PVL) is a very aggressive and rare form of oral leukoplakia (OL) with high morbidity. The first description has been made by Hansen et al. (1985) as a distinct form of OL which develops initially as a white plaque that eventually becomes multifocal slow-growing lesions resistant to all therapeutic procedures, including surgery, with a high recurrence rate and an oral cancer transformation trend. […] Hansen et al. (1985) described PVL as a disease with unclear etiology, but typically associated with tobacco use. However, the role of tobacco in PVL lesions is unknown since these lesions are seen in smokers and nonsmokers.

• #93 Proliferative Verrucous Leukoplakia Revisited: A Retrospective Clinicopathological Study

  https://www.mdpi.com/2039-7283/11/2/48

  The high rate of malignant transformation (60% to 100%) of PVL signifies an early and accurate diagnosis of the lesion. […] The diagnosis of PVL remains an enigma ever since its first report by Hansen et al. PVL progresses from an isolated leukoplakia to become multi-focal confluent or isolated exophytic/verrucous lesions. […] Cerero-Lapiedra et al. proposed a set of guidelines in 2010 to establish an objective and early diagnosis of PVL. They proposed that the early detection of PVL is adequate for the management of lesion. For the identification of PVL, they put forward that the lesion should fulfill certain specific combinations of criteria. […] We believe the diagnoses of PVL in the present study to be uncertain due to insufficient data on the follow-up of patients and the evolution of the disease. Thus, clinicians must ensure that they follow-up multi-focal oral leukoplakia, irrespective of the inert nature of their initial histopathology. Only thorough follow-up data would provide adequate evidence for a conclusive PVL diagnosis.

• #94 White Oral Lesions That Need Your Attention

  https://ostrowonline.usc.edu/white-oral-lesions-that-need-your-attention/

  Oral leukoplakia is a term used to describe a white patch or plaque in the oral cavity that cannot be clinically or pathologically categorized as any other specific disease. Studies have shown that leukoplakia can progress into a malignant disorder in the oral cavity. Plaques, erosive and ulcerative sites, especially on the soft palate, lateral, and ventral surface of the tongue or floor of the mouth, show more tendency for harboring dysplasia or carcinoma […] Proliferative verrucous leukoplakia (PVL) is a rare form characterized by progressive and multifocal white patches with a high rate of malignant transformation to either squamous cell cancer or verrucous carcinoma. It exhibits a predilection for women (female-to-male ratio, 2.7: 1 to 4: 1), with a mean age at diagnosis of 67 years. Even with treatment, recurrence rates range from 87% to 100%, and malignant transformation rates are 70%

• #95 Hairy Leukoplakia: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/279269-overview

  Oral hairy leukoplakia (OHL) is a disease of the mucosa first described in 1984. This pathology is associated with Epstein-Barr virus (EBV) and occurs mostly in people with HIV infection, including those who do not have a diagnosis of AIDS. […] The pathogenesis of hairy leukoplakia is clearly complex, potentially requiring a convergence of factors including EBV co-infection, productive EBV replication, EBV genetic evolution, expression of specific EBV „latent” genes, and immune escape. All of these factors are likely facilitated by local and systemic host immunodeficiency. […] In addition, a marked decrease or an absence of Langerhans cells occurs in hairy leukoplakia biopsy tissues. Langerhans cells are the antigen-presenting immune cells that are required for an immune system response to the viral infection and their deficiency may permit EBV to persistently replicate and escape immune recognition.

• #96 Hairy Leukoplakia: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/279269-overview

  Oral hairy leukoplakia (OHL) is a disease of the mucosa first described in 1984. This pathology is associated with Epstein-Barr virus (EBV) and occurs mostly in people with HIV infection, including those who do not have a diagnosis of AIDS. […] The pathogenesis of hairy leukoplakia is clearly complex, potentially requiring a convergence of factors including EBV co-infection, productive EBV replication, EBV genetic evolution, expression of specific EBV „latent” genes, and immune escape. All of these factors are likely facilitated by local and systemic host immunodeficiency. […] In addition, a marked decrease or an absence of Langerhans cells occurs in hairy leukoplakia biopsy tissues. Langerhans cells are the antigen-presenting immune cells that are required for an immune system response to the viral infection and their deficiency may permit EBV to persistently replicate and escape immune recognition.

