Matthias Widbiller

Prof. Dr. Matthias Widbiller

Department of Conservative Dentistry and Periodontology, University Hospital Regensburg, 93053 Regensburg, Germany
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Research Focus & Metrics

Academic Career Length

12Years (2015-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Journal Article
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KGKerstin M. Galler
Kerstin M. Galler
MWManuel Weber
Manuel Weber
YKYüksel Korkmaz
Yüksel Korkmaz
Matthias WidbillerMatthias Widbiller
Matthias Widbiller
MFMarkus Feuerer
Markus Feuerer
The macroscopic and microscopic anatomy of the oral cavity is complex and unique in the human body. Soft-tissue structures are in close interaction with mineralized bone, but also dentine, cementum and enamel of our teeth. These are exposed to intense mechanical and chemical stress as well as to dense microbiologic colonization. Teeth are susceptible to damage, most commonly to caries, where microorganisms from the oral cavity degrade the mineralized tissues of enamel and dentine and invade the soft connective tissue at the core, the dental pulp. However, the pulp is well-equipped to sense and fend off bacteria and their products and mounts various and intricate defense mechanisms. The front rank is formed by a layer of odontoblasts, which line the pulp chamber towards the dentine. These highly specialized cells not only form mineralized tissue but exert important functions as barrier cells. They recognize pathogens early in the process, secrete antibacterial compounds and neutralize bacterial toxins, initiate the immune response and alert other key players of the host defense. As bacteria get closer to the pulp, additional cell types of the pulp, including fibroblasts, stem and immune cells, but also vascular and neuronal networks, contribute with a variety of distinct defense mechanisms, and inflammatory response mechanisms are critical for tissue homeostasis. Still, without therapeutic intervention, a deep carious lesion may lead to tissue necrosis, which allows bacteria to populate the root canal system and invade the periradicular bone via the apical foramen at the root tip. The periodontal tissues and alveolar bone react to the insult with an inflammatory response, most commonly by the formation of an apical granuloma. Healing can occur after pathogen removal, which is achieved by disinfection and obturation of the pulp space by root canal treatment. This review highlights the various mechanisms of pathogen recognition and defense of dental pulp cells and periradicular tissues, explains the different cell types involved in the immune response and discusses the mechanisms of healing and repair, pointing out the close links between inflammation and regeneration as well as between inflammation and potential malignant transformation.

22 July 2015 in International Endodontic Journal
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KGKerstin M. Galler
Kerstin M. Galler
Matthias WidbillerMatthias Widbiller
Matthias Widbiller
WBW. Buchalla
W. Buchalla
AEA. Eidt
A. Eidt
KHK. ‐A. Hiller
K. ‐A. Hiller
GSG. Schmalz
G. Schmalz

8 March 2021 in International Endodontic Journal
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Journal Article
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Gabriel KrastlGabriel Krastl
Gabriel Krastl
RWR. Weiger
R. Weiger
AFA. Filippi
A. Filippi
HWH. Van Waes
H. Van Waes
KEK. Ebeleseder
K. Ebeleseder
KGK. Galler
K. Galler
The pulp plays a key role in the treatment of traumatic dental injuries (TDIs) and is strongly associated with the outcome, particularly in severe cases. A correct pulp diagnosis is essential as it forms the basis for developing the appropriate management strategy. However, many TDIs are complex, and their treatment requires a profound knowledge of the physiological and pathological responses of the affected tissues. This comprehensive review will look at the dentine–pulp complex and its interaction with the surrounding tissues following TDIs. The literature up to 2020 was reviewed based on several searches on PubMed and the Cochrane Library using relevant terms. In addition to the recently revised guidelines of the International Association of Dental Traumatology, this article aims to provide background information with a focus on endodontic aspects and to gather evidence on which a clinician can make decisions on the choice of the appropriate endodontic approach for traumatized permanent teeth.

29 October 2024 in Frontiers in Immunology
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SPSandra Pohl
Sandra Pohl
TATobias Akamp
Tobias Akamp
MSMartyna Smeda
Martyna Smeda
SUStefan Uderhardt
Stefan Uderhardt
DBDavid Besold
David Besold
Matthias WidbillerMatthias Widbiller
Matthias Widbiller
The pulp is a unique tissue within each tooth that is susceptible to painful inflammation, known as pulpitis, triggered by microbial invasion from carious lesions or trauma that affect many individuals. The host response involves complex immunological processes for pathogen defense and dentin apposition at the site of infection. The interplay of signaling between the immune and non-immune cells via cytokines, chemokines, neuropeptides, proteases, and reactive nitrogen and oxygen species leads to tissue reactions and structural changes in the pulp that escalate beyond a certain threshold to irreversible tissue damage. If left untreated, the inflammation, which is initially localized, can progress to pulpal necrosis, requiring root canal treatment and adversely affecting the prognosis of the tooth. To preserve pulp vitality and dental health, a deeper understanding of the molecular and cellular mechanisms of pulpitis is imperative. In particular, elucidating the links between signaling pathways, clinical symptoms, and spatiotemporal spread is essential to develop novel therapeutic strategies and push the boundaries of vital pulp therapy.

3 March 2019 in International Endodontic Journal
Verified
Journal Article
Closed access
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KGKerstin M. Galler
Kerstin M. Galler
VGV. Grubmüller
V. Grubmüller
RSR. Schlichting
R. Schlichting
Matthias WidbillerMatthias Widbiller
Matthias Widbiller
AEA. Eidt
A. Eidt
WBW. Buchalla
W. Buchalla

1 September 2020 in Journal of Endodontics
Verified
Journal Article
Closed access
GSGottfried Schmalz
Gottfried Schmalz
Matthias WidbillerMatthias Widbiller
Matthias Widbiller
KGKerstin M. Galler
Kerstin M. Galler