Xijiao Yu1,2, Hongmei Liu1, Shuang Liu2, Xue Chen2, Xinyu Zhao2, Yi Du1, Shu Li2. 1. Department of Endodontics, Jinan Stomatological Hospital, Jinan, China. 2. Shandong Provincial Key Laboratory of Oral Tissue Regeneration, School and Hospital of Stomatology, Shandong University, Jinan, China.
Abstract
BACKGROUND AND OBJECTIVE: Periodontal ligament-associated protein-1 (PLAP-1) is an important regulator of osteogenic differentiation of periodontal ligament cells and plays important role in the homeostasis of periodontal tissues. But the role of PLAP-1 in periodontitis is poorly understood. Expressions of PLAP-1 in experimental periodontitis are observed to elucidate whether PLAP-1 gets involved in the pathogenesis of periodontitis. MATERIAL AND METHODS: Wistar rats were randomly allocated to two groups (n = 6/group): Ligation group and Control group. PLAP-1 expression in experimental periodontitis was assessed by immunohistochemistry and collagen fibers in periodontal ligament were observed using picrosirius red staining. Expressions of PLAP-1 and CD68 in periodontitis were colocalized by double-labelled immunofluorescence. To further examine the relationship between PLAP-1 and osteoclastogenesis in experimental periodontitis, acute periodontal inflammatory infiltration and alveolar bone destruction were induced by administering ligated rats with 10 ng/mL tumor necrosis factor alpha (TNF-α; ligation + TNF-α group, n = 6). Alveolar bone loss was observed by micro-computed tomography (Micro-CT), and osteoclasts were identified by tartrate-resistant acid phosphatase staining (TRAP). Expressions of PLAP-1 in TNF-α stimulated human periodontal ligament cells were also detected at 24 and 48 hours by western blotting. RESULTS: PLAP-1 expression levels in periodontal ligament cells and collagen fibers were lower in the ligation group,compared with the control group. Similarly, TNF-α decreased PLAP-1 expression in human periodontal ligament cells in vitro. Degradation or destruction of collagen fibers accompanied the reduced PLAP-1 expression in the periodontal ligament in the ligation group. Colocalization of PLAP-1 and CD68 revealed the positive relationship between PLAP-1 and CD68+ infiltrating cells in periodontitis. More PLAP-1-positive inflammatory cells were found in the ligation + TNF-α group, compared with the ligation + saline group. CONCLUSION: PLAP-1-positive inflammatory cells are involved in the pathogenesis of periodontitis. An increase in PLAP-1-positive inflammatory cell number contributes periodontal inflammation and alveolar bone loss.
BACKGROUND AND OBJECTIVE: Periodontal ligament-associated protein-1 (PLAP-1) is an important regulator of osteogenic differentiation of periodontal ligament cells and plays important role in the homeostasis of periodontal tissues. But the role of PLAP-1 in periodontitis is poorly understood. Expressions of PLAP-1 in experimental periodontitis are observed to elucidate whether PLAP-1 gets involved in the pathogenesis of periodontitis. MATERIAL AND METHODS:Wistar rats were randomly allocated to two groups (n = 6/group): Ligation group and Control group. PLAP-1 expression in experimental periodontitis was assessed by immunohistochemistry and collagen fibers in periodontal ligament were observed using picrosirius red staining. Expressions of PLAP-1 and CD68 in periodontitis were colocalized by double-labelled immunofluorescence. To further examine the relationship between PLAP-1 and osteoclastogenesis in experimental periodontitis, acute periodontal inflammatory infiltration and alveolar bone destruction were induced by administering ligated rats with 10 ng/mL tumor necrosis factor alpha (TNF-α; ligation + TNF-α group, n = 6). Alveolar bone loss was observed by micro-computed tomography (Micro-CT), and osteoclasts were identified by tartrate-resistant acid phosphatase staining (TRAP). Expressions of PLAP-1 in TNF-α stimulated human periodontal ligament cells were also detected at 24 and 48 hours by western blotting. RESULTS:PLAP-1 expression levels in periodontal ligament cells and collagen fibers were lower in the ligation group,compared with the control group. Similarly, TNF-α decreased PLAP-1 expression in human periodontal ligament cells in vitro. Degradation or destruction of collagen fibers accompanied the reduced PLAP-1 expression in the periodontal ligament in the ligation group. Colocalization of PLAP-1 and CD68 revealed the positive relationship between PLAP-1 and CD68+ infiltrating cells in periodontitis. More PLAP-1-positive inflammatory cells were found in the ligation + TNF-α group, compared with the ligation + saline group. CONCLUSION:PLAP-1-positive inflammatory cells are involved in the pathogenesis of periodontitis. An increase in PLAP-1-positive inflammatory cell number contributes periodontal inflammation and alveolar bone loss.