FOOT AND ANKLE

CALCANEUS

Sever, in 1912, emphasized irregularity of the secondary calcaneal ossification centers and hypothesized that this change was due to apophysitis in this region producing pain and tenderness of the heel. In 1948, it was proposed that this condition was normal variation completely unrelated to the painful heels of adolescence. Current thought concludes that fragmentation and sclerosis of the secondary ossification center of the calcaneus can be entirely normal and is the result of proper weight bearing. Often times, soft tissue irritation at the Achilles' tendon insertion site of the calcaneal tuberosity is the site of the patient's pain and tenderness with can be elicited with careful clinical correlation. Though, radiographically, the sever's phenomenon may be clinically insignificant, it is often mistaken for a fracture.

NAVICULAR

In 1908, Kohler described a self limited condition of the tarsal navicular characterized by flattening, sclerosis and irregularity. The predominant theory of the pathogenesis is vascular insufficiency, however, normal or altered ossification may be impossible to distinguish from true Kohler's disease. Kohler's disease is more frequent in boys approximately three to seven years of age and is most commonly unilateral. Clinically, manifestations can be quite mild consisting of pain, tenderness, swelling, and decreased range of motion. Sometimes trauma can be elicited in the history. Radiographs demonstrate patchy increase in density and fragmentation with multiple ossific nuclei. Soft tissue swelling can be evident and over time the bone is diminished in size and may have a wafer-like appearance. Joint space narrowing in this region is not present. Typically over a period of two to four years the bone regains its normal size and shape consistent with its self limited and reversible nature. This has increased the speculation that this "disease" is really an altered sequence of tarsal ossification. Because of the great overlap between normal variation in ossification and true Kohler's disease, the following criteria must be used to establish a presence of Kohler's disease: changes are detected in previously normal navicular bone, alterations must be compatible with osteonecrosis, and clinical manifestations should be present. Kohler's disease may have a mechanical basis with the location of the tarsal navicular at the apex of the longitudinal arch which may lead to increased forces on this bone during normal locomotion. Compression forces could occlude vessels in the spongiosa of the bone producing osteonecrosis.