Research into surgical removal of calcifications is underway, however, this still remains an experimental procedure. Epidemiology
The condition is more common in older adults.CPPD is estimated to affect 4% to 7% of the adult populations of Europe and the United States. Previous studies have overestimated the prevalence by simply estimating the prevalence of chondrocalcinosis, which is found in many other conditions as well.It may cause considerable pain, but it is never fatal. Women are at a slightly higher risk than men, with an estimated ratio of occurrence of 1.4:1. History
CPPD crystal deposition disease was originally described over 50 years ago. Terminology
Calcium pyrophosphate dihydrate crystals are associated with a range of clinical syndromes, which have been given various names, based upon which clinical symptoms or radiographic findings are most prominent. A task force of the European League Against Rheumatism (EULAR) made recommendations on preferred terminology. Accordingly, calcium pyrophosphate deposition (CPPD) is an umbrella term for the various clinical subsets, whose naming reflects an emphasis on particular features. For example, pseudogout refers to the acute symptoms of joint inflammation or synovitis: red, tender, and swollen joints that may resemble gouty arthritis (a similar condition in which monosodium urate crystals are deposited within the joints). Chondrocalcinosis, on the other hand, refers to the radiographic evidence of calcification in hyaline and/or fibrocartilage. "Osteoarthritis (OA) with CPPD" reflects a situation where osteoarthritis  features are the most apparent. Pyrophosphate arthropathy refers to several of these situations. References


== External links ==
After one to two weeks, large, tense blisters typically develop on the red plaques, containing clear or blood-stained fluid. GP creates a histamine response that causes extreme relentless itching (pruritus). GP is characterized by flaring and remission during the gestational and sometimes post partum period. Usually after delivery, lesions will heal within months, but may reoccur during menstruation. Causes
Pathogenically, it is a type II hypersensitivity reaction where circulating complement-fixing IgG antibodies bind to an antigen (a 180-kDa protein, BP-180) in the hemidesmosomes (attach basal cells of epidermis to the basal lamina and hence to dermis) of the dermoepidermal junction, leading to blister formation as loss of hemidesmosomes causes the epidermis to separate from dermis. The immune response is even more highly restricted to the NC16A domain. The primary site of autoimmunity seems not to be the skin, but the placenta, as antibodies bind not only to the basement membrane zone of the epidermis, but also to that of chorionic and amniotic epithelia. Aberrant expression of MHC class II molecules on the chorionic villi suggests an allogenic immune reaction to a placental matrix antigen, thought to be of paternal origin. Recently, both IgA22 and IgE24 antibodies to either BP180 or BP230 have also been detected in pemphigoid gestationis. Risk
Pregnant women with GP should be monitored for conditions that may affect the fetus, including, but not limited to, low or decreasing volume of amniotic fluid, preterm labor, and intrauterine growth retardation.