Mouth and Tooth Diseases

Skin and Connective Tissue Diseases

All Conditions

Neoplasms

Symptoms and General Pathology

Rare Diseases

Lichen Planus, Oral

Lichen Planus

Leukoplakia

Leukoplakia, Oral

Erythroplasia

Lichenoid Eruptions

Exanthema

Skin Diseases

Skin Diseases, Papulosquamous

Mouth Diseases

Stomatognathic Diseases

Precancerous Conditions

Pathological Conditions, Anatomical

Mouth Neoplasms

Head and Neck Neoplasms

Erythroplakia

Oral Leukoplakia

Oral Cancer

all dental hygienists members in the trade union for dental hygienists

A web-based questionnaire will be send by the trade union for dental hygienists

questionnaire survey

Karin Gunnars Hellgren

Dental health professionals have a responsibility to perform routine intra- and extraoral inspection on their patients for detecting abnormalities. As dental hygienists (DH) and dentist (D) often see their patients on a regular basis, they have the opportunity to provide this screening, and at an early stage detect abnormalities.

In Sweden, education and training in intraoral inspection of the oral mucosa is a part of the curriculum in dental hygienists education, so there is an expectation that the dental hygienist routinely perform tactile and visual intraoral inspections in practice. However, DH are not trained in extra oral inspection and are not allowed to diagnose an oral mucosal lesion, but are trained to identify abnormalities and determine whether the patient needs referral to a dentist. It is also to expect that the DH are capable to identify risk behaviors, such as alcohol and smoking, and recommend, and offer smoking cessation or refer the patient to a certified profession for smoking cessation.

In 2007, The World Health Assembly (WHA) adopted a resolution to prevent oral cancer. The resolution urged the member states to ensure that measures against oral cancer was integrated into a national cancer control program by engaging and train dental personnel in screening, early diagnosis and treatment. Oral cancer is a severe oral health issue as it is potentially fatal and is the 5-6 most common tumor with approximately 275,000 cases for oral and 130,300 cases for pharyngeal cancers, excluding nasopharynx, globally. In Sweden,1000 new cases yearly is discovered and it is increasing. The explanation is an aging population and an increase in tonsil and tongue cancers caused by HPV, especially in younger subjects. Tumors caused by tobacco and alcohol are constant \[7-9\]. Despite the decreasing prevalence of smoking and certain smoking-associated cancers, an increased incidence of tonsillar cancer has been seen in both Finland and Sweden. High risk HPV (hrHPV) oral cancer is also increasing. The 5 year survival of oral cancer in Sweden is 55 % and only 3-4% in advanced cases. The etiology is hrHPV, exposure to tobacco and alcohol in 65% \[13\] and poor dental status. All are lifestyle factors so there are many opportunities for prevention and intervention. In 2016, 352 individuals in Sweden died in oral cancer compared with 135 individuals who died of cervical cancer. Leukoplakia (LP), erythroplakia (EP) and oral lichen planus (OLP) are the dominating oral premalignant entities. The diagnosis are clinical and often by biopsies. The nonhomogeneous have a risk of malignant transformation of 3.6-8.9% in Scandinavia. OLP is a chronic inflammatory lesion where the atrophic and erosive types have a risk of cancer development of 0.5-2%.

The potential for prevention is high, as the risk factors are well known. The Clinical examination discloses any potentially malignant lesions. Being aware of the increasing number of head, neck, and oral tumors we need to highlight the importance of inspection of the oral mucosa.

Intra and Extra Oral Inspection of Oral Mucosa

Dental Hygienists and Oral Mucosal Inspection - Extent, Knowledge and Perceived Barriers

A 27-item survey instrument using Likert-type and open-ended questions, constructed by dental hygienists and used in Canada, College of dental hygienists Nova Scotia, Canada is used. Frequency and comprehensiveness of intra- and extra-oral inspection is investigated and participants can answer always, usually, sometimes, rarely or never.

From a drop down meny participants get seven alternative barriers; • Someone else in my office performs the exam \[if selected drop down menu options appear: dentist, dental assistant, do not know, other

* Lack of knowledge and/or skills to perform the exam
* Lack of time
* Concern about patient compliance
* Concern over remuneration for services
* Not sure if it is within the dental hygiene scope of practice
* Other

Dalarna County Council, Sweden

Principal Investigator

Lip and Oral Cavity Cancer

Hypoglycemic Agents

All Drugs and Chemicals

Metformin

Patients receive extended release metformin hydrochloride PO QD for 24 weeks in the absence of disease progression or unacceptable toxicity. Patients will also undergo biopsies and blood collections on study.

