A comparative study of apoptosis in reticular and erosive oral lichen planus

Abstract

The oral lichen planus (OLP) is a chronic inflammatory disease, probably autoimmune, with different clinical forms. The most common types are the reticular and the erosive ones. Apoptosis participates in the destruction of basal keratinocytes, but its role in the perpetuation of the subepithelial lymphocytic infiltrates was not yet investigated. To evaluate the involvement of apoptosis in the epithelium and in subepithelial lymphocytic infiltrates, 15 samples of reticular and erosive OLP and 10 samples of healthy oral mucosa were collected and processed histologically. Apoptosis was quantified in the epithelium and in inflammatory cell infiltrates. TUNEL reaction was used to measure apoptosis in the infiltrates. Erosive OLP showed more intense epithelial apoptosis than reticular OLP and controls. In contrast, apoptosis in the inflammatory cell infiltrates was more frequent in reticular than in erosive OLP. Lymphocytes were the predominant cells within the inflammatory cell infiltrates and were more frequent in erosive OLP than in reticular type. These results suggest that different apoptotic levels are involved in the erosive/reticular switch in OLP, determining different clinical presentations. In conclusion, decreased apoptosis in inflammatory infiltrates may contribute to the persistence of T lymphocytes, worsening the attack to the epithelium in erosive OLP.

Increased cyclooxygenase 2 expression in association with oral lichen planus severity

“…Therefore, an increase in COX-2 expression in OLP epithelium in the clinical criteria scores 3, 4, and 5 (Figure 3) suggests that overwhelming COX-2 expression in these scores may cause a nonhealing wound in OLP epithelium. This speculation is consistent with the previous finding that demonstrated an increase in epithelial apoptosis in the ulcerative/erosive type of OLP 31 . Interestingly, COX-2 was also weakly expressed in the suprabasal cell layers of normal oral epithelium (Figure 1), which is in line with the findings from other studies in normal oral epithelium32, 33 and in normal epidermis 34 …”

“…The basement membrane destruction can thus lead to infiltration of T lymphocytes into the OLP epithelial layer, resulting in direct cell-to-cell contacts between epithelial cells and T lymphocytes that can lead to apoptosis of OLP epithelial cells 7, 30. Increased epithelial apoptosis was clinically observed as the atrophic and the ulcerative/erosive type of OLP, 31 in which they were scored as 2, 3, 4, and 5 according to the clinical criteria score. Therefore, an increase in COX-2 expression in OLP epithelium in the clinical criteria scores 3, 4, and 5 (Figure 3) suggests that overwhelming COX-2 expression in these scores may cause a nonhealing wound in OLP epithelium.…”

MicroRNA-26a/b have protective roles in oral lichen planus

“…Apoptosis is one of the most common features of OLP 6,23 , thus we evaluated apoptosis-related key factors using miR26a/b mimics or inhibitors in HOKs. As shown, miR26a/b levels were considerably upregulated or down-regulated with miR-26a/b mimic or inhibitor treatment respectively ( Supplementary Fig.…”

Apoptosis in immune-mediated diseases

“…[ 6 ] The pathogenesis of OLP is unclear,[ 7 8 ] but apoptosis has been evaluated in epidermal cells, indicating a role in epithelial destruction. [ 9 ] Histological degeneration of basal keratinocytes form colloid bodies and suggest that they are apoptotic keratinocytes. [ 1 ]…”