Defective binding of macrophages to bone in rodent osteomalacia and vitamin D deficiency. In vitro evidence for a cellular defect and altered saccharides in the bone matrix.

Abstract

A B S T R A C T In the osteomalacic as well as normal skeleton, few osteoclasts are associated with osteoidcovered bone surfaces. The reason for this particular cellular deficit is not clear, but may relate to the inability of osteoclasts and/or osteoclast precursors (monocyte-macrophages) to attach to immature, unmineralized bone matrix, a step apparently essential for normal resorptive activity and osteoclast differentiation. In this study, we have examined cell-bone binding using macrophages (MO) and bone isolated from vitamin D-deficient rats and hypophosphatemic, osteomalacic mice and from their normal counterparts. The data show that MO-bone attachment is greatly reduced (P < 0.001) in both vitamin D deficiency and hypophosphatemia, but that the mechanisms responsible for this reduction are apparently different in the two disorders. In hypophosphatemia, the reduction in binding appears solely attributable to the absence or inaccessibility of bone matrix oligosaccharides or glycoproteins essential to the attachment process. In vitamin D deficiency, on the other hand, not only is the bone matrix defective as a binding substrate, but the MO, per se, is limited in its capacity to attach to normal, vitamin D-deficient, and hypophosphatemic bone.

Effects of dietary vitamin D3 administration on innate immune parameters of seabream (Sparus aurata L.)

“…The phagocytic capacity also showed an increase at this time, but at the other two doses of vitamin tested. These results also agree with some in vitro studies carried out in mammals, including humans, in which vD 3 enhanced chemotaxis, phagocytosis and cytotoxic functions [47][48][49][50][51][52].…”

The calcium-sensing receptor and 25-hydroxyvitamin D–1α-hydroxylase interact to modulate skeletal growth and bone turnover

“…It has been reported previously, from studies in vitro, that macrophages, which are osteoclast precursors, bind poorly to demineralized bone. (36) However, other studies have reported that osteoclasts bind, in vitro and in vivo, to both demineralized and mineralized bone, (37) and although they will not form ruffled borders (38) and secrete acid, they can continue to release degradative enzymes and resorb bone matrix; that is, they adhere and remain at least partly functional. (37) In our studies, the reductions in osteoclasts appeared to be similar both on the nonmineralized and mineralized bone surfaces of these models when they were osteomalacic on a normal diet.…”

Circadian Rhythm and Cartilage Extracellular Matrix Genes in Osseointegration: A Genome-Wide Screening of Implant Failure by Vitamin D Deficiency

“…Vitamin D is a steroid hormone that participates in broad physiological actions [15] , [16] , [17] , [18] . Abnormal vitamin D-related regulations have resulted in skeletal diseases such as rickets and osteomalacia [19] , [20] , catabolic bone remodeling [20] , [21] , [22] , autoimmune diseases [23] , and increased susceptibility to infectious diseases [24] . However, the role of vitamin D in the establishment of osseointegration has not been addressed.…”