In the mucoperiosteum, the recruitment of BMDCs is increased upon wounding, whilst these cells are already present in the skin. These differences might be related to the larger repair capacity of oral mucosa.16 Much more myofibroblasts were present in the mucoperiosteal wounds than in the skin wounds. This could be related to the different course of wound healing in both tissues. The skin of rats is very loose and can contract

easily. Contraction will therefore not generate a high tension within the wound tissue, which limits selleckchem myofibroblast differentiation.29 The mucoperiosteum, however, is tightly attached to the palatal bone by Sharpey’s fibres.16 Therefore, contraction will generate higher mechanical tension, and hence more myofibroblasts appear.30 However, less than 10% of the myofibroblasts in both wound types is derived from BMDCs. This is similar to another study performed in mice.7 Myofibroblasts can originate from circulating fibrocytes which are part of the haematopoietic lineage but also have mesenchymal properties.31 BTK inhibitor Activated fibroblasts were also present in both types of wounds, as detected by staining for HSP47, a chaperone protein in collagen synthesis. This population of cells

probably includes the myofibroblasts, which are also producing large amounts of collagen. This is supported by double-staining for αSMA and HSP47 (data not shown). Especially in skin, the population of activated fibroblasts is much larger than that of myofibroblasts, both in the wound and in normal tissue. These cells might be more important in the healing of these

easily contracting wounds than the myofibroblasts. In contrast, in mucoperiosteal wounds, the population of activated fibroblasts was only slightly larger than that of myofibroblasts. The largest population of BMDCs is that of CD68-positive myeloid cells, notably Thymidylate synthase macrophages. In skin wounds, this population is about 40% of the total bone marrow-derived population. This is to be expected since bone marrow ablation followed by bone marrow grafting replaces most of the haematopoietic stem cells. Part of the local population of macrophages might already have been replaced by haematopoietic precursors in the recovery period after bone marrow transplantation, especially in the skin. In conclusion, the data indicate that a much larger population of local BMDCs is present in the skin than in the mucoperiosteum. The skin population of BMDCs seems to be able to resolve tissue damage, as no further BMDCs are recruited upon wounding at two weeks after wounding. In contrast, the small population of BMDCs in the mucoperiosteum is replenished with cells from the bone marrow during at the same time point. This might partly explain the rapid wound healing reported in oral mucosal wounds. Other important factors seem to be the growth factors present in saliva and the specific properties of oral fibroblasts.