Patients receive a placebo PO QD for 24 weeks in the absence of disease progression or unacceptable toxicity. Patients will also undergo biopsies and blood collections on study.

Biopsy

Biospecimen Collection

Extended Release Metformin Hydrochloride

Placebo Administration

Shethal Bearelly

Scott M. Lippman

Christine H. Chung

Jennifer Gross

Cherie-Ann O. Nathan

Justine Moe

Frank G. Ondrey

Alexander R. Kerr

Miriam Rosin

Leigha Rock

Scott M Lippman

This phase IIb trial tests whether metformin works in preventing oral cancer in patients with oral leukoplakia (white patches) or erythroplakia (red patches). Metformin is in a class of drugs called biguanides. Metformin helps to control the amount of glucose (sugar) in the blood. It decreases the amount of glucose patients absorb from food and the amount of glucose made by the liver. Metformin also increases the body's response to insulin, a natural substance that controls the amount of glucose in the blood. This trial may help researchers determine if metformin can stop changes in the mouth that are related to pre-cancer growths in the mouth.

PRIMARY OBJECTIVE:

I. To determine the histological response to metformin hydrochloride (metformin) intervention in the target lesion.

SECONDARY OBJECTIVES:

I. Clinical response to metformin intervention in the target lesion. II. Effect of metformin on cell proliferation (Ki67) and its molecular targets (pS6 and nuclear YAP) in the target lesion.

III. Metformin effect on serum metabolic markers (C-peptide, glucose and HbA1c).

IV. Trough plasma metformin concentrations.

EXPLORATORY OBJECTIVES:

I. Expression of dysregulated molecular mechanisms in the target lesion, including, in order of priority, p53, PTEN, p16, EGFR, and pEGFR.

II. Immune cell infiltration and markers of inflammation in the target lesion. III. Analysis of genomic alterations in the target lesion and blood deoxyribonucleic acid (DNA).

IV. Microbiome in oral rinses.

OUTLINE: Patients are randomized to 1 of 2 arms.

ARM I: Patients receive extended release metformin hydrochloride orally (PO) once daily (QD) for 24 weeks in the absence of disease progression or unacceptable toxicity. Patients also undergo collection of blood and biopsy at baseline and week 24.

ARM II: Patients receive a placebo PO QD for 24 weeks in the absence of disease progression or unacceptable toxicity. Patients also undergo collection of blood and biopsy at baseline and week 24.

After completion of study treatment, patients are followed for up to 3 weeks.

Metformin for the Prevention of Oral Cancer in Patients With Oral Leukoplakia or Erythroplakia

M4OC-Prevent 2.0: Phase IIb Trial of Metformin for Oral Cancer Prevention

NCI is committed to sharing data in accordance with NIH policy. For more details on how clinical trial data is shared, access the link to the NIH data sharing policy page

Histologic response will be evaluated by the following criteria: complete response (CR): Complete reversal of dysplasia or hyperplasia to normal epithelium in the target lesion. Partial response (PR): Improvement of the degree of dysplasia or hyperplasia in the target lesion. No change (NC): No change in the degree of dysplasia or hyperplasia in the target lesion, anything that is not CR, PR or PD. Progressive disease (PD): Increase in the severity of grade of histology in the target lesion.

Clinical response will be evaluated by the following criteria: CR: disappearance of all evidence of lesion(s). PR: greater than or equal to 50% reduction in the sum of the products of diameters of lesion(s) measurable at baseline. Non-measurable lesion(s) may not increase greater than or equal to 25% in size and no new lesion may appear. NC: no change in the size of the lesion(s) identified at baseline and no new lesions appearing, i.e., anything that is not CR, PR, or PD. PD: any increase greater than or equal to 25% in the product of the diameters of any lesion(s) measurable at baseline or in the estimated size of lesion(s) nonmeasurable at baseline or the appearance of an unequivocal new lesion.

Effect of metformin on cell proliferation (Ki67) and its molecular targets (pS6 and nuclear YAP) in the target lesion. The change (pre to post) will be compared between arms.

