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Do You Really Have Tendonitis - Or Is It Tendonosis?
By Owen Anderson, Ph. D.
Posted: May 13, 2005
The Two Conditions Have Quite-Different Recovery Processes
Tendonitis has a tenacious grip on the sports world. At least 25 percent of athletes treated for knee problems at major sports clinics are typically diagnosed with tendonitis (1), and 40 percent of competitive tennis players are thought to suffer from some form of elbow tendonitis (2). In the world of running, as many as 30 to 50 percent of all endurance runners experience tendonitis during a typical training year (3). Tendon injuries are among the most common "overuse" injuries - maladies which occur when an athlete's body is unable to adequately repair the insults it receives during strenuous or prolonged workouts (4).
Why are tendons such easy prey for the injury bug? Because tendons are constructed of strong, parallel, tightly packed bundles of a unique protein called collagen, tendons are rather stout structures, but they must transmit forces from muscle to bone and are thus subject to powerful tensile stresses. In addition, the linear arrangement of collagen fibers means that tendons resist shearing (side-to-side and/or rotational) forces rather poorly; such forces are a natural part of sporting activity, even during such "linear" sports as endurance running. Tendons are also not noted for their recovery prowess; although not as balky as the cartilage covers on the ends of bones or the cartilaginous pads which cushion the knees, tendons can take several days to mobilize the repair process fully after a damaging workout - days during which another red-hot training session may further aggravate the collagen bundles.
Of course, the majority of athletes who are part of the tendonitis plague take what are considered to be the appropriate steps to alleviate their problems. They ice, they stretch, they take their anti-inflammatory medications, and they attempt to strengthen the hurting areas; some athletes are even daring enough to take a short rest from their usual activities! There is just one little problem, however: There is strong evidence that the majority of athletes diagnosed with tendonitis are not really suffering from the disorder. In effect, they are treating something which does not exist.
Tendonitis, you see, is an inflammation of a tendon and/or the tendon's attachment point with a muscle, with characteristic white blood cells swarming through the red-hot tendon and leaky blood vessels infiltrating the tendonous area. And that's the problem: Most athletes diagnosed with tendonitis do not have these inflammatory reactions going on.
We know this because there have been 14 different studies carried out with human subjects in which the pathology of apparent "tendonitis" injuries was investigated by means of examination of biopsied tendon material. As Drs. Louis Almekinders and John Temple point out in a fascinating review article (5), almost all of these investigations have failed to find any inflammatory processes taking place in the examined tendons; what have been found instead are tendons undergoing degeneration (actual breakdowns and increased disorder of the collagen fibers), without inflammation. In other words, the "tendonitis plague" may actually be a severe outbreak of tendonosis, not tendonitis. Tendonosis is a degenerative problem in a tendon, not an inflammatory disorder.
So what, you might say? Why does the name we attach to a tendon problem make a difference, if the treatment is the same? And there is the hitch: The treatments for tendonitis and tendonosis are quite different. For example, a reasonable course of therapy for tendonitis, an inflammatory condition, would involve the use of anti-inflammatory drugs; in fact, non-steroidal anti-inflammatory medications have become the mainstay of treatment for so-called "overuse" injuries to tendons. The trouble is that there is evidence that anti-inflammatory drugs can actually have a negative impact on the progress of tendonosis, in effect retarding the healing process.
In ingenious research carried out at the University of North Carolina School of Medicine, Dr. Almekinders, along with Lynette Bracey and Dr. Albert Baynes, extracted human-tendon fibroblasts (the cells which actually produce collagen fibers) from the cores of normal tendons of individuals who were about to undergo surgery (6). These fibroblasts were then cultured in the laboratory and divided into four groups: (I) Control fibroblasts, which were not treated with anti-inflammatory medication and which were not subject to any repetitive strain, (II) Strain fibroblasts, subject to repetitive motion at 25 percent of maximal strain but exposed to no anti-inflammatory meds, (III) Strain-Med fibroblasts, subject to the same strain as group 2, along with 25 micromoles per liter of an anti-inflammatory medication called indomethacin, and (IV) Med fibroblasts, under no strain but getting the indomethacin. After 72 hours, the medium surrounding about 60 percent of the fibroblasts from each group was transferred and mixed with human macrophages (large white blood cells which are present in inflamed tissues). This transfer was accomplished to determine whether the presence of inflammatory cells (such as the macrophages) would alter the response of the fibroblasts to repetitive motion and strain. After 24 hours of macrophage contact, the medium was transferred back to the tendon fibroblasts for 12 final hours.
