Bone morphogenetic proteins: Periodontal regeneration

Abstract

Periodontitis is an infectious inflammatory disease that results in attachment loss and bone loss. Regeneration of the periodontal tissues entails de novo formation of cementum, periodontal ligament, and alveolar bone. Several different approaches are currently being explored to achieve complete, reliable, and reproducible regeneration of periodontal tissues. The therapeutic management of new bone formation is one of the key issues in successful periodontal regeneration. Bone morphogenetic proteins form a unique group of proteins within the transforming growth factor superfamily of genes and have a vital role in the regulation in the bone induction and maintenance. The activity of bone morphogenetic proteins was first identified in the 1960s, but the proteins responsible for bone induction were unknown until the purification and cloning of human bone morphogenetic proteins in the 1980s, because of their osteoinductive potential. Bone morphogenetic proteins have gained a lot of interest as therapeutic agents for treating periodontal defects. A systematic search for data related to the use of bone morphogenetic proteins for the regeneration of periodontal defects was performed to recognize studies on animals and human (PUBMED, MEDLINE, COCHRANE, and Google search). All the studies included showed noticeable regeneration of periodontal tissues with the use of BMP.

TGF-β/BMP signaling and other molecular events: regulation of osteoblastogenesis and bone formation

“…57 Three BMPRI (BMPRIA or ALK3, BMPRIB or ALK6, and ALK2: IA activin receptors) and three BMPRII (BMPRIIB, ACTRIIA, and ACTRIIB) are known to bind BMP. Out of the three BMPRI, ALK3 and ALK6 are structurally highly similar to each other, whereas ALK2 is less similar to the other two.…”

Chronic Periodontitis Is Associated With Spinal Dysmobility in Patients With Ankylosing Spondylitis

“…[46][47][48] Moreover, bone morphogenic proteins were reported to be increased in AS. [49][50][51] Conversely, the levels of sclerostin and DKK1 were upregulated in the periodontal tissue of CP, which is Wnt responsive. 16,52 Their expression levels were correlated with PD and AL, and circulating sclerostin levels were increased significantly in patients with CP.…”

“…The levels of a Wnt signaling inhibitor, sclerostin, were documented to be reduced in the serum and tissues, and dickkopf‐related protein 1 (DKK1), another Wnt signaling inhibitor, was suggested to be dysfunctional 46–48 . Moreover, bone morphogenic proteins were reported to be increased in AS 49–51 . Conversely, the levels of sclerostin and DKK1 were upregulated in the periodontal tissue of CP, which is Wnt responsive 16 , 52 .…”

Dentin regeneration by stem cells of apical papilla on injectable nanofibrous microspheres and stimulated by controlled BMP-2 release

“…Moreover, the presence of red vascularized thin fibrous connective tissue in BMP-2 release groups indicated abundant angiogenesis, one of the keys to successful tissue engineering. A reasonable explanation might be that BMP-2 acts as a differentiation factor and chemotactic agent, inducing chemotaxis of microvascular endothelial cells and stimulating angiogenesis [48, 49]. Notably, although odontoblast-like cells and dentin-like tissue formation were observed, the tissue formed on the NF-MS did not possess the typical tubular dentin structure.…”