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12/7/2024 Comments Regenerative aesthetics: Wound healing & growth factors for collagen biostimulation Interestingly, the biochemical pathways involved in skin rejuvenation and wound healing share notable similarities. This connection forms the basis for many clinical regenerative aesthetical treatments designed to stimulate collagen production. Interventions, such as chemical peelings and energy-based devices, work by creating controlled damage (wound) to trigger the skin's natural healing response, while topical treatments can include growth factors to boost collagen synthesis (biostimulation) and promote skin regeneration [1]. Wound healing is a complex biological process that relies on the synchronized actions of various cell types, guided by growth factors and cytokines [2]. Central to this regenerative process is collagen, a crucial component of the extracellular matrix (ECM) giving skin strenght and structure, however is declining as we age and therefore a primary target for skin (pre)rejuvenation treatments. Collagen's plays vital roles throughout the wound healing process [3]. The wound healing process has four distinct however overlapping phases (illustration): [3][4] 1. Hemostasis: ▌Platelets release growth factors including PDGF, IGF, TGF-α/β, and EGF, initiating the wound healing cascade and attracting immune cells to the wound site [3][5]. 2. Inflammation: ▌ Growth factors and cytokines released by platelets and immune cells promote inflammation and cellular migration [5]. ▌Macrophages produce additional growth factors, including FGF, which induces fibroblast activation and proliferation [5]. 3. Proliferation: ▌PDGF and TGF-β stimulate fibroblast migration, proliferation, and collagen production [4][5]. ▌FGF promotes fibroblast proliferation and angiogenesis [4]. ▌VEGF is crucial for angiogenesis and the formation of granulation tissue [5][6]. ▌KGF and EGF facilitate reepithelialization by stimulating keratinocyte migration and proliferation [6]. 4. Remodeling: ▌ TGF-β influences the transition from type III to type I collagen, improving wound strength [3][5]. ▌This phase can last from 3 weeks to 2 years post-injury [5]. This explains why biostimulation of collagen production is a gradual process and ultimate results can take weeks or even months. Initially, type III collagen is deposited in the granulation tissue, forming a loose matrix with other components like hyaluronic acid and fibronectin [3][5]. ▌During remodeling, type III collagen is gradually replaced by stronger type I collagen, increasing the mechanical strength of the tissue [3][5]. ▌The collagen fibers are rearranged into a more organized lattice structure, although newly formed scar tissue has only 70-80% of the tensile strength of intact skin [5]. ▌ Fibroblasts and myofibroblasts, stimulated by growth factors, are responsible for collagen production and remodeling [5][7]. Impairments in any phase of wound healing can lead to chronic, non-healing wounds, which is a growing concern in healthcare [3].  GROWTH FACTORS
Growth factors (GF) are naturally occurring polypeptides secreted by various cells including the dermal fibroblast, facilitating signaling pathways between and within cells throughout the healing phases [6]. These factors, including Platelet-Derived Growth Factor (PDGF), Vascular Endothelial Growth Factor (VEGF), Epidermal Growth Factor (EGF), Transforming Growth Factor-β (TGF-β), among others, function synergistically to guide the wound from injury to complete tissue regeneration [4]. Topical applied growth factors can support this skin rejuvenation healing process [8][9]. However, direct application of growth factors to wounds faces challenges such as rapid degradation in the wound environment and the need for high doses to achieve clinical efficacy [4]. COLLAGEN Collagen, whether in its natural fibrillar form or as soluble parts in the wound environment, closely interacts with these growth factors [3]. Collagen not only provides structural support to the skin, it also actively participates in cell signaling, influencing key processes such as hemostasis, inflammation resolution, angiogenesis, and matrix remodeling [3][10]. The interaction between growth factors and collagen creates