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Outpatient-based sharp debridement is considered an important element for the care of a chronic ulcer.The aim of this study is to evaluate the change in bacterial amounts with sharp debridement in a clinical setting.Bacterial autofluorescence, quantitative cultures, semiquantitative cultures, and qualitative speciation were performed predebridement and postdebridement during a single clinic visit.Thirty-six wounds were included in the analysis. The mean patient age was 62 years (range, 27-83 years), and there were 13 (36.11%) women and 23 (63.89%) men with an average body mass index of 33.8 kg/m² (range, 16.7-55.9 kg/m²). Of the 36 patients, 24 (66.67%) had type 2 diabetes and 19 (52.78%) had a prior history of lower extremity amputation. Majority of the ulcers were diabetic neuropathic (27, 75%); the most common location was on the plantar aspect of the foot (14, 41.67%) with a mean ulcer duration of 10 months (range, 1-36), mean ulcer area of 6.3 ± 12.8 cm² (range, 0.18-62.06 cm²), and mean volume of 2.2 ± 4.4 cm³ (range, 0.05-9.66 cm³). There was no statistically significant difference in bacterial autofluorescence between the predebridement (4.15 ± 8.82) and the postdebridement (4.65 ± 9.48) images (P = .32). There was a statistically significant difference in quantitative culture results between the predebridement (6.7 x 104 ± 1.4 x 106 CFU/cm²) and the postdebridement (1.7 x 104 ± 3.1 x 106 CFU/cm²) cultures (P = .04), although this is not a log reduction.There is no statistically significant difference between the predebridement versus postdebridement semiquantitative culture results or a detectable pattern of change for the most common bacterial species encountered. These results suggest little impact of clinic-based sharp debridement on bacteria.

Advanced age is associated with an increased risk of vascular morbidity, attributable in part to impairments in new blood vessel formation. Mesenchymal stem cells (MSCs) have previously been shown to play an important role in neovascularization and deficiencies in these cells have been described in aged patients. Here we utilize single cell transcriptional analysis to determine the effect of aging on MSC population dynamics. We identify an age-related depletion of a subpopulation of MSCs characterized by a pro-vascular transcriptional profile. Supporting this finding, we demonstrate that aged MSCs are also significantly compromised in their ability to support vascular network formation in vitro and in vivo. Finally, aged MSCs are unable to rescue age-associated impairments in cutaneous wound healing. Taken together, these data suggest that age-related changes in MSC population dynamics result in impaired therapeutic potential of aged progenitor cells. These findings have critical implications for therapeutic cell source decisions (autologous versus allogeneic) and indicate the necessity of strategies to improve functionality of aged MSCs.