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Bone marrow‐derived cells in palatal wound healing

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Oral Diseases (2010) 16, 788–794Objective:  Myofibroblasts are responsible for contraction and scarring after cleft palate repair. This leads to growth disturbances in the upper jaw. We hypothesized that cells from the bone marrow are recruited to palatal wounds and differentiate into myofibroblasts.Methods:  We transplanted bone marrow from green fluorescent protein (GFP)‐transgenic rats into lethally irradiated wild‐type rats. After recovery, experimental wounds were made in the palatal mucoperiosteum, and harvested 2 weeks later. GFP‐expressing cells were identified using immunostaining. Myofibroblasts, activated fibroblasts, endothelial cells, and myeloid cells were quantified with specific markers.Results:  After transplantation, 89 ± 8.9% of mononuclear cells in the blood expressed the GFP and about 50% of adherent cells in the bone marrow. Tissue obtained during initial wounding contained only minor numbers of GFP‐positive cells, like adjacent control tissue. Following wound healing, 8.1 ± 5.1% of all cells in the wound area were positive, and 5.0 ± 4.0% of the myofibroblasts, which was significantly higher than in adjacent tissue. Similar percentages were found for activated fibroblasts and endothelial cells, but for myeloid cells it was considerably higher (22 ± 9%).Conclusions:  Bone marrow‐derived cells contribute to palatal wound healing, but are not the main source of myofibroblasts. In small wounds, the local precursor cells are probably sufficient to replenish the defect.
Title: Bone marrow‐derived cells in palatal wound healing
Description:
Oral Diseases (2010) 16, 788–794Objective:  Myofibroblasts are responsible for contraction and scarring after cleft palate repair.
This leads to growth disturbances in the upper jaw.
We hypothesized that cells from the bone marrow are recruited to palatal wounds and differentiate into myofibroblasts.
Methods:  We transplanted bone marrow from green fluorescent protein (GFP)‐transgenic rats into lethally irradiated wild‐type rats.
After recovery, experimental wounds were made in the palatal mucoperiosteum, and harvested 2 weeks later.
GFP‐expressing cells were identified using immunostaining.
Myofibroblasts, activated fibroblasts, endothelial cells, and myeloid cells were quantified with specific markers.
Results:  After transplantation, 89 ± 8.
9% of mononuclear cells in the blood expressed the GFP and about 50% of adherent cells in the bone marrow.
Tissue obtained during initial wounding contained only minor numbers of GFP‐positive cells, like adjacent control tissue.
Following wound healing, 8.
1 ± 5.
1% of all cells in the wound area were positive, and 5.
0 ± 4.
0% of the myofibroblasts, which was significantly higher than in adjacent tissue.
Similar percentages were found for activated fibroblasts and endothelial cells, but for myeloid cells it was considerably higher (22 ± 9%).
Conclusions:  Bone marrow‐derived cells contribute to palatal wound healing, but are not the main source of myofibroblasts.
In small wounds, the local precursor cells are probably sufficient to replenish the defect.

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