Tohoku University · Medicine
Professor Takeru Kondo's research lab focuses on the molecular and cellular mechanisms underlying periodontitis and bone metabolism, with a particular emphasis on the role of fibroblasts and cathepsin K in early disease onset. The lab employs advanced technologies such as single-cell RNA sequencing and novel fluorescent probes (e.g., Osteoadsorptive Fluogenic Sentinel) to dissect immune and inflammatory responses in the oral microenvironment. Additionally, the lab explores biomaterials—especially bioactive glasses and surface-modified implants—for regenerative dentistry and metabolic bone disorders, aiming to bridge immunomodulation with tissue regeneration.
Figures are computed from collected data and may differ slightly.
Periodontitis is a highly prevalent disease leading to uncontrolled osteoclastic jawbone resorption and ultimately edentulism; however, the disease onset mechanism has not been fully elucidated. Here we propose a mechanism for initial pathology based on results obtained using a recently developed Osteoadsorptive Fluogenic Sentinel (OFS) probe that emits a fluorescent signal triggered by cathepsin K (Ctsk) activity. In a ligature-induced mouse model of periodontitis, a strong OFS signal is observ
Periodontitis, one of the most common non-communicable diseases, is characterized by chronic oral inflammation and uncontrolled tooth supporting alveolar bone resorption. Its underlying mechanism to initiate aberrant oral barrier immunity has yet to be delineated. Here, we report a unique fibroblast subpopulation a ctivated to g uide oral inflammation (AG fibroblasts) identified in a single-cell RNA sequencing gingival cell atlas constructed from the mouse periodontitis models. AG fibroblasts lo
Periodontitis, one of the most common non-communicable diseases, is characterized by chronic oral inflammation and uncontrolled tooth supporting alveolar bone resorption. Its underlying mechanism to initiate aberrant oral barrier immunity has yet to be delineated. Here, we report a unique fibroblast subpopulation <u>a</u>ctivated to <u>g</u>uide oral inflammation (AG fibroblasts) identified in a single-cell RNA sequencing gingival cell atlas constructed from the mouse periodontitis models. AG fi
Notably, circadian clock disruption reduces insulin secretion and insulin sensitivity and negatively affects glucose homeostasis. The circadian clock regulates the hypothalamic-pituitary-adrenal axis, an important factor that regulates glucose metabolism and influences T2D progression. Therefore, circadian clock regulation is an attractive, novel therapeutic approach for T2D, and various circadian clock stabilizers play therapeutic roles in T2D. Lastly, this review suggests novel therapeutic and
Bioglass 45S5, a silica-based glass, has pioneered a new field of biomaterials. Bioglass 45S5 promotes mineralization through calcium ion release and is widely used in the dental field, including toothpaste formulations. However, the use of Bioglass 45S5 for bone grafting is limited owing to the induction of inflammation, as well as reduced degradation and ion release. Phosphate-based glasses exhibit higher solubility and ion release than silica-based glass. Given that these glasses can be synth
Surface modification of implants aimed at regulating innate immunity may be useful in promoting further osteogenesis and overcoming the limitations encountered in severe situations, such as early loading protocol application.
Zirconia restorations are becoming increasingly common. However, zirconia reduces the polymerization of dual-cured resin cement owing to light attenuation, resulting in residual resin monomers. This study investigated the effects of dual-cured resin cement, with incomplete polymerization owing to attenuated light through zirconia, on the inflammatory response in vitro. The dual-cured resin cement (SA Luting Multi, Kuraray) was light-irradiated through zirconia with three thickness diameters (1.0
Compared with LC dual-cure resin-cements, SC dual-cure resin-cements show stronger cytotoxicity and elicit greater inflammatory responses in gingival cells owing to residual monomers (e.g., TEGDMA and UDMA) by activating MAP kinases in GFs and macrophages. Clinicians should ensure adequate light irradiation during prosthesis cementation and make efforts to remove the excess cement.
Tooth/skeletal dysplasia, such as hypophosphatasia (HPP), has been extensively studied. However, there are few definitive treatments for these diseases owing to the lack of an in vitro disease model. Cells differentiated from patient-derived induced pluripotent stem cells (iPSCs) demonstrate a pathological phenotype. This study aimed to establish a method for fabricating hard tissue-forming cells derived from human iPSCs (hiPSCs) for the pathological analysis of tooth/skeletal dysplasia. Healthy
Periodontitis, one of the most common non-communicable diseases, is characterized by chronic oral inflammation and uncontrolled tooth supporting alveolar bone resorption. Its underlying mechanism to initiate aberrant oral barrier immunity has yet to be delineated. Here, we report a unique fibroblast subpopulation activated to guide oral inflammation (AG fibroblasts) identified in a single-cell RNA sequencing gingival cell atlas constructed from the mouse periodontitis models. AG fibroblasts loca
A previously unrecognized subpopulation of fibroblasts that immediately responded to stimuli from mouse periodontitis models and activated the Toll-like receptor signaling and chemokine expression to guide oral barrier immunity and gingival inflammation was revealed by mouse gingival single-cell transcriptomic atlas.
Abstract Chronic cardiovascular and metabolic diseases have been linked with oral inflammation in the tooth-supporting gingiva. Therefore, elucidating the mechanisms underlying development of gingival inflammation may hold critical insight into the pathogenesis of these debilitating non-communicable diseases. Here, we report a unique fibroblast subpopulation activated to guide oral inflammation (AG fibroblasts), identified in a single-cell RNA sequencing-based gingival cell atlas constructed fro
Periodontitis, one of the most common non-communicable diseases, is characterized by chronic oral inflammation and uncontrolled tooth supporting alveolar bone resorption. Its underlying mechanism to initiate aberrant oral barrier immunity has yet to be delineated. Here, we report a unique fibroblast subpopulation activated to guide oral inflammation (AG fibroblasts) identified in a single-cell RNA sequencing gingival cell atlas constructed from the mouse periodontitis models. AG fibroblasts loca
Periodontitis, one of the most common non-communicable diseases, is characterized by chronic oral inflammation and uncontrolled tooth supporting alveolar bone resorption. Its underlying mechanism to initiate aberrant oral barrier immunity has yet to be delineated. Here, we report a unique fibroblast subpopulation activated to guide oral inflammation (AG fibroblasts) identified in a single-cell RNA sequencing gingival cell atlas constructed from the mouse periodontitis models. AG fibroblasts loca
症例の概要：63歳男性．歯冠の形態や色調に対する不満を主訴に来院した．ブラキシズムの自覚があり，全顎的に著しい咬耗を認めた．全顎的プロビジョナルレストレーションを装着し，約1年間かけて咬合調整や形態調整を行った．Computer-aided design (CAD)を用いて，プロビジョナルレストレーションの形態を正確に再現した最終補綴装置を作製した．
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