Vitamin D Level Between Calcium-Phosphorus Homeostasis and Immune System: New Perspective in Osteoporosis

Abstract

Vitamin D is a key molecule in calcium and phosphate homeostasis; however, increasing evidence has recently shown that it also plays a crucial role in the immune system, both innate and adaptive. A deregulation of vitamin D levels, due also to mutations and polymorphisms in the genes of the vitamin D pathway, determines severe alterations in the homeostasis of the organism, resulting in a higher risk of onset of some diseases, including osteoporosis. This review gives an overview of the influence of vitamin D levels on the pathogenesis of osteoporosis, between bone homeostasis and immune system.

Vitamin D and Calcium Are Required during Denosumab Treatment in Osteoporosis with Rheumatoid Arthritis

“…At present, the mechanism of this enhanced H-BMD gain is unknown, but may be related to the lumbar region being less solicited than the hips; increased H-BMD may be linked to the fact that hip osteoblasts have mechanoreceptors that become more fully activated combined with increased mobility of the analyzed are (i.e., greater in the hips and lower in the lumber area). Also, the reasons why H-BMD in the combination group were significantly greater than those in the denosumab monotherapy group were due to the effects of vitamin D (anti-inflammatory phenomena and bone synthesis) [21]. …”

“…Bellavia et al have described that vitamin D is a key player in calcium and phosphate homeostasis and an important immunoregulatory molecule [21]. They found that in RA patients, low 25(OH)D levels were significantly associated with clinical parameters of disease activity as well as with high serum levels of IL-17 and IL-23 and bone loss.…”

“…They found that in RA patients, low 25(OH)D levels were significantly associated with clinical parameters of disease activity as well as with high serum levels of IL-17 and IL-23 and bone loss. Accordingly, vitamin D deficiency may play a role in the pathogenesis of osteoporotic patients with RA [21]. Although serum 25(OH)D levels were not measured in this study, vitamin D and calcium supplementation can inhibit the decrease of calcium and improve BMD due to the potential increase of 25(OH)D. Antoniucci et al reported that vitamin D status at therapy initiation did not affect the BMD response to ALN when co-administered with vitamin D [22].…”

“…Whether vitamin D sufficiency or administration influences the effects on BMD during BP therapy is controversial [22,23,24,25], although it remains generally supported that vitamin D addition is desirable during BP treatment. Reported discrepancies may be due to such population characteristics as age and physical activity and/or genetic factors, such as mutations or polymorphisms in genes of vitamin D [21]. …”

MiR-33a Controls hMSCS Osteoblast Commitment Modulating the Yap/Taz Expression Through EGFR Signaling Regulation

“…The imbalance between these two processes leads to several diseases, such as osteopenia, osteoporosis, etc. [1,2]. Bone regeneration is mediated by a well-orchestrated process that involves external and internal elements to promote formation of new mineralized tissues as receptor tyrosine kinase (RTK) signaling pathways, including epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and fibroblast growth factor (FGF) [3].…”