Metformin effect on serum metabolic markers (C-peptide, glucose and HbA1c). The change (pre to post) in serum metabolic markers will be compared between arms.

The plasma metformin concentrations will be determined in the pre- and post-intervention samples.

National Cancer Institute (NCI)

University of Arizona

Brusch biopsy at baseline and at 3 or 6 months

Control at 3 or 6 month, surgical biopsy when needed

Brush sampling instead of surgical biopsy for control of reaccurance

Brush sampling

Kristina Edman, PhD

Jan-Michael Hirsch

Public dental care

Cancer is a complex disease; its different causes and types have a strong impact on patient treatment and prognosis. To improve understanding of the disease, its causes and progression, the investigators will develop a simple, cost-effective system for continuous control of mucosal lesions with non-invasive brush biopsy that can be managed in primary dental care, as an alternative to tissue biopsy in order to reduce the number of oral cavity cancers.

In Sweden, about 1,200 cases of cancer of the oral cavity, lips and throat are diagnosed each year. This is significantly higher than the global age-standardized incidence of 6.1 per 100,000 inhabitants, including all ages and genders. Oral cancer is a serious and growing public health problem and leads to significantly reduced quality of life after extensive treatment that usually includes radiation therapy and surgery. Patients often have pain, swallowing problems, dry mouth that causes tooth status, negatively affected appearance, family life and social interaction. Although it is well known that early diagnostic screening is of great importance for increasing survival, there is a lack of a nationally organized screening program of high-risk individuals, tobacco users and individuals with overconsumption of alcohol. As a result, many cases are diagnosed late and therefore have poor prognosis. The five-year survival rate in Sweden for the diagnosis of oral cancer is about 60%. If the tumor is small when diagnosed, without lymph node involvement or metastases,and treated correctly, a survival rate of 90% can be achieved while in a late diagnosis with the presence of lymph node involvement and metastases, survival drops drastically and is only 36%. A large proportion of oral cancer originates from potentially malignant oral mucosal lesions (PMOD) that occur in a prevalence of about 2-3% globally and over time are at risk of malignification. Of PMOD, oral leukoplakia (OL) is the most prevalent and most common in the group of middle-aged or older men. Swedish prevalence figures for OL have been reported to range from 0.7% to 3.5%. As patients with PMOD such as OL, erythroplakia (EP) or proliferative verrukös are at a significantly increased risk of developing oral cancer, it is important to include these patients in a functioning control system. This is especially true for risk individuals, those with an overconsumption of alcohol, with tobacco use, and those with chronic infection of tonsil and tongue base with high-risk human papillomavirus. About 80% of the adult population in Sweden is regularly examined at private dental care or public dental care, which means that general dental care can take a great responsibility for identifying and carrying out continuous checks on risk groups. A routine examination of the patient should include assessment of the oral mucosa according to clinical practice. Oral mucosal changes should be diagnosed and, if necessary, treatment initiated. In the case of a clinical diagnosis of OL, EP or verrukös leukoplakia, the clinical diagnosis should be verified with a tissue biopsy performed at a specialist clinic in orofacial medicine, oral surgery or ear-nose-throat clinic. Based on the diagnosis and degree of cell changes, it is decided according to current practice whether the continued treatment and the patient is included in a system for continuous checks. Oral cancer must be diagnosed early because mortality is high, especially in late diagnosis, and quality of life after treatment is very poor with significant pain, speech, chewing and swallowing difficulties with a strong impact on both family life and social contacts and working life. The solution is early detection and early treatment, which can be achieved if follow-up are performed in primary dental care with non-invasive brush biopsies for cytological diagnostics in a similar way to cervical cancer screening managed by midwives. Cytological diagnosis of oral mucosal changes is a safe, simple and rapid method with high sensitivity and specificity. With the present series of studies, the investigators intend to evaluate different possibilities to identify PMOD with high-grade dysplasias, and tumors early in order to improve prognosis.

Oral Cancer Screening for Early Detection of Premalignant Disorders (PMOD)

Screening for Oral Cancer for Early Detection of Premalignant Disorders

Uppsala University

Carcinoma

Hyperplasia

Patients receive extended-release metformin hydrochloride PO QD for 2 weeks and then BID for 10-12 weeks. Treatment continues in the absence of disease progression or unacceptable toxicity.

