Inflammation-regeneration interplay in the dentine-pulp complex.
OBJECTIVE
Dental tissue disease and trauma provides an excellent model for the interaction between tissue defence and regenerative processes and has application to many of the body's other tissues. Following dental tissue infection, characterised by caries, the molecular and cellular mediators of the immune/inflammatory processes clearly impact on the dental tissues' natural regenerative responses. This review of the literature was performed to better understand how these two processes interact and identify whether cross-talk may provide novel areas for future research and subsequent translation into clinical application.


METHODS
A review of the literature was performed using the PubMed database resource and this was followed by extensive hand searching using reference lists from relevant articles.


CONCLUSIONS
Frequently, the dental tissue inflammatory and regenerative processes are seen as both distinct and antagonistic and subsequently have often been studied in isolation; however, both direct and indirect data are now emerging which indicate significant inter-relationship. Whilst the ensuing inflammatory process will result in dental tissue breakdown and molecular signalling which may impede regeneration, low grade inflammation, potentially induced by mechanical trauma and tissue necrosis, may promote regenerative mechanisms, including angiogenic and stem cell processes. Notably, the locally derived growth factors, neuropeptides, cytokines and chemokines, released from the host dentine matrix and by resident pulpal cells, immune cells, neurons and/or dying cells, will modulate defence and repair processes within the tissue.
Cooper
Paul R
PR
Oral Biology, School of Dentistry, University of Birmingham, St Chad's Queensway, Birmingham B4 6NN, UK. p.r.cooper@bham.ac.uk
Takahashi
Yusuke
Y
Graham
Lee W
LW
Simon
Stephane
S
Imazato
Satoshi
S
Smith
Anthony J
AJ
D003731:Dental Caries / Q000276:immunology / Q000503:physiopathology; D003782:Dental Pulp / Q000276:immunology / Q000503:physiopathology*; D003804:Dentin / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000276:immunology / Q000502:physiology; D011671:Pulpitis / Q000276:immunology / Q000503:physiopathology*; D012038:Regeneration / Q000502:physiology*; D015398:Signal Transduction / Q000276:immunology / Q000502:physiology
D018836:Inflammation Mediators