Abstract Purpose of review To give an overview of the current knowledge regarding the aetiology, epidemiology, and classification of laryngeal dysplasia (LD) and to highlight the contributions of recent literature. As most cases of dysplasia occur at the glottic level and data on diagnosis and management are almost exclusively from this location, laryngeal dysplasia in this position paper is taken to be synonymous with dysplasia of the vocal folds. Summary LD has long been recognized as a precursor lesion to laryngeal squamous cell carcinoma (SCC). Tobacco and alcohol consumption are the two single most important etiological factors for the development of LD. There is currently insufficient evidence to support a role of reflux. Although varying levels of human papillomavirus have been identified in LD, its causal role is still uncertain, and there are data suggesting that it may be limited. Dysplasia has a varying presentation including leukoplakia, erythroleukoplakia, mucosal reddening or thickening with exophytic, “tumor-like” alterations. About 50% of leukoplakic lesions will contain some form of dysplasia. It has become clear that the traditionally accepted molecular pathways to cancer, involving accumulated mutations in a specific order, do not apply to LD. Although the molecular nature of the progression of LD to SCC is still unclear, it can be concluded that the risk of malignant transformation does rise with increasing grade of dysplasia, but not predictably so. Consequently, grading systems are inherently troubled by the weak correlation between the degree of the dysplasia and the risk of malignant transformation. The best data on LD grading and outcomes come from the Ljubljana group, forming the basis for the World Health Organization classification published in 2017.