Theories about tendon disorders in athletes
Physical Therapy in Branson for Tendonitis
Sports injuries command a lot of attention in the orthopedic world. Keeping athletes in tip top shape and in playing or competitive mode is a top priority for sports medicine specialists. Toward that end, researchers are trying to understand what causes tendon problems (called tendinopathies) in this group of individuals. If we can understand how and why tendon disorders develop, then maybe we can prevent them from occurring in the first place. The authors of this review article on tendinopathies offer some perspective on how these injuries occur and what can be done to prevent them as well as how to manage tendon disorders when they do occur.
Research has clearly shown that chronic overuse tendon disorders affecting the knee (patellar tendon), ankle (Achilles tendon), shoulder (rotator cuff), and thigh (adductor tendons) are common. In the past, it was assumed that these were acute, inflammatory injuries. But studies of cells from the affected areas show minimal or no inflammation. That's not to say there aren't changes seen. But these changes are at the cellular level and point more to what is now referred to as a failed healing response.
There may be an inflammatory response at first but it doesn't last. Instead, the local cells expand and the individual collagen fibers start to spread out. Exactly why this failed healing response happens or even why it leads to tendon problems remains a mystery. Some experts have wondered why tendons don't hold up under stress and strain -- after all, that's what they are built for. But evidently, the design of most tendons isn't meant for repeated loading as occurs with competitive athletes who practice daily and perform or compete regularly. The tendons are exposed to more load or mechanical overload than they can handle.
That's the extent of what we know about the cause and underlying pathology of tendon injuries. From here on, it's just theory about what might be happening. In the mechanical theory of tendinopathy, the tendon gets weak after too much load over too much time. At first, it's a problem at the microscopic level, but with repetitive microtrauma, eventually repeated stress causes enough tendon breakdown to result in painful symptoms. There really isn't a single event or specific injury -- it's more of an accumulation of tiny traumas occurring over and over.
There are some problems with this theory. For one thing, soft tissues and bone normally respond to stress by building up of the tissues, resulting in a strengthening of the muscle or bone. So, why don't the ligaments respond the same way? Perhaps it's because the ligaments don't have a rich blood supply naturally. Heavy training or overload might compress the tendon, cutting off blood supply even more. This is called the vascular insufficiency theory.
Here again, there are some holes in this theory. Microscopic examination of the tendons has shown an even and full blood supply even in tendons exhibiting tendinopathies. There just isn't enough evidence to show there's a loss of blood supply to the area so this theory hasn't been confirmed. Okay, then -- maybe all that exercise is creating a local heat response in the tissues. This is the exercise-induced localized hyperthermia theory. The theory suggests it's not so much a lack of blood supply to the cells as it is too much heat building up inside the tissues and threatening tenocyte (tendon cell) survival.
Two more theories of how and why tendinopathies develop include the neural theory and the underuse theory. The neural theory proposes that the nervous system is somehow at the center of these injuries. A finger has been pointed to the role of pain-producing chemicals such as substance P, glutamate, and calcitonin gene-related peptide. Each of these substances has been found in higher levels than normal in affected tendons. But the fact that not everyone with tendinopathy has pain leaves scientists scratching their heads and going back to the drawing board over this theory.
The underuse theory suggests that there are some tenocytes that don't get stimulated enough and remain underdeveloped. That idea might not make sense at first when we are talking about overuse or overloading injuries in athletes. But a closer look at where in the tendon the problem is developing has suggested that not all tendinopathies affect the same area. Some disorders appear to affect the main body of the tendon, while others occur where the tendon inserts into the bone. Tendon insertion is called the enthesis or the osteotendinous junction. Stimulation may differ depending on the type of activity involved in each sport. For example, soccer players seem to be at increased risk for Achilles and patellar tendon injuries. Is this because of functional overload or underload?
Whatever theory proves right in the end, a few risk factors have been identified. Older age, gender (female) with hormonal links, and decreased joint motion and tendon/muscular flexibility seem to contribute to the problem. Achilles tendon ruptures have been reported with the use of a particular family of antibiotics (the quinolones) and with prolonged use of steroids. Running or training on concrete surfaces will also increase the risk of tendon problems, especially of the patellar (knee) tendon. Being aware of risk factors and reducing or eliminating as many as possible may be able to prevent the start of tendinopathies. If a tendon injury does occur, preventing a recurrence is also important.
That leaves us with one final area to review: the management of tendinopathies. Since we don't exactly know what's going on, the first approach in caring for the individual with tendinopathy is to control the pain. Conservative measures have been tried such as taping, rest, exercise, cold packs, and nonsteroidal antiinflammatory drugs (NSAIDs) with varying success. Correcting any training errors and flexibility or biomechanical problems is advised.
Exercise is quickly becoming a central focus of rehab for tendinopathies. Researchers have been able to show that eccentric muscle contractions seem to help normalize tendons. With eccentric exercise, the affected body part is moved through a range of motion that begins with the at-risk tendon fully contracted and under some load. The muscle is slowly lengthened back to its normal resting position.
The best example of this is eccentric loading of the gastrocnemius (calf) muscle. The patient stands on a stair (facing the stair as if going up stairs) with just the toes in contact with the stair. From a position up on raised toes (shortened or contracted calf muscle), the person slowly lowers the heel down past the edge of the stair. The knee is kept straight throughout the first set of exercises. The exercise is repeated keeping the knee bent throughout the raising and lowering motion.
Surgery remains a last resort when all attempts at nonoperative care have failed. Almost one-third of all patients with chronic tendinopathies end up having surgery. This is true despite the fact that there is no evidence to support this approach or show which surgical procedure works best. Surgical options include removing scar tissue and adhesions, repairing tendon tears, removing areas of obvious tendon degeneration, and tenotomy (cutting the tendon). If a large portion of the tendon is removed, it may be necessary to transfer a tendon from some other area of the body to the affected site. Surgical options vary according to which tendon is the problem.
When it's all said and done, the athlete may or may not achieve healing or full recovery. Strength may still be limited. As a result, scientists are turning their attention to other types of treatment. In the future, it may be possible to fully repair tendons with growth factors or stem cells. Finding ways to manipulate the biologic process of healing at the cellular level may be our only hope of complete regeneration of damaged tendons.
Reference: Jonathan D. Rees, MSc,MRCP (UK), FFSEM (UK), et al. Management of Tendinopathy. In The American Journal of Sports Medicine. September 2009. Vol. 37. No. 9. Pp. 1855-1867.