Osteoclast precursors do not express <scp>CD</scp>68: results from <scp>CD</scp>68 promoter‐driven <scp>RANK</scp> transgenic mice

Jackson, Melissa F.; Scatena, Marta; Giachelli, Cecilia M.

doi:10.1002/1873-3468.12588

Cited by 9 publications

(9 citation statements)

References 35 publications

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“…Moreover, during GBR procedures a variety of other biomaterials are routinely used such as collagen membranes. Collagen membranes can cause immigration of macrophages, which might not necessarily become osteoclasts . Antagonizing this process by the addition of PRF could potentially inhibit osteoclastogenesis under inflammatory conditions thereby enhancing biomaterial integration.…”

Section: Discussionmentioning

confidence: 99%

Platelet‐rich fibrin suppresses in vitro osteoclastogenesis

Kargarpour

Nasirzade

Strauß

et al. 2019

Journal of Periodontology

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Background Platelet‐rich fibrin (PRF) membranes can preserve alveolar ridge dimension after tooth extraction. Thus, it can be presumed that PRF suppresses the catabolic events that are caused by osteoclastic bone resorption. Methods To address this possibility, we investigated the impact of soluble extracts of PRF membranes on in vitro osteoclastogenesis in murine bone marrow cultures. Osteoclastogenesis was induced by exposing murine bone marrow cultures to receptor activator of nuclear factor kappa B ligand (RANKL), macrophage colony‐stimulating factor (M‐CSF) and transforming growth factor‐beta 1 (TGF‐β1) in the presence or absence of PRF. Osteoclastogenesis was evaluated based on histochemical, gene expression, and resorption analysis. Viability was confirmed by formation of formazan crystals, live‐dead staining and caspase‐3 activity assay. Results We report here that in vitro osteoclastogenesis is greatly suppressed by soluble extracts of PRF membranes as indicated by tartrate‐resistant acid phosphatase (TRAP) staining and pit formation. In support of the histochemical observations, soluble extracts of PRF membranes decreased expression levels of the osteoclast marker genes TRAP, Cathepsin K, dendritic cell‐specific transmembrane protein (DCSTAMP), nuclear factor of activated T‐cells (NFATc1), and osteoclast‐associated receptor (OSCAR). PRF membranes, however, cannot reverse the process once osteoclastogenesis has evolved. Conclusion These in vitro findings indicate that PRF membranes can inhibit the formation of osteoclasts from hematopoietic progenitors in bone marrow cultures. Overall, our results imply that the favorable effects of PRF membranes in alveolar ridge preservation may be attributed, at least in part, by the inhibition of osteoclastogenesis.

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Section: Discussionmentioning

confidence: 99%

Platelet‐rich fibrin suppresses in vitro osteoclastogenesis

Kargarpour

Nasirzade

Strauß

et al. 2019

Journal of Periodontology

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“…The macrophage marker CD-68 (log 2 = -1.34) is also upregulated in functional teeth (Fig 2A, S2B). CD68 is expressed in fully differentiated osteoclasts and not their precursors (Jackson et al 2017). TGF β - 1 was at the edge of the significant genes described by edgeR analysis (Fig.…”

Section: Resultsmentioning

confidence: 99%

Transcriptomic profiling of the adult reptilian dentition sheds light on the genes regulating indefinite tooth replacement

Henriquez

Flibotte

et al. 2022

Preprint

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The aim of this study is to profile the transcriptomes of teeth and the surrounding tissues of an adult lizard dentition (Eublepharis macularius) that is actively replacing teeth throughout life. Bulk RNAseq was used to compare teeth that are in function versus unerupted, developing teeth and single cell RNA-seq was carried out on jaw segments containing the dental forming tissues. In bulk RNAseq data, we found that functional teeth expressed genes involved in bone and tooth resorption. Indeed, multinucleated odontoclasts were abundant in tissue sections of functional teeth undergoing resorption. These are the first steps towards characterizing odontoclasts that participate in physiological resorption. Unexpectedly, chemotaxis gene SEMA3A was expressed within odontoblasts and in adjacent mesenchyme, confirmed using RNAscope. Semaphorins may be involved in regulating odontoclasts during tooth resorption. The scRNA-seq experiment successfully isolated dental mesenchyme and epithelial cells. We confirmed that some of these genes are expressed in the earliest tooth buds within the tooth forming field. In addition, we found evidence of convergent evolution in the tooth eruption trait. Geckos evolved a means for second generation teeth to communicate with the functional teeth. Instead of a dental follicle inducing an eruption pathway as in the mammal, the gecko and other squamate reptiles use the enamel organ of the successional teeth to trigger tooth resorption of the functional teeth, thus creating an eruption pathway. New molecules such as SEMA3A may also participate in this process. Future studies on the gecko will uncover the molecular basis of convergent evolution in the dentition.

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“…Furthermore, CD11b expression is found on both resident and inflammatory monocyte populations in mice and humans, therefore, CD11b represents a reliable marker of osteoclast precursors that may be derived from either tissue-resident or migratory monocyte populations [41]. Additionally, commonly used macrophage markers such as CD68 and F4/80 may not be ideal markers for our purposes due to demonstrations that their expression may inhibit OCG [42,43]. We also rely on coexpression of CD11b and TRAP to identify TPMs in this study, as cells of the monocyte/macrophage lineage are the primary cell type known to express high levels of TRAP [44].…”

Section: Discussionmentioning

confidence: 99%

Cigarette Smoke Extract Activates Tartrate-Resistant Acid Phosphatase-Positive Macrophage

Igari¹,

Kelly²,

Yamanouchi³

2019

J Vasc Res

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Background: It has been reported that smoking is one of the strongest positive risk factors for abdominal aortic aneurysms (AAAs). Although many studies have been directed to decipher the effect of smoking on AAA, its effect on macrophage activation has not yet been explored. Objectives:We have reported the importance of osteoclastogenesis (OCG) in aneurysm formation. Therefore, we examined the effect of cigarette smoking on OCG and arterial aneurysmal formation by using cigarette smoke extract (CSE) in this study.Methods: Macrophage cell lines were stimulated with CSE, and their activation and differentiation were examined in vitro. Since macrophages activated through the OCG pathway are identified by tartrate-resistant acid phosphatase (TRAP) expression, these cells are referred to as TRAP-positive macrophages (TPMs) in this study. We also applied CSE-contained PBS in the calcium chloride-induced mouse carotid aneurysm model in vivo.Results: Macrophages stimulated with CSE expressed significantly higher levels of nuclear factor of activated T-cells cytoplasmic 1 (NFATcl), TRAP, cathepsin K, matrix metalloproteinase-9 and membrane-type metalloproteinase (MT1-MMP). CSE-treated mouse aneurysms showed increased aneurysm size with increased TPM infiltration and protease expression compared to non-CSE-treated mouse aneurysms.Conclusions: These results suggest that CSE intensifies OCG in macrophages and promotes arterial aneurysmal progression.

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Osteoclast precursors do not express CD68: results from CD68 promoter‐driven RANK transgenic mice

Cited by 9 publications

References 35 publications

Platelet‐rich fibrin suppresses in vitro osteoclastogenesis

Platelet‐rich fibrin suppresses in vitro osteoclastogenesis

Transcriptomic profiling of the adult reptilian dentition sheds light on the genes regulating indefinite tooth replacement

Cigarette Smoke Extract Activates Tartrate-Resistant Acid Phosphatase-Positive Macrophage

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