Acceleration of Wound Healing With Topically Applied Deoxyribonucleosides

Chen, E. A.

doi:10.1001/archsurg.134.5.520

Cited by 14 publications

(8 citation statements)

References 27 publications

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“…In trying to address these deficiencies, we have developed the aforementioned rabbit ear wound biofilm model, which we believe is the most accurate representation of biofilm‐infected human chronic wounds to date. Our model utilizes an adaptation of the rabbit dermal ulcer model, 21 an FDA‐recognized model of wound healing that has been utilized by our lab and others for 20 years 22–30 . In this model, full‐thickness, circular punch‐wounds are made in the ears of New Zealand White rabbits down to cartilage, affording a number of important advantages.…”

Section: Discussionmentioning

confidence: 99%

Development of a novel, highly quantitative in vivo model for the study of biofilm‐impaired cutaneous wound healing

Gurjala

Geringer

Seth

et al. 2011

Wound Repair Regeneration

163

149

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A growing body of evidence suggests that in addition to hypoxia, ischemia-reperfusion injury, and intrinsic host factors, bacterial biofilms represent a fourth major pillar in chronic wound pathogenesis. Given that most studies to date rely on in vitro or observational clinical data, our aim was to develop a novel, quantitative animal model enabling further investigation of the biofilm hypothesis in vivo. Dermal punch wounds were created in New Zealand rabbit ears, and used as uninfected controls, or inoculated with green fluorescent protein-labeled Staphylococcus aureus to form wounds with bacteria predominantly in the planktonic or biofilm phase. Epifluorescence and scanning electron microscopy revealed that S. aureus rapidly forms mature biofilm in wounds within 24 hours of inoculation, with persistence of biofilm viability over time seen through serial bacterial count measurement and laser scanning confocal imaging at different time points postwounding and inoculation. Inflammatory markers confirmed that the biofilm phenotype creates a characteristic, sustained, low-grade inflammatory response, and that over time biofilm impairs epithelial migration and granulation tissue in-growth, as shown histologically. We have established and validated a highly quantitative, reproducible in vivo biofilm model, while providing evidence that the biofilm phenotype specifically contributes to profound cutaneous wound healing impairment. Our model highlights the importance of bacterial biofilms in chronic wound pathogenesis, providing an in vivo platform for further inquiry into the basic biology of bacterial biofilm-host interaction and high-throughput testing of antibiofilm therapeutics.

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Section: Discussionmentioning

confidence: 99%

Development of a novel, highly quantitative in vivo model for the study of biofilm‐impaired cutaneous wound healing

Gurjala

Geringer

Seth

et al. 2011

Wound Repair Regeneration

163

149

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“…Moreover, our knowledge of the precise cellular changes that characterize delayed healing is at present scarce, this being in part due to the lack of easily reproducible experimental models. The models described so far 30–32 do not entirely mimic the clinical problems encountered in chronic ulcers of the lower limb. Some of them involve linear incisions that obviously do not take into account wound contraction, others involve denervation, and some require the use of flaps.…”

Section: Discussionmentioning

confidence: 99%

Persistent ischemia impairs myofibroblast development in wound granulation tissue: A new model of delayed wound healing

Alizadeh¹,

Pepper

M³

et al. 2007

Wound Repair Regeneration

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We describe a new animal model designed to assess the impact of ischemia on wound healing. Eight patterns of arterial lesion in the limb were first tested in 24 Wistar rats. Resection of the external iliac artery down to the femoral artery at the level of the knee was chosen as the reference model and performed on the left limb of 45 rats; the right limb was used as the control. Skin wounds measuring 1.2 x 0.8 cm were created on both feet. Ischemia was assessed by blood flow measurement, which decreases dramatically in the ischemic limb. A significant delay in wound closure with a decrease in wound contraction was observed in the ischemic limb. Myofibroblast quantification showed a significant delay in appearance as well as a decrease in the number of these cells in the ischemic wound. Vascular endothelial growth factor-A appearance and evolution were qualitatively similar in both situations. However, collagen type I mRNA was markedly decreased in ischemic granulation tissue 10 days after wounding. These findings suggest that decreased wound contraction plays an important role in delayed ischemic wound healing, probably due to reduced myofibroblast development and activity.

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“…In vivo animal models have been developed to study the mechanisms of wound healing in both normal and impaired states (Rothe & Falanga, 1992). Studies have shown that topological application of cod liver oil ointment, vitamin A, deoxyribonucleosides, and some proteins can accelerate wound healing (Shah et al ., 1995; Chen et al ., 1999; Terkelsen et al ., 2000). However, up to now we know very little about the inheritance of the rate of wound healing and the mode of its inheritance.…”

Section: Introductionmentioning

confidence: 99%

Genetic control of the rate of wound healing in mice

Masinde

et al. 2001

Heredity

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There have been few studies of the inheritance of wound healing in mammals. In this study, we demonstrate that inbred strains of mice differ significantly in the rate of wound healing. Of the 20 strains tested, fast healers (MRL/MpJ‐Faslpr and LG/J) healed wounds four times faster than slow healers (Balb/cByJ and SJL/J). The genetic basis underlying the difference in the healing capacity was analysed using F2 populations of two different crosses. We show that the wound healing is a polygenically determined quantitative trait with an average estimated heritability of 86%. The modes of gene action in these two crosses are different. In the (MRL/MpJ × SJL/J) cross, genes regulating fast healing in MRL/MpJ mice exhibited additive effects, whereas these effects were suppressed by a dominant repressor gene in CBA/J mice in the (MRL/MpJ‐Faslpr× CBA/J) cross. Information gained from this investigation provides insight into further study of molecular mechanisms underlying the rate of wound healing in mammals.

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Acceleration of Wound Healing With Topically Applied Deoxyribonucleosides

Abstract: We hypothesized that a topical mixture of purified deoxyribonucleosides would accelerate wound healing in an open wound model.

Cited by 14 publications

References 27 publications

Development of a novel, highly quantitative in vivo model for the study of biofilm‐impaired cutaneous wound healing

Development of a novel, highly quantitative in vivo model for the study of biofilm‐impaired cutaneous wound healing

Persistent ischemia impairs myofibroblast development in wound granulation tissue: A new model of delayed wound healing

Genetic control of the rate of wound healing in mice

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