• #97 Hairy Leukoplakia: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/279269-overview

  Oral hairy leukoplakia (OHL) is a disease of the mucosa first described in 1984. This pathology is associated with Epstein-Barr virus (EBV) and occurs mostly in people with HIV infection, including those who do not have a diagnosis of AIDS. […] The pathogenesis of hairy leukoplakia is clearly complex, potentially requiring a convergence of factors including EBV co-infection, productive EBV replication, EBV genetic evolution, expression of specific EBV „latent” genes, and immune escape. All of these factors are likely facilitated by local and systemic host immunodeficiency. […] In addition, a marked decrease or an absence of Langerhans cells occurs in hairy leukoplakia biopsy tissues. Langerhans cells are the antigen-presenting immune cells that are required for an immune system response to the viral infection and their deficiency may permit EBV to persistently replicate and escape immune recognition.

• #98 Hairy Leukoplakia | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/22489

  Hairy leukoplakia is commonly found in association with HIV infection and/or immunosuppression. […] The pathophysiology of this condition is complex, requiring an interplay of various factors such as EBV coinfection along with its productive replication, virulence, genetic evolution in association with expressing specific EBV genes that are in a latent state. All these factors enhanced by local as well as systemic deficiency of the host immune system lead to hairy leucoplakia. […] A marked reduction or an absence of Langerhans cells (antigen-presenting immune cells necessary for the response of the immune system to the viral infection) has also been found in hairy leukoplakia biopsy tissues. […] Impaired immune status of the host along with a marked reduction of Langerhans cells then contribute to the successful establishment of EBV in the oral epithelium.

• #99 Hairy leukoplakia

  https://dermnetnz.org/topics/oral-hairy-leukoplakia

  Oral hairy leukoplakia is caused by Epstein-Barr virus (EBV) infection of the tongue epithelium where there are few or no Langerhans cells. EBV delays apoptosis resulting in epithelial cell proliferation and hyperplasia. In OHL EBV is seen as intact virions and does not incorporate into the cell genome. […] Oral hairy leukoplakia associated with HIV infection is a sign of severe immunosuppression and progression to AIDS. […] OHL is not a premalignant lesion. […] Treatment is not usually required as oral hairy leukoplakia is asymptomatic and not premalignant. […] Oral hairy leukoplakia is not cured by treatment. It may resolve spontaneously. OHL does not progress to oral cancer.

• #100 Hairy leukoplakia

  https://dermnetnz.org/topics/oral-hairy-leukoplakia

  Oral hairy leukoplakia is caused by Epstein-Barr virus (EBV) infection of the tongue epithelium where there are few or no Langerhans cells. EBV delays apoptosis resulting in epithelial cell proliferation and hyperplasia. In OHL EBV is seen as intact virions and does not incorporate into the cell genome. […] Oral hairy leukoplakia associated with HIV infection is a sign of severe immunosuppression and progression to AIDS. […] OHL is not a premalignant lesion. […] Treatment is not usually required as oral hairy leukoplakia is asymptomatic and not premalignant. […] Oral hairy leukoplakia is not cured by treatment. It may resolve spontaneously. OHL does not progress to oral cancer.

• #101 The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-023-01217-0

  The onset of oral leukoplakia (OLK), the most common oral lesion with a high risk of malignant transformation, is closely associated with the exposure of cigarette smoke. […] The complicated pathogenic impacts of CS are considered as the attribution that leads to OLK and even its malignant transformation. […] Recent evidence identify that the oxidative stress contributes to the release of extracellular vesicles (EVs). […] Currently, emerging evidence have attempted to explain how CS affects the generation and release of EVs, and what is the specific molecular mechanism or pathways they interfered that cause the disease occurrence, especially for lung, cardiovascular and cancer-related diseases. […] The health of oral mucosal epithelial is prone to be damaged, because it is the first affected site by CS. Exposure to CS is identified as a major risk factor for OLK and its malignant transformation to OSCC. However, evidence done on the role of EVs in CS-induced OLK is still in its infancy. Based on the prior literature, upon CS stimulation, the biogenesis of EVs is significantly elevated, the composition of EVs and the signaling transduction via EVs are obviously changed, which is closely associated with the occurrence and progression of disease. Exposure to cigarette smoke contributes to the production of EVs from different types of cells including epithelial cells, macrophages, T cells, and monocytes. The bioactive cargo (proteins, cytokines, RNAs, and DNAs) of these EVs induced by CS stimulation are significantly changed, which acts as mediators for intra/inter-cellular communication. When these EVs are engulfed, they can change the biological behavior of the recipient/target cells and finally lead to the onset of OLK pathogenesis or even carcinogenesis. […] Elucidating the functions of CS-induced EVs in the pathophysiological processes of OLK is of great significance for the development of diagnostic biomarkers, prognostic evaluation, and therapeutic targets of OLK.

