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inflammation in tendons and other new tendon research


For more than three decades, the peer-reviewed scientific literature has said that most tendinopathies (TENDINOSIS included) are not inflammatory — in other words, when the tendons were biopsied, there were no inflammatory cells present.   I reported this but always said that even though these tendinopathies might not contain inflammation, inflammation undoubtedly helps drive the process.  It seems the science is changing in this area and that tendinosis is inflammatory after all.   What’s the evidence for this assertion and what difference does it make as far as your issues are concerned? Follow along.

  • Last year’s book, Metabolic Influences on Risks for Tendon Disorders, carried a chapter called Inflammation in Tendon Disorders which described the criteria for inflammation to be an issue in tendon disorders.  “The role of inflammation in tendon disorders has long been a subject of considerable debate. Developments in our understanding of the basic science of inflammation have provided further insight into its potential role in specific forms of tendon disease, and the circumstances that may potentiate this. Such circumstances include excessive mechanical stresses on tendon and the presence of systemic inflammation associated with chronic diseases.”  The last half of the last sentence is paramount.  Not sure what SYSTEMIC INFLAMMATION is or what causes it?  Just click the link. Remember this concept because we will briefly revisit it at the end of the post.
  • Remember the famous tendon researcher and orthopedic surgeon Dr. GA Murrell that I have quoted many times (see “tendinosis” link above)?  Here is one of his more recent studies.  This January’s issue of the journal Nature Reviews: Rheumatology (Inflammatory Mechanisms in Tendinopathy – Towards Translation) concluded, “These disorders are common, account for a high proportion (30%) of referrals to musculoskeletal practitioners, and confer a large socioeconomic burden of disease.  The advent of modern molecular techniques has highlighted the presence of immune cells and inflammatory mechanisms throughout the spectrum of tendinopathy in both animal and human models of disease. Key inflammatory mediators — such as cytokines, nitric oxide, prostaglandins and lipoxins — play crucial parts in modulating changes in the extracellular matrix within tendinopathy.”  In other words, the ECM is “scarred” and there are inflammatory markers in the tendons.   Thanks to METABOLOMICS we can now see this. 
  • April’s issue of the inflammation journal Cytokine (The Influence of Chronic IL-6 Exposure, in Vivo, on Rat Achilles Tendon Extracellular Matrix) simply stated in its abstract that, “Elevated levels of IL-6 are associated with tendinopathy.”  IL-6 (interleukin six) is probably the most common and well known of the numerous biomarkers of inflammation.
  • March’s Frontier in Aging Neuroscience (Commentary: Role of VEGF, Nitric Oxide, and Sympathetic Neurotransmitters in the Pathogenesis of Tendinopathy: A Review of the Current Evidences) provided a comment by a researcher, arguing by listing numerous other studies, that yes, tendinosis is indeed inflammatory.
  • March’s issue of PLoS One (The Effects of Substance P and Acetylcholine on Human Tenocyte Proliferation Converge Mechanistically Via TGF-β1) showed how certain inflammatory mediators caused a thickening of the tendons via “proliferation” of the cells that make tendon material (tenocytes).  While a degree of this is needed, when the process gets out of kilter the tendons get too thick, which makes them less functional and weaker.
