In dental implantology, vitamin D has been investigated almost exclusively as influencing factor of the bone to implant contact and implant stability. Vitamin D demonstrates several effects on bone metabolism: it upregulates the gene expression of osteocalcin, osteopontin, calbindin, and 24-hydroxylase, increases extracellular matrix protein formation by osteoblasts, and stimulates osteoclast activity. But beyond modulation of bone formation, vitamin D has an impact on the innate and adaptive immune response in the field of osteoimmunology and could therefore influence early implant healing.

Bone necrosis during implant bed preparation or placement is considered as a reason for early implant failures. An additional vitamin D deficiency might disrupt the sensitive balance between the immune system and bone metabolism during implant healing due to direct or indirect alteration of osteoclast function. For instance, the removal of bone debris through osteoclasts could be hampered since vitamin D controls osteoclast precursor monocyte migration. On the other hand, in vitro studies demonstrated that vitamin D inhibits dendritic cell maturation and function as well as T cell proliferation and influences B cell responses, inhibiting proliferation and plasma cell differentiation. An altered cytokine release by immune cells caused by a low vitamin D level could lead to a dysregulation of osteoclast activation and differentiation via associated immunoreceptors in osteoclasts.