It is generally assumed that vitamin D plays an intimate role in healing fractures. However, very little data exists on how it does so, nor on how activated vitamin D, called calcitriol, levels fluctuate after a fracture. It is assumed that calcitriol is localized at the repair site (callus). In humans it is further assumed that the intracellular calcitriol levels will not vary much as serum calcitriol is an adaptive hormone that varies with the amount of calcium in the intestine.
However, fracture repair studies have never been done in humans. In rats, calcitriol levels have been measured after rats were purposefully given femoral fractures.
Jingushi S, Iwaki A, Higuchi O, Azuma Y, Ohta T, Shida JI, Izumi T, Ikenoue T, Sugioka Y, Iwamoto Y. Serum 1alpha,25-dihydroxyvitamin D3 accumulates into the fracture callus during rat femoral fracture healing. Endocrinology. 1998 Apr;139(4):1467-73.
The above study showed that in rats, blood calcitriol levels rapidly decreased by day 3 and continued to decrease up to 10 days after the fracture. When radioactive calcitriol was injected in such rats, radioactivity in the fractured femurs was higher than that of a control group without fractures. Furthermore, the radioactivity was concentrated at the callus.
This study indicated that in rats, the rapid reduction in serum calcitriol is due to increased consumption of calcitriol at the fracture site and suggests that calcitriol may regulate cellular events in the process of fracture healing.
When fractures in humans do not heal, called nonunion, sometimes vitamin D deficiency is the culprit. Sometimes nonunion becomes union when vitamin D deficiency is treated.
So what do we know about vitamin D physiology and human fracture healing? Just about nothing until January of 2013, when Dr. Christoph Woelfl and fellow German researchers studied 25(OH)D and PTH levels in 30 humans with fractures, 15 of whom had osteoporosis and 15 who did not.
Woelfl C, Englert S, Moghaddam AA, Zimmermann G, Schmidt-Gayk G, Höner B, Hogan A, Lehnhardt M, Grützner PA, Kolios L. Time course of 25(OH)D3 vitamin D3 as well as PTH (parathyroid hormone) during fracture healing of patients with normal and low bone mineral density (BMD). BMC Musculoskelet Disord. 2013 Jan 3;14(1):6.
They took blood every several weeks for 8 weeks after the fracture. Unfortunately, they did not measure serum calcitriol levels to see if that varied after fractures like it does in rats. However, the German researchers found that 25(OH)D levels fell a little after fractures, from about 18 ng/ml to 16 ng/ml, and then started to inch up again by 8 weeks. There was no difference in 25(OH)D or PTH changes between osteoporotic patients and normal controls.
As both groups were deficient, we still don’t know what vitamin D levels do in patients with adequate vitamin D levels. When 25(OH)D levels are in the teens, the body is probably beginning to triage 25(OH)D into the line that says “let’s save 25(OH)D so we can make calcitriol in the future to maintain serum calcium.” That is, at most vitamin D levels in modern humans, the body is conserving vitamin D for its life saving role in preventing blood calcium from falling.
So while we still don’t know much about vitamin D and fracture healing, we know more than we did, thanks to the contribution of Dr. Woelfl and his colleagues.