Toll-like receptor-2 induced inflammation causes local bone formation and activates canonical Wnt signaling

It is well established that inflammatory processes in the vicinity of bone often induce osteoclast formation and bone resorption. Effects of inflammatory processes on bone formation are less studied. Therefore, we investigated the effect of locally induced inflammation on bone formation. Toll-like r...

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Published in:	Frontiers in immunology 2024, Vol.15, p.1383113-1383113
Main Authors:	Henning, Petra, Kassem, Ali, Westerlund, Anna, Lundberg, Pernilla, Engdahl, Cecilia, Lionikaite, Vikte, Wikström, Pernilla, Wu, Jianyao, Li, Lei, Lindholm, Catharina, de Souza, Pedro P C, Movérare-Skrtic, Sofia, Lerner, Ulf H
Format:	Article
Language:	eng
Subjects:	Adaptor Proteins Adaptor Proteins, Signal Transducing Animals bone formation Bone Resorption Bone Resorption - metabolism drug effects Endocrinology and Diabetes Endokrinologi och diabetes genetics immunology Inbred C57BL Inflammation Inflammation - metabolism Lipopolysaccharides Male metabolism Mice Mice, Inbred C57BL Osteoblasts Osteoblasts - immunology Osteoblasts - metabolism Osteoclasts Osteoclasts - immunology Osteoclasts - metabolism Osteocytes Osteocytes - metabolism Osteogenesis Osteogenesis - drug effects Porphyromonas gingivalis Signal Transducing Skull Toll-Like Receptor 2 Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - metabolism toll-like receptors Wnt Proteins Wnt Proteins - metabolism Wnt signaling Wnt Signaling Pathway
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Summary:	It is well established that inflammatory processes in the vicinity of bone often induce osteoclast formation and bone resorption. Effects of inflammatory processes on bone formation are less studied. Therefore, we investigated the effect of locally induced inflammation on bone formation. Toll-like receptor (TLR) 2 agonists LPS from and PAM2 were injected once subcutaneously above mouse calvarial bones. After five days, both agonists induced bone formation mainly at endocranial surfaces. The injection resulted in progressively increased calvarial thickness during 21 days. Excessive new bone formation was mainly observed separated from bone resorption cavities. Anti-RANKL did not affect the increase of bone formation. Inflammation caused increased bone formation rate due to increased mineralizing surfaces as assessed by dynamic histomorphometry. In areas close to new bone formation, an abundance of proliferating cells was observed as well as cells robustly stained for Runx2 and alkaline phosphatase. PAM2 increased the mRNA expression of , and , and decreased the expression of and . hybridization demonstrated decreased mRNA expression in osteocytes present in old bone. An abundance of cells expressed in Runx2-positive osteoblasts and ß-catenin in areas with new bone formation. These data demonstrate that inflammation, not only induces osteoclastogenesis, but also locally activates canonical WNT signaling and stimulates new bone formation independent on bone resorption.
ISSN:	1664-3224 1664-3224