a lively environment that is essential for effective wound healing. Some studies suggest potential benefits of oral collagen supplements [11][12][13] and topical collagen products [14] for wound healing. A high quality collagen powder does have right building blocks (amino acids: proline, glycine and hydroxyproline) for collagen production. The effects may vary depending on the type of wound, collagen formulation, and application method. Exosomes [15] Exosomes isolated from stem cell cultures contain various growth factors, including EGF, VEGF, TGF, HGF, FGF, IGF, and PDGF. These growth factors play crucial roles in skin regeneration, anti-aging effects, and wound healing by promoting fibroblast proliferation and collagen synthesis. The use of skin´s own healing power via a regenerative aesthetic treatment causing controlled injury is collagen biostimulatory and the use of topical growth factors, exosomes and oral collagen powders may enhance the outcome. Always consult a qualified healthcare professional to determine what the most suitable approach is for your needs and goals. Take care Anne-Marie References: [1] Goldman R. Growth factors and chronic wound healing: past, present, and future. Adv Skin Wound Care. 2004 Jan-Feb;17(1):24-35. doi: 10.1097/00129334-200401000-00012. PMID: 14752324. [2] Barrientos S, Brem H, Stojadinovic O, Tomic-Canic M. Clinical application of growth factors and cytokines in wound healing. Wound Repair Regen. 2014 Sep-Oct;22(5):569-78. doi: 10.1111/wrr.12205. PMID: 24942811; PMCID: PMC4812574. [3] Mathew-Steiner SS, Roy S, Sen CK. Collagen in Wound Healing. Bioengineering (Basel). 2021 May 11;8(5):63. doi: 10.3390/bioengineering8050063. PMID: 34064689; PMCID: PMC8151502. [4] Vaidyanathan, L. (2021). Growth Factors in Wound Healing – A Review. Biomedical and Pharmacology Journal, 14(3). DOI: https://dx.doi.org/10.13005/bpj/2249 [5] Park JW, Hwang SR, Yoon IS. Advanced Growth Factor Delivery Systems in Wound Management and Skin Regeneration. Molecules. 2017 Jul 27;22(8):1259. doi: 10.3390/molecules22081259. PMID: 28749427; PMCID: PMC6152378. [6] Barrientos, S., Stojadinovic, O., Golinko, M.S., Brem, H., & Tomic-Canic, M. (2008). Growth factors and cytokines in wound healing. Wound Repair and Regeneration, 16(5), 585–601. [7] Hochstein, A. O., & Bhatia, A. (2014). Collagen: Its Role in Wound Healing. Podiatry Management, 33(6), 103-110. [8] Zarei, F., & Soleimaninejad, M. (2018). Role of growth factors and biomaterials in wound healing. Artificial Cells, Nanomedicine, and Biotechnology, 46(sup1), 906–911. [9] La Monica, F.; Campora, S.; Ghersi, G. Collagen-Based Scaffolds for Chronic Skin Wound Treatment. Gels 2024, 10, 137. https://doi.org/10.3390/gels10020137 [10] Shi, S., Wang, L., Song, C. et al. Recent progresses of collagen dressings for chronic skin wound healing. Collagen & Leather 5, 31 (2023). https://doi.org/10.1186/s42825-023-00136-4 [11] Bagheri Miyab K, Alipoor E, Vaghardoost R, Saberi Isfeedvajani M, Yaseri M, Djafarian K, Hosseinzadeh-Attar MJ. The effect of a hydrolyzed collagen-based supplement on wound healing in patients with burn: A randomized double-blind pilot clinical trial. Burns. 2020 Feb;46(1):156-163. doi: 10.1016/j.burns.2019.02.015. Epub 2019 Dec 16. PMID: 31859087. [12] Choi FD, Sung CT, Juhasz ML, Mesinkovsk NA. Oral Collagen Supplementation: A Systematic Review of Dermatological Applications. J Drugs Dermatol. 2019 Jan 1;18(1):9-16. PMID: 30681787. [13] Katayoun Bagheri Miyab, Elham Alipoor, Reza Vaghardoost, Mohsen Saberi Isfeedvajani, Mehdi Yaseri, Kurosh Djafarian, Mohammad Javad Hosseinzadeh-Attar, The effect of a hydrolyzed collagen-based supplement on wound healing in patients with burn: A randomized double-blind pilot clinical trial, Burns, Volume 46, Issue 1, 2020, Pages 156-163,ISSN 0305-4179, https://doi.org/10.1016/j.burns.2019.02.015. [14] Friedman, A., et al. (2019). A Head-to-Head Comparison of Topical Collagen Powder to Primary Closure for Acute Full-Thickness Punch Biopsy-Induced Human Wounds: An Internally Controlled Pilot Study. Journal of Drugs in Dermatology. [15] Kim, J. Y., & Park, Y. H. (2017). Stem cell-derived exosome containing high amount of growth factors (World Intellectual Property Organization Patent No. WO2017123022A1). Google Patents.