  • Last July’s issue of Scientific Reports (A Possible Link Between Loading, Inflammation and Healing: Immune Cell Populations During Tendon Healing….) revealed that the link discussed in the study’s title is present. “Loading influences tendon healing, and so does inflammation. We hypothesized that the two are connected….  Mechanical loading has a profound influence on tendon healing. Reduced loading has been shown in numerous models to impair healing.  Recently, we have noticed that anti-inflammatory drugs impair tendon healing mainly by impairing the response to loading or microdamage, and also that the expression of inflammation-related genes was involved. This points to a possible connection between loading, inflammation and healing.  By analyzing the cell populations from healing tissue by flow cytometry with markers for several inflammatory and regulatory cell types, we can describe the composition of the population and use it as an “inflammatory signature”. Changes in the signature over time can then show how the inflammatory reaction is influenced under varying conditions.”  BTW, the idea that anti-inflammation drugs impair healing is not new and will be discussed at the end of the post.
  • The term “apoptosis” refers to a cell’s propensity to die in a pre-programed fashion, and is controlled by a part of the immune system known as the TH-17 SYSTEM, which, by the way, is heavily associated with AUTOIMMUNE DISEASES.  In fact, the Polish journal Archivum Immunologiae et Therapiae Experimentalis (The Role of IL-17 and Th17 Lymphocytes in Autoimmune Diseases) concluded that, “The identification of the new subpopulation of T helper cells producing IL-17 modified our model of the Th1–Th2 paradigm and it was named Th17. High abilities to stimulate acute and chronic inflammation made these cells an ideal candidate to be the crucial player in the development of autoimmune disorders.”  Last June’s issue of Scientific Reports (IL-17A Mediates Inflammatory and Tissue Remodeling Events in Early Human Tendinopathy) talked about the heavy-hitters of the inflammatory modulator community, saying that, “Increasingly, inflammatory mediators are considered crucial to the onset and perpetuation of tendinopathy.  Endogenous expression of TNFα, IL-1β, IL-6, IL-10, VEGF and TGFβ has been demonstrated in tenocytes.  Increased expression of IL-17A was detected in ‘early tendinopathy’ compared to both matched samples and non-matched control samples. Double immunofluoresence staining revealed IL-17A expression in leukocyte subsets including mast cells, macrophages and T cells. IL-17A treated tenocytes exhibited increased production of proinflammatory cytokines, altered matrix regulation with increased Collagen type III, and increased expression of several apoptosis related factors.”  I have said forever that Systemic Tendinosis, which we will discuss shortly, is almost always autoimmune —even though it does not have an official name because the specific auto-antigen remains unknown.
  • As I have shown you many times, inflammation always leads to fibrosis — the medical word for Scar Tissue (HERE).  Thus, when last November’s issue of Arthritis Research and Therapy (Profibrotic Mediators in Tendon Disease: A Systematic Review) started talking about fibrosis in tendinopathies, I was interested.  Their conclusions; “Tendon disease is characterized by the development of fibrosis,” were not surprising as we were already aware of this.  The fact that the authors linked any number of inflammatory mediators to the process was, however, interesting.  Especially considering that for decades this was believed not to be the case.  Be aware that the progression of virtually all disease, tendinopathies included, is Inflammation, Fibrosis, Degeneration (REPEAT).

