Section 3 of 4
Discussion
Ramachandra Reddy Gowda Venkatesha, Karthik Rajaram Mohan, Saramma Mathew Fenn, Reethikarathan Rathanswamy Thiruneervannan, and Sindhuja Rajalingam · about 3 minutes
Leukoplakia is of clinical significance due to the presence of dysplasia at some point in development [1]. Oral leukoplakia is the most prevalent form of oral potentially malignant disorder and has been extensively researched [1]. The malignant transformation of oral leukoplakia has always remained a clinical concern. The rate of malignant transformation increases with large size, older age group, location on the tongue, non-homogeneous leukoplakia, and the habit of smoking or smokeless tobacco chewing with or without betel nut [1]. Yang et al. stated that among 144 patients, 44 (25.48%) had leukoplakia lesions on the tongue dorsum [2].
Leukoplakia on the dorsum of the tongue is less commonly observed clinically than leukoplakia on the ventrolateral surface of the tongue. The behavior of leukoplakia on the tongue's dorsum and the tongue's ventrolateral surface concerning carbon dioxide (CO₂) laser treatment is similar in malignant transformation and rate of recurrence. Clinicians must adopt a more aggressive approach to oral tongue leukoplakia with a more severe grade of dysplasia. The cumulative malignant transformation rate is 7.41% [2]. The period of malignant transformation of dorsal tongue leukoplakia is 1.25 to 5.13 years [2].
A bifid tongue, or cleft or forked tongue, is a congenital anomaly that occurs in a small percentage of the population and is characterized by a split or divided tongue, usually resulting from a failure of the embryonic tissues to fuse appropriately during development [4]. A bifid tongue's etiology and related factors are the inadequate fusion of lateral lingual swellings and a median swelling (tuberculum impar) from the first three or four branchial arches during embryogenesis. Inadequate fusion of these structures may lead to a bifid tongue [4]. The bifid tongue occurs with various genetic syndromes, including oral-facial-digital syndrome type I, Opitz syndrome, Klippel-Feil anomaly, Larsen syndrome, and hereditary sensory and autonomic neuropathy type IV [4,5]. Proliferative verrucous leukoplakia is not much attributed to tobacco and alcohol use and has a high mortality, whereas leukoplakia is attributed to tobacco use [5]. Careful monitoring of the lesion is essential, as it is likely to become dysplastic. Patients with a non-homogeneous type of leukoplakia on the tongue develop cancer earlier than those with a homogeneous type. In conclusion, leukoplakia on the tongue dorsum should be closely monitored and potentially treated to avoid future complications. Cessation of risk factors such as tobacco and alcohol consumption and regular dental visits are key preventive strategies.
For non-homogeneous oral leukoplakia, Erbium:Yttrium Aluminium Garnet (Er:YAG), Erbium, Chromium-doped Yttrium, Scandium, Gallium, and Garnet laser (Er:Cr:YSGG), and CO₂ laser with photodynamic therapy (PDT) provide potential alternatives to surgical removal, likely decreasing recurrence and increasing patient comfort [6]. More high-quality randomized controlled trials (RCTs) are needed to verify these results and identify the most appropriate laser-PDT combination for treating oral leukoplakia [6]. More RCTs are required to identify the CO₂ laser as beneficial in treating oral leukoplakia [7,8]. The management for oral leukoplakia includes observation or surveillance, laser or excision by surgery, and local, systemic chemoprevention approaches [9]. A CO₂ laser is used to treat vocal cord leukoplakia and has the advantage of being minimally invasive, having low recurrence post-treatment, and improving phonation after surgery [9]. Laser-assisted or activated photodynamic therapy (LA-PDT) is an effective treatment method for dysplastic oral leukoplakia, which must be treated first with topical aminolevulinic acid, a photosensitizer. Aminolevulinic acid photodynamic therapy (ALA-PDT) uses light-emitting diode (LED) or laser light for a favorable clinical outcome. In addition, ALA-PDT is a non-surgical method that can treat recurrent or refractory lesions without producing significant short- or long-term adverse effects [10].