PLATELET-DERIVED GROWTH-FACTOR IN FIBROUS MUSCULOSKELETAL DISORDERS -A STUDY OF PATHOLOGICAL TISSUE-SECTIONS AND IN-VITRO PRIMARY-CELL CULTURES

Citation
Ba. Alman et al., PLATELET-DERIVED GROWTH-FACTOR IN FIBROUS MUSCULOSKELETAL DISORDERS -A STUDY OF PATHOLOGICAL TISSUE-SECTIONS AND IN-VITRO PRIMARY-CELL CULTURES, Journal of orthopaedic research, 13(1), 1995, pp. 67-77
Citations number
28
Categorie Soggetti
Orthopedics
ISSN journal
07360266
Volume
13
Issue
1
Year of publication
1995
Pages
67 - 77
Database
ISI
SICI code
0736-0266(1995)13:1<67:PGIFMD>2.0.ZU;2-S
Abstract
Despite the great variability in the clinical behavior of fibrous lesi ons of the musculoskeletal system, they are composed of cytologically similar fibrocytes. Receptors for estrogen or progesterone, or both, a re present in some of these lesions and some increase their rate of gr owth during periods of high levels of sex steroid hormones. The platel et-derived growth factor-B (PDGF-B) proto-oncogene encodes the B chain of PDGF, a mitogen for fibrocytes. Tissue from aggressive fibromatosi s, fibrous dysplasia, plantar fibromatosis, and recurrent plantar fibr omatosis was analyzed with use of the polymerase chain reaction and in situ hybridization for the expression of PDGF-B and PDGF beta recepto r. Cell culture was used to determine if estrogen and progesterone sti mulation modulated the expression of PDGF-B. Aggressive fibromatosis, fibrous dysplasia, and recurrent plantar fibromatosis expressed PDGF-B ; plantar fibromatosis, normal plantar fascia, normal fascia lata, and mature scar did not. All of the tissues expressed PDGF beta receptor. The level of expression in aggressive fibromatosis and fibrous dyspla sia was four times that in the recurrent plantar fibromatosis. Estroge n and progesterone stimulation in aggressive fibromatosis resulted in an increase in the level of expression. Therefore, the detection of PD GF-B may be an adjunct in the pathologic identification of locally inv asive lesions. Its production may be a common mechanism leading to a f ibroproliferative response through deregulation of the control of grow th by both paracrine and autocrine mechanism.