Elevated expression of JAK1 and pJAK1 in oral lichen planus: a retrospective study.

BACKGROUND

Janus kinase (JAK) inhibitors have recently emerged as potential therapeutic agents for oral lichen planus (OLP). In OLP, cytokine-mediated immune activation is thought to involve the JAK/STAT signaling pathway; however, the precise role of this pathway remains incompletely understood. Therefore, this study aimed to investigate the expression of JAK1 and its activated form, pJAK1, in OLP.

METHODS

In this retrospective study, forty-four formalin-fixed, paraffin-embedded OLP and nineteen normal oral mucosa (NOM) specimens were analyzed using immunohistochemistry to assess JAK1 and pJAK1 expression. The number of JAK1 and pJAK1 positive cells in the epithelium and inflammatory infiltrate, as well as the total number of epithelial and inflammatory cells, were counted. The percentage of JAK1 and pJAK1 expression in OLP and NOM was then compared.

RESULTS

JAK1 and pJAK1 expression was significantly increased in both epithelial cells (p = 0.007 and p = 0.001, respectively) and infiltrating inflammatory cells (p < 0.001 and p = 0.017, respectively) in OLP compared with NOM. In epithelial cells, the median percentages of JAK1 and pJAK1 positive cells in OLP were 63.62 (42.77, 96.01) and 55.68 (44.72, 59.22), respectively, compared with 32.51 (10.77, 89.95) and 24.25 (12.54, 66.20) in NOM. Similarly, median JAK1 and pJAK1 expression in infiltrating inflammatory cells was higher in OLP (65.40 (40.45, 81.31) and 44.18 (19.40, 66.96), respectively) than in NOM (14.71 (7.69, 66.91) and 14.54 (8.88, 28.37)).

CONCLUSIONS

The significant overexpression of JAK1 and pJAK1 in OLP suggests an involvement in its pathogenesis. However, given the retrospective design, further prospective studies and functional analyses are necessary to confirm these findings and to explore the potential role of JAK inhibitors in the management of OLP.