The Skin and Science Series
In this blog series, we unravel the intricate science behind it all. Our aim is to empower you with knowledge so that you can make well-informed decisions about your skincare routine. From exploring the intricate workings of various skin types to understanding the powerful ingredients that transform our complexion - each instalment of this series promises to provide you with valuable insights and practical advice.
TL;DR
Most aesthetic procedures induce some form of 'wound' and that is entirely the intention! Wounds are the starting point for new collagen formation. However, inefficient wound healing may have undesirable effects such as reduction in efficacy of treatment, increased risk of post-procedure hyperpigmentation and even infection. Some individuals are more at-risk of delayed wound healing than others but thankfully there are new (and old) approaches that not only improve wound healing but may even improve the outcome of aesthetic procedures themselves.
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Wounds are a common business in skincare
Wounds are a common business in aesthetics procedures, after all the most effective way to boost collagen and other components of the extracellular matrix in skin is by taking advantage of our wound healing response – specifically designed through evolution to rapidly restore the skin barrier by remodelling the extracellular matrix.
While we may think of wounds as physical breaches to the skin (i.e. scratches, open cuts, lacerations etc), a wound is an injury that damages skin or the underlying components of skin.
Understanding this, we then include bruises, excessive UV light exposure and burns to the list. Irrespective of the cause, we can describe wound healing in 4 stages.
Wound healing is a 4-stage process
The first stage of wound healing occurs in mere minutes! It is where blood clotting (haemostasis) occurs and the inflammatory signals are set up for the next stage to come – that is, Inflammation.
Inflammation is the stage in wound healing where we can see the effect under our naked eye. Redness ensues around the area and it often feels hot to the touch. Both these features are the effect of increased blood flow – vital in wound healing.
Blood carries nutrients/gases, and in an area that needs to be rebuilt following a wound, the nutrient requirement is high. The Inflammation stage generally lasts 1-3 days, depending on the magnitude of the wound however this is also the stage where we would expect delays in wound healing to occur.
Immune cells are recruited during this stage and the key immune cell, macrophages become activated and release growth factors that lead to the next stage - Proliferation.
4 stages of wound healing
Proliferation is where the magic of wound healing occurs – the dominant cell types in the skin divide, including keratocytes and fibroblast and the wound begins to seal. This also coincides with the ramped-up production of collagen – type III collagen. Generally, this process takes 3-5 days.
The final stage is where collagen matures, the skin matrix remodels and the debri is removed. This stage is called Remodelling or Organisation because the skin reorganises. It is perhaps the most critical part of wound healing when it comes to aesthetics because it is this stage where mature collagen is produced and older/weaker collagen fibres are dissolved.
Remodelling takes many weeks and months and this explains why the effects of aesthetics procedures often take months to fully appreciate their effects on the skin.
Collagen III is reabsorbed and eventually replaced by stronger collagen IFactors that delay wound healing
Wound healing is an inflammatory process – though too much inflammation (hyperinflammation) or too little inflammation (immunosuppression) can affect the wound healing process and often this results in delay and inefficient wound healing. While excessive inflammation delays the proliferation stage of wound healing, too little inflammation limits the release of growth factors and this too slows the proliferation stage and thus keratocytes and fibroblasts are unable to close the wound in a timely manner.
Poor blood supply is the major cause for delayed wound healing. Simply put, there just isn’t enough nutrients reaching the affected area for efficient wound healing to occur as blood is the way our body carries nutrients. Wounds are nutrient-hungry zones and understandably require more nutrients than unaffected tissue. Protein malnourishment is well-documented in delayed wound healing.
Risk factors for delayed wound healing
The following are risk factors for delayed wound healing
- Diabetes
- Obesity
- Anorexia nervosa (protein malnourishment)
- Smokers
- Chronic conditions/immunosuppression
Uncontrolled diabetes can result in poor blood supply, and we established earlier that blood supply is critical for wound healing. For example, it is not uncommon to see foot ulcers that persist for weeks and months in individuals with diabetes. These are wounds that have delayed healing and require clinical intervention.
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Individuals in a hyperinflammatory state (i.e obesity) or individuals who are immunosuppressed (chronic illness, immunosuppressive medications, chemotherapies) are also likely to experience delayed wound healing.
Even as we age, our general biological processes become less efficient and this includes processes of wound healing.
The question is, what are the consequences of delayed wound healing and can we intervene to improve the outcome?
Consequences of delayed wound healing
Reduction in the efficacy of aesthetic treatment is a likely outcome of delayed wound healing (apart from opportunistic infections as a more serious complication of delayed wound healing).
Almost all clinic aesthetic procedures are designed in one way or another to elicit a wound and to lay down new collagen. However, just as important is the quality of collagen deposited. In the early stages of wound healing (i.e. during proliferation), fibroblast quickly lay down type III collagen.
Type III collagen is a clumsy disorganised type of collagen that has poor tensile strength and is randomly deposited. However, the speed by which we can produce this type of collagen makes it ideal to seal the wound rapidly – often within days!
In the final remodelling phase of wound healing (also known as ‘organisation’), the type III collagen is slowly dissolved and replaced by well-formed and mature collagen type I which is the dominant skin collagen - boasting a much greater mechanical strength at the expense of weeks and months to produce!
Delaying the transition from collagen type III to collagen type I due to delayed wound healing may result in insufficient replacement of these collagen types. From an aesthetic perspective, we may have lost the purpose of our treatment which was to create new and strong collagen fibres.
