FASCIA, INFLAMMATION, FIBROSIS, AND CHRONIC PAIN / CHRONIC DISEASE
Doc, I have a bone to pick with you and the rest of the medical profession: I am real tired of hearing about pain. I have no pain. I have loss of functionality without pain. I am also real tired of hearing about injury, There is no injury, just a lifetime of assymetrical usage. My mother did the same thing, but much worse. She actually gave herself severe scoliosis without injury, just by bending over her work asymmetrically for 60 years. I'm not that bad yet, but it's real hard to fight alone, ad it's very difficult to find help, because all anyone wants to talk about is pain and injury, whereas all I want is not to end up in a wheelchair (like my mother). From Suzie via a blog comment (I got this after I put this up today).
Making sure that you do not end up with soft tissue fibrosis is a big deal. This fact really hits home once you realize what fibrosis really is. Spine Health reveals that, "Fibrosis is the replacement of normal tissue with scar tissue." News Medical (What is Fibrosis?) describes it thusly. "The term fibrosis describes the development of fibrous connective tissue as a reparative response to injury or damage. Fibrosis may refer to the connective tissue deposition that occurs as part of normal healing or to the excess tissue deposition that occurs as a pathological process. When fibrosis occurs in response to injury, the term “scarring” is used." Merriam Webster defines fibrosis as "a condition marked by increase of interstitial fibrous tissue." The Oxford Dictionary says this of fibrosis. "Fibrosis is the thickening and scarring of connective tissue, usually as a result of injury."
I've talked at length on my site about fibrosis, the debate as to whether it's really "scar tissue" or not (HERE), as well as a characteristic mentioned above --- "THICKENING" ("DENSIFICATION"). There is an inaccuracy above that I must clear up as well. When Oxford says that fibrosis is usually the result of injury, this is simply not true. Or at least not true in the sense that most people think of an injury as a physical trauma. Listen to what the authors of a study published earlier this month in Advanced Drug Delivery Reviews (Scarring vs. Functional Healing: Matrix-Based Strategies to Regulate Tissue Repair) showing that fibrosis goes way beyond CONNECTIVE TISSUES.
"All vertebrates possess mechanisms to restore damaged tissues with outcomes ranging from regeneration to scarring. Unfortunately, the mammalian response to tissue injury most often culminates in scar formation. Accounting for nearly 45% of deaths in the developed world, fibrosis is a process that stands diametrically opposed to functional tissue regeneration. Wound healing is guided by precise deposition and remodeling of the extracellular matrix (ECM). The ECM, comprising the non-cellular component of tissues, is a signaling depot that is differentially regulated in scarring and regenerative healing. Strategies to improve wound healing outcomes therefore require methods to limit fibrosis."
Allow me to take you through this bit by bit. First off, I've shown you previously that fibrosis is the number one cause of death, not just in America, but worldwide (HERE), directly accounting for almost one death in two. Secondly, bear in mind that there is a known reason for this --- inflammation always results in fibrosis (HERE). And while this inflammation can certainly be the result of a physical trauma, it can also be driven by other things, including food sensitivities (HERE is a common one), sugar and junk carbs (HERE), PARASITES, BLACK MOLD, DYSBIOSIS, POLLUTION, TOXIC METALS, OCCULT INFECTIONS, POOR POSTURE, CHEMICAL EXPOSURE, and on, and on, and on. And ultimately, it all leads to inflammation, which in turn leads to fibrosis (HERE), which itself leads to various sorts of dysfunction(s) depending on where it's found (heart, lungs, liver, kidneys, etc, etc), with the ultimate dysfunction being death. Today, however, we are going to focus on inflammation and fibrosis of the connective tissue fascia.
FASCIA is the tough membranous cover that permeates muscles (it's also the covering for nerves, blood vessels, bones, etc, etc). It can become "fibrous" (fibrotic) due to either local inflammation from an injury (HERE) or systemic inflammation from the many causes mentioned earlier (HERE). Either way, as joints become dysfunctional (even slightly so), BIOMECHANICS can become screwed up enough to start causing degenerative changes. While DEGENERATIVE CHANGES in and of themselves are not typically enough to cause pain in their earlier stages, few would argue that the less degeneration you have, the better. Enter TISSUE REMODELING.
As you can see from watching a few of our VIDEO TESTIMONIALS, it is important --- scratch that; it's imperative --- to get injured / insulted tissues moving and keep them moving in order to prevent fibrosis and the subsequent problems that follow. A study from the Tissue Repair Laboratory of the State University of Rio de Janerio (Mechanical Tension Prevents Fibrosis by Reducing Collagen Deposition After Injury On Subcutaneous Layer In Mice) provided some proof. Two groups of mice had their THORACOLUMBAR FASCIA "injured" by a microsurgical procedure. The first group underwent specific stretches, while the second did not. After later looking at the tissues under a microscope the authors concluded that, "Microinjury resulted in a significant increase on collagen deposition in the absence of stretch, but not in the presence of stretch. Brief tissue stretch attenuated the collagen deposition following tissue injury. These results have potential relevance to propose treatments of different types of excessive scars."
