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Review
. 2021 Dec 6:9:788461.
doi: 10.3389/fbioe.2021.788461. eCollection 2021.

Functional Hydrogel Dressings for Treatment of Burn Wounds

Affiliations
Review

Functional Hydrogel Dressings for Treatment of Burn Wounds

Wentao Shu et al. Front Bioeng Biotechnol. .

Abstract

The therapy of burns is a challenging clinical issue. Burns are long-term injuries, and numerous patients suffer from chronic pain. Burn treatment includes management, infection control, wound debridement and escharotomy, dressing coverage, skin transplantation, and the use of skin substitutes. The future of advanced care of burn wounds lies in the development of "active dressings". Hydrogel dressings have been employed universally to accelerate wound healing based on their unique properties to overcome the limitations of existing treatment methods. This review briefly introduces the advantages of hydrogel dressings and discusses the development of new hydrogel dressings for wound healing along with skin regeneration. Further, the treatment strategies for burns, ranging from external to clinical, are reviewed, and the functional classifications of hydrogel dressings along with their clinical value for burns are discussed.

Keywords: antibacterial; burn wound; emergency temporary coverage; factors promoting wound healing; hydrogel dressing; stem cells.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have influenced this work.

Figures

FIGURE 1
FIGURE 1
Burn wounds. (A) First degree. (B) Superficial second degree. (C) Deep second degree. (D) Third degree.
FIGURE 2
FIGURE 2
Classification of burn dressings: Traditional dressings, Natural biological dressings, and Synthetic dressings.
FIGURE 3
FIGURE 3
Functional classification of hydrogel dressings for burns: Imitating extracellular matrix hydrogel, Hydrogel loaded with stem cells, Hydrogel loaded with healing promoting factors, and New technology of hydrogel dressing.
FIGURE 4
FIGURE 4
“On demand” dissolvable hydrogels for the healing of deep partial-thickness burns. (A) How on-demand dissolvable self-healing hydrogels are used to treat wounds (schematic). (B) Representative images of wound sites in each treatment group over time. (C) Unclosed wound area rate of initial wound as a function of time. ns p > 0.05, *p ≤ 0.05, **p ≥ 0.01, ***p ≤ 0.001. Reproduced with permission from (Huang et al., 2018).
FIGURE 5
FIGURE 5
Hydrogel-based localized release of colistin for antimicrobial treatment of infections from burn wounds. (A) Treatment of a burn wound with a colistin-loaded hydrogel (schematic). (B) Synthesis of a colistin-containing hydrogel (schematic). (C) Disk diffusion assay of a colistin-loaded hydrogel against colistin-sensitive (left) and colistin-resistant (right) P. aeruginosa strains (D) Test of colistin-loaded hydrogel against colistin-sensitive (left) and colistin-resistant (right) strains of P. aeruginosa in a model of burn infection. Reproduced with permission from (Zhu et al., 2017).
FIGURE 6
FIGURE 6
Delivery of silver sulfadiazine and adipose-derived stem cells using fibrin hydrogel improves infected burn wounds. (A) Photographs of the burn device and burn wound. (B) Burn wounds treated with SSD-CSM-ASC-FPEG had significantly thicker granulation tissue than those treated with SSD-CSM-FPEG. (C) SSD-CSM-ASC-FPEG facilitates neo-vascularization on day-21. p < 0.05. (D) Maturation of collagen. Picrosirius staining images on day-28. Reproduced with permission from (Banerjee et al., 2019).
FIGURE 7
FIGURE 7
In situ-formed anti-inflammatory hydrogel loaded with plasmid DNA encoding VEGF for healing of burn wounds. (A) Application of this hydrogel in a model of a splinted excisional wound (schematic). (B) Immunohistochemical staining showing expression of the proinflammatory cytokines IL-1β and TNF-α. (C) Immunohistochemical staining showing expressions of the angiogenic factors VEGF, CD31, and α-SMA. Scale bar = 100 μm. (D) RT-qPCR of mRNA expression for inflammatory and angiogenic factors (IL-1β, TNF-α, VEGF). **p ≤ 0.01, *p ≤ 0.05. Reproduced with permission from (Wang et al., 2019).

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