Oral Potentially Malignant Disorders (OPMDs) – Review Flashcards

These flashcards cover key definitions, classifications, risk factors, molecular alterations, clinical presentations, diagnostic methods, treatment options and surveillance principles for oral potentially malignant disorders as discussed in the lecture.

What is the WHO working-group definition of an oral potentially malignant disorder (OPMD)?

Any oral mucosal abnormality associated with a statistically increased risk of developing oral cancer.

Name five OPMDs with sufficient epidemiological evidence for malignant potential (2020 WHO list).

Leukoplakia, proliferative verrucous leukoplakia, erythroplakia, oral submucous fibrosis, oral lichen planus.

Which two new conditions were added to the 2020 OPMD classification?

Oral lichenoid lesions (OLL) and oral graft-versus-host disease (OGVHD).

Identify the main lifestyle risk factors most strongly linked to OPMDs.

Tobacco use and alcohol consumption (synergistic effect).

Which chewing habit is associated with oral submucous fibrosis and lichen planus?

Areca (betel) nut chewing.

How can alterations in the oral microbiome contribute to OPMD development?

Dysbiosis leads to chronic inflammation, mutagenic bacterial metabolites, immune suppression and promotion of malignant transformation.

Which high-risk HPV types are recognised risk factors for oropharyngeal SCC but have insufficient evidence in OPMDs?

HPV-16 and HPV-18.

List two inherited syndromes that raise OPMD/cancer risk due to genomic instability.

Dyskeratosis congenita and Fanconi anaemia (others include Bloom syndrome, xeroderma pigmentosum).

Define loss of heterozygosity (LOH) and its significance in OPMDs.

LOH is deletion/inactivation of one parental allele; frequent LOH at key loci predicts malignant transformation risk in OPMDs.

Which oncogene’s copy-number gain is often observed in high-risk OPMDs?

Epidermal growth factor receptor (EGFR).

High levels of which three microRNAs correlate with progression of OPMDs?

miR-21, miR-345 and miR-181b.

What epigenetic change affecting p16 (CDKN2A) is documented in OPMDs?

Promoter hypermethylation leading to gene silencing.

Describe the protective vs promotive roles of immune infiltration in OPMDs.

Increased CD4+/CD8+ T-cells protect; elevated PD-1/PD-L1 expression, reduced CD3+ T-cells and TH1 skew promote progression.

Which three transcriptomic clusters of OPMDs carry higher malignant risk?

Hypoxia, mesenchymal and classical clusters.

Provide the recommended clinical definition of leukoplakia.

A predominantly white plaque of questionable risk having excluded other known diseases or disorders that carry no increased risk for cancer.

How does proliferative verrucous leukoplakia (PVL) typically behave?

Progressive, multifocal, warty lesions that are persistent, irreversible and show a high rate of malignant transformation.

What clinical colour and definition characterise erythroplakia?

A predominantly fiery red patch that cannot be characterised clinically or pathologically as any other definable disease.

Give two examples of white oral lesions that must be excluded before diagnosing leukoplakia.

Oral lichen planus (plaque type) and chronic hyperplastic candidosis (others: leukoedema, frictional keratosis, OHL).

Which OPMD is classically linked to progressive trismus due to fibrous bands?

Oral submucous fibrosis (OSF).

State two hallmark oral findings of oral lichen planus (OLP).

Bilateral white reticular (lace-like) striae; may coexist with atrophic, erosive or plaque areas.

What sun-related OPMD affects the vermilion of the lower lip?

Actinic cheilitis (actinic keratosis of the lip).

Which connective-tissue disorder can present orally as erythematous ‘target’ lesions with white striae?

Oral lupus erythematosus.

Define dyskeratosis congenita in one sentence.

A rare inherited bone-marrow-failure syndrome with nail dystrophy, reticular skin pigmentation and oral leukoplakia due to defective telomere biology.

What is the current gold standard for definitive OPMD diagnosis?

Scalpel or punch biopsy followed by histopathologic examination.

Where should a biopsy be taken in a heterogeneous white lesion?

From speckled, indurated, erosive or ulcerated areas and include a small margin of normal tissue.

Name four chair-side adjuncts that can aid early detection or biopsy site selection for OPMDs.

Toluidine blue vital staining, chemiluminescent light (Vizilite), tissue autofluorescence (VELscope), brush cytology (OralCDx).

What colour change signifies abnormal mucosa with VELscope autofluorescence?

Abnormal areas lose the pale green fluorescence and appear dark.

Give one major advantage and one disadvantage of Vizilite screening.

Advantage: simple, non-invasive, immediate results. Disadvantage: expensive single-use and unable to specify exact biopsy location.

Why is habit cessation the first-line intervention for many OPMDs?

Lesions in tobacco users often regress after quitting; stopping known carcinogenic habits lowers transformation risk.

List two common surgical modalities used to excise dysplastic OPMDs.

Cold-blade scalpel excision and CO₂ laser ablation.

What is the main advantage of CO₂ laser over scalpel excision?

Less postoperative pain/edema, better hemostasis and reduced scarring.

How does photodynamic therapy (PDT) work in treating OPMDs?

A photosensitiser accumulates in lesion cells; light activation generates reactive oxygen species causing selective cytotoxicity.

Name two topical or systemic agents under investigation for chemoprevention of OPMDs.

Celecoxib (COX-2 inhibitor) and green-tea extract (antioxidant).

Which receptor is targeted by the chemopreventive drug erlotinib?

EGFR (epidermal growth factor receptor).

Are any chemopreventive drugs currently approved for routine clinical use in OPMDs?

No—none have yet gained regulatory approval.

Explain ‘field cancerization’ in the context of OPMDs.

Exposure to carcinogens creates genetically altered mucosal fields, predisposing to multiple primary and second cancers even after lesion removal.

Why are there no fixed evidence-based surveillance intervals for OPMDs?

Transformation risk is unpredictable; follow-up must be tailored to lesion dysplasia grade, patient habits, site, and other risk factors.

What dysplastic grade typically warrants more frequent follow-up visits?

Moderate to severe epithelial dysplasia.

Which optical adjunct combines a blue excitation light with direct visualisation without rinses?

VELscope tissue autofluorescence device.

What are two primary limitations of the OralCDx brush biopsy?

Cannot provide definitive diagnosis (only detects atypia) and still requires confirmatory scalpel biopsy if positive.

State one key molecular pathway commonly deregulated in OPMDs alongside PI3K/AKT.

Fibroblast growth factor (FGF) signalling pathway.

Which microRNA levels are typically low in OPMDs that progress to cancer?

miR-142-5p.

What are the sensitivity and specificity ranges reported for toluidine-blue staining?

Sensitivity 0.78–1.00; specificity 0.31–1.00.

Give two advantages of cryotherapy for OPMDs.

Bloodless field with minimal bleeding, low postoperative pain and scarring.

Why might PD-1/PD-L1 expression in OPMD tissue be clinically relevant?

High expression promotes immune evasion and progression; it is a potential target for checkpoint-inhibitor chemoprevention trials.