Its proposed pathogenesis is the following:
It begins with an inciting event at the level of the vasculature, probably the endothelium. The inciting event is yet to be elucidated, but may be a viral agent, oxidative stress, or autoimmune. Endothelial cell damage and apoptosis ensue, leading to the vascular leakiness that manifests in early clinical stages as tissue oedema. At this stage, it is predominantly a Th1- and Th17-mediated disease. After this, the vasculature is further compromised by impaired angiogenesis and impaired vasculogenesis (fewer endothelial progenitor cells), likely related to the presence of antiendothelinal cell antibodies (AECA). Despite this impaired angiogenesis, elevated levels of pro-angiogenic growth factors such as PDGF and VEGF is often seen in persons with the condition. The balance of vasodilation and vasoconstriction becomes askew, and the net result is vasoconstriction. The damaged endothelium then serves as a point of origin for blood-clot formation and further contributes to ischaemia-reperfusion injury and the generation of reactive oxygen species. These later stages are characterised by Th2 polarity. The damaged endothelium upregulates adhesion molecules and chemokines to attract leucocytes, which enables the development of innate and adaptive immune responses, including loss of tolerance to various oxidised antigens, which includes topoisomerase I. B cells mature into plasma cells, which furthers the autoimmune component of the condition. T cells differentiate into subsets, including Th2 cells, which play a vital role in tissue fibrosis. Anti–topoisomerase 1 antibodies, in turn, stimulate type I interferon production. Fibroblasts are recruited and activated by multiple cytokines and growth factors to generate myofibroblasts.
Pes anserinus ("goose foot") refers to the conjoined tendons of three muscles of the thigh. It inserts onto the anteromedial (front and inside) surface of the proximal tibia. The muscles are the sartorius, gracilis and semitendinosus sometimes referred to as the guy ropes. The name "goose foot" arises from the three-pronged manner in which the conjoined tendon inserts onto the tibia. Structure
The three tendons, from front to back, that conjoin to form the pes anserinus come from the sartorius muscle, the gracilis muscle, and the semitendinosus muscle. It inserts onto the proximal anteromedial surface of the tibia.The pes anserinus is around 5 cm below the medial tibial joint line. It lies superficial to the tibial insertion of the medial collateral ligament of the knee. Clinical significance
Pes anserine bursitis is a cause of chronic knee pain and weakness. It occurs when the medial portion of the knee is inflamed. If the bursa underlying the tendons of the sartorius, gracilis, and semitendinosus gets irritated from overuse or injury, a person can develop this ailment. This condition usually occurs in athletes from overuse. This pathology is characterized by pain, swelling, and / or tenderness.The semitendinosus tendon can be used in certain techniques for reconstruction of the  anterior cruciate ligament. History
The name "goose foot" arises from the three-pronged manner in which the conjoined tendon inserts onto the tibia. Additional Images
References
External links
Pes anserinus at the Duke University Health Systems Orthopedics program