Clinical evaluation of photodynamic therapy for oral leukoplakia: a retrospective study of 50 patients

Abstract

Background Topical photodynamic therapy (PDT) has demonstrated encouraging results in the treatment of oral leukoplakia (OLK). However, data on the clinical efficacy of PDT in Chinese patients with OLK are still limited. Methods Fifty patients diagnosed with OLK were enrolled, including patients with various dysplastic tissues. All patients received topical PDT with 5-aminolevulinic acid (5-ALA) as a photosensitizer. Clinical efficacy was evaluated 4 weeks after treatment. Follow-up was performed every 3 months during the first year and every 6 months during the second year. Results The overall response rate was 68% (34/50): 12% (n = 6) complete and 56% (n = 28) partial responses. Aneuploidy was reduced in the patients with dysplastic lesions. Oral pain and local ulcers developed in 52% of the patients (n = 26). Patients with a long history of OLK including hyperplasia and dysplastic lesions, as well as those with non-homogenous lesions, were more likely to develop pain and ulcer. During follow-up, the recurrence rate of hyperplasia and dysplastic lesions was 32% (n = 16) and the malignant transformation rate of dysplastic lesions was 4% (n = 2). Lesions on the buccal mucosa were associated with recurrence (P = 0.044; OR: 0.108, 95% CI: 0.013–0.915). Conclusion Topical 5-ALA-mediated PDT is an effective treatment for OLK, particularly for homogenous leukoplakia, with few side effects. The buccal mucosa may be a protective factor that can reduce recurrence.

Epidemiological Trends and Clinicopathological Characteristics of Oral Leukoplakia: A Retrospective Analysis From a Single Institution in Chennai, Tamil Nadu, India

“…Previous studies in an in vitro setting suggested that human neoplastic cellular growth has been inhibited by the usage of lycopene [ 27 ]. Surgical excision remains one of the most common treatment modalities for oral leukoplakia and includes conventional surgery, cryosurgery, laser excision, and electrocoagulation [ 6 ]. This was concordant with the results of the present study and surgical excision was predominantly performed for patients with oral leukoplakia.…”

“…The pathogenesis of leukoplakia remains an enigma. Previous studies have proposed that the pathogenesis of leukoplakia is driven by somatic genetic mutations that affect the growth, survival, and cycle control of keratinocytes, reflecting as hyperkeratosis, hyperplasia, and dysplasia histopathologically, which translates clinically as changes in color and texture of the mucosa [ 6 ]. Genetic alterations in various oncogene drivers such as EGFR , MYC , CCND1 , and CDKN2A have been found.…”