The pubic symphysis is a secondary cartilaginous joint between the left and right superior rami of the pubis of the hip bones. It is in front of and below the urinary bladder. In males, the suspensory ligament of the penis attaches to the pubic symphysis. In females, the pubic symphysis is close to the clitoris. In most adults it can be moved roughly 2 mm and with 1 degree rotation. This increases for women at the time of childbirth.The name comes from the Greek word symphysis, meaning growing together. Structure
The pubic symphysis is a nonsynovial amphiarthrodial joint. The width of the pubic symphysis at the front is 3–5 mm greater than its width at the back. This joint is connected by fibrocartilage and may contain a fluid-filled cavity; the center is avascular, possibly due to the nature of the compressive forces passing through this joint, which may lead to harmful vascular disease. The ends of both pubic bones are covered by a thin layer of hyaline cartilage attached to the fibrocartilage. The fibrocartilaginous disk is reinforced by a series of ligaments. These ligaments cling to the fibrocartilaginous disk to the point that fibers intermix with it. Two such ligaments are the superior pubic ligament  and the inferior pubic ligament, which provide the most stability; the anterior and posterior ligaments are weaker. The strong and thicker superior ligament is reinforced by the tendons of the rectus abdominis muscle, the abdominal external oblique muscle, the gracilis muscle, and by muscles of the hip.
However, it has been shown to have comparable affinity with calcitriol for the vitamin D receptor (VDR), while being less than 1% as active as the calcitriol in regulating calcium metabolism. The vitamin D receptor belongs to the steroid/thyroid receptor superfamily, and is found on the cells of many different tissues including the thyroid, bone, kidney, and T cells of the immune system. T cells are known to play a role in psoriasis, and it is thought that the binding of calcipotriol to the VDR modulates the T cells gene transcription of cell differentiation and proliferation related genes. In mouse studies, topical calcipotriol administration to the ear and dorsal skin led to a dose-dependent increase in the production of the epithelial cell-derived cytokine TSLP by keratinocytes, and triggered atopic dermatitis at high concentrations. This upregulation of TSLP production due to calcipotriol application is thought to be mediated through the coactivation of vitamin D receptor/RXRα and vitamin D receptor/RXRβ heterodimers. As psoriasis is typically thought to be partially driven by Th1/Th17 inflammatory cytokines, calcipotriol treatment at appropriate concentrations may alleviate psoriasis symptoms by repressing Th1/Th17 inflammation through TSLP production, which is linked to a Th2 response. However, it is important to note that this has not yet been confirmed. Pharmacokinetics
After application and systemic uptake, calcipotriol undergoes rapid hepatic metabolism. Calcipotriol is metabolized to MC1046 (the α,β−unsaturated ketone analog), which is subsequently metabolized to its primary metabolite, the saturated ketone analog MC1080.