In our last blog, we had discussed the five classifications of Debridement including sharp debridement. As noted, sharp debridement is one of the quickest and most effective means of debridement especially for wound slough, devitalized, escharotic and non-viable tissue. This also includes Biofilm.
Although Biofilm is not readily seen atop of wound beds, rest assure it is there as well as its protective shield or glycocalyx. When describing Biofilm, I often times refer to our favorite Marvel comic heroes who can generate an impenetrable shield to protect not only themselves, but others within the vicinity. That’s exactly what Biofilm can do in wounds. In essence Biofilm is a conglomerate of bacteria living in the extracellular polymeric substance or EPS composed of polysaccharides, proteins, extracellular DNA and lipids. This environment provides biofilm the protection it needs from adverse environmental factors and the hosts immunological responses, thus making it virtually impervious to topical wound products and agents, cleansing solutions, and antibiotics. That is why sharp debridement remains the gold standard in the treatment of Biofilm.
Biofilm is also composed of multiple aggregates and colonies across the wound surface, with the more mature colonies living within the superficial strata and immature groupings below. The colonies contain different properties and phenotypical characteristics creating challenges in treatment. Not to mention the bacteria also change their phenotype both from production and also the host. Biofilm is very energy efficient in production and perpetuates the inflammatory phase in wound healing leading to chronic wounds. Therefore, chronic wounds cannot progress to the fibro-proliferative and remodeling phases.
Biofilm therefore leads to changes in normal cellular DNA syntheses and increases the formation of Metalloproteases (MMPs). MPPs impede the fundamental building blocks of cellular function including chemotactic factors, growth factors, and mitogens. The disruptive nature of Biofilm also phenotypically alters Fibroblasts by delaying replication which ultimately leads to impaired and dysfunctional granulation tissue. Peripheral keratinocytes are also altered and therefore cannot differentiate and therefore migrate across the wound: a very important step needed for wound contracture and secondary intent healing.
As you can see, Biofilm and chronic wounds can be extremely detrimental in the wound care space as the longevity of the wound continues to progress. The wounds which continue to wax and wane with exacerbations, or respond incompletely to antibiotics with symptomatology reemerging following withdrawal rapidly are becoming a surging social-economic problem. Are there methods or a combination of tenants that will thwart this ongoing problem and if so, what are the next steps?
In my next installment of wound bed preparation, we will take an in-depth look at the literature in regards to sharp debridement and Biofilm. Please check back often and until next time, fair winds and following sees.
In our last blog, we had discussed the five classifications of Debridement including sharp debridement. As noted, sharp debridement is one of the quickest and most effective means of debridement especially for wound slough, devitalized, escharotic and non-viable tissue. This also includes Biofilm.
Although Biofilm is not readily seen atop of wound beds, rest assure it is there as well as its protective shield or glycocalyx. When describing Biofilm, I often times refer to our favorite Marvel comic heroes who can generate an impenetrable shield to protect not only themselves, but others within the vicinity. That’s exactly what Biofilm can do in wounds. In essence Biofilm is a conglomerate of bacteria living in the extracellular polymeric substance or EPS composed of polysaccharides, proteins, extracellular DNA and lipids. This environment provides biofilm the protection it needs from adverse environmental factors and the hosts immunological responses, thus making it virtually impervious to topical wound products and agents, cleansing solutions, and antibiotics. That is why sharp debridement remains the gold standard in the treatment of Biofilm.
Biofilm is also composed of multiple aggregates and colonies across the wound surface, with the more mature colonies living within the superficial strata and immature groupings below. The colonies contain different properties and phenotypical characteristics creating challenges in treatment. Not to mention the bacteria also change their phenotype both from production and also the host. Biofilm is very energy efficient in production and perpetuates the inflammatory phase in wound healing leading to chronic wounds. Therefore, chronic wounds cannot progress to the fibro-proliferative and remodeling phases.
Biofilm therefore leads to changes in normal cellular DNA syntheses and increases the formation of Metalloproteases (MMPs). MPPs impede the fundamental building blocks of cellular function including chemotactic factors, growth factors, and mitogens. The disruptive nature of Biofilm also phenotypically alters Fibroblasts by delaying replication which ultimately leads to impaired and dysfunctional granulation tissue. Peripheral keratinocytes are also altered and therefore cannot differentiate and therefore migrate across the wound: a very important step needed for wound contracture and secondary intent healing.
As you can see, Biofilm and chronic wounds can be extremely detrimental in the wound care space as the longevity of the wound continues to progress. The wounds which continue to wax and wane with exacerbations, or respond incompletely to antibiotics with symptomatology reemerging following withdrawal rapidly are becoming a surging social-economic problem. Are there methods or a combination of tenants that will thwart this ongoing problem and if so, what are the next steps?
In my next installment of wound bed preparation, we will take an in-depth look at the literature in regards to sharp debridement and Biofilm. Please check back often and until next time, fair winds and following sees.
Cheers,
Dr. F. Derk
