Hyaluronic acid (HA), an important component of the tissue extracellul
ar matrix, is a ubiquitous glycosaminoglycan (GAG) that forms a perice
llular coat on the surface of cells. It has been speculated that this
pericellular HA boundary may localize cytokines, such as transforming
growth factor-beta 1, which is known to stimulate collagen production.
The purpose of this study was to examine the role of HA and its cell
surface receptor (CD44), an active participant in HA degradation, as t
hey relate to keloid formation. Dermal excisions from both normal pati
ents (n = 13) and keloid patients (n = 13) were analyzed for HA conten
t using an alcian blue staining technique. Fibroblast cell cultures we
re used to quantitate HA synthesis and CD44 receptor density. Histolog
ical analyses showed a greater HA content in keloid tissue compared wi
th normal dermal tissue. In agreement with this observation, keloid fi
broblasts were found to synthesize significantly more HA than normal d
ermal fibroblasts (2469 +/- 483 cpm versus 1122 +/- 256 cpm, P =.02).
Treatment of keloid fibroblasts with triamcinolone acetonide reduced t
he level of HA synthesis to that of normal fibro blasts (1560 +/- 477
cpm versus 1293 +/- 264 cpm, P =.6). However, there was no significant
difference in HA receptor density on keloid cells compared with norma
l skin fibroblasts. Therefore, the increased HA deposits found in kelo
ids are attributable to increased synthesis rather than to decreased d
egradation mediated by the CD44 receptor. Copyright (C) 1995 by W.B. S
aunders Company.