Wound healing connective tissue proliferation

Taken together, the identification of mast cell hyperplasia and mediator release at sites of tissue fibrosis and wound healing, observations in animal models, and study of the actions of mast cell products, has provided much circumstantial evidence that mast cells are involved in tissue remodelling, healing and fibrosis. It is unlikely that mast cells are essential in these responses, but more likely that they augment them. Complex interactions between different connective tissue components, mast cells and other inflammatory cells are likely to operate, and are unlikely to be fully delineated in humans in vivo. It seems reasonable to hypothesize however that initial mast cell mediator release has the potential to activate fibroblasts, which may then promote the recruitment at d proliferation of further mast cells, explaining the mast cell hyperplasia often witnessed at sites of chronic inflammation. 

As a natural constituent of connective tissue and major structural protein, collagen is implicated in all phases of the wound healing process (hemostasis, inflammation, migration, proliferation and maturation) and controls the cellular functions such as cell shape and differentiation, migration, and synthesis of a number of proteins [100]. The use of collagen dressings may seem attractive in view of their functions to ... 

MMP-9 is preferentially expressed in UIP (46). The concentrations of MMP-9 and tissue inhibitors of metalloproteinases (TIMPs) are more increased in BAL fluid of patients with OP than in those with UIP (47). These data suggest that an imbalance between MMPs and TIMPs may play a role in the connective tissue remodeling of OP. Laminin-5, a glycoprotein involved in cell attachment, migration, proliferation, differentiation, and apoptosis expressed in epithelial cells of wound healing, is also expressed in regenerating epithelial cells in OP and UIP (48). 

---