Symposium: Tendon and ligament remodelling and regeneration

摘要: An international symposium entitled ‘Tendon and ligament remodelling regeneration’ was held on the 9 April 2006 at Queens’ College Cambridge. This one day meeting a satellite to main British Society for Matrix Biology Annual General Meeting, which 10–11 April. The organized by Dr Graham Riley Helen Birch, genererously sponsored Logres Trust, Biochemical Flexcell International Corporation. attended 60 delegates, maximum capacity of venue, included scientists from Denmark, Italy, Australia, USA as well UK. All plenary speakers were given opportunity prepare an article based their talk publication in Journal Experimental Pathology, four resultant manuscripts are published this issue. All have excellent reputation, is reflected very high quality papers, provide overview current research thinking important aspects tendon physiology pathology. In first paper, Birch describes how tendons show remarkable variation molecular composition mechanical properties that closely related specialized function specific sites body. Her studies equine forelimb superficial digital flexor (SDFT) has similar strength compared common extensor (CDET), but SDFT more compliant, with lower elastic modulus. Data human confirm hypothesis energy-storing such Achilles compliant than positional anterior tibialis. These differences material must arise variations matrix organization. Differences so far reported include mass average fibril diameter tendons, proteoglycan content collagen cross-linking. academic interest, since surgical procedures routinely involve reconstruction transfer tissue site another. It therefore potentially utmost importance match donor recipient tissues. will also be emerging technology engineering understand structure determined function. A key aspect regulation turnover mediated cells (tenocytes). Dr Clegg addresses his paper. He reviews central role metalloproteinases (MMP) enzymes ADAMTS (a disintegrin metalloproteinase thrombospondin motifs) respectively. His study normal pathological identified several perturbations gene expression, including decrease MMP-3 marked elevation MMP-13 chronic lesions. major aggrecanase enzyme ADAMTS-5 decreased, consistent changes turnover. clearly determine different proteinase genes regulated tendon. Furthermore, he shown there expression disease transformation towards fibrochondrogenic phenotype. response tenocytes shear forces or compression, although precise mechanism not known. Further work required characterize cell populations tendon, particular identify putative progenitor population actively involved repair, future therapies may designed promote improved healing regeneration tendon. Dr Kjaer described recent adaptability men women. been women sustain soft injury during physical activity, reason Measurements cross-sectional area (CSA) trained versus untrained individuals larger CSA no difference between Studies synthetic activity using radiolabelled precursors showed rates synthesis men, (unlike men) do respond exercise elevated rate protein synthesis. However, tendency early follicular phase menstrual cycle when circulating oestradiol low, hormonal influence activity. further supported greater ultimate stress tangent modulus fascicles Thus, addition gender-specific metabolism go some way explain increased susceptibilty men. In final Arnoczky laboratory's ground-breaking strain. widely overuse injuries consequence over stimulation tissue. thought modified degraded produced repeated co-workers conducted interesting experiments rat tail model, collagen-degrading stimulated suddenly released strain after breakage fibre bundles. They suggest catabolic responses triggered result under-stimulation microscopic damage fibres. At end session, six short presentations researchers around UK, followed dinner elegant college dining rooms. Overall I believe can report truthfully great success, enthusiasm interest all delegates heartening encouraging. agreed universally scientific pathology truly ‘coming age’, growing clinicians who wish challenging, yet rewarding, area. We beginning elucidate mechanisms underlying pathology, regular meetings type only serve enhance progress improvement therapy disabling condition.