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Cited by 329

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Infection, Inflammation, and Bone Regeneration: a Paradoxical Relationship

Open access
Thomas, M.V., Puleo, D.A.·2011·Journal of Dental Research

Abstract

Various strategies have been developed to promote bone regeneration in the craniofacial region. Most of these interventions utilize implantable materials or devices. Infections resulting from colonization of these implants may result in local tissue destruction in a manner analogous to periodontitis. This destruction is mediated via the expression of various inflammatory mediators and tissue-destructive enzymes. Given the well-documented association among microbial biofilms, inflammatory mediators, and tissue destruction, it seems reasonable to assume that inflammation may interfere with bone healing and regeneration. Paradoxically, recent evidence also suggests that the presence of certain pro-inflammatory mediators is actually required for bone healing. Bone injury (e.g., subsequent to a fracture or surgical intervention) is followed by a choreographed cascade of events, some of which are dependent upon the presence of pro-inflammatory mediators. If inflammation resolves promptly, then proper bone healing may occur. However, if inflammation persists (which might occur in the presence of an infected implant or graft material), then the continued inflammatory response may result in suboptimal bone formation. Thus, the effect of a given mediator is dependent upon the temporal context in which it is expressed. Better understanding of this temporal sequence may be used to optimize regenerative outcomes.

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Crossref · 10.1177/0022034510393967

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Metadata

Authors
Thomas, M. V., & Puleo, D. A.
Venue
Journal of Dental Research
Published
2011-01-19
Volume
90
Issue
9
Pages
1052-1061
ISSN
  • 0022-0345 (ISSN-L)
  • 1544-0591
OpenAlex
W2159314490
Cited by
329
References
4
FWCI
8.75
Type
journal article
Language
en
Open access
green

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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