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Review
. 2021 Feb;14(1):43-49.
doi: 10.21053/ceo.2020.00416. Epub 2020 Sep 4.

Crosstalk Between Mucosal Inflammation and Bone Metabolism in Chronic Rhinosinusitis

Affiliations
Review

Crosstalk Between Mucosal Inflammation and Bone Metabolism in Chronic Rhinosinusitis

Roza Khalmuratova et al. Clin Exp Otorhinolaryngol. 2021 Feb.

Abstract

Chronic rhinosinusitis (CRS) is a multifactorial and highly heterogeneous upper airway disease that affects approximately 12% of the general population. There is increasing evidence supporting the impact of osteitis on the pathophysiology of CRS. Osteitis is frequently observed in patients with CRS, and is associated with severe sinonasal inflammation and recalcitrant cases. The overlying inflammatory sinonasal mucosa plays a critical role in the initiation of osteitis; however, the underlying molecular mechanisms and functional significance remain unclear. Increasingly many studies have suggested that immune cells play a crucial role in the bone remodeling process in CRS. The purpose of this review is to summarize the current state of knowledge regarding the specific role of sinonasal inflammation in bone remodeling in CRS patients.

Keywords: Chronic Rhinosinusitis; Cytokine; Inflammation; Osteitis; Osteoblasts; Osteoclasts.

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Conflict of interest statement

Hyun Woo Shin is an editorial board member of the journal but did not involve in the peer reviewer selection, evaluation, or decision process of this article. No other potential conflicts of interest relevant to this article were reported.

Figures

Fig. 1.
Fig. 1.
The interplay between immune cells and bone in chronic rhinosinusitis (CRS). Immune cells are involved in shaping the CRS pathophysiology and directly impact osteogenic cells. IL-13 is a pleiotropic type 2 cytokine that contributes to bone remodeling in patients with eosinophilic CRS through its effects on the activity of osteoblasts. IL-17A is a cytokine secreted primarily by Th17 cells that regulates the activity of osteoblasts in non-eosinophilic CRS. IL, interleukin; Th, T helper; ILC2, type 2 innate lymphoid cells.

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