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measures of therapy such as joint

replacements through full or partial prosthesis

may become necessary.

Although research in this field of osteoarthritis

is extensive and has elucidated many

important mechanisms about how the

homeostasis of the hyaline cartilage is

imbalanced, it is not yet possible to stop the

degenerative processes, nor can full

regeneration of the cartilage surface be

achieved. Chondroprotective supplements or

anti-inflammatory drugs can partially slow

down the mechanism and take some of the

pain away. Some approaches have engaged in

cell-based therapies, but even these cannot

fully restore joint integrity. Like in chronic

wounds, one of the major problems in joint

disease is also the local distribution of

medication and keeping a therapeutic drug

level over a longer period of time in the

affected tissues.

Although non-steroidal anti-inflammatory drugs

(NSAID) or cortison derivates may decrease the

degree of chronic inflammation and pain, they

cannot put a halt to the degradation process.

In contrast, NSAIDs may dose-dependently

accelerate the activity of metalloproteinases

and cortison derivates may completely inhibit

the synthesis of new macromolecules.

Furthermore, chronic systemic application of

NSAIDs and particularly cortison derivates may

cause complications, such as gastric ulcers,

liver and kidney failures.

For both deep wound infections and joint

diseases, alternative and innovative drug

C

hronic deep wounds and chronic joint disease are always a

problem for patients due to the constant pain and restrictions

in daily living, for both people and animals. Chronic wounds

may prove difficult to heal for many reasons. Among them one of the

major inhibitions is scarce distribution of drugs to wound beds and edges

due to excess fibrosis and scar formation. Missing vascularity, often

alongside chronic infection within the scar tissue, is just one of the major

underlying problems.

Hyaline cartilage damage within the joint, often resulting from synovial

membrane inflammation or small lesions, will worsen over time and result

in irreversible changes. Matrix destruction is the end-result for both

chronic inflammation and small lesions. In both cases, matrix-degrading

enzymes such as metalloproteinases, aggrecanases, hyaluronidases and

cathepsins are triggered by inflammatory mediators (nitric oxide (NO),

prostaglandin (PGE2)) and cytokines (interleukins (IL1, IL6) and tumour

necrosis factor) and will finally degrade the collagen network and

proteoglycans, thus changing the hydro-osmotic pressure of the hyaline

cartilage. It is then only a question of time until fibrillation of the cartilage

surface occurs, followed by fissures and cleft formation down to the

subchondral bone plate. Erosion of cartilage down to the subchondral

bone is the devastating result for patients, at which point stronger

I S S U E E I G H T

H O R I Z O N 2 0 2 0 P R O J E C T S : P O R T A L

www.horizon2020projects.com

114

B I O M E D I C A L S C I E N C E S

Transcutaneous drug delivery

The CABMM’s Professor Dr Brigitte von Rechenberg and her fellow

researchers outline their studies into transcutaneous drug delivery using a

novel transdermal application technology

Fig. 1 MedDrop device

Fig. 2 Valeoskin scaffold