Fibromyalgia is considered the second most common rheumatologic disorder, second to osteoarthritis. It is a disorder that causes severe, chronic pain throughout the body, as well as chronic fatigue. Secondary symptoms include sore throat, tender nodes, cognitive difficulty, and headache and sleep difficulties.
Patients often report at least 11 tender points at the side of the neck, top of the shoulder blade, outside of the hip joint, and inside the knee. Despite affecting millions, researchers do not fully understand its cause. It is thought to be caused by dysfunction at the hypothalamic-pituitary axes, a control center for endocrine and immunomodulation.
Additionally, several autoimmune system mechanisms have been associated with fibromyalgia, and the thymus plays a critical role in mediating these mechanisms. An imbalance between two lymphocytes, immune cells, which mature in the thymus, Th1 and Th2, and their local effects is thought to cause many of the symptoms associated with this disease. Th1 and Th2 cells are self-regulating. Th1 cells promote the maturation of additional Th1 cells, while suppressing the maturation of Th2 cells. Th2 self-regulates in the same way. However, Th1 cells have a pro-inflammatory effect, and inflammation is the leading cause of pain. An imbalance which promotes Th1 maturation and suppresses Th2 maturation will lead to the inflammation and pain characteristic of fibromyalgia.
The thymus’ role is to maintain the appropriate balance between these two cell types. It does this though the action of cytokines (interleukins), chemicals which control the maturation process. Cells within the thymus secreting Interleukin-10 (IL-10) will suppress Th1 formation and promote Th2 formation. Cells secrete Interleukin-12 (IL-12) or another cytokine known as Tumor Necrosis Factor-alpha (TNF-a), will promote Th1 formation and suppress Th2 formation. In this way, the thymus is able to regulate the inflammatory response properly.