Ergocalciferol (D2) and cholecalciferol (D3) are considered to be equivalent for vitamin D production, as both forms appear to have similar efficacy in ameliorating rickets and reducing the incidence of falls in elderly patients. Conflicting reports exist, however, concerning the relative effectiveness, with some studies suggesting that ergocalciferol has less efficacy based on limitations in absorption, binding, and inactivation. A meta-analysis concluded that evidence usually favors cholecalciferol in raising vitamin D levels in blood, although it stated more research is needed. Mechanism
Ergocalciferol is a secosteroid formed by a photochemical bond breaking of a steroid, specifically, by the action of ultraviolet light (UV-B or UV-C) on ergosterol, a form of provitamin D2.Like cholecalciferol, ergocalciferol is inactive by itself. It requires two hydroxylations to become active: the first in the liver by CYP2R1 to form 25-hydroxyergocalciferol (ercalcidiol or 25-OH D2), and the second in the kidney by CYP27B1, to form the active 1,25-dihydroxyergocalciferol (ercalcitriol or 1,25-(OH)2D2), which activates the vitamin D receptor. Unlike cholecalciferol, 25-hydroxylation is not performed by CYP27A1 for ergocalciferol.Ergocalciferol and metabolites have lower affinity to the vitamin D-binding protein compared to the D3 counterparts. The binding affinity of ercalcitriol to the vitamin D receptor is similar to that of calcitriol. Ergocalciferol itself and metabolites can be deactivated by 24-hydroxylation.
Chondrolysis [ICD Code M94.3] is the process of breakdown of cartilage. It can occur as a result of trauma (traumatic chondrolysis). Intra-articular infusions of certain local anesthetic agents such as bupivacaine, lidocaine, ropivacaine and levobupivacaine can also lead to this effect. See also
Chondritis
Osteochondritis
Relapsing polychondritis

References
External links
Chondrolysis at Radiopedia