The Expression Of TGF-β₁and α-SMA In Human Chronic Periapical Lesions

Background and objectivePeriapical lesions are a response of the host, which actively prevents disseminationof bacteria from an infected root canal into the surrounding tissue. Although it has beenwell recognized that the immune response participates in the formation of periapicallesions, their pathogenicity has not been clearly defined.Transforming growth factor-β1(TGF-β1) is one of the cytokines released duringtissue injury and by inflammatory cells exposed to bacteria and their products. It hasproinflammatory properties, triggering the production of bone-resorptive cytokines. In avariety of fibrotic diseases and wound healing studies, it has been shown that thedifferentiation of myofibroblast induced by TGF-β1is the key to tissue repair, canaccelerate the injury healing and tissue reconstruction.α-smooth muscle actin (α-SMA), as the most used marker of myofibroblast, has beenstudied in wound healing and fibrotic diseases. It is widely accepted that after tissue injury,fibroblasts expressing α-SMA stimulated by TGF-β1, causing excessive extracellularmatrix synthesis and accumulation, lead to fibrous lesions of organs and tissue.Whether the expression of TGF-β1and α-SMA takes part in the pathogenesis ofperiapical diseases has not been reported. Therefore, we examined the expression anddistribution of TGF-β1and α-SMA in different types of human chronic periapical diseasesusing immunohistochemistry stainingMethodsSixty specimen, including healthy control (n=20), periapical cyst(n=20) andperiapical granuloma(n=20), were involved in this study. Tissue material was fixed in10%buffered formalin for at least48h, and then embedded in paraffin. Serial5μm thicksections were deposited onto SuperFrost/Plus microscope glasses. Routine staining ofsections using hematoxylin and eosin (HE) was performed for histopathology. Theexpression and distribution of TGF-β1and α-SMA in different types of human chronicperiapical diseases were identified by immunohistochemistry staining.Results 1. Histological observationsHealthy control group showed normal periapical periodontal ligament structure andno inflammatory cell infiltration was found. Periapical granuloma group showed severeinflammatory cell infiltration. Periapical cyst group showed intercellular edema inepithelial layer, slight inflammatory cell infiltration below the epithelial layer and densecollagen fibers in fibrous tissue layer of cyst wall.2. TGF-β1immunohistochemistry staining resultsThe expression of TGF-β1in healthy control group was not detected. The expressionof TGF-β1was found on capillary endothelial cells and some inflammatory cells inperiapical granuloma group. In periapical cyst group, the expression of TGF-β1was foundin epithelial cells, inflammatory cells and capillaries of epithelial layers. In cystic fibroustissue layer, the expression of TGF-β1was found in fibroblasts, fibrous tissue, bloodvessels and inflammatory cell around vessels. The expression of TGF-β1in periapical cystwas significantly higher than that of periapical granuloma（P＜0.05）.3. α-SMA immunohistochemistry staining resultsThere was no expression of α-SMA in healthy control group. The expression ofα-SMAin periapical cyst group was mainly found in capillary endothelial cells. Inepithelial layer of periapical cyst group, α-SMA was slightly expressed in epithelial cellsand moderately expressed in capillary endothelial cells. In fibrous tissue layer ofperiapical cyst group, high expression of α-SMA was found in the fibrous layer of cystwall. The results showed that the expression of α-SMA in periapical cyst group weresignificantly stronger than that of the periapical granuloma group（P＜0.05）.Conclusions1. Compared with healthy control group, the expression of TGF-β1and α-SMA inboth periapical granuloma group and periapical cyst group was significantly stronger.2. The expression of TGF-β1and α-SMA in periapical cyst group were significantlyhigher than that of periapical granuloma group.TGF-β1may play a role in the pathogenesis of chronic periapical disease,particularly in periapical cyst formation, the precise mechanism of action still needsfurther study.