Interestingly enough, the synthesis of DNA (the chemical from which genes are made) was significantly elevated in Group-II fibroblasts (compared with the beginning of the experiment), and it was higher still in the Group-II fibroblasts which had been in contact with the macrophage medium. In other words, there was something about repetitive motion and strain which stimulated fibroblasts to begin making significant quantities of new DNA, presumably to provide genetic material for the new fibroblasts which would be created as part of a tendon-strengthening process. It seems clear that new-DNA creation is an adaptive response to physical stress and repeated motion. In contrast, DNA synthesis was suppressed in both of the anti-inflammatory-treated groups (III and IV from above), compared with group II. The anti-inflammatory medication acted to stop the creation of new genetic material - and presumably new tendon cells, potentially thwarting healing.
As it turned out, anti-inflammatory treatment did enhance protein synthesis in groups III & IV, compared with I & II. This would seem to be a good thing, since the protein could be used to form new collagen fibers (a process called matrix formation). However, matrix creation often occurs somewhat late in the healing process of a tendon injury, after the worst pain has subsided. In effect, an athlete using anti-inflammatory medication to control tendon pain might be likely to stop taking the medicament before its potentially positive effect (augmented protein synthesis) could be exhibited.
In addition to the directly negative effect mentioned above (the blocking of DNA production), anti-inflammatory medications have a variety of unpleasant side effects; they can be very hard on the digestive system and can increase the risk of abnormal bleeding, for example. Anti-inflammatory meds can produce a centrally induced analgesia which can make many injured athletes feel more comfortable, but they have not been proven to be effective for the treatment of tendonosis (remember that tendonosis does not involve inflammation, the condition for which anti-inflammatory drugs have been designed). Tendonosis has its own unique treatment modalities (which we will describe in a moment).
Let's return to our original contention that most tendon injuries probably represent tendonosis, rather than tendonitis. If this is really the case, it raises a legitimate question: How could so many athletes be misdiagnosed? As Almekinders and Temple point out in their review article (5), exercise scientists and physicians may not have a very good understanding of what produces tendon maladies in the first place. The traditional view in endurance sports is that tendons become injured because of "overuse" (i. e., due to repetitive, damaging strain on a tendon which exceeds its capacity for repair), leading to the development of tendonitis. To put it another way, the conventional belief is that cumulative microtrauma leads to an inflammatory reaction.
The trouble is that this reasonable-sounding scenario remains absolutely unproven, because very few prospective scientific studies have been able to demonstrate that this is what really happens. Most research concerning tendon injury is retrospective, with sports scientists looking back in time to try to figure out why the members of their study group have so many tendon problems. After gazing into the past, the researchers attribute the "tendonitis" to training errors, inappropriate shoes, anatomic predispositions, inflexibility, and so on, but there is no real evidence to back up these claims (without control subjects in these retrospective analyses, the "evidence" is very hard to interpret). In addition, the subjects in these studies may be suffering from a variety of tendon disorders, including tendonitis, tendonosis, and tenosynovitis (a distinct disorder in which the connective-tissue sheath around a tendon becomes inflamed), and the etiologies of these difficulties may be quite different.
Unfortunately, animal studies are not much help; in fact, there is no reliable animal "model" available. A difficulty which bedevils researchers is that most animals, aside from race horses, do not seem to develop tendonitis; investigations carried out with animals have failed to show that even extraordinarily repetitive use of a tendon will produce true tendon inflammation. In a classic study conducted at the Neurobiological Research Unit in Marseille, France, researchers dramatically overloaded the plantaris muscles in the legs of experimental rats by removing both the soleus and gastrocnemius muscles in both posterior appendages, leaving only the plantaris muscles to plantar-flex the poor-rats' ankles (7). Within one week after the surgery, the rats' plantaris tendons began undergoing major changes. The fibroblasts (tendon cells) increased their activity dramatically and became much larger than usual, while arranging themselves in linear columns in between existing collagen fibers (they were getting ready to "lay down" new collagen tendrils). In the junction between the tendon and muscle, the fibroblasts began to project thick processes directly into the muscle tissue. In effect, the plantaris tendons were undergoing remodeling, with old collagen fibers breaking down and new collagen being created to strengthen the tendons. There was no trace of inflammatory cells or the inflammation process in general.
The Marseille study was a good one. It helped to explain why athletes often are weaker after a very severe workout or following a period of very strenuous training (for one thing, their affected tendons may be breaking down as part of the process of tendon renewal; during this breakdown period, the tendons are less strong and less resistant to stretch). It also showed that - at least in the rat - overuse of a muscle and a tendon does not lead to tendonitis but rather to something which looks much more like tendonosis.