Again, the questions we’ll answer at the end of the post; does it matter, and what can we do about this other than simply prescribe more drugs to MOP UP the inflammation rather than shutting off the Systemic Inflammation at its source?


Further evidence that inflammation is involved in tendinopathies comes in the form of just how many studies are talking not only about inflammatory markers, but about the numerous inflammatory comorbidites (concurrent diseases caused by inflammation — HERE is a list of some of them) that are commonly found in folks struggling with tendinosis.  In other words, if you are fighting tendinosis, your chances of having some serious health issues, CANCER INCLUDED, go up dramatically.

  • SHOULDER ARTHRITIS AND TENDINOSIS:  The suffix “itis” lets you know that something is inflammatory as it is the Latin term for inflammation.  A recent study from PLoS One (TREM-1, HMGB1 and RAGE in the Shoulder Tendon: Dual Mechanisms for Inflammation Based on the Coincidence of Glenohumeral Arthritis) revealed that, “Rotator cuff injury is a major disorder in the adult population where inflammation and pain are contributing factors. Coincidence of other clinical conditions like glenohumeral arthritis aggravates inflammation and delays the healing response.  The principal findings in this study reveal significant expression of TREM-1, RAGE and HMGB1 in the shoulder tendon tissue with respect to severity of glenohumeral arthritis.”  As you might suspect, these substances are yet other inflammatory biomarkers / mediators that we have not discussed previously.
  • DIABETES AND TENDINOSIS:  March’s issue of Scientific Reports stated that, “People with diabetes are susceptible to tendinopathy and tendon rupture. Diabetic tendons are characterized by weaker mechanical properties than non-diabetic tendons, including lower stiffness, maximum load, Young’s modulus, and strain at break point. Tendons are mainly composed of highly organized collagen fibers as well as various minor structural molecules, such as proteoglycans and glycoproteins. In tendons, tenocyte is the fundamental cell population responsible for maintaining tissue homeostasis, and loss of its genetic traits can cause tendon dysfunction.”  The same month the cancer journal Oncotarget concluded, “Patients with diabetes are at great risk to suffer many musculoskeletal disorders, such as tendinopathy, tendon rupture and impaired tendon healing.  In this study, we found that high glucose could inhibit cell proliferation and induce cell apoptosis of TDSCs (tendon-derived stem cells) in vitro. The tenogenic differentiation ability of TDSCs was decreased in the initial stage in vitro. All these findings proved our hypothesis and accounted for the potential pathogenesis of diabetic tendon disorders including diabetic tendinopathy, tendon rupture and impaired tendon healing.” By the way, most of this is not really new information.
  • NEUROPATHY AND TENDINOSIS:  While certainly not the only reason for neuropathic pain, DIABETES is by far the most common.  February’s British Journal of Pain concluded that, “This study suggests that neuropathic pain as identified by the painDETECT questionnaire may be common in patients with chronic lower limb tendinopathy conditions.  28% of respondents scored 19 or higher with painDETECT (neuropathic component to pain likely), 29% scored 13-18 (equivocal result).” 
  • HEART DISEASE AND TENDINOPATHY:   February’s issue of the Journal of Occupational and Environmental Medicine (Association Between Cardiovascular Disease Risk Factors and Rotator Cuff Tendinopathy: A Cross-Sectional Study) revealed that, “Recent evidence has found potential associations between cardiovascular disease (CVD) risk factors and common musculoskeletal disorders.  A strong association was observed between CVD risk scores and both glenohumeral joint pain and rotator cuff tendinopathy. The results show a dose-response trend of increasing risk.  Individual risk factors were associated with both outcomes. Combined, CVD risk factors demonstrated a strong correlation with glenohumeral joint pain and an even stronger correlation with rotator cuff tendinopathy. Results suggest a potentially modifiable disease mechanism.”  I’ve talked about this particular link before HERE).
  • DYSBIOSIS AND/OR INFECTIONS CAUSE TENDON RUPTURE?  We know that virtually all forms of DYSBIOSIS and INFECTION are inflammatory.  March’s copy of The American Journal of Sports Medicine (Presence of Bacteria in Spontaneous Achilles Tendon Ruptures) showed that, “The structural pathology of Achilles tendon (AT) ruptures resembles tendinopathy.  Recently, a number of diseases were found to be attributed to bacterial infections, resulting in low-grade inflammation and progressive matrix disturbance [fibrosis / scar tissue].  AT rupture samples exhibited histopathological features characteristic of tendinopathy, and most healthy hamstring tendon samples displayed normal tendon features.  The authors have demonstrated the presence of bacterial DNA in ruptured AT samples.”  You need to be aware that not only is sugar one of the most inflammatory things you can consume (HERE), but that it actually feeds both dysbiosis and infection (HERE).
  • OBESITY AND TENDINOSIS:  What do we know about OBESITY?  Only that it is one of the chief of the myriad of inflammatory conditions.  One of last year’s copies of Advances in Experimental Medicine and Biology (How Obesity Affects Tendons?) had this to say on the subject.  “Several epidemiological and clinical observations have definitely demonstrated that obesity has harmful effects on tendons.”  Notice, however, that this is not simply a “weight” issue. “In addition to overload, attributable to the increased body weight, which significantly affects load-bearing tendons, systemic factors play a relevant role. Several bioactive peptides (chemerin, leptin, adiponectin and others) are released by adipocytes, and influence tendon structure by means of negative activities on mesenchymal cells.”  This is very similar to what we saw in THIS POST where I showed you how adipose tissue becomes it’s own endocrine gland. “The ensuing systemic state of chronic, sub-clinicical, low-grade inflammation can damage tendon structure. Metabolic disorders (diabetes, impaired glucose tolerance, and dislipidemia), frequently associated with visceral adiposity [BELLY FAT], are concurrent pathogenetic factors. Indeed, high glucose levels increase the formation of Advanced Glycation End-products, which in turn form stable covalent cross-links within collagen fibers, modifying their structure and functionality.”  We are warned all the time about AGES from grilled foods, when the biggest form of AGES comes from inflammatory sugar.


Here are a few of the tidbits gleaned from recent peer-review (mainstream journals, one and all), showing what’s being studied and contemplated as far as solving tendon issues are concerned.