There are only about a million and one ways to mechanically load your soft tissues, including many that you can do on your own (HERE, HERE, HERE, HERE, or HERE). What does moving injured or inflamed soft tissues do besides fire off PROPRIOCEPTON? Let's take a look at an issue of Molecular Basis of Disease (Tissue Mechanics and Fibrosis) that was published 5 years ago this month (everything in today's post is cherry-picked due to restraints on time and space). The study kicks off with the statement "Mechanical forces are essential to the development and progression of fibrosis." This means that if you can control (or at least manage) said forces, you will ultimately change the progression of the healing process and control / manage deposition of collagen (fibrosis) that I usually refer to as "SCAR TISSUE FORMATION".
The authors talked about the many different forces at work in tissue --- pushing forces, pulling forces, hydraulic forces, etc. What do these forces do and why is it important to learn how to harness them? "These forces collectively regulate the phenotype and proliferation of myofibroblasts and other cells in damaged tissues, the activation of growth factors, and the structure and mechanics of the matrix – all of which are central to fibrosis." This is why understanding FIBROBLASTIC ACTIVITY as it related to both normal and abnormal fibroproliferation is a big deal. And as for the fibroblasts, the authors state "It is important to note that changes in the mechanical properties of tissues can both cause and result from fibrosis." In other words, biomechanical / biochemical changes cause fibrosis, and fibrosis causes biomechanical / biochemical changes. And in similar fashion to compound interest, you can either make these changes work for you or they will likely work against you; quite possibly for the rest of your life (can anyone say 'Vicious Cycle'?). The authors ended by concluding....
"Mechanical forces are increasingly appreciated to play a role in fibrosis on a par with soluble [chemical] factors. Matrix stiffness is so far the best-appreciated mechanical stimulus in fibrosis, and liver and lung are the tissues best studied. Even for these tissues and stimuli, our understanding of forces, their effects, and mechanotransduction in fibrosis is rudimentary."
The first thing I want you to grasp is the concept of MECHANOTRANSDUCTION --- the process of turning mechanical energy into electrical / chemical messages that the body understands. As you might have guessed, it's compromised in fibrotic tissues. And as for the "soluble factors," this would not only cover INFLAMMATION (a chemical process that is not synonymous with either swelling or infection), but all sorts of growth factors and enzymes as well. Speaking of enzymes, thirteen researchers from the surgical departments of Stanford and the Oregon Health and Science University teamed up to publish a study (Focal Adhesion Kinase Links Mechanical Force to Skin Fibrosis via Inflammatory Signaling) in Nature Medicine.
The study kicked things off by saying, "Traditional cytokine-based paradigms for fibrosis largely overlook the role of cell-matrix interactions and physical cues in disease pathogenesis." In English, this means that although mainstream scientists have known about the effects of CYTOKINES (inflammation) on the development and proliferation of fibrosis for a very long time, only recently are researchers appreciating mechanical effects on the ECM (the gel part of the connective tissue). Listen as these authors talk about potential causes and solutions for "exuberant fibroproliferation ---- a common complication after injury."
Because inflammatory mechanisms are strongly implicated in fibrosis, we examined whether FAK modulates cytokine/chemokine signaling. One key component of wound repair that is often overlooked is mechanical force, which regulates cell-matrix interactions through intracellular focal adhesion components, including focal adhesion kinase (FAK). Here we report that FAK is activated after cutaneous injury and that this process is potentiated by mechanical loading. Fibroblast-specific FAK knockout mice have substantially less inflammation and fibrosis than control mice in a model of hypertrophic scar formation. Inflammatory chemokine pathways are a major mechanism by which FAK mechanotransduction induces fibrosis.
In other words, FAK --- an enzyme that controls, regulates, and essentially causes "focal adhesions" (can anyone say FASCIAL ADHESIONS?) is not only found in great concentrations in said adhesions, but is "activated" by injury, and "potentiated" by loading said tissues in a mechanical fashion (this process is known as TISSUE DEFORMATION). What does tissue loading entail? Tissue loading is any sort of mechanical stimulus that pushes or pulls tissue, and is accomplished by the very things mentioned earlier; exercise, stretching, bodywork, etc, etc. "It is possible that in addition to these chemokine-mediated mechanisms, FAK may also control fibrosis by directly activating fibroblast collagen production... Based on these studies, we propose a model for load-induced fibrosis whereby mechanical force activates both MCP-1 secretion and collagen production through FAK to perpetuate a ‘vicious cycle’ of fibroproliferation after injury." Stimulating the production of collagen through INCREASING FIBROBLASTIC ACTIVITY is a good thing, but in cases where inflammation (cytokines, chemokines, etc) is rampant or the mechanical loading is "abnormal," the end result can be crazy amounts of Scar Tissue.
SCAR TISSUE AND FASCIAL ADHESIONS
Dr. Schierling completed four years of Kansas State University's five-year Nutrition / Exercise Physiology Program before deciding on a career in Chiropractic. He graduated from Logan Chiropractic College in 1991, and has run a busy clinic in Mountain View, Missouri ever since. He and his wife Amy have four children (three daughters and a son).