Table 2.

MBG‐based delivery systems for cancer treatment

Bioglass/MBGs	Cancer cell type	Drug	Bone‐conduction capacity	Biocompatibility	Drug loading properties	Drug release properties	Drug delivery effect on cancer cell lineage	Conclusion	Refs.
MBG	Osteosarcoma cell line (MG63)	Imatinib (IMT)	Considerable hydroxycarbonate apatite formation and bioactivity	Not reported (N.R.)	Drug loading amount and efficiency increased with drug loading concentrations increase (from 0.2 mg mL−1 to 1.0 mg mL−1), with maximum of 77.59% for 1.0 mg mL−1 concentration	Drug release rate and cumulative drug release are in contrast with pH values Drug loading concentration influences the drug release profile	IMT‐MBG showed a significant inhibitory effect on MG63 cell lineage compared to MBG	IMT‐MBG has the potential for bone tissue regeneration and bone cancer treatment	[115]
MBG	Metastatic breast cancer cell line MDA‐MB‐231	Silibinin	N.R.	Relatively low cytotoxicity effect on Noncancerous breast endothelial cell line (MCF‐10A)	Optimal drug loading efficiency (61%) was obtained at 40 µg mL−1 silibinin concentration	Silibinin release has a burst at first hours (cumulative 16% release of the loaded drug in the initial 5 h), which continues with sustained drug release	MBG nanoparticles with silibinin can induce cytotoxicity and cause growth inhibition in breast cancer cell line MDA‐MB‐231	MBG nanoparticles loaded with silibinin has a high potential for clinical application	[34]
MBG	MG‐63 osteoblast‐like cell's	Alendronate (AL)	HA formation on the surface detected, MBG promoted ECM mineralization	MBG showed no toxicity to MG‐63 osteoblast‐like cells before loading AL	The optimal loading efficiency of 60% was obtained	AL drug delivery rate of MBG can be adjusted by MBG particles pore size	AL release from MBG potentially inhibited MG63 cell line proliferation, even at lower concentrations	MBG–AL demonstrated dual efficacy in bone regeneration and anticancerous drug delivery	[116]
MBG nanospheres	Osteosarcoma cell line (MG63)	Alendronate (AL)	MBG nanospheres and AL‐MBG promote mineralization in SBF	N.R.	MBG was able to load AL up to 17% wt. in optimal drug concentration of 1 mg mL−1	N.R.	Alendronate‐loaded MBG was effective in decreasing tumor cell viability even at lower alendronate concentration	MBG is a promising tool for bone regeneration and osteosarcoma treatment	[117]
Ag2O‐MBG	Osteosarcoma cell line (MG63)	DOX	Considerable apatite formation	Normal human fibroblast cell line in vitro biocompatibility in contrast with Ag2O‐MBG concentration (I IC50:178 µg mL−1)	Drug loading amount and efficiency increased with drug loading concentrations increase (from 0.2 mg mL−1 to 1.0 mg mL−1), with maximum of 83.5% for 1.0 mg mL−1 concentration increase and decrease in release media pH	Drug release rate and cumulative drug release amount increases with loading concentration	DOX‐Ag2O‐MBG significantly inhibited MG63 osteosarcoma cells viability	Ag2O‐MBG Nanoparticles are efficient for bone tissue regeneration and drug delivery	[118]
Fe3O4–MBG	Osteosarcoma cell line (MG63)	Mitomycin C (Mc)	Hydroxycarbonate apatite (HCA) formation	No significant cytotoxicity on normal human fibroblast (NHFB) cells at any concentration	The optimum drug loading efficiency of 93% was measured	Fe3O4–MBG cumulative release was in contrast with pH values	Mc–Fe3O4–MBG has a significant inhibitory effect on MG63 osteosarcoma cell line viability in a dose‐dependent manner (IC50: 12.19 µg mL−1)	Fe3O4–MBG is a nontoxic, biocompatible biomaterial with potential for bone tissue regeneration and drug delivery	[119]
