Anne Eriksson Agger successfully defended her PhD thesis today, 15 September, at the Faculty of Dentistry, University of Oslo.
Her thesis, 3D Models of Inflammation: The Future of Oral In Vitro Pathophysiology?, addresses an important challenge in oral and biomaterials research: how can we more realistically recreate human inflammatory disease more realistically in the laboratory?
Chronic inflammation in the tissues surrounding teeth is a major cause of tissue destruction and tooth loss. Research has traditionally relied on animal experiments and two-dimensional cell cultures. However, neither fully reproduces the complex environment of human tissue. Anne's work, therefore, focused on developing laboratory models using human cells that more closely mimic what occurs during inflammation in the body.
From patient samples to human 3D models
The research progressed from understanding inflammation in patients to reproducing key aspects under controlled laboratory conditions.
Initially, Anne studied tissue samples from patients with persistent apical periodontitis and identified distinct patterns of inflammatory cytokines and chemokines.
The next step was to reproduce chronic inflammation in human gingival fibroblasts in the laboratory. Anne and her colleagues established conditions that combined bacterial lipopolysaccharide and the inflammatory signalling molecule IL-1β, under reduced-serum conditions, and demonstrated that the resulting gene expression and cytokine profiles were relevant to chronic inflammation in human tissue.
The work then shifted from conventional 2D cell culture to the development of a reproducible 3D model. In a recently published Scientific Reports study, Anne and colleagues characterised human gingival fibroblast 3D spheroids and investigated the interplay between inflammation and hypoxia. The combination affected the organisation of the extracellular matrix and cell cytoskeleton and triggered strong inflammatory signalling, while overall cell viability was largely maintained.
These findings establish a human 3D model that captures key interactions among inflammation, hypoxia, extracellular matrix remodelling, and cytokine secretion. The model could provide a platform for studying chronic inflammatory disease and, in future, testing therapeutic strategies in more physiologically relevant human systems.
Towards more human-relevant disease models
Anne's work demonstrates a stepwise development from characterising inflammatory disease in patient samples, through establishing robust 2D models, to building more controlled 3D systems.
This approach may help bridge the gap between simplified laboratory experiments and human disease development by using models and methods that can reduce reliance on animals.
Anne has been part of the Department of Biomaterials since 2019, first as a researcher and, since 2021, as a PhD candidate.
Before the defence, she delivered her trial lecture. The evaluation committee consisted of Professor Umber Cheema from University College London, Dr Lucia Gabriele, Head of the Tumour Immunology Section at the Istituto Superiore di Sanità in Rome, and Professor Thomas Küntziger from the University of Oslo.
The defence was chaired by Dean Hans Jacob Rønold. Associate Professor Athina Samara was Agger's principal supervisor.
The Department warmly congratulates Dr Anne Eriksson Agger on the successful completion of her doctoral degree.
Publications from the thesis
Agger AE, Hlinkova J, Reseland JE, Samara A. 3D models for oral inflammation using gingival fibroblasts, lipopolysaccharides and hypoxia. Scientific Reports, 2026; 16:17190. DOI: 10.1038/s41598-026-47648-7.
Agger AE, Samara A, Geng T, Olstad OK, Reseland JE. Mimicking and in vitro validating chronic inflammation in human gingival fibroblasts. Archives of Oral Biology, 2025; 169:106113. DOI: 10.1016/j.archoralbio.2024.106113.
Agger AE, Reseland JE, Hjelkrem E, Lian A-M, Hals EKB, Zandi H, Sunde PT. Are comorbidities associated with the cytokine/chemokine profile of persistent apical periodontitis? Clinical Oral Investigations, 2023; 27:5203–5215. DOI: 10.1007/s00784-023-05139-3.
