- CConnexion
![]()
RééDOC
75 Boulevard Lobau 54042 NANCY cedex Christelle Grandidier Documentaliste 03 83 52 67 64 0
|
Myofibroblast numbers are elevated in human elbow capsules after trauma
HILDEBRAND KA; ZHANG M; VANSNELLENBERG W
CLIN ORTHOP RELAT RES , 2004, n° 419, p. 189-197 Doc n°: 112784 Localisation : Documentation IRR Descripteurs : DD54 - TRAUMATISMES - COUDE Elbow contractures, a frequent problem after injury, can be treated by excision of the joint capsule. However, the underlying changes in the joint capsule are poorly understood. Based on skin healing work, we examined the hypotheses that myofibroblast numbers and expression of a myofibroblast marker a-smooth muscle actin, are elevated in patients with posttraumatic joint contractures. Anterior capsules were obtained from six patients who had operative release of posttraumatic contractures greater than 5 months after injury and six elbows of organ donors free of contractures. Immunohistochemical studies revealed that myofibroblast numbers and percentage of total cells that were myofibroblasts were significantly elevated in the joint capsules from patients with contractures (326 +/- 61 cells per field, 36% +/- 4% total cells) when compared with similar tissues of the organ donors (69 +/- 41 cells per field, 9% +/- 4% total cells). Western blot analysis showed that protein levels of a-smooth muscle actin were significantly elevated in patients with posttraumatic joint contractures. However, analysis with reverse transcription-polymerase chain reaction determined that messenger ribonucleic acid levels for smooth muscle actin normalized to the housekeeping gene glyceraldehyde-3-phosphate dehydrogenase were not significantly different between the two groups. An association between increased numbers of myofibroblasts and posttraumatic joint contractures has been established in the human elbow capsule. Additional work is required to determine whether myofibroblast regulators may be targets for adjuvant therapies of posttraumatic contractures. Langue : ANGLAIS |
0
|