• #102 The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-023-01217-0

  The onset of oral leukoplakia (OLK), the most common oral lesion with a high risk of malignant transformation, is closely associated with the exposure of cigarette smoke. […] The complicated pathogenic impacts of CS are considered as the attribution that leads to OLK and even its malignant transformation. […] Recent evidence identify that the oxidative stress contributes to the release of extracellular vesicles (EVs). […] Currently, emerging evidence have attempted to explain how CS affects the generation and release of EVs, and what is the specific molecular mechanism or pathways they interfered that cause the disease occurrence, especially for lung, cardiovascular and cancer-related diseases. […] The health of oral mucosal epithelial is prone to be damaged, because it is the first affected site by CS. Exposure to CS is identified as a major risk factor for OLK and its malignant transformation to OSCC. However, evidence done on the role of EVs in CS-induced OLK is still in its infancy. Based on the prior literature, upon CS stimulation, the biogenesis of EVs is significantly elevated, the composition of EVs and the signaling transduction via EVs are obviously changed, which is closely associated with the occurrence and progression of disease. Exposure to cigarette smoke contributes to the production of EVs from different types of cells including epithelial cells, macrophages, T cells, and monocytes. The bioactive cargo (proteins, cytokines, RNAs, and DNAs) of these EVs induced by CS stimulation are significantly changed, which acts as mediators for intra/inter-cellular communication. When these EVs are engulfed, they can change the biological behavior of the recipient/target cells and finally lead to the onset of OLK pathogenesis or even carcinogenesis. […] Elucidating the functions of CS-induced EVs in the pathophysiological processes of OLK is of great significance for the development of diagnostic biomarkers, prognostic evaluation, and therapeutic targets of OLK.

• #103 The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-023-01217-0

  The onset of oral leukoplakia (OLK), the most common oral lesion with a high risk of malignant transformation, is closely associated with the exposure of cigarette smoke. […] The complicated pathogenic impacts of CS are considered as the attribution that leads to OLK and even its malignant transformation. […] Recent evidence identify that the oxidative stress contributes to the release of extracellular vesicles (EVs). […] Currently, emerging evidence have attempted to explain how CS affects the generation and release of EVs, and what is the specific molecular mechanism or pathways they interfered that cause the disease occurrence, especially for lung, cardiovascular and cancer-related diseases. […] The health of oral mucosal epithelial is prone to be damaged, because it is the first affected site by CS. Exposure to CS is identified as a major risk factor for OLK and its malignant transformation to OSCC. However, evidence done on the role of EVs in CS-induced OLK is still in its infancy. Based on the prior literature, upon CS stimulation, the biogenesis of EVs is significantly elevated, the composition of EVs and the signaling transduction via EVs are obviously changed, which is closely associated with the occurrence and progression of disease. Exposure to cigarette smoke contributes to the production of EVs from different types of cells including epithelial cells, macrophages, T cells, and monocytes. The bioactive cargo (proteins, cytokines, RNAs, and DNAs) of these EVs induced by CS stimulation are significantly changed, which acts as mediators for intra/inter-cellular communication. When these EVs are engulfed, they can change the biological behavior of the recipient/target cells and finally lead to the onset of OLK pathogenesis or even carcinogenesis. […] Elucidating the functions of CS-induced EVs in the pathophysiological processes of OLK is of great significance for the development of diagnostic biomarkers, prognostic evaluation, and therapeutic targets of OLK.

• #104 The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-023-01217-0

  The onset of oral leukoplakia (OLK), the most common oral lesion with a high risk of malignant transformation, is closely associated with the exposure of cigarette smoke. […] The complicated pathogenic impacts of CS are considered as the attribution that leads to OLK and even its malignant transformation. […] Recent evidence identify that the oxidative stress contributes to the release of extracellular vesicles (EVs). […] Currently, emerging evidence have attempted to explain how CS affects the generation and release of EVs, and what is the specific molecular mechanism or pathways they interfered that cause the disease occurrence, especially for lung, cardiovascular and cancer-related diseases. […] The health of oral mucosal epithelial is prone to be damaged, because it is the first affected site by CS. Exposure to CS is identified as a major risk factor for OLK and its malignant transformation to OSCC. However, evidence done on the role of EVs in CS-induced OLK is still in its infancy. Based on the prior literature, upon CS stimulation, the biogenesis of EVs is significantly elevated, the composition of EVs and the signaling transduction via EVs are obviously changed, which is closely associated with the occurrence and progression of disease. Exposure to cigarette smoke contributes to the production of EVs from different types of cells including epithelial cells, macrophages, T cells, and monocytes. The bioactive cargo (proteins, cytokines, RNAs, and DNAs) of these EVs induced by CS stimulation are significantly changed, which acts as mediators for intra/inter-cellular communication. When these EVs are engulfed, they can change the biological behavior of the recipient/target cells and finally lead to the onset of OLK pathogenesis or even carcinogenesis. […] Elucidating the functions of CS-induced EVs in the pathophysiological processes of OLK is of great significance for the development of diagnostic biomarkers, prognostic evaluation, and therapeutic targets of OLK.

