FASCIA, INFLAMMATION, FIBROSIS, AND CHRONIC PAIN / CHRONIC DISEASE
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
WHY DOES IT MATTER?
“It is fairly common for people to have an anesthetic, or numb, area around an operation site owing to inevitable damage to superficial sensory nerves in the skin; this usually recovers in time. Extreme sensitivity is most unusual. Your GP’s reassurance suggests that this condition is not indicative of anything nasty. However, the pain sounds very unpleasant so do go and impress this on your doctor if the situation is still causing concern. Yours sincerely, The NetDoctor Medical Team.”
Not common? Most unusual? Not nasty? Allow me to show you that if you are struggling with some sort of adhesion-induced pain issue (whether you realize it or not), it’s not only common, it’s common enough that numerous experts in the field are discussing it in some form or fashion. Below are some random quotes from the first couple pages of a Google search.
- “Scar tissue pain occurs, for example, after an operation, and can result in chronic pain in and around the scar area. The cause of scar tissue pain is damage to a small skin nerve, or when a nerve is squeezed by the scar tissue. In scar tissue pain, which can occur after an operation, there sometimes mention of neuroma formation at the end of a damaged skin nerve. After some interventions, such as inguinal hernia, lung, heart, kidney, and shoulder operations, as well as breast amputations, scar tissue pain is more common.” The Maastricht University Pain Centre in the Netherlands (Scar Tissue Pain)
- “Every time an injury to the skin penetrates through to the dermis layer, a scar will occur as a result of the healing process, this is the body’s way of naturally repairing itself. In response to a wound, the body produces collagen, a protein of which the rest of our skin is made from. Scar tissue however, looks and feels different – some researchers suggest that this is due to its alignment, which differs from that of normal skin tissue. Although many scars are trivial, some are extremely unpleasant causing not only aesthetic displeasure but also chronically painful symptoms. Scar pain, whether it be from an operative, or traumatic cause, is very common. The symptoms and signs can be similar to those of Complex Regional Pain Syndrome. They include pain, itching, swelling, tightness, restriction of movement, skin colour changes, allodynia or hypersensitivity to touch, and hyperalgesia or marked pain to deeper palpation. Scar tissue pain is usually caused by damage to the nerves or when a nerve is compressed by the scar. In some cases….. firing uncontrollable pain signals to the brain.” Dr. Mark Miller, owner of a number of Pain Management clinics in England, from an article called Scar Pain
- “Wounds take a variable amount of time to heal. The location of the wound makes a difference, as peripheries like your foot heal slower than your shoulder for example. Other factors such as smoking, using steroids, diabetes or low protein levels also slow wound healing. Scars are not just skin deep. They may involve several layers beneath the skin which are stuck together.” My Ortho Clinic dot com (Stitches, Wounds & Sensitive Scars)
- “Many people have scars as a result of accidents, injuries and surgeries. While scar tissue is extremely helpful at repairing cells quickly to prevent further damage and/or injury, the characteristics of scars and their presence in the body can restrict and inhibit movement. This can lead to myofascial pain, musculoskeletal imbalances and ultimately impede athletic performance. Since the configuration of scar tissue is not the same as the surrounding muscle fibers it can alter the way these structures work.” From an article on PT On the Net (How Scar Tissue Affects Pain and Performance) by therapist Justin Price
- “As of 2012, 33% of births ended in C-section. A common complaint after a C-section is the sensitivity of the scar itself. In addition, the scar may cause a slight postural change… that could result in back pain. But the possible consequences don’t stop there. The scarring can cause the adjacent muscles to develop trigger points that refer pain…. In addition, the adjacent connective tissue can become restricted also causing pain. Lastly, the scarring can irritate superficial nerves in the area of the scar. What’s more, the round ligament that attaches from the sides of the uterus to the labia can be caught in scar tissue after a C-section because the incision is also right over the area where the round ligament crosses the pelvic brim. Another symptom we have seen with our patients who have had C-sections is that they may have issues with lower digestion such as irritable bowel syndrome or constipation. This occurs because of the tightening created by the scar tissue pulls within the abdominal cavity and thus affects the organs.” Cherry-picked from an article called C-Section Scar: Problems and Solutions by the physical therapists at the Pelvic Health and Rehabilitation Centers of California
- “After a trauma, a large cut or surgery around the nerves, scar tissue forms. Scar tissue is both good and bad. It helps the nerve attach to nearby structures, but when the patient moves, pressure is placed on the nerve because the scar tissue can pull on the nerve. Even without movement, the scar tissue can reduce the nerve’s blood supply. All of this can cause significant nerve pain. The main symptom is constant, unrelenting pain coming from the nerve tissue.” The University of Michigan’s Medical School (Scarred Nerves)
- “Scars can be a big pain… When there is an initial injury (and yes, a surgical incision is an “injury”), the body goes through three phases of healing: Inflammation, Proliferation and Remodeling. Through this process, the body creates scarring to close up the initial injury. Scars are composed of a fibrous protein (collagen)…. The difference, however, is that scars are not quite organized the same way as the tissues they replace, and they don’t really do the job quite as well. Scars can form in all tissues of the body. Scars are not super selective when it comes to tissues they adhere to. So, sometimes, scars will adhere to lots of tissues around them and this pull can lead to discomfort. Sometimes, small nerves can be pulled on by the scar which can lead to irritation.” From Dr. Jessica Reale’s (she’s a DPT in Atlanta) article about Painful Scars….