Laboratory Biomarker Analysis

Metformin Hydrochloride

This phase IIa trial studies how well metformin hydrochloride works in preventing oral cancer in patients with an oral premalignant lesion (oral leukoplakia or erythroplakia). Oral premalignant lesions look like red or whitish plaques or lesions in the mouth that do not rub off and can be associated with a higher risk of cancer. Metformin hydrochloride may help prevent oral cancer from forming in patients with an oral premalignant lesion.

PRIMARY OBJECTIVES:

I. To determine the clinical response of oral premalignant lesions to 12-14 weeks of metformin (metformin hydrochloride) intervention.

SECONDARY OBJECTIVES:

I. Histologic response to metformin intervention in the target lesion. II. Tissue-based biomarkers: metformin effect on cell proliferation and its molecular targets in the target lesion and in the normal tissue (marker of cell proliferation, Ki67, molecular targets of metformin, including, in order of priority, phosphorylated ribosomal protein S6 kinase \[pS6\], phosphorylated v-akt murine thymoma viral oncogene homolog 1 \[pAKT\]S473, phosphorylated eukaryotic translation initiation factor 4E-binding protein 1 \[p4EBP\], phosphorylated acetyl-CoA carboxylase alpha \[pACC\]).

III. Tissue-based biomarkers: expression of dysregulated molecular mechanisms and organic cation transporter 3 (OCT 3) in the target lesion and in the normal tissue, including, in order of priority, epidermal growth factor receptor (EGFR), phosphorylated (p)EGFR, tumor protein 53 (p53), phosphatase and tensin homolog (PTEN), phosphorylated mitogen-activated protein kinase 1 (pERK), cyclin-dependent kinase inhibitor 2A (p16), and OCT3.

IV. Tissue-based biomarkers: targeted analysis of cancer-associated genes in the target lesion and blood deoxyribonucleic acid (DNA).

V. Serum and saliva based biomarkers: metformin effect on serum metabolic markers (C-peptide, glycosylated hemoglobin \[HbA1c\]).

VI. Serum and saliva based biomarkers: metformin concentrations in serum and saliva.

VII Serum and saliva based biomarkers: metformin effect on serum and saliva inflammatory and angiogenic cytokines, including interleukin (IL)-6, IL-8, growth-related oncogene-1 (GRO-1), and vascular endothelial growth factor (VEGF).

EXPLORATORY OBJECTIVES:

I. To characterize changes in the saliva microbiome before and after metformin intervention, including both the absolute microbial load and taxonomic composition.

II. To evaluate the potential microbiome signatures that are correlated with treatment response.

OUTLINE:

Patients receive extended-release metformin hydrochloride orally (PO) once daily (QD) for 2 weeks and then twice daily (BID) for 10-12 weeks. Treatment continues in the absence of disease progression or unacceptable toxicity.

After completion of study treatment, patients are followed up for 2-4 weeks.

Metformin Hydrochloride in Preventing Oral Cancer in Patients With an Oral Premalignant Lesion

M4OC-Prevent: Metformin for Oral Cancer Prevention

This will characterize changes in the saliva microbiome before and after metformin intervention, including both the absolute microbial load and taxonomic composition. Will first evaluate changes in alpha diversity among matched pairs using non-parametric analogous Wilcoxon rank-sum test (Mann-Whitney test). To test for significant differences in beta diversity (e.g. if pretreatment and post-treatment samples cluster in principle coordinates analysis space), permutational multivariate analysis of variance (PERMANOVA) will be used.

Will first evaluate changes in alpha diversity among matched pairs using non-parametric analogous Wilcoxon rank-sum test (Mann-Whitney test). To test for significant differences in beta diversity (e.g. if pretreatment and post-treatment samples cluster in principle coordinates analysis space), PERMANOVA will be used.

Number of participants with complete and partial clinical response to metformin intervention.

Criteria for complete and partial clinical response are:

Complete Response (CR): Disappearance of all evidence of lesion(s). Partial Response (PR): Greater than or equal to 50% reduction in the sum of the products of diameters of lesion(s) measurable at baseline. Non-measurable lesion(s) may not increase greater than or equal to 25% in size and no new lesion may appear.

Number of participants with complete and partial histologic response to metformin intervention.