• #105 The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-023-01217-0

  The onset of oral leukoplakia (OLK), the most common oral lesion with a high risk of malignant transformation, is closely associated with the exposure of cigarette smoke. […] The complicated pathogenic impacts of CS are considered as the attribution that leads to OLK and even its malignant transformation. […] Recent evidence identify that the oxidative stress contributes to the release of extracellular vesicles (EVs). […] Currently, emerging evidence have attempted to explain how CS affects the generation and release of EVs, and what is the specific molecular mechanism or pathways they interfered that cause the disease occurrence, especially for lung, cardiovascular and cancer-related diseases. […] The health of oral mucosal epithelial is prone to be damaged, because it is the first affected site by CS. Exposure to CS is identified as a major risk factor for OLK and its malignant transformation to OSCC. However, evidence done on the role of EVs in CS-induced OLK is still in its infancy. Based on the prior literature, upon CS stimulation, the biogenesis of EVs is significantly elevated, the composition of EVs and the signaling transduction via EVs are obviously changed, which is closely associated with the occurrence and progression of disease. Exposure to cigarette smoke contributes to the production of EVs from different types of cells including epithelial cells, macrophages, T cells, and monocytes. The bioactive cargo (proteins, cytokines, RNAs, and DNAs) of these EVs induced by CS stimulation are significantly changed, which acts as mediators for intra/inter-cellular communication. When these EVs are engulfed, they can change the biological behavior of the recipient/target cells and finally lead to the onset of OLK pathogenesis or even carcinogenesis. […] Elucidating the functions of CS-induced EVs in the pathophysiological processes of OLK is of great significance for the development of diagnostic biomarkers, prognostic evaluation, and therapeutic targets of OLK.

• #106 The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-023-01217-0

  The onset of oral leukoplakia (OLK), the most common oral lesion with a high risk of malignant transformation, is closely associated with the exposure of cigarette smoke. […] The complicated pathogenic impacts of CS are considered as the attribution that leads to OLK and even its malignant transformation. […] Recent evidence identify that the oxidative stress contributes to the release of extracellular vesicles (EVs). […] Currently, emerging evidence have attempted to explain how CS affects the generation and release of EVs, and what is the specific molecular mechanism or pathways they interfered that cause the disease occurrence, especially for lung, cardiovascular and cancer-related diseases. […] The health of oral mucosal epithelial is prone to be damaged, because it is the first affected site by CS. Exposure to CS is identified as a major risk factor for OLK and its malignant transformation to OSCC. However, evidence done on the role of EVs in CS-induced OLK is still in its infancy. Based on the prior literature, upon CS stimulation, the biogenesis of EVs is significantly elevated, the composition of EVs and the signaling transduction via EVs are obviously changed, which is closely associated with the occurrence and progression of disease. Exposure to cigarette smoke contributes to the production of EVs from different types of cells including epithelial cells, macrophages, T cells, and monocytes. The bioactive cargo (proteins, cytokines, RNAs, and DNAs) of these EVs induced by CS stimulation are significantly changed, which acts as mediators for intra/inter-cellular communication. When these EVs are engulfed, they can change the biological behavior of the recipient/target cells and finally lead to the onset of OLK pathogenesis or even carcinogenesis. […] Elucidating the functions of CS-induced EVs in the pathophysiological processes of OLK is of great significance for the development of diagnostic biomarkers, prognostic evaluation, and therapeutic targets of OLK.

