Role of osteopontin in bone remodeling and orthodontic tooth movement: a review

Abstract

In this review, most of the known and postulated mechanisms of osteopontin (OPN) and its role in bone remodeling and orthodontic tooth movement are discussed based on available literature. OPN, a multifunctional protein, is considered crucial for bone remodeling, biomineralization, and periodontal remodeling during mechanical tension and stress (orthodontic tooth movement). It contributes to bone remodeling by promoting osteoclastogenesis and osteoclast activity through CD44- and αvβ3-mediated cell signaling. Further, it has a definitive role in bone remodeling by the formation of podosomes, osteoclast survival, and osteoclast motility. OPN has been shown to have a regulatory effect on hydroxyapatite crystal (HAP) growth and potently inhibits the mineralization of osteoblast cultures in a phosphate-dependent manner. Bone remodeling is vital for orthodontic tooth movement. Significant compressive and tensional forces on the periodontium induce the signaling pathways mediated by various osteogenic genes including OPN, bone sialoprotein, Osterix, and osteocalcin. The signaling pathways involved in the regulation of OPN and its effect on the periodontal tissues during orthodontic tooth movement are further discussed in this review. A limited number of studies have suggested the use of OPN as a biomarker to assess orthodontic treatment. Furthermore, the association of single nucleotide polymorphisms (SNPs) in OPN coding gene Spp1 with orthodontically induced root resorption remains largely unexplored. Accordingly, future research directions for OPN are outlined in this review.

Hydroxylapatite-collagen hybrid scaffold induces human adipose-derived mesenchymal stem cells to osteogenic differentiation in vitro and bone regrowth in patients

“…SPP1 gene that codifies for the osteopontin was modulated by the biomaterial. Osteopontin protein is considered to play an important role in bone regrowth, as well …”

“…Osteopontin protein is considered to play an important role in bone regrowth, as well. 39 Among DEGs, modulated by the biomaterial, there are BMPR1b and SOX9. The knockdown of BMPR1b by siRNA inhibited the osteogenic differentiation of human bone marrow-derived mesenchymal stem cells 40 ; BMPRIB appears primarily expressed in mesenchymal precartilage condensations, in differentiated osteoblasts and chondrocytes.…”

The Administration of 4-Hexylresorcinol Accelerates Orthodontic Tooth Movement and Increases the Expression Level of Bone Turnover Markers in Ovariectomized Rats

“…At 16 h, 4HR induced overexpression of RANKL (osteoclast differentiation factor) [29], RUNX2 (a key transcription factor associated with osteoblast differentiation) [30], osterix (a transcription factor for osteoblast differentiation) [31], aggrecan (a cartilage-specific proteoglycan core protein) [32], and calmodulin-dependent kinase II (a key regulator of osteoblast differentiation) [33], which co-operatively stimulated osteoblast differentiation. At 24 h, 4HR induced overexpression of BMP-3 (a negative regulator for bone density) [34], OPG (a regulator for bone density) [35], osteocalcin (a calcium-binding protein) [36], and osteopontin (bone sialoprotein I) [37], which simultaneously regulated osteoid matrix deposition. These results corresponded with those of the Western blot (Figures 1 and 2).…”

An Extract of <i>Eisenia Bicyclis</i> Stimulates Mineralized Nodule Formation by Osteoblasts

“…Bone sialoprotein anchors osteoblasts to the bone, and supports cell attachment and binding to calcium ion 2,29,30) . Osteopontin, which contains potential phosphorylation sites, such as serine-and aspartate-rich motifs, is associated with both downregulation and upregulation during the calcification process in tissues 2,[30][31][32] . Phosphorylated osteopontin is considered an inhibitor of mineral deposition 32,33) , whereas treatment of osteopontin with ALPase reduces the inhibitory effects of osteopontin on hydroxyapatite formation 32,34) .…”