In these articles, there’s a common thread: injury or insult leads to scarring, which in many cases leads to pain and various sorts of dysfunction. If you are struggling with CHRONIC PAIN, there were terms used in these articles that you really need to be familiar with. HYPERAGLIA, ALLODYNIA, CRPS, Hypersensitivity — uncontrolled firing of pain signals to the brain (CENTRAL SENSITIVITY), are just a few of the more common. And if you’ve been following my site(s) for the past decade or so (DCP is where I started), you are already aware of the fact that Scar Tissue is different from normal tissues in any number of ways, including both its physical structure and its increased propensity to act as a pain generator (HERE), via an almost infinite number of causal mechanisms. And on top of everything else, it’s dysfunction is being touted as a “universal” cause of disease (HERE).
For instance, the August 2015 issue of Muscle & Nerve (Comparison of Nerve Growth Factor-Induced Sensitization Pattern in Lumbar and Tibial Muscle and Fascia) concluded, after injecting NGF into various areas of human fascia that, “Nerve growth factor (NGF) induces profound hyperalgesia. The mechanical hyperalgesia area was larger in tibial fascia than in muscle. Pressure pain thresholds were lower, tonic pressure pain ratings, and citrate buffer evoked pain higher in fascia than in muscle.” This is all well and good, but the next sentence is where the rubber meets the road as far as chronic low back pain is concerned. “Thoracolumbar fasciae appear more sensitive than tibial fasciae and may be major contributors to low back pain.” Once you start to understand the THORACOLUMBAR FASCIA, this all starts making sense.
This is doubly true if you recall that the amount of degenerative change (HERE) or presence of disc herniations (HERE), are poor indicators not only of whether or not a person will have back pain at all, but how severe said back pain may be. Check out the results of a study from the University of Heidelberg’s Dissertaitions Kurzfassung (Pain Sensitivity of Human Fascia and Muscle Sensory Findings After Chemical and Electrical Stimulation). And if you are one of the millions of Americans suffering from CHRONIC LOW BACK PAIN, be sure and read the paragraph until you understand it.
“ln many patients, chronic low back pain cannot be explained by abnormalities in the bony structures of the vertebral column. Due to their dense innervation, fascia and muscles of the lower back are potential alternative sources of nociceptive input in these patients with “non-specific low back pain”. These studies suggest that the fascia of the lower back might be a key structure in the genesis of nonspecific low back pain, because of its high innervation density, its high pain sensitivity to several stimuli, and substantial pain amplification after its stimulation. Effects of muscle nerve stimulation in previous studies may have been at least partly due activation of afferents from the fascia that run through these nerves. Therefore, treatment of the fascia may be an important target for prevention and treatment of back pain.”
We are seeing this phenomenon is studies over and over again. If you want another example, take a look at Dr. Stecco’s, The Role of Fascia in Non-Specific Low Back Pain. And what do we see when we go to current peer review as far as treatment is concerned? We see that while far from perfect, bodywork of various sorts (stretching, MANIPULATION, exercise, etc — things that move joints and fascia) is at least as good, or in most cases, better, than other treatments designed to get these people get out of pain and return to function. And they’re certainly better than drugs (HERE). If you are interested in lowering your level of systemic inflammation and addressing the various roots of many, if not most of your fascial adhesions, I would suggest you take a moment to read THIS SHORT POST.