• #107 The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-023-01217-0

  The onset of oral leukoplakia (OLK), the most common oral lesion with a high risk of malignant transformation, is closely associated with the exposure of cigarette smoke. […] The complicated pathogenic impacts of CS are considered as the attribution that leads to OLK and even its malignant transformation. […] Recent evidence identify that the oxidative stress contributes to the release of extracellular vesicles (EVs). […] Currently, emerging evidence have attempted to explain how CS affects the generation and release of EVs, and what is the specific molecular mechanism or pathways they interfered that cause the disease occurrence, especially for lung, cardiovascular and cancer-related diseases. […] The health of oral mucosal epithelial is prone to be damaged, because it is the first affected site by CS. Exposure to CS is identified as a major risk factor for OLK and its malignant transformation to OSCC. However, evidence done on the role of EVs in CS-induced OLK is still in its infancy. Based on the prior literature, upon CS stimulation, the biogenesis of EVs is significantly elevated, the composition of EVs and the signaling transduction via EVs are obviously changed, which is closely associated with the occurrence and progression of disease. Exposure to cigarette smoke contributes to the production of EVs from different types of cells including epithelial cells, macrophages, T cells, and monocytes. The bioactive cargo (proteins, cytokines, RNAs, and DNAs) of these EVs induced by CS stimulation are significantly changed, which acts as mediators for intra/inter-cellular communication. When these EVs are engulfed, they can change the biological behavior of the recipient/target cells and finally lead to the onset of OLK pathogenesis or even carcinogenesis. […] Elucidating the functions of CS-induced EVs in the pathophysiological processes of OLK is of great significance for the development of diagnostic biomarkers, prognostic evaluation, and therapeutic targets of OLK.

• #108 Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and M2 polarization of macrophage | International Journal of Oral Science

  https://www.nature.com/articles/s41368-021-00128-2

  Oral immunosuppression caused by smoking creates a microenvironment to promote the occurrence and development of oral mucosa precancerous lesions. This study aimed to investigate the role of metabolism and macrophage polarization in cigarette-promoting oral leukoplakia. […] The results also showed that the supernatant of Raw cells stimulated by CSE could induce excessive proliferation of Leuk-1 and inhibit apoptosis. Glutamine abundance can facilitate this process. Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and macrophage M2 polarization. […] However, the mechanism by which smoking promotes OLK pathogenesis is unclear. […] It incorporates the activation of M1 innate response at a low dose but suppresses the M1 innate response at high-dose particle exposures.

• #109 Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and M2 polarization of macrophage | International Journal of Oral Science

  https://www.nature.com/articles/s41368-021-00128-2

  The significant increase in arginine metabolism in the stimulation suggested tissue repairment. […] Therefore, it is concluded that in the process of smoke cigarettes promoting OLK, glutamine metabolism and M2 polarization of macrophage play important roles for regulating oral mucosa immune microenvironment and epithelial dysplasia and keratosis.

• #110 Cigarette smoke promotes oral leukoplakia via regulating glutamine metabolism and M2 polarization of macrophage | International Journal of Oral Science

  https://www.nature.com/articles/s41368-021-00128-2

  The significant increase in arginine metabolism in the stimulation suggested tissue repairment. […] Therefore, it is concluded that in the process of smoke cigarettes promoting OLK, glutamine metabolism and M2 polarization of macrophage play important roles for regulating oral mucosa immune microenvironment and epithelial dysplasia and keratosis.

• #111 Quantitative Risk Stratification of Oral Leukoplakia with Exfoliative Cytology | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0126760

  In this study, we developed a statistical modeling method for quantitative risk stratification of OLK patients. […] OLK, as a definite premalignant lesion of OSCC, is known to carry a cancer risk higher than normal subjects. […] The major advantages are its being minimally invasive and inexpensive, and thus better acceptance by patients. […] Therefore there is a need of quantitative risk stratification of OLK. […] In this study, using DI values of exfoliative cytology we successfully developed EdTAR as a method for data transformation and reconstruction. […] After EdTAR, the signal of aneuploid cell population is amplified. […] Reconstruction of data of three cell populations allows SVM for pattern recognition and calculation of OCRI. […] One of our OLK cases had a high OCRI and was found to develop OSCC 40 months later during follow-up.

• #112 Quantitative Risk Stratification of Oral Leukoplakia with Exfoliative Cytology | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0126760

  In this study, we developed a statistical modeling method for quantitative risk stratification of OLK patients. […] OLK, as a definite premalignant lesion of OSCC, is known to carry a cancer risk higher than normal subjects. […] The major advantages are its being minimally invasive and inexpensive, and thus better acceptance by patients. […] Therefore there is a need of quantitative risk stratification of OLK. […] In this study, using DI values of exfoliative cytology we successfully developed EdTAR as a method for data transformation and reconstruction. […] After EdTAR, the signal of aneuploid cell population is amplified. […] Reconstruction of data of three cell populations allows SVM for pattern recognition and calculation of OCRI. […] One of our OLK cases had a high OCRI and was found to develop OSCC 40 months later during follow-up.

