Tag Archives: Achilles tendinopathy

The Great Toe

When you think of the most common lower body injuries, you think ankle sprains, shin splints, runner’s knee, jumper’s knee, fasciitis, or Achilles tendinitis. When you have these injuries, you treat the injured area. We might be overlooking a little, but big deal.  Dysfunction in the big toe influences every step you take, every lunge, every jump, and every stride of every run. Ultimately, it can be a direct result in many of the aforementioned common lower body injuries. If you have dysfunction (pain, instability, or hypomobility) at the first big toe joint (MTP joint), it could wreak havoc on the entire kinetic chain.

Normal range of motion of the big toe is 40° flexion, 80-90° extension, and 10-20° abduction and adduction. Lack of motion, especially extension, will create compensatory movement at other joints. Common big toe issues such as, hallux valgus (bunion), hallux rigidus, turf toe, sesamoiditis, and gout will limit toe mobility. Below is an image of a client who demonstrates normal range or motion on the right and limited toe extension on the left.

N ROM   Limited ROM

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Causes and Treatment of Achilles Tendinopathy

Overview and etiology:

Pain and injury to the Achilles tendon is often thought to be a result of inflammation.

Pain and injury to the Achilles tendon is often thought to be a result of inflammation.

The term “tendinitis” or any [insert any body part] with “itis” is tossed around as if it is the only possible cause for musculoskeletal pain. However, the “itis” is not really true. A tendon, specifically the Achilles tendon, is not really inflamed, rather it is deranged (tendiopathic / tendinopathy). In January 2013 the Annals of Human Genetics published an article that demonstrated Achilles Tendinopathy is associated with gene polymorphism (Abrahams, et al., 2013). COL51A is a gene that encodes the development and organization of Type V collagen. This collagen can be found in ligaments, tendons, and connective tissue. COL51A plays an integral role in development and maintenance of connective tissue. Abrahams, et al. (2013) demonstrated that polymorphisms occur in the COL51A gene causing altered structure of collagen resulting in tendinopathy.

The tendon may become fusiform or thickened, but it is due to cellular derangement rather than inflammation. Kannus and Jozsa in a controlled study of 891 patients with Achilles tendon rupture found that 97% of patients had degenerative changes in the ruptured tendon. The study also found that 34% of asymptomatic tendons also had degenerative changes (2) Continue reading