In this review we consider diseases associated with pathological mineralization/ossification, namely, ankylosing spondylitis (AS), osteoarthritis (OA), generalized artery calcification of infancy (GACI), vascular calcification as well as chondrocalcinosis (CC) and pseudo gout. Deciphering the key enzymes implicated in the calcification process is an objective of prime importance and the ultimate goal is to synthesize inhibitors of these enzymes in order to provide efficient alternate therapeutic strategies that will slow down the pathologic mineralization and complement the arsenal of anti-inflammatory drugs. One of the difficulties in the definition of diseases associated with pathologic mineralization/ossification lies in the controversial relationship between the type of calcification and the nature of the disease. Here, we propose to clarify this relationship by making a distinction between diseases associated with hydroxyapatite (HA) and calcium pyrophosphate dihydrate (CPPD) deposits. AS, OA, GACI and vascular calcification are usually characterized by mineralization/ossification associated with HA deposits, while CC and pseudo gout are mostly characterized by CPPD deposits. Although both HA and CPPD deposits may occur concomitantly, as in chronic pyrophosphate arthritis or in OA with CPPD, they are formed as a result of two antagonistic processes indicating that treatment of distinct diseases can be only achieved by disease-specific drug therapies. The hydrolysis of PPi, an inhibitor of HA formation, is mostly controlled by tissue non-specific alkaline phosphatase TNAP, while PPi production in the extracellular medium is controlled by ANK, a PPi transporter, and/or NPP1 which generates PPi from nucleotide triphosphates. Low PPi concentration may lead to a preferential deposition of HA while high PPi concentration will favor the formation of CPPD deposits. Thus, HA and CCPD deposition cannot occur concomitantly because they are determined by the Pi/PPi ratio which, in turn, depends on the relative activities of antagonistic enzymes, TNAP hydrolyzing PPi or ANK and NPP1 producing PPi. TNAP inhibitors could prevent HA formation in AS, in late OA, in GACI, as well as in vascular calcifications, while ANK or NPP1 inhibitors could slow down CCPD deposition in CC and pseudo gout.

Patients with atopic dermatitis (AD) often present with dry skin, and the reduced secretion of sebum may be responsible for the impaired skin barrier function. A sebum check film enables the patient to self-evaluate the skin sebum content. This study compared the sebum check film with a sebumeter. The skin sebum content of the forehead was measured using a sebum check film and a sebumeter. The findings of the sebum content of healthy controls showed that the sebum dot fields on the sebum check film were significantly correlated with the sebum content measured using the sebumeter (r = 0.774, p < 0.001). In addition, the sebum fields on the sebum check film of AD patients (n = 26) were significantly less than those on the sebum check film of the controls (n = 30; p < 0.05). Furthermore, the analysis of the sebum fields on the sebum check film of the AD patients was significantly correlated with their sebum content findings that were obtained using a sebumeter (r = 0.592, p < 0.01). These findings indicate that the sebum check film is easy to use for measuring the sebum secretion and is suitable for self-checking the sebum contents by AD patients for daily skin care.

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