In yet another piece of interesting research, investigators repeatedly overloaded the Achilles tendons of rabbits. The experimental bunnies developed significant cases of tenosynovitis (inflammation in the sheaths surrounding the tendons), but there was virtually no inflammation within the Achilles tendons, i. e., there was no sign of tendonitis (8). Overall, there is little experimental evidence to support the idea that tendonitis is truly a repetitive-load, "overuse" tendon injury.
True, the real-world experiences of many endurance athletes seem to suggest that repetitive loads can induce tendonitis. Almost any runner who has developed Achilles pain, ITB syndrome, or patellar-tendon discomfort, for example, after he/she has expanded training mileage significantly can attest to that. However, in these cases it is possible that the hurting athletes are like the overworked bunnies and the French rats; there may be no tendonitis present at all, and tendonosis, tenosynovitis, or some other abnormality may be the real problem.
Almekinders also likes to point out one other unsettling fact: Although the rate of tendon malady appears to be high in athletes, many studies have shown that it is not much different from the frequency of tendon disorder in the completely sedentary population (5). If overuse is the key cause of tendon problems, why do underused tendons have about the same rate of injury as their overused cousins?
Of course, understanding what is really happening to tendons when they suddenly become painful during training is extremely important; as mentioned earlier, the appropriate course of treatment depends entirely on whether the problem is really tendonitis, tenosynovitis, or tendonosis. Ice and anti-inflammatory medications would seem to be appropriate treatments for tendonitis, although solid scientific support for these therapies is weaker than one would think. For example, there have been over 30 studies published in English in the scientific literature concerning the effects of non-steroidal anti-inflammatory medications on the outcome of tendon injuries; however, only nine of these studies included a placebo group and were prospective in nature (5). In addition, the true nature of the tendon problems was unknown; in most cases, researchers simply assumed that tendonitis was present. In effect, the anti-inflammatory medications may have been used to treat a plethora of problems. Five of the nine prospective, placebo-controlled investigations documented improved pain scores at the final follow-up in individuals taking an anti-inflammatory medication, but (and it's a big "but") the duration of the follow-up periods ranged from just seven to 28 days, and so it is unclear if there were long-term benefits associated with use of the anti-inflammatory medication. It is possible that the anti-inflammatory medicines provide some pain relief but have no positive impact (and may indeed have a negative impact) on the long-term healing process.
Physical therapy is often prescribed for tendon discomfort, and there is evidence in the scientific literature that physical therapy can be helpful in the treatment of tendon problems (physical therapists will be relieved to know this). Bear in mind, though, that there are lots of reports of the positive effects of physical therapy, but few of these accounts are prospective and actually include control groups. One controlled study found that physical therapy was useful for the treatment of supraspinatus "tendonitis" (9), compared with a laser placebo, and another investigation detected upgraded range of motion in patients suffering from shoulder tendonitis who were treated with physical therapy (10). However, note that no proof was offered that tendonitis was the real problem in either of these studies; as mentioned, an entirely different disorder may have been the primarily malady. It's possible that everyone in these investigations had not a trace of tendonitis - and that tendonosis was the aggravator.
As noted, there is no point in treating a tendonosis with anti-inflammatory medication (especially since such medication might block DNA synthesis and harm tendon healing, as in Almekinders' fibroblast study). To be on the safe side, it would seem to make sense to take a simple analgesic such as acetaminophen to control tendon pain, if necessary.
So, what should you do if one of your tendons suddenly flares up? Ice the darned thing, take acetaminophen if necessary, and reduce your activity for awhile. If the problem persists for more than two weeks, it's a reasonable bet that you have tendonosis. That's the bad news: The good news is that there are three solid treatments for tendonosis. Dr. Almekinders is in the forefront of the first treatment; he cultures blood platelets in his laboratory, extracts growth factors from the platelets, and then injects the growth factors into the damaged tendon. The growth compounds then seem to block further degeneration and appear to spur the reconstruction of the tendon. Dr. Almekinders' e-mail address is email@example.com
Noted Swedish researcher H. Alfredson and his colleagues at the University of Umea have been experimenting with a very interesting, second technique for treating tendonosis, also with excellent success. The Swedes noticed that troubled tendons seem to be excessively vascularized, i. e., they have an abnormally large number of blood vessels leading into them. At first, this was thought to be a good thing; it was felt that the extra capillaries could bring supplemental nutrients, growth factors, and oxygen to a damaged tendon, spurring recovery. However, the Swedes gradually began to realize that the expansive blood supply might in fact be stimulating too much "turnover" within the harmed tendons, in effect causing the breakdown portion of the remodeling process to be occurring at too high a rate, ultimately preventing repair of the tendon. So, the Swedes have been chemically destroying a large percentage of the blood vessels leading into hurting, damaged tendons, and the results have been outstanding. Pain relief is dramatic, and athletes treated with the technique return to close-to-normal training with surprising rapidity. The technique is called Swedish sclerotization.