Selenium–MBG	Osteosarcoma cell line (MG63)	DOX	Se4+ improves HA‐mineralization ability of Se/MBG	5Se/MBG at concentrations higher than 20 µg mL−1 showed significant toxicity to MC3T3‐E1 preosteoblast cells at 48 h Se/MBG and 3Se/MBG showed no toxicity toward MC3T3‐E1 preosteoblast cells	Se doping enhances the specific surface area and nanospheres pore volume; thus, 5Se/MBG and 3Se/MBG showed a higher drug loading rate	DOX release adjusted by pH and Se concentrations; lower pH values of release environment cause higher drug release rate, and Doping Se ions decrease DOX release rate	Se/MBG at different concentrations induces apoptosis in osteosarcoma cells (MG63); furthermore, Se and DOX codoped MBG nanospheres exhibit a long‐term inhibition on the viability of osteosarcoma cells (MG63)	Se/MBG has the potential in diagnostics, therapy, and clinical application owing to its tunable intrinsic toxicity, high surface area, and adjustable surface chemistry	[120]
Europium(Eu)/MBG	Osteosarcoma cell line (MG63)	DOX	Apatite formed; Eu changed the morphology of formed apatite from sheet to rod in a dose‐dependent manner	Eu/MBG enhanced viability of osteosarcoma MG 63 cells	DOX loading is dependent on specific surface area and pore size of MBG/Eu	DOX release increases with a decrease in pH Proper Eu content improves DOX release behavior besides its loading properties	Eu/MBG‐DOX shows controlled release of DOX, which inhibits MG 63 cells in long term	Eu/MBGs are a prospective candidate owing to their mesoporous structure, unique apatite formation, and controlled and adjustable drug delivery properties	[121]
Aminated MBG (AMBG)	MG‐63 osteoblast‐like cell's	Alendronate (AL)	AMBG promoted ECM mineralization	AMBG showed no toxicity to MG‐63 osteoblast‐like cells before loading AL	The optimal loading efficiency of 63% was obtained	AMBG Drug release profile was more controlled and sustained comparing MBG; furthermore, reducing mesopore size and creating attachment sites on AMBG causes a more sustained drug release	AL release from AMBG potentially inhibited MG63 cell line proliferation, even at lower concentrations	AMBG‐AL showed dual efficacy in bone regeneration and anticancerous drug delivery	[116]
Rice husk MBG (rMBG)	HeLa cancer cells	Camptothecin (CPT)	N.R.	rMBG has No toxicity up to a dose of 200 µg mL−1 after 24 h on normal fibroblasts (L929)	rMBG has a higher CPT loading capacity compare with MBG due to its higher pore volume CPT loading capacity of rMBG was measured 13.8% in PBS (pH 7.4) at 37 °C	A rapid drug release within the first week followed by sustained release after day 7	rMBG/CPT was cytotoxic to HeLa cancer cells after incubation for 3 h	rMBG can be used as a drug delivery vehicle, which increases CPT solubility as a hydrophobic anticancer drug	[41]
Dendritic MBG	Tumor (HepG2) cells	DOX	N.R.	Minimal damage to human normal (LO2) in vitro MBG–DOX has the potential to reduce cardiac and systemic toxicity caused by free DOX in vivo	Increase in DOX to MBG ratio increases loading amount while decreases loading efficiency	DOX and Ca2+ release was dependent on pH of release solution; release increases with pH decrease	Dendritic MBG have controlled drug delivery potential and shows a synergism effect with loaded DOX in tumor growth inhibition Tumor volume significantly decreased following injection of dendritic MBG nanospheres to animal model (mice) in vivo	Dendritic MBG nanospheres potentially can be used as a superior delivery system for cancer treatment	[122]
Fluorescent MBG nanoparticles (fBGn)	HeLa cancer cells	DOX	N.R.	fBGn showed no significant toxicity to HeLa cells up to 320 µg mL−1 fBGn in a varying dosage of (0, 5, 10, and 20 mg kg−1) were IV injected to nude mice, and the result showed high histocompatibility to almost all organs with no significant difference between doses and saline control group	Drug loading increased with drug concentration increase with the optimum of ≈92% Ca2+ ions improved loading efficiency	Drug release rate increases in an acidic environment, and Ca2+ enhances sustained drug release properties	fBGn‐DOX drug release has the potential to destroy the HeLa cancer cells	Drug release based on fBGn can be used for future cancer drug delivery	[123]

IMT: imatinib; N.R; not reported; IC₅₀: half maximal inhibitory concentration; DOX: doxorubicin; Mc: mitomycin C; HCA: hydroxycarbonate apatite; AL: alendronate; Eu: europium; rMBG: rice husk MBG; CPT: camptothecin.