Wound Healing: Tensional Factor Pathomechanism In Occurance Of Abnormal Scar

Gerardo AK Laksono, Paul L Tahalele, Jose L Anggorwasito, HYL Wihastyoko

Abstract


Wound healing is a series of biophysiological processes, beginning with tissue injury, and ending with repairs from the wound tissue itself to a complete state consisting of several phases including inflammation, proliferation and remodeling. Every process of wound healing always leaves a scar. Hypertrophic and keloid is a product of abnormal wound healing. This abnormal scar formation is influenced by several factors, one of which is the
wound stress. A tension that is too large in a wound will cause a hypoxic state in the wound itself. This hypoxic state will cause recurrent inflammation which leads to abnormal scar formation. One of abnormal scars formation prevention is reduction in wound tension. Reduction in wound tension reduce the inflammation process.

Save to Mendeley


Full Text:

PDF

References


Gosain, A., Dipietro, M. D. L. A. & Ph, D. Aging and Wound Healing. World J. Surg. 28, 321–326 (2004).

Diegelmann, R. F. Wound healing: an overview of acute, fibrotic and delayed healing. Front. Biosci. 9, 283 (2004).

Li, J., Chen, J. & Kirsner, R. Pathophysiology of acute wound healing. Clin. Dermatol. 25, 9–18 (2007).

Keast, D. H. & Orsted, H. The basic principles of wound care. Ostomy. Wound. Manage. 44, 24–8, 30–1 (1998).

Guo, S. & DiPietro, L. A. Critical review in oral biology & medicine: Factors affecting wound healing. J. Dent. Res. 89, 219–229 (2010).

Willenborg, S. et al. Genetic Ablation of Mast Cells Redefines the Role of Mast Cells in Skin Wound Healing and. Soc. Investig. Dermatology 134, 2005–2015 (2014).

Landén, N. X., Li, D. & Ståhle, M. Transition from inflammation to proliferation: a critical step during wound healing. Cell. Mol. Life Sci.

, 3861–3885 (2016).

Flanagan, M. The physiology of wound healing. J. Wound Care 9, 25–26 (2000).

Velnar, T., Bailey, T. & Smrkol, J. The Wound Healing Process: an Overview of the Cellular and Molecular Mechanisms. J. Int. Med. Res. 37, 1528–42 (2009).

Cristina, A. & Gonzalez, D. O. Wound healing - A literature review*. An Bras Dermatol 91, 614–620 (2016).

Li, B. & Wang, J. H. . Fibroblast and Myofibroblast in Wound Healing: Force Generation and Measurement. J Tissue Viability 4, 108–120 (2012).

Huang, C., Murphy, G. F., Akaishi, S. & Ogawa, R. Keloids and hypertrophic scars: Update and future directions. Plast. Reconstr. Surg. 1, (2013).

Perdanakusuma, D. Penanganan Parut Hipertrofik dan Keloid. (Airlangga University Press, 2017).

Wynn, T. A. Fibrotic Disease And The Th1/Th2 Paradigm. Nat. Rev. Immunol. 4, 583–294 (2004).

Wolfram, D., Tzankov, A., Pülzl, P. & Piza-Katzer, H. Hypertrophic scars and keloids - A review of their pathophysiology, risk factors, and therapeutic management. Dermatologic Surg. 35, 171–181 (2009).

Yoshimoto, H. et al. Overexpression of insulin-like growth factor-1 (IGF-I) receptor and the invasiveness of cultured keloid fibroblasts. Am. J. Pathol. 154, 883–889 (1999).

Bock, O. et al. Aberrant expression of transforming growth factor β -1 (TGF β -1 ) per se does not discriminate fibrotic from nonfibrotic chronic myeloproliferative disorders. J. Pathol. 205, 548–557 (2005).

George J, Y. Y. et al. Mast Cells Are Required in the Proliferation and Remodeling Phases of Microdeformational Wound Therapy. Plast. Reconstr. Surg. 128, 649–658 (2011).

Wulff, B. C. & Wilgus, T. A. Mast cell activity in the healing wound : more than meets the eye ? Exp. Dermatol. 22, 507–510 (2013).

Gauglitz, G. & Korting, H. Hypertrophic Scarring and Keloids: Pathomechanism and current emerging treatment strategies. Mol. Med. 17, 113–125 (2011).

Artuc, M., Steckelings, U. M. & Henz, B. M. Mast Cell±Fibroblast Interactions: Human Mast Cells as Source and Inducers of Fibroblast and Epithelial Growth Factors. Soc. Investig. Dermatology 391–395 (2002).

Son, D. & Harijan, A. Overview of surgical scar prevention and management. J. Korean Med. Sci. 29, 751–757 (2014).

Suarez, E. et al. Skin equivalent tensional force alters keloid fibroblast behavior and phenotype Wound Repair Regen. 22, 557–568 (2014).

Ogawa, R. et al. Clinical Applications of Basic Research that Shows Reducing Skin Tension Could Prevent and Treat Abnormal Scarring: The Importance of Fascial/Subcutaneous Tensile Reduction Sutures and Flap Surgery for Keloid and Hypertrophic Scar Reconstruction. J Nippon Med Sch 78, 68–76 (2011).

Jeong, W. et al. Scar prevention and enhanced wound healing induced by polydeoxyribonucleotide in a rat incisional wound-healing model. Int. J. Mol. Sci. 18, 1–12 (2017).

Balin, A. K. & Pratt, L. Oxygen Modulates the Growth of Skin Fibroblasts. Soc. Vitr. Biol. 38, 305–310 (2016).

Hong, W. X. et al. The Role of Hypoxia-Inducible Factor in Wound Healing. Adv. Wound Care 3, 390–399 (2014).

Ruthenborg, R. J., Ban, J. J., Wazir, A., Takeda, N. & Kim, J. W. Regulation of Wound Healing and Fibrosis by Hypoxia and Hypoxia-Inducible Factor-1. Mol. Cells 37, 637–643 (2014).




DOI: https://doi.org/10.33508/jwmj.v1i3.2101

Refbacks

  • There are currently no refbacks.