Abstract: Evolving dynamics of vascular blood supply and ulceration of otherwise absorptive mucosal epithelium appear to primarily implicate intercellular adhesion molecules such as cadherin. An increased permeability of mucosa would progress in terms of injury to enterocytes with translocation transcytolically and paracellularly of fluid and macromolecules. Intense congestion with mucosal ulceration would develop as a multiplicity of involvement of blood vessels constituting granulation tissue and ulcer base. Also, a loss of effective epithelial barriers of the gut mucosa would progress largely as increased vascular wall permeability that further damages adjacent mucosal epithelium. Vascularity and disease progression would allow for a delineation of active processes that promote inflammation and ongoing injury to the bowel wall centered particularly on the lamina propria. Cytokine and chemokine derivatives would impair the vascular response patterns to injury of bowel mucosa in terms characteristically of a stereotyped lamina propria response. Variable mucosal injury induces a stereotyped response in attempted repair of the injury that further progresses as a superimposed series of changes in proliferation of enterocytes coupled to vascular permeability effects and transformed adhesion dynamics of epithelial cell junctions.