How To Stimulate Fibrobla?

How to stimulate fibrobla?
Stimulation of fibroblastic activity
For chronic pain, dysfunction, and fascial adhesion
Ryan hoyme - pixabay

Fibroblasts are dispersed in connective tissue throughout the body, where they secrete a nonrigid extracellular matrix that is rich in type I and/or type iii collagen. When a tissue is injured, the fibroblasts nearby proliferate, migrate into the wound, and produce large amounts of collagenous matrix. Fibroblasts also seem to be the most versatile of connective-tissue cells, displaying a remarkable capacity to differentiate into other members of the family. From the book molecular biology of the cell

You gotta be cruel to be kind, in the right measure
Nick lowe from 1979's cruel to be kind

A few days ago I did a post on fibroblasts, what they are, and why understanding them is critical to figuring out why you may be stuck as far as solving your particular chronic pain syndrome (or maybe even your chronic illness --- here) is concerned. Which begs the question; what can be done to stimulate these cells? I will get around to answering that momentarily. But before we address the what part of this question, let's take just a moment to discuss why. In other words, why would we care whether or not we activate fibroblasts? to understand this better, let's take a look at fgf's (fibroblastic growth factors). According to a popular online encyclopedia's listing, we see that.

" fgfs are important players in wound healing. They are multifunctional proteins with a wide variety of effects; they are most commonly mitogens [having to do with increased tissue proliferation via cell division] but also have regulatory, morphological, and endocrine effects. They have been alternately referred to as" pluripotent" [extremely potent] growth factors and as" promiscuous" growth factors due to their multiple actions on multiple cell types. One important function of fgf1 and fgf2 is the promotion ofendothelial cell proliferation and the physical organization of endothelial cells into tube-like structures. They promoteangiogenesis, the growth of new blood vessels from the pre-existing vasculature. Fgf1 and fgf2 are more potent angiogenic factors than vascular endothelial growth factor (vegf) orplatelet-derived growth factor (pgf). Fgf1 and fgf2 stimulate the proliferation of fibroblasts that give rise to granulation tissue [new connective tissue and tiny blood vessels] which fills up a wound space/cavity early in the wound-healing process. During the development of the central nervous system, fgfs play important roles in neural stem cell proliferation, neurogenesis, axon growth, and differentiation" 

Think of it this way. Insulin-like growth factors (igf's) are so powerful that they are considered to be peds (performance enhancing drugs) in the athletic community, and due to their extreme anabolic (tissue building) nature, are thus banned. In many ways, fgf's are even more potent than igf's. As you can gather from the paragraph above, they promote a natural form of prp, as well as the proliferation of collagen's" tube-within-a-tube" structure (here). And on top of all this, they greatly enhance the body's ability to build more blood vessels (angiogenesis), meaning there is more available oxygen available for tissue repair, regeneration, and healing. The question now becomes, how can we naturally harness the power of fgf's, not only for the professional athlete, but for the everyday joe who has been injured and is living in chronic pain? at least in theory, it's easy. All we have to do is figure out what sort of treatments might cause fgf's to be manufactured and released in injured cells.

There are any number of brand new studies showing that a wide array of exposures to various forms of electric fields as well as a number of the newer forms of electrical stimulation can stimulate fibroblastic activity and fgf's. If you read 1985's amazing body electric by the va's blacklisted researcher, robert becker (md), you would know that this is nothing new. Likewise, there are a number of studies showing the benefit of low level laser (both cold and class iv) on wound healing and fibroblastic activity. 

There are also any number of chemical factors that stimulate fibroblastic activity; many of which are the chemical factors (cytokines, chemokines, interleukins, no, etc) that are broadly characterized as inflammation. This is why taking nsaids after a workout is counterproductive. It's also important to remember that there are times when fibroblastic activity can be too strong. For example, the august 2017 issue of the journal of physiology (human skeletal muscle fibroblasts stimulate in vitro myogenesis and in vivo muscle regeneration) revealed that" accumulation of skeletal muscle extracellular matrix is an unfavourable characteristic of many muscle diseases, muscle injury and sarcopenia" in other words, there are situations where a pathological" thickening" occurs in injured or diseased tissues. The authors state, however, that" it thus appears, in humans, that fibroblasts exert a strong positive regulatory influence on myogenic precursor cell activity, in line with observations during skeletal muscle regeneration" 

As you'll soon see, there is a fine line between stimulating ecm (extracellular matrix) and cranking out too much ecm. What can be done to drive local (as opposed to systemic) fibroblastic activity in the person who has been injured and is living with either chronic pain or chronic dysfunction? that is the subject of today's post