Comments
 The widespread belief that the epidermis renews itself every 28 days is inaccurate. Epidermal turnover primarily involves keratinocytes, the predominant cell type in the epidermis with 90%. These cells originate in the basal layer (stratum germinativum) and progressively move upward through the epidermal layers, undergoing various changes before being shed from the skin's surface as dead, flaky cells - a process known as desquamation [1]. The keratinocyte journey has several stages:
Epidermal turnover rates vary significantly with age: ▌In young adults: approximately 28-40 days [2] ▌In more mature adults: 60+ days [2] This age-related slowdown is attributed to decreased cell proliferation [3] KERATINOCYTE LIFESPAN The keratinocyte lifecycle can be divided into two main phases: 1. Active life: Approximately 8 to 10 days from mitosis (in the basal layer) to arrival in the stratum corneum [1]. 2. Stratum corneum transit: The period spent in the outermost layer as corneocytes (dead keratinocytes) before shedding [1].  Epidermal turnover dynamics The total epidermal turnover time, which includes both active life and stratum corneum transit, varies with age: ▌In young adults: The stratum corneum transit time is approximately 20 days [3] ▌In more mature adults: This transit time is lengthened by more than 10 days (approximately 30+ days) [3] This increase in transit time reflects a slowdown in epidermal cell proliferation rather than an increase in cell layers [3] On average, it takes an estimated 40 to 56 days for the keratinocytes in the epidermis to completely turn over [1] Overall epidermal turnover times Total turnover time (including both active life and stratum corneum transit) varies significantly with age. The decline in epidermal cell renewal is not constant throughout adulthood, remaining relatively stable in younger years before dropping more dramatically after age 50 [3]. Several factors influence the epidermal turnover of keratinocytes 1. Age: Epidermal turnover slows with age. In young adults, the process takes approximately 28-40 days, while in older adults it can extend to 60+ days [4]. 2. Growth factors: Epidermal growth factor (EGF) and keratinocyte growth factor (KGF) play crucial roles in regulating keratinocyte proliferation, migration, and differentiation [5]. 3. Transcription factors: p63, particularly the ΔNp63α isoform, is critical for maintaining keratinocyte proliferation and regulating the switch from proliferation to differentiation [4]. 4. Signaling pathways: Notch signaling, IKKα, and IRF6 are involved in regulating keratinocyte differentiation and epidermal turnover [4]. 5. Matrix stiffness: Increased extracellular matrix stiffness promotes keratinocyte proliferation through enhanced EGF signaling [5]. 6. Vitamin D: 1,25-dihydroxyvitamin D3 regulates keratinocyte proliferation and differentiation by modulating calcium concentrations and gene expression [6]. 7. Cell adhesion: Contact with the basal lamina, mediated by integrins, regulates keratinocyte proliferation and differentiation [7]. These factors work in concert to maintain the balance between keratinocyte proliferation in the basal layer and terminal differentiation in the upper layers, ensuring proper epidermal homeostasis and turnover.  Improving epidermal turnover can be beneficial for several skin conditions, including:
1. Aging: Enhanced epidermal turnover can help reduce visible signs of aging such as: ▌ Wrinkles and fine lines ▌ Skin sagging ▌ Dull, rough skin texture (the size or the corneocytes is increased - see graph) 2. Acne: Faster skin cell turnover can help prevent acne by: ▌ Reducing the accumulation of dead skin cells that can clog pores ▌ Decreasing the risk of bacteria buildup on the skin surface 3. Hyperpigmentation and age spots: Improved turnover can address patches of darkened skin by promoting the removal of older, pigment-producing cells 4. Dry skin: Enhanced cell turnover can help improve skin hydration and barrier function [8] 5. Sun damage: Accelerated epidermal renewal can aid in repairing and replacing sun-damaged skin cells [9] Several in-office procedures and cosmetic ingredients have been shown to accelerate keratinocyte renewal and epidermal turnover: 1. Hyaluronic acid (HA) production enhancers: ▌1-ethyl-β-N-acetylglucosaminide (β-NAG2) has been shown to increase HA production in the epidermis, leading to accelerated keratinocyte proliferation and differentiation [10]. 2. Retinoids: ▌Topical retinoids, such as tretinoin, can increase epidermal turnover and promote keratinocyte proliferation [11]. 3. Chemical peels: ▌Various chemical peeling agents can stimulate epidermal renewal by inducing controlled damage to the skin [11]. 4. Microdermabrasion: ▌This procedure can promote skin turnover by physically removing the outermost layer of dead skin cells [11] 5. Laser treatments: ▌Certain laser therapies can stimulate epidermal regeneration and increase keratinocyte turnover [11] 6. Liquid Crystal Gel (LCG): ▌A study showed that low concentration LCG can increase epidermal thickness and potentially promote skin turnover [11] Excessive stimulation may lead to adverse effects. Therefore, these treatments should be used under professional guidance and with careful consideration of individual skin conditions. Always consult a qualified healthcare professional to determine what the most suitable approach is for your needs and goals. Take care Anne-Marie References: [1] Iizuka H. Epidermal turnover time. J Dermatol Sci. 1994 Dec;8(3):215-7. doi: 10.1016/0923-1811(94)90057-4. PMID: 7865480. [2] Maeda, K. New Method of Measurement of Epidermal Turnover in Humans. Cosmetics 2017, 4, 47. [3] Grove GL, Kligman AM. Age-associated changes in human epidermal cell renewal. J Gerontol. 1983;38(2):137-42. doi:10.1093/geronj/38.2.137 [4] Koster MI, Roop DR. J Invest Dermatol. 2007;127(11):2432-8. PMID: 17934504. [5] Wickert LE, et al. J Cell Sci. 2018;131(10):jcs215780. PMID: 29661845. [6] Wikipedia contributors. "Keratinocyte." Wikipedia, The Free Encyclopedia. [7] Megías M, et al. "Keratinocyte." Atlas of Plant and Animal Histology. University of Vigo. [8] Farage MA, Miller KW, Elsner P, Maibach HI. Aging Clin Exp Res. 2008;20(3):195-204. doi:10.1007/BF03020230. [9] Yaar M, Gilchrest BA. J Investig Dermatol Symp Proc. 2007;12(1):1-10. doi:10.1038/sj.jidsymp.5650020. [10] Yoshida H, et al. J Dermatol Sci. 2021;101(2):122-131. PMID: 33358097. [11] Musashi M, et al. Cosmetics. 2014;1(3):202-210. doi:10.3390/cosmetics1030202. |
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