The third method of treating tendonosis is a tried-and-true one, described on several occasions in the pages of Running Research News (http://www.rrnews.com). This therapy involves the deliberate, eccentric loading of a painful tendon and its muscle, a process which seems to accelerate strengthening of both the tendon and its associated sinew. A runner with Achilles tendonosis, for example, would rely on heel-drop exercises, in which the balls of the feet were placed at the edge of a step or bench and the heels were allowed to drop down suddenly to below the level of the step, with the Achilles tendons and calf muscles attempting to control such plummeting.
How about rest? Shouldn't you always treat a tendon problem with rest - until the symptoms go away? Strangely, the scientific literature is almost completely silent on this issue. While it might seem that rest would give an injured tendon an opportunity to heal, it might also give a tendon suffering from tendonosis a chance to degenerate further. In fact, it is clear that a tendon needs to be mechanically stimulated in order to begin the process of activating its fibroblasts and synthesizing significant quantities of new collagen fibers; complete rest would prevent this from happening (recall Almekinders' study in which the fibroblasts which were subject to strain were the ones which hiked DNA synthesis, as long as they were not exposed to anti-inflammatory medication). Thus, it is probably good to carry out reasonable numbers of eccentric exercises for a calling-out tendon, pain permitting, as soon as it is possible to do so.
Of course, before you get too carried away and start booking your flights to Raleigh-Durham or Umea, make sure that you really do have a tendon problem; bear in mind that other conditions may masquerade as tendon difficulties. An arch strain, for example, might disguise itself as a case of tibialis posterior tendonitis, and what appears to be a chronic, non-tractable Achilles-tendon problem might actually be nothing more than retrocalcaneal bursitis. If you are a serious athlete, it is important to have an extremely wise, skilled, sports-medicine physician who can make the right diagnosis and recommend the proper treatment.
It's now time for our final apothegm? Have you been plagued by "tendonitis" for a long time? One reason that your plague might be continuing is that your malady might not be tendonitis - you could have tendonosis, which is not well treated by the conventional therapies for tendonitis. Almekinders' growth factors, the Swedes' blood-vessel sclerosis, or systematic eccentric exercise might be what you really need to remove yourself from the ranks of "tendonitis" victims. ?
(1) "Knee Injuries in Athletes: Review of Exertion Injuries and Retrospective Study of Outpatients Sports Clinic Material," Sports Medicine, Vol. 3, p. 447, 1986
(2) "An Epidemiologic Study of Tennis Elbow: Incidence, Recurrence, and Effectiveness of Prevention Strategies," American Journal of Sports Medicine, Vol. 7, pp. 234-238, 1979
(3) "Sports Traumatology Today: A Review of Common Current Sports Injury Problems," Ann. Chir. Gynaecol., Vol. 80, pp. 81-93, 1991
(4) "Tendons - A Source of Major Concern in Competitive and Recreational Athletes," Scandinavian Journal of Medicine and Science in Sports, Vol. 7, pp. 53-54, 1997
(5) "Etiology, Diagnosis, and Treatment of Tendonitis: An Analysis of the Literature," Medicine and Science in Sports and Exercise, Vol. 30(8), pp. 1183-1190, 1998
(6) "An In Vitro Investigation into the Effects of Repetitive Motion and Nonsteroidal Antiinflammatory Medication on Human Tendon Fibroblasts," The American Journal of Sports Medicine, Vol. 23(1), pp. 119-123, 1995
(7) "Tendon and Myo-Tendinous Junction in an Overloaded Skeletal Muscle of the Rat," Anatomy and Embryology, Vol. 179, pp. 89-96, 1988
(8) "Chronic Achilles Paratenonitis with Tendinosis: An Experimental Model in the Rabbit," Journal of Orthopaedic Research, Vol. 8, pp. 541-547, 1990
(9) "Arthroscopic Surgery Compared with Supervised Exercises in Patients with Rotator Cuff Disease (Stage II Impingement)," British Medical Journal, Vol. 307, pp. 899-903, 1993
(10) "Periarthritis of the Shoulder: A Controlled Clinical Trial of Physiotherapy," Physiotherapy, Vol. 59, pp. 312-315, 1973
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