Bioactive-Glass-Based Materials with Possible Application in Diabetic Wound Healing: A Systematic Review

Abstract

Diabetes affected 537 million adults in 2021, costing a total of USD 966 billion dollars in healthcare. One of the most common complications associated with diabetes corresponds to the development of diabetic foot ulcers (DFUs). DFUs affect around 15% of diabetic patients; these ulcers have impaired healing due to neuropathy, arterial disease, infection, and aberrant extracellular matrix (ECM) degradation, among other factors. The bioactive-glass-based materials discussed in this systematic review show promising results in accelerating diabetic wound healing. It can be concluded that the addition of BG is extremely valuable with regard to the wound healing rate and wound healing quality, since BG activates fibroblasts, enhances M1-to-M2 phenotype switching, induces angiogenesis, and initiates the formation of granulation tissue and re-epithelization of the wound. In addition, a higher density and deposition and better organization of collagen type III are seen. This systematic review was made using the PRISMA guideline and intends to contribute to the advancement of diabetic wound healing therapeutic strategies development by providing an overview of the materials currently being developed and their effect in diabetic wound healing in vitro and in vivo.

Keywords: angiogenesis; bioactive glass; diabetic wounds; osteomyelitis; wound healing.

Figure 1

Wound healing stages. (a) Processes that occur during the different wound healing stages. I. Hemostasis: occurs immediately after tissue damage to stop bleeding by platelet aggregation and the coagulation cascade. II. Inflammation: removal of the bacteria and dead cells in wound bed by inflammatory cells (neutrophils and macrophages). Triggers the proliferation stage. III. Proliferation: proliferation and migration of fibroblasts, keratinocytes, and endothelial cells. Re-epithelialization, angiogenesis, and granulation tissue formation. IV. Remodeling: reorganization of ECM, where collagen type III is replaced by collagen type I. This can last one year or more [13]. ECM: extracellular matrix; MP: metalloproteinases; TIMP: tissue inhibitors of metalloproteinases [11]. (b) Four phases of wound healing. Each stage is key in order to ensure a proper wound healing response [14].

Figure 2

Full text screening illustrated by the PRISMA flow diagram.