Vitamin D deficiency can cause secondary hyperparathyroidism and bone loss, mineralization defects, and in the long term rickets and osteomalacia. Vitamin D stimulates calcium and phosphate absorption from the gut, making these available for bone mineralization which mainly is a passive process. New laboratory observations show effects of vitamin D metabolites on osteoblast function and possibly mineralization. The prevalence of rickets is low in affluent countries but higher in some countries in Asia and Africa, and also in non-western immigrants. The global prevalence of osteomalacia depends on definition and can be estimated from biopsy and autopsy series, conservatively at about 1%. Osteomalacia has been observed as a cause of hip fractures in the elderly. Vitamin D status is estimated according to serum 25-hydroxyvitamin D as deficient (<25 nmol/l) or insufficient (2550 nmol/l) or adequate (>50 nmol/l). Low serum 25(OH)D (<50 nmol/l) has been observed in 5080% of older persons, and in about 50% of all adults at least during winter. This results in a seasonal increase of parathyroid hormone and bone loss. The deficit of bone mineral density as a consequence of elevated PTH can be estimated at 12.5%. Clinical trials with vitamin D vs placebo in older persons have shown an increase of BMD of about 2%. Randomized clinical trials with vitamin D with or without calcium have shown a decrease of fracture incidence in seven of 19 trials, no effect in ten and an increase of fracture incidence in two trials. Most meta-analyses showed a decrease of fracture incidence with the combination of vitamin D and calcium, but no effect of vitamin D alone. The effect on fracture incidence could result from an increase of bone mineralization or a decrease of fall incidence.