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1.
Int J Mol Sci. 2016 Dec 11;17(12). pii: E2085.

Inflammation in Chronic Wounds.

Author information

1
Sutton Arthritis Research Laboratory, Kolling Institute of Medical Research, University of Sydney, NSW 2065, Australia. rzha9073@uni.sydney.edu.au.
2
Sutton Arthritis Research Laboratory, Kolling Institute of Medical Research, University of Sydney, NSW 2065, Australia. helena.liang@sydney.edu.au.
3
Murray Maxwell Biomechanics Laboratory, Kolling Institute of Medical Research, University of Sydney, NSW 2065, Australia. elizabeth.clarke@sydney.edu.au.
4
Sutton Arthritis Research Laboratory, Kolling Institute of Medical Research, University of Sydney, NSW 2065, Australia. chris.jackson@sydney.edu.au.
5
Sutton Arthritis Research Laboratory, Kolling Institute of Medical Research, University of Sydney, NSW 2065, Australia. meilang.xue@sydney.edu.au.

Abstract

Non-healing chronic wounds present a major biological, psychological, social, and financial burden on both individual patients and the broader health system. Pathologically extensive inflammation plays a major role in the disruption of the normal healing cascade. The causes of chronic wounds (venous, arterial, pressure, and diabetic ulcers) can be examined through a juxtaposition of normal healing and the rogue inflammatory response created by the common components within chronic wounds (ageing, hypoxia, ischaemia-reperfusion injury, and bacterial colonisation). Wound bed care through debridement, dressings, and antibiotics currently form the basic mode of treatment. Despite recent setbacks, pharmaceutical adjuncts form an interesting area of research.

KEYWORDS:

ageing; arterial ulcer; bacterial colonisation; chronic wound; diabetic ulcer; hypoxia; inflammation; ischaemia-reperfusion; pressure ulcer; venous ulcer

PMID:
27973441
PMCID:
PMC5187885
DOI:
10.3390/ijms17122085
[Indexed for MEDLINE]
Free PMC Article
Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
2.
Adv Wound Care (New Rochelle). 2013 Sep;2(7):389-399.

Biofilms and Inflammation in Chronic Wounds.

Author information

1
Division of Dermatology, University of Washington , Seattle, Washington.
2
Department of Genome Sciences, University of Washington , Seattle, Washington.
3
Center for Biofilm Engineering, Montana State University , Bozeman, Montana.

Abstract

SIGNIFICANCE:

The incidence, cost, morbidity, and mortality associated with non-healing of chronic skin wounds are dramatic. With the increasing numbers of people with obesity, chronic medical conditions, and an increasing life expectancy, the healthcare cost of non-healing ulcers has recently been estimated at $25 billion annually in the United States. The role played by bacterial biofilm in chronic wounds has been emphasized in recent years, particularly in the context of the prolongation of the inflammatory phase of repair.

RECENT ADVANCES:

Rapid high-throughput genomic approaches have revolutionized the ability to identify and quantify microbial organisms from wounds. Defining bacterial genomes and using genetic approaches to knock out specific bacterial functions, then studying bacterial survival on cutaneous wounds is a promising strategy for understanding which genes are essential for pathogenicity.

CRITICAL ISSUES:

When an animal sustains a cutaneous wound, understanding mechanisms involved in adaptations by bacteria and adaptations by the host in the struggle for survival is central to development of interventions that favor the host.

FUTURE DIRECTIONS:

Characterization of microbiomes of clinically well characterized chronic human wounds is now under way. The use of in vivo models of biofilm-infected cutaneous wounds will permit the study of the mechanisms needed for biofilm formation, persistence, and potential synergistic interactions among bacteria. A more complete understanding of bacterial survival mechanisms and how microbes influence host repair mechanisms are likely to provide targets for chronic wound therapy.

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