Publications by authors named "Yutaro Ando"

Treponema denticola is frequently isolated together with Porphyromonas gingivalis from the lesions seen in cases of chronic periodontitis and is considered a major pathogen of this disease. It has several virulence factors, including a major surface protein (Msp) and a major surface protease, dentilisin. The effect of these virulence factors on the host immune response remains to be elucidated, however.

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The periosteum is the layer of cells that covers nearly the entire surface of every bone. Upon infection, injury or malignancy the bone surface undergoes new growth-the periosteal reaction-but the mechanism and physiological role of this process remain unknown. Here we show that the periosteal reaction protects against cancer invasion into the bone.

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Article Synopsis
  • Treponema denticola is linked to chronic periodontitis, and the study examines the role of the gene TDE_0259 (oxtR1) in its environmental adaptability.
  • Using an oxtR1-deficient mutant, researchers found that inactivating oxtR1 sped up bacterial growth and altered its susceptibility to antibacterial agents, revealing changes in gene expression related to stress response mechanisms.
  • The study concludes that OxtR1 is an oxygen-sensing regulator that influences genes for ferrodoxin and likely helps T. denticola cope with oxygen-related stresses.
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The immune-stromal cell interactions play a key role in health and diseases. In periodontitis, the most prevalent infectious disease in humans, immune cells accumulate in the oral mucosa and promote bone destruction by inducing receptor activator of nuclear factor-κB ligand (RANKL) expression in osteogenic cells such as osteoblasts and periodontal ligament cells. However, the detailed mechanism underlying immune-bone cell interactions in periodontitis is not fully understood.

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The bony skeleton is continuously renewed throughout adult life by the bone remodeling process, in which old or damaged bone is removed by osteoclasts via largely unknown mechanisms. Osteocytes regulate bone remodeling by producing the osteoclast differentiation factor RANKL (encoded by the TNFSF11 gene). However, the precise mechanisms underlying RANKL expression in osteocytes are still elusive.

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Periodontal disease is characterized by inflammation of the periodontal tissue and subsequent destruction of the alveolar bone. It is one of the most common infectious diseases in humans, being the leading cause of tooth loss in adults. Recently, it has been shown that the receptor activator of NF-κB ligand (RANKL) produced by osteoblasts and periodontal ligament fibroblasts critically contributes to the bone destruction caused by periodontal disease.

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The ontogeny and fate of stem cells have been extensively investigated by lineage-tracing approaches. At distinct anatomical sites, bone tissue harbors multiple types of skeletal stem cells, which may independently supply osteogenic cells in a site-specific manner. Periosteal stem cells (PSCs) and growth plate resting zone stem cells (RZSCs) critically contribute to intramembranous and endochondral bone formation, respectively.

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We investigated shifts in growth rates and cell size reduction-restoration processes in two species of diatoms, Skeletonema japonicum and Skeletonema dohrnii. Growth rates greatly fluctuated from 1.0 to 2.

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