The proliferation stage of wound healing begins when the inflammation winds down
How ß-glucans promote wound healing
Β-glucans are a type of sugar molecule that we do not produce, nor does it occur naturally in our bodies. This is a key bit of information as our immune cells, namely macrophages recognise β-glucans as being foreign and belonging to bacteria or fungi.
As a result, these macrophages activate on contact with β-glucans (via Dectin-1 and TLR2/6 receptors) and release a growth factor called IL-1.
Topical beta-glucans activate macrophages to produce IL-1 (Sousa et al., 2023)
IL-1 activates fibroblasts to produce collagen and instructs keratocytes to divide.
Does this sound familiar? Yes, this is the same effect which occurs during the proliferation stage of wound healing.
Applying β-glucan on a fresh wound is a quick way to transition more effectively into the proliferation stage, effectively limiting the inflammation window.
This can have drastic effects, particularly in individuals with risk factors of delayed wound healing.
Ideal forms of ß-glucans
Not all β-glucans are created equal for the purpose of wound healing. There are 3 major sources of β–glucan – cereals (e.g. oats, barely), fungi (yeast and mushrooms), bacteria.
So, what are the differences between the sources of β-glucans and their effectiveness in wound healing?
Different structures of beta-glucans (Biomacromolecules, 2020)
It comes down to the shape of β-glucan. Generally, the longer and more complex the structure of β-glucans, the more likely our macrophages recognise through their receptors, Dectin-1 and TLR2/6 and thus the more likely they become activated.
β-glucans can either appear as a random coil, linear with a single, double or triple helix or may be rod-like. For macrophage activation, the triple helix β-glucan structure is most superior!
These are found in fungi, including bakers yeasts and various types of mushrooms (split gill and shiitake mushrooms) – but not the more common oats and barley!
In fact, there are specific techniques and skills required to extract β-glucans from yeast and mushrooms that preserve their triple helix structure!
Without this, even the correct source of β-glucans may result in less than ideal outcomes.
How NAC & EGF promote wound healing
While a good deal of this article is dedicated towards β-glucans, they are by no means the only approach to enhancing the wound healing process.
As mentioned earlier, good wound healing has a healthy degree of inflammation – just enough to initiate the process but not excessive enough to delay its outcome. Inflammation and reactive oxygen species (ROS) come hand-in-hand and often excessive ROS can perpetrate the inflammatory cycle.
Knowing this, the approach of applying topical antioxidants has gained the interests of researchers.
N-acetyl cysteine (NAC) is an antioxidant precursor found in meat, fish, chicken and seafood. When absorbed, it is converted to a powerful antioxidant – glutathione.
Recent research has shown that topical NAC assists in wound healing by virtue of its unique antioxidant properties, reducing the presence of free radicals in wounds and increasing keratinocytes cell proliferation (Wiktor Paskal et al., 2021) (Tsai et al., 2014)
Another ingredient shown to increase the proliferation of keratinocytes is Epidermal Growth Factor (EGF). This is an oldie but goodie, first used to manage wound healing clinically since the late 1980s.
EGF not only increases dermal cell proliferation, but also increases vascularisation of the wound-affected area, thereby increasing blood and nutrient supply to support wound healing (Cheng et al., 2020).
Summary
While we all may reap the benefits of improved wound healing outcomes, individuals affected by chronic diseases or older in age may find the greatest benefits.
Outcomes of improved wound healing in the clinic include reduced client down-time following aesthetic procedures, reduced infection risk, reduced risk of post-procedural pigmentation and increased efficacy of treatment.
However, selecting the right post-procedure care product is imperative – simply, the incorrect source or extraction technique of β-glucan (i.e. oats or barely) will provide little to no benefit in wound healing.
Instead, opt for β-glucans sourced from mushrooms (lentinan or schizophyllan) or yeast and from a reputable brand with a strong scientific background.
Reference
Biomacromolecules. (2020). Recent Advances in Chain Conformation and Bioactivities of Triple-Helix Polysaccharides.
Cheng, Y., Li, Y., Huang, S., Yu, F., Bei, Y., Zhang, Y., Tang, J., Huang, Y. and Xiang, Q. (2020). Hybrid Freeze-Dried Dressings Composed of Epidermal Growth Factor and Recombinant Human-Like Collagen Enhance Cutaneous Wound Healing in Rats. Frontiers in bioengineering and biotechnology, [online] 8. doi:https://doi.org/10.3389/fbioe.2020.00742.
Tsai, M.-L., Huang, H.-P., Hsu, J.-D., Lai, Y.-R., Hsiao, Y.-P., Lu, F.-J. and Chang, H.-R. (2014). Topical N-Acetylcysteine Accelerates Wound Healing in Vitro and in Vivo via the PKC/Stat3 Pathway. International journal of molecular sciences, [online] 15(5), pp.7563–7578. doi:https://doi.org/10.3390/ijms15057563.
Wiktor Paskal, Paskal, A.M., Piotr Pietruski, Stachura, A., Kacper Pełka, Woessner, A.E., Quinn, K.P., Kopka, M., Galus, R., Jarosław Wejman and Paweł Włodarski (2021). N-Acetylcysteine Added to Local Anesthesia Reduces Scar Area and Width in Early Wound Healing—An Animal Model Study. International journal of molecular sciences, [online] 22(14), pp.7549–7549. doi:https://doi.org/10.3390/ijms22147549.
Sousa, P., Tavares-Valente, D., Amorim, M., João Azevedo-Silva, Pintado, M., & Fernandes, J. (2023). β-Glucan extracts as high-value multifunctional ingredients for skin health: A review. Carbohydrate Polymers, 322, 121329–121329.
