Research news: DEL-1's one-two punch may pave the way to a new class of endogenous therapeutics for treating periodontitis and other inflammatory disorders

Researchers have recently identified a mechanism within DEL-1 whereby bone loss is stopped and immune cell infliltration into the periodontium is blocked. This news offers great hope for a new class of therapeutics to treat periodontitis and possibly other inflammatory disorders as well.

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It is well supported in the literature that untreated periodontitis can increase an individual’s chance of developing other inflammatory diseases such as cardiovascular disease and rheumatoid arthritis. Since such a large number of people suffer from rampant caries, the ongoing research into reducing inflammation is, for a number of reasons, a justifiable focus in the quest to promote oral-systemic health.

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On the scientific front, researchers have identified a novel regulatory mechanism of DEL-1 (developmental endothelial locus-1)—an endothelial cell-secreted protein that regulates LFA-1 (lymphocyte function-associated antigen-1) integrin-dependent leukocyte recruitment and inflammation in various tissues—in osteoclast biology. According to a summary published by the American Association for the Advancement of Science, study authors Shin, et al. (1) “capitalized on the natural anti-inflammatory activity of the protein DEL-1, finding that it not only blocked excessive immune cell infiltration into the periodontium, but also had innate anti-osteoclastogenic activity; that is, it stopped bone loss by interrupting the signaling pathways to osteoclasts, the bone-resorbing cells.

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“In vitro, in human and mice osteoclast precursor cells, DEL-1 prevented osteoclast differentiation by inhibiting NFATc1 activity. In vivo, in mouse and nonhuman primate models of periodontitis, giving DEL-1 locally reduced inflammation and tissue destruction, thus halting any tissue loss. The mechanism appears to be two-pronged: working “upstream” in disease-signaling pathways to prevent inflammatory cell recruitment to the teeth and gums, as well as acting “downstream” to stop osteoclastogenesis. With data in a monkey model that represents the human disease, anatomy, and immune system closely, it is likely that DEL-1–based therapeutics could translate soon once safety of this endogenous molecule is confirmed.” (1)

Read the abstract from PubMed here.

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Reference
1. Shin J, Maekawa T, Abe T, Hajishengallis E, Hosur K, Pyaram K, Mitroulis I, Chavakis T, Hajishengallis G. DEL-1 restrains osteoclastogenesis and inhibits inflammatory bone loss in nonhuman primates. Sci Transl Med. 2015;7(307):307ra155. doi: 10.1126/scitranslmed.aac5380.

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