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As he body degrades he stuffed of acid hyaluronic

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By Unilaser Médica blog laser rejuvenation treatments September 8, 2024
Dr. Daniel Rivera Resident II plastic, reconstructive and aesthetic surgery at the Nueva Granada Military University, Bogotá, Colombia, year 2018. Published 6 November 2018 New writing by Adrian Rios 26 September 2023 The degradation of hyaluronic acid by the body occurs through gradual mechanisms. Hyaluronic acid or hyaluronan (HA) is a polysaccharide that is found naturally in multiple tissues and cells of most organisms and whose molecular structure is highly conserved between species, 1,6 . This allows it to be extracted from multiple sources, usually specific colonies of bacteria 2,6 . The molecule consists of a basic unit of two sugars: glucuronic acid and N-acetyl-glucosamine, which are repeated in groups of 30,000 units 1 . Glucuronic acid is strongly hydrophilic due to its carboxyl group which contains two electronegative oxygen atoms which attract electrons from the hydrogen atom of water. Acetyl glucosamine gives it the structure. In nature, it is formed on the cell surface of fibroblasts by extrusion to the extracellular membrane. To reduce water solubility and therefore increase the duration of the filler, cross-links are generated by adding hydroxyl groups 4 (esterification) in varying degrees, such that a greater number of links decreases solubility 2,3 . This type of esterification decreases the reaction of fibroblasts for cellular degradation 1,2 . Exposing the material to the body may atypically result in both a sudden loss of effect instead of a progressive decrease 4. as well as the reverse effect: a replacement of part of the filler by autogenous tissue 3 .
Narins, R.S., & Mariwalla, K. (2018). 4 – NASHA family.  Soft Tissue Augmentation  (Fourth Edition, pp. 17–24). Elsevier Inc. http://doi.org/10.1016/B978-0-323-47658-4.00004-6
The degradation of hyaluronic acid by the body occurs through staggered mechanisms via 3 different pathways 5,6 : Local hyaluronic acid replacement: Fibroblasts migrate and proliferate in the hyaluronic acid application space and form reticular structures for several reasons:
  • The injection generates mechanical stress in the dermis which activates fibroblasts and increases constituents such as collagen, elastin and proteoglycans in the dermis 3 .
  • Fibroblasts are also activated by hyaluronic acid per se .
  • The cells express CD44 and CD168 as hyaluronan receptors causing proliferation and migration of these cells 3 .
  • Fibroblasts also produce hyaluronidase (HYAL1 and HYAL2, the most important in humans 5 ), an enzyme that degrades HA, and are capable of internalizing both HA and its lysis products 1 .
  • Enzymatic degradation splits the hyaluronic acid macromolecule into small polymers with variable lengths of 1,5 dimeric chains . 
Systemic replacement of hyaluronic acid: Accounts for 85% of total catabolism.
  • It differs in the epidermis from the dermis.
  • In the epidermis, local degradation takes only 2-3 hours, while in the dermis it takes 1-2 days. This is why topical application of HA does not achieve effects for more than two hours, while intradermal injections will end up being diluted by the body in a few days.
  • HA is eliminated by lymphatic drainage via receptors on the endothelium 5 with the final steps of elimination occurring in the liver, kidneys and possibly the spleen 6 .
  • Extracellular degradation is thought to initiate following release from the extracellular matrix network by non-enzymatic mechanisms 5,6 .
HA cleavage by free radicals: Degradation can also occur by non-enzymatic mechanisms related to cellular stress leading to the production of free radicals. The actual proportion of HA that undergoes turnover by this mechanism is unknown. References
  1. Price, R.D., Berry, M.G., & Navsaria, H.A. (2007). Hyaluronic acid: the scientific and clinical evidence. Journal of Plastic, Reconstructive & Aesthetic Surgery , 60 (10), 1110–1119. http://doi.org/10.1016/j.bjps.2007.03.005
  2. Carruthers, J.D.A., Glogau, R.G., & Blitzer, A. (2008). Advances in Facial Rejuvenation: Botulinum Toxin Type A, Hyaluronic Acid Dermal Fillers, and Combination Therapies???-Consensus Recommendations. Plastic and Reconstructive Surgery , 121 (SUPPLEMENT), 5S–30S. http://doi.org/10.1097/PRS.0b013e31816de8d0
  3. Mochizuki, M., Aoi, N., Gonda, K., Hirabayashi, S., & Komuro, Y. (2018). Evaluation of the In Vivo Kinetics and Biostimulatory Effects of Subcutaneously Injected Hyaluronic Acid Filler. Plastic and Reconstructive Surgery , 142 (1), 112–121. http://doi.org/10.1097/PRS.0000000000004496
  4. Narins, R.S., & Mariwalla, K. (2018). 4 – NASHA family. Soft Tissue Augmentation (Fourth Edition, pp. 17–24). Elsevier Inc. http://doi.org/10.1016/B978-0-323-47658-4.00004-6
  5. Anderegg, U., Simon, J.C., & Averbeck, M. (2014). More than just a filler – the role of hyaluronan for skin homeostasis. Experimental Dermatology , 23 (5), 295–303. http://doi.org/10.1111/exd.12370
  6. Coleman, S. R. (2006). Cross-Linked Hyaluronic Acid Fillers. Plastic and Reconstructive Surgery , 117 (2), 661–665. http://doi.org/10.1097/01.prs.0000200913.34368.79

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