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Vitamin D is critical for musculoskeletal health and has been implicated in the risk of extraskeletal diseases, including cancer, cardiovascular diseases, and autoimmune diseases, as well as overall mortality. Although numerous studies deal and have dealt with vitamin D deficiency and its consequences, experts cannot agree on the right 25-hydroxyvitamin D levels. This survey aims to shed light on the ongoing vitamin D controversy from different angles.We discuss the minimum threshold for the 25-hydroxyvitamin D level to guarantee optimal health, why vitamin is D critical to musculoskeletal and extraskeletal functions, and new evidence for the success of prevention measures such as food fortification.We searched PubMed, Google Scholar, and reference lists of articles using several keywords. The most recent search was in February 2011.While the use of parathyroid hormone as a surrogate measure did not lead to a consensus concerning the required 25-hydroxyvitamin D serum level, the combined analysis of bone mineralization and vitamin D status has established minimum levels of more than 75 nmol/L (30 ng/mL) to guarantee at least skeletal health. An effective measure to approach this status is food fortification, which has been demonstrated by countries such as Canada, the United States, and Finland.Given the health economic implications of failure to maintain a balanced vitamin D status, action is recommended to integrate current scientific knowledge on vitamin D into physicians' treatment of patients and governmental policies on food fortification.

Background: The distal radius is the most frequent fracture localization in humans. Although younger patients receive a distal radius fracture after an adequate trauma, elderly patients suffer fractures through low-energy mechanisms. Low-energy fractures are hallmarks of osteoporosis. Osteoporotic changes of the distal radius are well described by DXA and peripheral quantitative computed tomography measurements. However, to date, the effects of aging on the microarchitecture of the distal radius have not been investigated. Methods: To investigate whether the microarchitecture of the human distal radius shows osteoporotic changes in bone mass and structure during aging, we dissected out 60 complete human distal radii from 30 age- and gender-matched patients at autopsy. Each of the three different age groups (group I: 20-40 years, group II: 41-60 years, group III: 61—80 years) was represented by 10 autopsy cases and 20 specimens (double-sided extraction), respectively. The specimens were analyzed by peripheral quantitative computed tomography, contact-radiography, and histomorphometry. Results: We observed a significant age-related decrease in bone mass, bone mineral density and an increase in typical osteoporotic changes of the bone microarchitecture in female distal radius specimens. Comparable observations of age-related changes have not been made in male specimens. Conclusions: The distal radius is a location of osteoporosis-specific bone changes. Our data provide evidence for the occurrence of typical osteoporotic changes, especially postmenopausal osteoporotic changes, in the distal radius during aging.

Hypophosphatasia is a rare inherited disorder characterized by defective skeletal mineralization and low alkaline phosphatase activities in the serum. The genetic cause of hypophosphatasia is believed related to inactivating mutations in the TNSALP gene, encoding tissue-nonspecific alkaline phosphatase. Another rare inheritable disease, Saethre-Chotzen syndrome, leads to premature fusion of the cranial sutures caused by heterozygous mutations of the human TWIST1 gene. Because the two disorders apparently are not genetically related (only reported individually) yet both involve defective skeletal formation, we believe it is important to report our findings on a patient harboring mutations of TNSALP and TWIST1.