Sesamoiditis is inflammation of the sesamoid bones. Humans
Sesamoiditis occurs on the bottom of the foot, just behind the big toe. There are normally two sesamoid bones on each foot; sometimes sesamoids can be bipartite, which means they each comprise two separate pieces. The sesamoids are roughly the size of jelly beans. The sesamoid bones act as a fulcrum for the flexor tendons, the tendons which bend the big toe downward. Symptoms include inflammation and pain. Sometimes a sesamoid bone is fractured. This can be difficult to pick up on X-ray, so a bone scan or MRI is a better alternative.Among those who are susceptible to the malady are dancers, catchers and pitchers in baseball, soccer players, and football players. Horses
In the horse it occurs at the horses fetlock. The sesamoid bones lie behind the bones of the fetlock, at the back of the joint, and help to keep the tendons and ligaments that run between them correctly functioning. Usually periostitis (new bone growth) occurs along with sesamoiditis, and the suspensory ligament may also be affected. Sesamoiditis results in inflammation, pain, and eventually bone growth. Causes
In humans, excessive forces caused by sudden bending upwards of the big toe, high heels, or a stumble can contribute to sesamoiditis. Once the sesamoid bone is injured it can be very difficult to cure, because additional pressure is put on the sesamoid bone during walking.
All pathways culminate in the production of a C3 convertase, which catalyses C3 into its constitutive parts (better detailed here – classical complement pathway).In brief, the crucial role of C1q in the pathway is its importance as the first protein to start the complement cascade (which ends in the destruction of the invading bacteria or virus), and its ability to link the two important arms of the immune system – the innate immune system: a broad defence system; and the adaptive immune system: the strong immune response capable of remembering previous infections, allowing fast response against recurrent infections, meaning that people with a normal immune system dont continually catch the same cold or same strain of flu repeatedly.Case studies of individuals with HUV have also highlighted other potential complicating factors which it seems the anti-C1q antibodies play a role in. This can mean in some cases the deposition of large immune complexes in the kidney which cannot be cleared by the usual cells of the immune system (e.g. macrophages which are unable to bind the Fc portion of the C1q antibody), leading to further complications. This seems to be rare, but can occur when a pre-existing renal condition is apparent. Also, there has been some speculation as to an additional autoantibody against an inhibitor protein (in the complement pathway) named C1-inhibitor. The inhibition of C1-inhibitor leads to over-activation of the complement pathway and one protein that builds up controls angioedema (vessel – swelling), resulting in excess water building up under the skin (the weal appearance).