Criteria for complete and partial histologic response are:

Complete Response (CR): Complete reversal of dysplasia or hyperplasia to normal epithelium in the target lesion.

Partial Response (PR): Improvement of the degree of dysplasia or hyperplasia in the target lesion.

Nonparametric methods, e.g. signed rank test, will be performed to evaluate each of the changes in tissue, serum, and saliva markers.

Nonparametric methods, e.g. signed rank test, will be performed to evaluate each of the changes in tissue, serum, and saliva markers. A univariate logistic regression model with the clinical response as the outcome variable will be fitted to explore if any of the expression of frequent dysregulated mechanisms and OCT3 level are associated with the clinical response to metformin hydrochloride.

Nonparametric methods, e.g. signed rank test, will be performed to evaluate each of the changes in tissue, serum, and saliva markers. A univariate logistic regression model with the clinical response as the outcome variable will be fitted to explore if any genomic alterations are associated with the clinical response to metformin hydrochloride.

Patients receive extended-release metformin hydrochloride PO QD for 2 weeks and then BID for 10-12 weeks. Treatment continues in the absence of disease progression or unacceptable toxicity.

Laboratory Biomarker Analysis: Correlative studies

Metformin Hydrochloride: Given PO

Prevention (Extended-release Metformin Hydrochloride)

Age, Continuous

Sex: Female, Male

Ethnicity (NIH/OMB)

Race (NIH/OMB)

Canada

United States

Region of Enrollment

Dr. Sherry Chow

Clinical Response to Metformin Intervention

Histologic Response to Metformin Intervention

Changes in Cell Proliferation and Its Molecular Targets

Changes in Frequent Dysregulated Molecular Mechanisms and OCT Expression

Impact of Genomic Alterations on the Biological and Biochemical Consequences and Clinical Response to Metformin Hydrochloride

Change in Measurements of Metformin Hydrochloride Concentrations in Serum and Saliva

Change in Serum Metabolic Markers

Change in Serum and Saliva Inflammatory and Angiogenic Cytokines

Change in Saliva Microbiome Analyzed Using Flow Cytometry

Microbiome Signatures Correlated With Treatment Response

Overall Study

Keratosis

No dysplasia, mild, moderate, severe dysplasia, CIS

Assessment for risk of progression to oral cancer

STRATICYTE™ Test

Jody Filkowski, BSc, MSc, PhD

Jason TK Hwang, HBSc, MSc, PhD

Andrew G Sikora, MD, PhD

Simon W Young, DDS, MD, PhD

The purpose of this study is to validate the ability of the STRATICYTE™ predictive model to predict the transformation of oral potentially malignant disorders (OPMDs) to oral squamous cell carcinoma (OSCC) in a retrospective cohort of patients who received biopsies.

The study objectives are to:

1. Evaluate STRATICYTE™ sensitivity and specificity in a cohort of patients that meet the inclusion/exclusion criteria.
2. Identify patient and clinical characteristics influencing the sensitivity and specificity of the STRATICYTE™ model.
3. Estimate the correlation between STRATICYTE™ outcome and time to a positive diagnosis of oral cancer.

FFPE specimens immunohistochemically stained with S100A7

Evaluation of Oral Potentially Malignant Disorders (OPMDs) With STRATICYTE™

Standard measures of accuracy calculated using cross-tabulation of predicted risk category and confirmed cancer progression over a 5-year period from biopsy

Kaplan-Meier analyses to compare time to a positive diagnosis of oral cancer between patients/biopsies with a STRATICYTE™ classification of Low- and Elevated-Risk.

From all possible pairs of patients, compute the number of concordant and discordant pairs. Compute C-index as the proportion of all possible pairs that are concordant.

The University of Texas Health Science Center, Houston

Loma Linda University

Minnesota Oral & Facial Surgery

University of Alabama at Birmingham

Proteocyte Diagnostics Inc.

Cheilitis

Actinic Cheilitis

Dermatologic Agents

Aminolevulinic Acid

Photosensitizing Agents

Metil 5-aminolevulinate arm with photo activation.

Placebo (without metil 5-aminolevulinate) arm with photo activation.

Scrubbing lip vermillion and applying the medication or placebo that is activated (or not, in case of placebo) with red light.

