Bisphosphonate-related osteonecrosis of the jaw

Almoghazy, Safwat

doi:10.53347/rid-54147

Cited by 1 publication

(1 citation statement)

References 2 publications

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“…Overall, the observed pattern of periodontal tissue degradation was consistent with that reported in previous studies (24), (25) . Left-side palatal gingiva tissue was harvested from mice on Day 0 (i.e., healthy gingiva without ligature placement) and on Days 1, 4, and 7 after ligature placement, and gingival cells were dissociated for single-cell RNA sequencing (scRNA-seq) (22), (26) . On Days 0 and 1, the major cell types identified included epithelial cells expressing cadherin 1 (Cdh1) (27) and type XVII collagen (Col17a1) (28) , fibroblasts expressing type I collagen (Col1a1) (29) and lumican (Lum) (30) , B cells expressing membrane spanning 4 domains A1 (Ms4a1) (31) and cluster of differentiation 79A (Cd79a) (32) , T cells expressing epsilon subunit of T cell receptor complex (Cd3e) (33) and cluster of differentiation 5 (Cd5) (34) , and myeloid cells expressing lysozyme 2 (Lyz2) (35) and integrin subunit alpha M (Itgam) (36) (Figure 1E and F-figure supplement 2).…”

Section: Alterations In Major Cell Type Proportions During Periodonti...mentioning

confidence: 99%

Mouse gingival single-cell transcriptomic atlas identified a novel fibroblast subpopulation activated to guide oral barrier immunity in periodontitis

Kondo

Gleason

Okawa

et al. 2023

eLife

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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 from the mouse ligature-induced periodontitis model. Collagen-XIV-positive AG fibroblasts localized beneath gingival epithelium express chemokine ligands and Toll-like receptor-related molecules upon ligature placement, which were linked to receptors expressed by neutrophils and lymphocytes, including innate lymphoid cells (ILCs). We further identify ILCs as the primary source of proinflammatory interleukin-17 cytokines and show that cervical alveolar bone resorption is absent in Rag2-/-γc-/-, but not Rag2-/-, mice suggesting ILC3s mediate the human periodontitis-like phenotype. We therefore propose AG fibroblasts function as a previously unrecognized surveillant to orchestrate chronic gingival inflammation in periodontitis.

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