Abstract

Periodontalligament-associated protein-1 (PLAP-1) is an important regulator of osteogenic differentiation ofperiodontalligament 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. 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 10ng/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 48hours by western blotting. 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 revealedthe 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. 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.

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