Metil 5-aminolevulinate

Daniel Cohen Goldemberg, PhD

Brazil is a tropical country, with high incidence of ultraviolet radiation throughout the year. Many Europeans migrated to Brazil escaping either war or economic crisis to live in the country searching for opportunities. Low phototype combined with high incidence of UV light is a combination that not only affect the skin but also the lips. The current study was designed to use photodynamic therapy with metil 5-aminolevulinate for actinic cheilitis in a phase 2 clinical trial.

Photodynamic Therapy With Metil 5-aminolevulinate for Actinic Cheilitis - Phase 2 Clinical Trial

Photodynamic Therapy With Metil 5-aminolevulinate for Actinic Cheilitis - A Phase 2 Randomized Double-blind Placebo Controlled Clinical Trial

The Informed Consent Form (ICF) will be read and explained to each patient informing about all the risks and potential benefits. Clinical Study Report (CSR) is going to be registered for all patients, although data will not be shared.

Expected complete clinical response in 60% of cases

Expected histological cure in 40% of cases

Expression of immunohistochemical markers of cancer progression

Instituto Nacional de Cancer, Brazil

Photodynamic therapy with methyl aminolevulinate in the treatment of actinic cheilitis

Substance Related Disorders

Behaviors and Mental Disorders

Blood and Lymph Conditions

Urinary Tract, Sexual Organs, and Pregnancy Conditions

Diseases and Abnormalities at or Before Birth

Nutritional and Metabolic Diseases

Tobacco Use Disorder

Anemia

Fanconi Syndrome

Fanconi Anemia

Substance-Related Disorders

Chemically-Induced Disorders

Mental Disorders

Psychotic Disorders

Anemia, Hypoplastic, Congenital

Anemia, Aplastic

Hematologic Diseases

Syndrome

Bone Marrow Failure Disorders

Pancytopenia

Congenital Bone Marrow Failure Syndromes

Bone Marrow Diseases

Genetic Diseases, Inborn

DNA Repair-Deficiency Disorders

Metabolic Diseases

Congenital Aplastic Anemia

Participants' oral cavities are inspected by a clinician using a standard white light headlamp. Participants then undergo oral mucosa examination using wide-field reflectance and fluorescence imaging, and/or fluorescence spectroscopy imaging. Standard oral brush biopsies are also performed and examined microscopically. Participants may undergo repeated imaging procedures and biopsy during subsequent follow up visits.

Cytology Specimen Collection Procedure

Mouth tissue examined microscopically for cytologic features

Diagnostic Microscopy

Undergo standard white light headlamp oral examination

Diagnostic Procedure

Undergo widefield fluorescent and reflectance imaging

Fluorescence Imaging

Fluorescence Spectroscopy

Ann M Gillenwater

This clinical trial studies widefield fluorescence and reflectance imaging, fluorescence spectroscopy, and tissue samples in regularly examining (monitoring) participants at risk for developing oral cancer. All tissue and cells are made of tiny particles. Some of these particles give off small amounts of light. This light is called fluorescence. Fluorescent imaging use instruments that shine different wavelengths (colors) of light in the mouth taking fluorescence pictures through a portable head light or by taking fluorescent and reflectance pictures through a dental microscope using a digital camera. Fluorescent spectroscopy uses a small probe placed gently against the lining of the mouth and the tissue is exposed to small amounts of fluorescent light that is then collected with a special camera and a computer to be analyzed. Checking mouth tissue samples under a microscope may also help detect abnormal cells. Diagnostic procedures, such as fluorescence and reflectance imaging, fluorescence spectroscopy imaging, and tissue samples, may help doctors detect pre-cancer or early cancer when it may be easier to treat.

PRIMARY OBJECTIVES:

I. To compare images of oral mucosa, obtained at various wavelength combinations including 350 nm, 380 nm, 400 nm, and 450 nm excitation, to standard white light images, pathologic analysis of any biopsied tissue when available, and carcinogenic progression.

OUTLINE:

Participants' oral cavities are inspected by a clinician using a standard white light headlamp. Participants then undergo oral mucosa examination using wide-field reflectance and fluorescence imaging, and/or fluorescence spectroscopy imaging. Standard oral brush biopsies are also performed and examined microscopically. Participants may undergo repeated imaging procedures and biopsy during subsequent follow up visits.