• #113 Quantitative Risk Stratification of Oral Leukoplakia with Exfoliative Cytology | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0126760

  In this study, we developed a statistical modeling method for quantitative risk stratification of OLK patients. […] OLK, as a definite premalignant lesion of OSCC, is known to carry a cancer risk higher than normal subjects. […] The major advantages are its being minimally invasive and inexpensive, and thus better acceptance by patients. […] Therefore there is a need of quantitative risk stratification of OLK. […] In this study, using DI values of exfoliative cytology we successfully developed EdTAR as a method for data transformation and reconstruction. […] After EdTAR, the signal of aneuploid cell population is amplified. […] Reconstruction of data of three cell populations allows SVM for pattern recognition and calculation of OCRI. […] One of our OLK cases had a high OCRI and was found to develop OSCC 40 months later during follow-up.

• #114 Quantitative Risk Stratification of Oral Leukoplakia with Exfoliative Cytology | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0126760

  In this study, we developed a statistical modeling method for quantitative risk stratification of OLK patients. […] OLK, as a definite premalignant lesion of OSCC, is known to carry a cancer risk higher than normal subjects. […] The major advantages are its being minimally invasive and inexpensive, and thus better acceptance by patients. […] Therefore there is a need of quantitative risk stratification of OLK. […] In this study, using DI values of exfoliative cytology we successfully developed EdTAR as a method for data transformation and reconstruction. […] After EdTAR, the signal of aneuploid cell population is amplified. […] Reconstruction of data of three cell populations allows SVM for pattern recognition and calculation of OCRI. […] One of our OLK cases had a high OCRI and was found to develop OSCC 40 months later during follow-up.

• #115 Quantitative Risk Stratification of Oral Leukoplakia with Exfoliative Cytology | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0126760

  In this study, we developed a statistical modeling method for quantitative risk stratification of OLK patients. […] OLK, as a definite premalignant lesion of OSCC, is known to carry a cancer risk higher than normal subjects. […] The major advantages are its being minimally invasive and inexpensive, and thus better acceptance by patients. […] Therefore there is a need of quantitative risk stratification of OLK. […] In this study, using DI values of exfoliative cytology we successfully developed EdTAR as a method for data transformation and reconstruction. […] After EdTAR, the signal of aneuploid cell population is amplified. […] Reconstruction of data of three cell populations allows SVM for pattern recognition and calculation of OCRI. […] One of our OLK cases had a high OCRI and was found to develop OSCC 40 months later during follow-up.

• #116 Quantitative Risk Stratification of Oral Leukoplakia with Exfoliative Cytology | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0126760

  In this study, we developed a statistical modeling method for quantitative risk stratification of OLK patients. […] OLK, as a definite premalignant lesion of OSCC, is known to carry a cancer risk higher than normal subjects. […] The major advantages are its being minimally invasive and inexpensive, and thus better acceptance by patients. […] Therefore there is a need of quantitative risk stratification of OLK. […] In this study, using DI values of exfoliative cytology we successfully developed EdTAR as a method for data transformation and reconstruction. […] After EdTAR, the signal of aneuploid cell population is amplified. […] Reconstruction of data of three cell populations allows SVM for pattern recognition and calculation of OCRI. […] One of our OLK cases had a high OCRI and was found to develop OSCC 40 months later during follow-up.

• #117 Quantitative Risk Stratification of Oral Leukoplakia with Exfoliative Cytology | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0126760

  In this study, we developed a statistical modeling method for quantitative risk stratification of OLK patients. […] OLK, as a definite premalignant lesion of OSCC, is known to carry a cancer risk higher than normal subjects. […] The major advantages are its being minimally invasive and inexpensive, and thus better acceptance by patients. […] Therefore there is a need of quantitative risk stratification of OLK. […] In this study, using DI values of exfoliative cytology we successfully developed EdTAR as a method for data transformation and reconstruction. […] After EdTAR, the signal of aneuploid cell population is amplified. […] Reconstruction of data of three cell populations allows SVM for pattern recognition and calculation of OCRI. […] One of our OLK cases had a high OCRI and was found to develop OSCC 40 months later during follow-up.

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