The word “all” is dangerous territory in scientific discussions. I used it in the book and now, in these blogs. It will undoubtedly raise objections and some punctilious readers (scientists and lay people) voicing disagreement. I guess the fact that I’m willing to withstand the slings and arrows suggests my commitment and belief in the premise. I also believe my defense in the book (and briefly here in this blog) will provide some succor for my logic.
So what is chronic inflammation (CI)? We all are pretty comfortable with acute inflammation, the clinical (immune) reaction that occurs rapidly (acutely) in response to an antigen (foreign, non-self substance or stress). It includes the classic (described originally by a first-century Roman physician, Celsus in 38AD) redness (“rubor”), heat or fever (“calor”), pain (“dolor”), swelling (“tumor”), and loss of tissue or organ function (“functio laesa”). We’ll be discussing in greater depth just how acute inflammation is produced through an immune reaction with all sorts of cells (lymphocytes, PMN [polymorphonuclear] cells) and cytokines (chemicals and proteins) in Chapters 1 and 2. But here, I want to establish a distinction between acute and chronic inflammation. It is often assumed that chronic (prolonged, enduring) inflammation is simply an extension of the acute form. In fact, though one may flow from the other or present de novo, they are 2 entirely separate pathological processes with distinctly different clinical effects. In the book, I made a suggestion that we should consider a separate and distinct name for chronic inflammation, maybe “pathomelitis” (Etymology: patho = disease; ome = complete set of; [l]itis = inflammation). Fat chance that will ever happen!
The distinct differences between acute and chronic inflammation include: (1) a difference in the pathophysiology and histopathology (cells and tissue) between the two; (2) a difference between the pharmacology and pharmacodynamics between the two; and (3) perhaps of greatest consequence, a dramatic difference between the clinical course, beyond duration, of acute versus CI disease. The clinical basis for this thesis of CI as the progenitor or originating cause of all major human disease categories lies in the diffuse and destructive nature of its pathophysiologic process. As opposed to the acute inflammatory reaction being a localized tissue process, in chronic inflammation the persistent inflammatory mediators and cellular components can damage tissue locally (e.g., psoriasis, a skin disease) or throughout the entire body (e.g., systemic lupus erythematosus [SLE], rheumatoid arthritis, and the vast array of autoimmune diseases). Perhaps, the most devastating pathophysiological changes in chronic inflammation (which can also be part of acute inflammation) are the diffuse changes in blood vessel walls throughout the entire body (perivasculitis). Both the localized and more so, diffuse nature of these diffuse vascular changes are what makes CI the foundation of the pathological etiologies that precipitate “all” resultant disease states. So when you hear about “inflammation” associated with a specific disease, it’s chronic, not acute, inflammation.
A more in-depth discussion of the bioscience and pathophysiology of CI will be addressed in the blogs under "The Enemy Within Us." However, most blogs will present case-by-case reasoning for CI as the basis for autoimmune diseases, cancers, infectious disease, and in fact, all categories of human disease.
Discussion Questions:
In your opinion, should acute inflammation be considered a precursor to CI or are they, in fact, distinct and separate clinical entities?
Do you believe the pathophysiology and diffuse vascular changes associated with CI qualify it as the basis of all diseases? (This is a bit of a “loaded” question, the nature of which will be further explicated in the first blog under "The Enemy Within Us.")
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