PolySciTech (
www.polyscitech.com)
provides a wide array of PLGA polymers and related biodegradable polyesters. Recently PLGA has been used along with other
components to generate a bone scaffold that allows for repairing large defects or
substantial fractures. This scaffold was
loaded with an anti-inflammatory drug which were found to aid in the healing
process when loaded at the correct dose. Read more: Sidney, Laura E., Thomas RJ
Heathman, Emily R. Britchford, Arif Abed, Cheryl V. Rahman, and Lee D. Buttery.
"Investigation of localised delivery of diclofenac sodium from PLGA/PEG
scaffolds using an in vitro osteoblast inflammation model." Tissue
Engineering ja (2014). http://online.liebertpub.com/doi/abs/10.1089/ten.TEA.2014.0100
“ABSTRACT: Non-union fractures and large bone
defects are significant targets for osteochondral tissue engineering
strategies. A major hurdle in the use of these therapies is the foreign body
response of the host. Herein, we report the development of a bone tissue engineering
scaffold with the ability to release anti-inflammatory drugs, in the hope of
evading this response. Porous, sintered scaffolds composed of poly(DL-lactic
acid-co-glycolic acid) (PLGA) and poly(ethylene glycol) (PEG) were prepared
with and without the anti-inflammatory drug diclofenac sodium. Analysis of drug
release over time demonstrated a profile suitable for the treatment of acute
inflammation with approximately 80% of drug released over the first 4 days and
a subsequent release of around 0.2% per day. Effect of drug release was
monitored using an in vitro osteoblast inflammation model, comprised of mouse
primary calvarial osteoblasts stimulated with proinflammatory cytokines
interleukin-1β (IL-1β), tumour necrosis factor-α (TNF-α) and interferon-γ
(IFN-γ). Levels of inflammation were monitored by cell viability and cellular
production of nitric oxide (NO) and prostaglandin E2
(PGE2). The osteoblast inflammation model revealed that
proinflammatory cytokine addition to the medium reduced cell viability to 33%,
but the release of diclofenac sodium from scaffolds inhibited this effect with
a final cell viability of approximately 70%. However, releasing diclofenac
sodium at high concentrations had a toxic effect on the cells. Proinflammatory
cytokine addition led to increased NO and PGE2
production; diclofenac sodium releasing scaffolds inhibited NO release by
approximately 64% and PGE2 production by approximately
52%, when the scaffold was loaded with the optimal concentration of drug. These
observations demonstrate the potential use of PLGA/PEG scaffolds for localised
delivery of anti-inflammatory drugs in bone tissue engineering applications.”
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