Abstract
Chronic wounds, including pressure ulcers, foot ulcers, and venous leg ulcers, have a detrimental impact on the health and well-being of an estimated 2% of people in the UK. Chronic wounds are normally colonized by bacteria and in some instances bacterial load increases sufficiently for infection to ensue. Once a chronic wound becomes infected it is difficult to resolve and a combination of continuous inflammation and bacterial proliferation makes these wounds difficult to manage. A state of prolonged inflammation can occur as a result of impaired homeostatic pathways, which are exacerbated by bacterial growth. Chronic, infected wounds can persist for many months or even years, sometimes requiring surgical intervention in the form of regular debridement or amputation when other strategies such as antimicrobial treatments fail. The complex relationships between both oral microbiota and the host have been extensively characterized, including the shift from health to disease, and this has allowed the development of numerous control strategies. This knowledge, combined with contemporary studies of chronic infected wounds, can be used to develop an understanding of the relationship between the host and microorganism in the chronic wound environment. Such information has the potential to inform wound management including strategies to control infection and promote wound healing.
Highlights
In developed countries, it has been estimated that 1 to 2% of the population will experience a chronic wound during their lifetime (Gottrup, 2004)
Elevated apoptosis of keratinocytes and mesenchymal stromal cells combined with a general reduction in viability and impaired migration is observed in response to biofilms of a wide genera of microorganisms including S. aureus and P. aeruginosa, which impedes early stage angiogenesis and consequent wound healing (Kirker et al, 2009, Secor et al, 2011, Ward et al, 2015, Zhao et al, 2010) It has been proposed that these effects are mediated by reduced cytokine expression resulting from suppressed JNK (c-Jun N-terminal kinases) and p38 phosphorylation (Ward et al, 2015, Secor et al, 2011)
Typical microbial profiles associated with “normal skin microbiota” are sometimes observed within chronic wounds but once infection has established, these diminish to be replace by a few pathogenic bacteria; this is indicative of dysbiosis as observed in the oral cavity
Summary
It has been estimated that 1 to 2% of the population will experience a chronic wound during their lifetime (Gottrup, 2004). Elevated apoptosis of keratinocytes and mesenchymal stromal cells combined with a general reduction in viability and impaired migration is observed in response to biofilms of a wide genera of microorganisms including S. aureus and P. aeruginosa, which impedes early stage angiogenesis and consequent wound healing (Kirker et al, 2009, Secor et al, 2011, Ward et al, 2015, Zhao et al, 2010) It has been proposed that these effects are mediated by reduced cytokine expression resulting from suppressed JNK (c-Jun N-terminal kinases) and p38 phosphorylation (Ward et al, 2015, Secor et al, 2011).
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