  • PRP IS A MICROBIOME THING:  There are lots of studies on PRP INJECTIONS for tendinosis, some saying it works, just as many saying not so much.  Interestingly, a new study from March’s issue of Acta Orthopedica (Effect of Platelet-Rich Plasma on Rat Achilles Tendon Healing is Related to Microbiota) concluded — as might be imagined from the study’s title — that, “In 3 papers in Acta Orthopaedica 10 years ago, we described that platelet-rich plasma (PRP) improves tendon healing in a rat Achilles transection model. Later, we found that microtrauma has similar effects, probably acting via inflammation.”  This is exactly why potentially “HARSH” methods such as TISSUE REMODELING have merit, and why GUT HEALTH is so blamed critical to truly solve your issue.  BTW, the authors concluded that rats with Staph (not an active infection but as part of their normal MICROBIOME) actually healed better than those without.
  • LOW LEVEL LASER THERAPY IS HELPFUL FOR TENDINOSIS: This month’s issue of the Dutch / German journal Zeitschrift für Rheumatologie (Low Level Laser Therapy : A Narrative Literature Review on the Efficacy in the Treatment of Rheumatic Orthopaedic Conditions) concluded that, “While earlier studies often failed to demonstrate the efficacy of LLLT, several recent studies of increasing quality proved the efficacy of LLLT in the treatment of multiple musculoskeletal pain syndromes like neck or lower back pain, tendinopathies (especially of the Achilles tendon) and epicondylolpathies, chronic inflammatory joint disorders like rheumatoid arthritis or chronic degenerative osteoarthritis of the large and small joints. In addition, there is recent evidence that LLLT can have a preventive capacity and can enhance muscle strength and accelerate muscle regeneration.  LLLT shows potential as an effective, noninvasive, safe and cost-efficient means to treat and prevent a variety of acute and chronic musculoskeletal conditions.”  Interested in my LOW LEVEL LASER THERAPY posts?  Just click the link.
  • TREATING TENDINOPATHIES WITH SUPPLEMENTS:  A group of six Italian orthopedists published a study in a 2016 copy of Muscles, Ligaments, and Tendons called Nutraceutical Supplement in the Management of Tendinopathies: A Systematic Review, in which they looked at 46 studies concerning the popular joint supplements glucosamine and chondroitin sulphate, vitamin C, hydrolazed type 1 collagen, arginine alpha-keto-glutarate, bromelain, curcumin, boswellic acid, and methil-sulfonil-methane.  The authors concluded that, “In the last years, the increase of sport activities, life expectancy, and other factors such as environment, diet, systemic diseases and some drug therapies have led to a rise in the incidence of tendinopathies.  Nutraceuticals are not only used in the general population, but also in athletes.  Preclinical results are very encouraging…”  As noted in this paper, certain drugs (THESE ANTIBIOTICS ARE THE MOST DANGEROUS AND BRUTAL) actually cause inflammation.  And once again we see that Systemic Inflammation / Systemic Disease is a big deal.
  • INJECTING TENDONS WITH VARIOUS HORMONES CAUSES?  There are tons of studies on DRY NEEDLING techniques, with most of them showing promise for tendinopathies and similar musculoskeletal issues.  A study from the February issue of Muscles, Ligaments, and Tendons (Therapeutic Use of Hormones on Tendinopathies: A Narrative Review) looked at the efficacy of injecting various hormones (ESTROGEN, TESTOSTERONE, THYROID, etc, etc) directly into tendons.  Conclusions?  “At present, experimental studies and preliminary observations in humans suggest that parathyroid and growth hormones, locally administered, are promising therapeutic tools in specific tendon disorders. Local injections of glucocorticoids are useful in several tendinopathies, exploiting their anti-inflammatory and anti-proliferative properties, but carry the risk of further tendon degeneration and ruptures, due to the detrimental direct effect of glucocorticoids on the tendon structure.”  Speaking of glucocorticoid (corticosteriods and cortisone) risks………..

We’ve repeatedly seen that tendinopathy accounts for about 1/3 of the visits to the doctor’s office in people going in with musculoskeletal issues.  And while there are a few cutting-edge doctors and clinics out there that are using these and other not-quite-mainstream treatment methods, the standard medical fare for tendinosis is still anti-inflammation medication —- CORTICOSTEROIDS and NSAIDS.  I have shown you study after study and textbook after MEDICAL TEXTBOOK that say in various ways just how bad these drugs are as far as fouling the healing process is concerned.  Here are a couple more (I could have given you dozens, if not hundreds).

