From chronic wounds to tooth loss - when skin cells behave badly
This research was completed on 30 April 2008
Published on 7 October 2005
Tooth loss and chronic wounds that don't heal properly - these are just two of the problems that can result when the cells covering the gum or skin, called epithelial cells, behave abnormally. They affect the health of vast numbers of people. Researchers hope to reveal what's going wrong at a molecular level, with the ultimate aim of developing new treatments.
What's the problem and who does it affect?
When wounds won't heal...
Around three percent of people over 60 suffer from chronic skin wounds, such as bed sores and leg ulcers.1,2
Some people's wounds don't heal despite weeks of treatment. Even when successfully treated, they tend to recur. It can seem like there's no escape from the pain and distress.
Chronic wounds cost the UK over £1 billion each year. 3 They strike people whose mobility is limited - the elderly, wheelchair users and the bed ridden. Certain health problems, such as diabetes and poor circulation, also put people at increased risk.
Wound healing is normally highly organised. In skin, epithelial cells move, or migrate, to the wound where they proliferate - that is they increase rapidly in numbers to repair the damaged skin. In non-healing wounds, epithelial cells don't migrate, or proliferate, enough.
The opposite defect - excessive proliferation and migration of epithelial cells, this time in the gum - also causes health problems in vast numbers of people. It contributes to teeth becoming loose in a dental disorder called periodontal disease. This insidious disease affects some 10-15% of adults, though many people don't realise they've got it. 4
What is the project trying to achieve?
What controls the behaviour of epithelial cells during healing?
Researchers are investigating what controls the healing process in skin and gum at a molecular level. They are concentrating on how a particular type of cell, called a connective tissue cell or fibroblast, controls the behaviour of epithelial cells.
The team will grow fibroblasts and epithelial cells from skin together in the laboratory. They hope to reveal how the two types of cells communicate with each other by looking, for example, for molecules that act as messengers by moving between the cells. They will use specially designed equipment - for example, they will watch the epithelial cells moving using a video microscopy system.
The project team will also study tissue from people who are having teeth extracted to compare the mechanisms that regulate the behaviour of epithelial cells in gum with those in skin.
What are the researchers' credentials?
|Project Leader||Professor D Aeschlimann PhD and Dr Locke PhD|
|Location||Matrix Biology and Tissue Repair Research Unit and Department of Adult Dental Health, Dental School at Cardiff University, Cardiff|
|Grant awarded||7 July 2005|
|Start date||1 May 2006|
|End date||30 April 2008|
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The project team is in a unique position to carry out this study. They have internationally established expertise, a laboratory equipped with cutting-edge facilities and direct access to clinics treating patients - with both periodontal disease and non-healing wounds.
Having worked in this area of research for over 15 years, Professor Aeschlimann has both the knowledge and resources needed to succeed, including access to a large panel of unique reagents that he has accumulated. A long list of articles published in well-respected journals documents his achievements in improving understanding of basic science, while a series of patents reveals how he's applied that understanding to help solve clinical problems.
Important insights into the regulation of connective tissue cells have recently been made by Professor Aeschlimann's laboratory and underpin this study. 5 Dr Locke is a clinician scientist associated with this study who has specialised in understanding the role of epithelial cells in the initiation and progression of periodontal disease.
Who stands to benefit from this research and how?
Uncovering targets for new drugs
We already know that non-healing wounds and periodontal disease are caused by opposite defects - epithelial cells don't migrate enough in wounds that fail to heal, whereas they migrate too much in the gums of people with periodontal disease. But we don't understand what controls the errant behaviour of those cells.
Researchers hope their studies will reveal what controls epithelial cells at a molecular level. They hope to determine the defects in communication between cells that cause both non-healing wounds and periodontal disease.
The ultimate goal is to use this information to design new treatments for the vast numbers of people with wound healing defects. Such treatments could, for example, correct the response of epithelial cells by targeting a specific molecule that controls their behaviour.
Potential benefits are huge. Wound healing deficiencies severely affect quality of life, particularly in the elderly, and are a growing problem in an ageing population. Each year, diabetic foot ulceration and venous leg ulcers alone cost the NHS some £17 million and £400 million, respectively.3 And treatment of periodontal disease cost the NHS in excess of £30 million in 2004. 6
1. Baker, S, Fletcher, A, Glanville, J, Press, P, Sharp, F, Sheldon, T, Cullum, N, and Semlyn, A. "Compression therapy for venous leg ulcers." Effective Health Care 3 (4): 1-12, 1997 (ISSN:0965-0288)
2. "Healing chronic wounds: technologic solutions for today and tomorrow." Adv Skin Wound Care 13 (2 Suppl): 4-22, 2000
3. Harding, KG, Morris, HL and Patel, GK. "Healing chronic wounds." BMJ 324: 160-163, 2002 [back to main article]
4. Miyazaki, H, Pilot, T, Leclercq, MH, and Barmes, DE. "Profiles of periodontal conditions in adults measured by CPITN." Int Dent J 41(2): 74-80, 1991
5. Stephens, P, Grenard, P, Aeschlimann, P, Langley, M, Blain, E, Errington, R, Kipling, D, Thomas, D, and Aeschlimann, D. Crosslinking and G-protein functions of transglutaminase 2 contribute differentially to fibroblast wound healing responses. J. Cell Sci. 117, 3389-3403, 2004
6. Dental practice board 2003 http://www.dpb.nhs.uk/download/digest/digest_2003.pdf