- A transition to a pattern of chronic inflammation develops following weeks of an unresolved inflammatory process and can last months or even years. The molecular mechanisms by which this transition occurs is poorly understood and only a few clues are beginning to be understood. What is clear is that the basic demographic of immune cells changes at the site of injury as inflammation evolves into a chronic phase. Following the initial injury, tissue repair processes are also activated; however, in settings of chronic inflammation these repair processes become engaged chronically and thus can lead to significant architectural distortion of the affected tissue.
- A wide variety of etiologies can result in chronic inflammation with the key theme being that the initiating source of cell injury remains unresolved. The source of injury may be a persistent microbial infection, persistence of toxic particles, or the continuation of autoimmune pathogenic mechanisms. Whatever the case, chronic inflammation evolves when the initial, acute inflammatory response cannot eliminate the source of cellular injury.
- The prime feature of chronic inflammation is the prominent presence of macrophage and lymphocytes, including \B-cells, Plasma Cells, and T-cells, at the site of injury. Consequently, chronic inflammation is characterized primarily by a mononuclear cell infiltrate with a small contribution from or completely absent presence of Neutrophils. When chronic inflammation is due to a parasitic infection, eosinophil and mast cell may be a prominent feature of the infiltrate. Concomitant with the inflammatory process, histological features of tissue repair are also observed. This may include features of angiogenesis as well as deposition of extracellular matrix by fibroblasts which over time may lead to overt fibrosis.