Widefield Fluorescence and Reflectance Imaging Systems and Oral Tissue Samples in Monitoring Participants at Risk for Developing Oral Cancer

Fluorescence &Amp; Reflectance Imaging to Detect Oral Neoplasia

Oral mucosa obtained at various wavelength combinations including 350 nm, 380 nm, 400 nm, and 450 nm excitation will be compared to standard white light images, pathologic analysis of any biopsied tissue when available, and carcinogenic progression. Diagnostic methods will be compared with each other by forming 2x2 tables and computing the chi-square statistics for the McNemar test. Kappa statistic will also be calculated for comparing the chance corrected agreement between various diagnostic methods.

M.D. Anderson Cancer Center

Pharmaceutical Solutions

During Phase I, to determine the maximum tolerated energy density of the Pulse Dye Laser operated at 585 nm with a pulse time of 1.5 ms (PDL-585), when used in combination with 5-aminolevulinic acid (5-ALA) applied topically to the premalignant lesion.

The maximum tolerated energy density will be called the Maximum Tolerated Dose (MTD). Procedure: Fluorescence Diagnosis Imaging Interventions: Application of 5-ALA to lesion followed by activation with high power 585 nm pulsed dye laser (PDL-585, ScleroPLUS laser) at 6, 7 and 8 J/cm2.

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Intra and Extra Oral Inspection of Oral Mucosa	NCT04079491	Oral Lichen Pla... Oral Leukoplaki... Erythroplakia	questionnaire s...	-	Dalarna County Council, Sweden
Metformin for the Prevention of Oral Cancer in Patients With Oral Leukoplakia or Erythroplakia	NCT05237960	Erythroplakia Oral Leukoplaki...	Biopsy Biospecimen Col... Extended Releas... Placebo Adminis...	21 Years -	University of Arizona
Oral Cancer Screening for Early Detection of Premalignant Disorders (PMOD)	NCT05296941	Mouth Neoplasms	Brush sampling	18 Years -	Dalarna County Council, Sweden
Oral Cancer Screening for Early Detection of Premalignant Disorders (PMOD)	NCT05296941	Mouth Neoplasms	Brush sampling	18 Years -	Dalarna County Council, Sweden
Metformin Hydrochloride in Preventing Oral Cancer in Patients With an Oral Premalignant Lesion	NCT02581137	Erythroplakia Hyperplasia Oral Cavity Car... Oral Leukoplaki...	Laboratory Biom... Metformin Hydro...	18 Years -	National Cancer Institute (NCI)
Evaluation of Oral Potentially Malignant Disorders (OPMDs) With STRATICYTE™	NCT05853783	Mouth Diseases	STRATICYTE™ Tes...	18 Years -	Proteocyte Diagnostics Inc.
Photodynamic Therapy With Metil 5-aminolevulinate for Actinic Cheilitis - Phase 2 Clinical Trial	NCT03990636	Actinic Cheilit... Leukoplakia Erythroplakia	Metil 5-aminole...	18 Years -	Instituto Nacional de Cancer, Brazil
Widefield Fluorescence and Reflectance Imaging Systems and Oral Tissue Samples in Monitoring Participants at Risk for Developing Oral Cancer	NCT00542373	Erythroplakia Fanconi Anemia Lichen Planus Oral Cavity and... Oral Cavity Leu... Oral Neoplasm Premalignant Le... Tobacco Use Dis...	Cytology Specim... Diagnostic Micr... Diagnostic Proc... Fluorescence Im... Fluorescence Sp...	18 Years -	M.D. Anderson Cancer Center
Treatment of Oral Premalignant Lesions With 5-ALA PDT	NCT00571974	Leukoplakia Erythroplakia	PDL-585, Sclero... 5-Aminolevulini... Fluorescence Di...	18 Years - 80 Years	University of Arkansas
Photodynamic Therapy With Metil 5-aminolevulinate for Actinic Cheilitis - Phase 2 Clinical Trial	NCT03990636	Actinic Cheilit... Leukoplakia Erythroplakia	Metil 5-aminole...	18 Years -	Instituto Nacional de Cancer, Brazil
Early Prediction of Oral Cancer by S100A7 Immunohistochemistry Signature-based Assessment	NCT04622462	Oral Neoplasm	Standard of Car... STRATICYTE Asse...	15 Years - 90 Years	Proteocyte Diagnostics Inc.

Spots Global Cancer Trial Database for erythroplakia