Keratin 17-positive Civatte bodies in oral lichen planus—distribution variety, diagnostic significance and histopathogenesis

Abstract

Although emergence of keratin 17 (K17) and reciprocal loss of K13 are immunohistochemical hallmarks for oral mucosal malignancy, we report here findings of K17-positive (+) speckles, possibly equivalent to Civatte bodies, in benign oral lichen planus. Sixty-two biopsy samples from oral lichen planus cases were subjected to immunohistochemical examinations to analyze the distribution as well as histopathogenesis of Civatte bodies. K17 was irregularly positive among oral lichen planus-affected epithelial cells, and K17-positive (+) filamentous structures were irregularly distributed within the cytoplasm in confocal images. K17+ speckles were identified as Civatte bodies, and they were mainly distributed in the interface between epithelial cells and lymphocytic infiltrates (type A, 52.8%), followed by distribution within the epithelial layer (type B, 24.7%) or within the lamina propria with lymphocytic infiltration (type C, 22.5%). Apoptotic figures were often engulfed by macrophages and clearly distinguished from Civatte bodies by the presence TUNEL signals. These results indicate that K17 is a sensitive immunohistochemical marker for Civatte bodies and useful for differential diagnosis of oral lichen planus from other oral mucosal lesions. Civatte bodies are generated from denucleation of K17+ epithelial cells during the process of cell death via dyskeratosis, which is possibly related to blood capillary collapse.

Increased expression of keratin 17 in oral lichen planus and its correlation with disease severity

“… 13 , 25 In addition, we observed KRT17 was widely distributed in the epithelial layer, which was in accordance to the previous study. 26 …”

Evaluating the Frequency of Histopathological Features of Oral and Cutaneous Lichen Planus Lesions: A Retrospective- Comparative Study

“…The CBs represent necrotic keratinocytes, measure about 20 μm in diameter and have a homogeneous, eosinophilic appearance. Other lesions in which CBs may be present include any interfacial dermatitis in which basal cell damage occurs, such as lupus erythematosus, graft versus host disease (GvHD), and inflammatory keratoses such as actinic lichenoid keratosis, and LP-like keratosis [22,23]. There might be a huge number of CBs in LPs in the form of a cluster [24].…”

Antimicrobial peptide nisin induces spherical distribution of macropinocytosis-like cytokeratin 5 and cytokeratin 17 following immediate derangement of the cell membrane

“…In epithelial cells, CK may participate in macropinocytosis instead of vimentin. In general, CK17 distribution has many unsolved questions compared to CK17 protein expression [ 45 ]. Therefore, together with the nisin study, CK17 distribution requires further research.…”