  • NSAIDS EFFECTS ON TENDON HEALING:  Two medical doctors (one a Ph.D as well) wrote a well-bibbed article (48 sources) for Rhematology Network called Do NSAIDs Impair Healing of Musculoskeletal Injuries?NSAIDs are among the most frequently used and prescribed medications in the management of musculoskeletal pain and injury. Many physicians consider them to be the medication of choice.  However, a number of studies have questioned the value of NSAIDs in the healing process of bone, muscle, tendon, and ligament injuries. Studies have demonstrated that prostaglandins and leukotrienes are produced during the acute phase of a tendon injury… In the first few days after acute tendon injury, there is an initial inflammatory phase and entry of inflammatory cells into the injury site.  There appears to be little role for NSAIDs outside of the initial symptomatic pain relief during the first few days after injury.”  This is an interesting paper because while actually acknowledging PGE2, LEKOTRIENES, and other inflammatory mediators, the authors are not high on the long-term effects of blocking these mediators we refer to as “inflammation”.
  • INJECTING TENDONS / JOINTS WITH STEROIDS: Listen folks; I’ve only shown you about a hundred times how bad this stuff is over the long haul.  Here’s one more for those who may have missed the rest.  December’s Expert Opinion on Drug Safety (Clinical Benefits and Drawbacks of Local Corticosteroid Injections in Tendinopathies) showed us yet again that the short-term relief sometimes provided by corticosteroids is not worth the long term grief.  “Local glucocorticoids injections are widely administered for the treatment of tendinopathies. positive results have been observed in some tendinopathies but not in others. moreover, worsening of symptoms, and even spontaneous tendon ruptures has been reported. Several experimental studies suggest that the direct action of glucocorticoids on tendons is detrimental. Loss of collagen organization, impaired viability of fibroblasts, depletion of stem cells pool, and reduced mechanical properties have been observed.”   How about boosting COLLAGEN production and FIBROBLASTIC ACTIVITY instead of suppressing it!  This bullet helps explain why I’ve repeatedly argued that that IMMUNE SYSTEM SUPPRESSION is America’s number one form of medical treatment.


Have you ever been so far behind you thought you were in the lead?  For decades, the research side of the medical community told us that TENDINOSIS is not an inflammatory condition — it’s purely mechanical (fibrosis).  Since most docs never got that memo — continuing to treat with their usual array of drugs — the fact that the science has changed yet again didn’t affect them one iota.  But what does this information mean to you, the individual struggling with tendinosis, who does not want the drugs? 

It means that as I just showed you, the “alternatives” are every bit as effective as mainstream care (drugs, chiefly steroids and NSAIDS).  And while inflammation is certain a factor in tendinosis, addressing the inflammation (the “itis“) without addressing the fibrotic changes (the “osis“) is just as ineffective today as it was yesterday, last week, last year, or back in the 20th century.  Sure, I want you to deal with the inflammation. 

What you have to remember, however, is that the local inflammation is a critical part of the healing process (HERE).  It’s the SYSTEMIC INFLAMMATION that must be addressed, and unfortunately, you can’t take care of this kind of inflammation with a pill, potion, or lotion.  Remember the last part of the last sentence of the very first bullet point of this post that I said I would come back to? Local inflammation is probably not your problem —- it’s the presence of systemic inflammation associated with chronic diseases that is making your tendon train go off the rails in so many different ways.

What you need to do is deal with underlying systemic inflammation like you would for any other inflammatory problem (HERE) — after all, study after study (as I showed you again today) reveals just how inter-related these disease processes really are.  That’s why they refer to these as “comorbidites” (Co = “along with or beside; concurrent” and Morbidity = “illness or sickness“). 

A failure to address the systemic inflammation means that you will probably be repeating the whole tendinopathy thing over and over again along with at least some of THESE DISEASES.  However, address the systemic inflammation successfully and you end up taking care of any number of “comorbidites”.  HERE’S a really cool example of someone who addressed a handful at the same time.

As for treating tendinosis in my clinic, this information doesn’t really change anything I’ll be doing other than warning people about the relationship between diet / lifestyle and their chronic pain by handing out more copies of my CLINIC’S “ONLINE” WEB CHECKLIST.  In other words, it’s not like this information completely snuck up on me — I’ve been increasingly talking about the role of inflammation in tendinopathy for awhile now (HERE and HERE). 

And for those of you struggling with SYSTEMIC TENDINOSIS (not the stuff caused by fluoroquinolone antibiotics such as Cipro), I have plenty of info for you as well.  Not surprisingly, I have always maintained that it’s largely an autoimmune issue driven by — you guessed it — inflammation.  And truthfully, if you swapped out the word FASCIA for tendon in this post, it would probably all still be true.

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