From silicosis to sarcoid-like reaction: a continuum model of silica-induced lung disease
- 1Department of Pulmonary Diseases, Faculty of Medicine, Ağrı İbrahim Çeçen University, Ağrı, Turkey
- 2Department of Pulmonary Diseases, Atatürk University School of Medicine, Erzurum, Turkey
- 3Department of Occupational Medicine, Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, University of Health Sciences, İstanbul, Turkey
Abstract
The term “sarcoidosis”, coined in 1899 from the Greek sarx (flesh) and -oid (resembling), is descriptive and conveys no aetiological information. When a trigger has been identified for a granulomatous condition previously considered idiopathic, nomenclature has tended to shift from descriptive to aetiological, as when “Salem sarcoid” was reclassified as chronic beryllium disease (CBD). Crystalline silica exposure has been associated with sarcoidosis in several occupational cohorts, and partially overlapping immunopathogenic pathways have been described, notably NLR family pyrin domain containing 3 (NLRP3) inflammasome activation and T-helper cell 17.1 (Th17.1) polarisation, neither of which is disease-specific. The available evidence is consistent with a continuum model of silica-induced lung disease spanning a silicotic fibrotic phenotype (classical silicosis, driven by NLRP3 and transforming growth factor-β1 signalling), a granulomatous phenotype (silica-induced sarcoid-like reaction (SISLR), driven by NLRP3, interleukin-1β and Th17.1 signalling in susceptible individuals) and a mixed phenotype in which both processes coexist. The silica lymphocyte proliferation test (Si-LPT) has detected in vitro immunoreactivity in a subset of patients with sarcoidosis but is not standardised. The CBD paradigm offers useful analogies, although beryllium-driven adaptive and silica-driven innate mechanisms differ in important respects. SISLR may serve as a working classification that identifies the putative trigger, supports occupational disease recognition and situates the granulomatous response within a broader continuum; we discuss it alongside the alternative “silicosarcoidosis” terminology. On the evidence reviewed, crystalline silica should no longer be treated as an incidental co-exposure in a patient with sarcoid-type granulomas. A documented exposure warrants classification as occupationally related granulomatous lung disease and standardising the Si-LPT is the immediate priority.
Related
- Hodgkin Lymphoma With Sarcoid-Like Reaction: Importance of Clinicopathological Correlation in Granulomatous Lymphadenopathy.
- Artificial Stone Silicosis: New Face of an Old Disease
- MRI-Negative Sarcoid Myelitis Revealed by Spinal ¹⁸F-FDG-PET Hypermetabolism.
- Memantine-Induced Sialorrhea: A Rare Adverse Reaction and Review of Pathophysiological Mechanisms
- 1141 Spatial immune profiling across the lobular breast cancer continuum reveals progressive immune exclusion from precursor lesion to invasive disease
BibTeX
@article{akgun2026from,
title = {{From silicosis to sarcoid-like reaction: a continuum model of silica-induced lung disease}},
author = {Metin Akgün and Alperen Aksakal and Ozlem Kar Kurt},
journal = {European Respiratory Review},
year = {2026},
month = nov,
doi = {10.1183/16000617.0153-2026},
url = {https://doi.org/10.1183/16000617.0153-2026},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - From silicosis to sarcoid-like reaction: a continuum model of silica-induced lung disease
AU - Metin Akgün
AU - Alperen Aksakal
AU - Ozlem Kar Kurt
PY - 2026
DA - 2026/11/04
JO - European Respiratory Review
DO - 10.1183/16000617.0153-2026
UR - https://doi.org/10.1183/16000617.0153-2026
AB - The term “sarcoidosis”, coined in 1899 from the Greek sarx (flesh) and -oid (resembling), is descriptive and conveys no aetiological information. When a trigger has been identified for a granulomatous condition previously considered idiopathic, nomenclature has tended to shift from descriptive to aetiological, as when “Salem sarcoid” was reclassified as chronic beryllium disease (CBD). Crystalline silica exposure has been associated with sarcoidosis in several occupational cohorts, and partially overlapping immunopathogenic pathways have been described, notably NLR family pyrin domain containing 3 (NLRP3) inflammasome activation and T-helper cell 17.1 (Th17.1) polarisation, neither of which is disease-specific. The available evidence is consistent with a continuum model of silica-induced lung disease spanning a silicotic fibrotic phenotype (classical silicosis, driven by NLRP3 and transforming growth factor-β1 signalling), a granulomatous phenotype (silica-induced sarcoid-like reaction (SISLR), driven by NLRP3, interleukin-1β and Th17.1 signalling in susceptible individuals) and a mixed phenotype in which both processes coexist. The silica lymphocyte proliferation test (Si-LPT) has detected in vitro immunoreactivity in a subset of patients with sarcoidosis but is not standardised. The CBD paradigm offers useful analogies, although beryllium-driven adaptive and silica-driven innate mechanisms differ in important respects. SISLR may serve as a working classification that identifies the putative trigger, supports occupational disease recognition and situates the granulomatous response within a broader continuum; we discuss it alongside the alternative “silicosarcoidosis” terminology. On the evidence reviewed, crystalline silica should no longer be treated as an incidental co-exposure in a patient with sarcoid-type granulomas. A documented exposure warrants classification as occupationally related granulomatous lung disease and standardising the Si-LPT is the immediate priority.
SN - 0905-9180
SN - 1600-0617
ER -