The expression of plasminogen activator system in a rat model of periodontal wound healing.
BACKGROUND
The plasminogen activator system has been proposed to play a role in proteolytic degradation of extracellular matrices in tissue remodeling, including wound healing. The aim of this study was to elucidate the presence of components of the plasminogen activator system during different stages of periodontal wound healing.


METHODS
Periodontal wounds were created around the molars of adult rats and healing was followed for 28 days. Immunohistochemical analyses of the healing tissues and an analysis of the periodontal wound healing fluid by ELISA were carried out for the detection of tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), and 2 plasminogen activator inhibitors (PAI-1 and PAI-2).


RESULTS
During the early stages (days 1 to 3) of periodontal wound healing, PAI-1 and PAI-2 were found to be closely associated with the deposition of a fibrin clot in the gingival sulcus. These components were strongly associated with the infiltrating inflammatory cells around the fibrin clot. During days 3 to 7, u-PA, PAI-1, and PAI-2 were associated with cells (particularly monocytes/macrophages, fibroblasts, and endothelial cells) in the newly formed granulation tissue. During days 7 to 14, a new attachment apparatus was formed during which PAI-1, PAI-2, and u-PA were localized in both periodontal ligament fibroblasts (PDL) and epithelial cells at sites where these cells were attaching to the root surface. In the periodontal wound healing fluid, the concentration for t-PA increased and peaked during the first week. PAI-2 had a similar expression to t-PA, but at a lower level over the entire wound-healing period.


CONCLUSIONS
These findings indicate that the plasminogen activator system is involved in the entire process of periodontal wound healing, in particular with the formation of fibrin matrix on the root surface and its replacement by granulation tissue, as well as the subsequent formation of the attachment of soft tissue to the root surface during the later stages of wound repair.
Xiao
Y
Y
School of Dentistry, The University of Queensland, Brisbane, Australia.
Li
H
H
Bunn
C
C
Bartold
P M
PM
D000818:Animals; D001777:Blood Coagulation / Q000502:physiology; D002448:Cell Adhesion; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells / Q000473:pathology; D005337:Fibrin / Q000032:analysis; D005347:Fibroblasts / Q000473:pathology; D005500:Follow-Up Studies; D005883:Gingival Crevicular Fluid / Q000737:chemistry; D006097:Granulation Tissue / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D008264:Macrophages / Q000473:pathology; D008297:Male; D009000:Monocytes / Q000473:pathology; D010510:Periodontal Diseases / Q000378:metabolism* / Q000503:physiopathology; D010513:Periodontal Ligament / Q000473:pathology / Q000503:physiopathology; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D017396:Plasminogen Activator Inhibitor 2 / Q000032:analysis; D010960:Plasminogen Activators / Q000032:analysis*; D051381:Rats; D011917:Rats, Inbred Lew; D015842:Serine Proteinase Inhibitors / Q000032:analysis; D010959:Tissue Plasminogen Activator / Q000032:analysis*; D014092:Tooth Root / Q000473:pathology; D014568:Urokinase-Type Plasminogen Activator / Q000032:analysis*; D014945:Wound Healing / Q000502:physiology
D017395:Plasminogen Activator Inhibitor 1; D017396:Plasminogen Activator Inhibitor 2; D015842:Serine Proteinase Inhibitors; D005337:Fibrin; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator