title: Alteration of fracture stability influences chondrogenesis, osteogenesis and immigration of macrophages.
abstract: Mechanical conditions at the fracture line determine the mode of fracture healing (osteonal versus non-osteonal bone union). The aim of this study was to investigate the influence of differing degrees of fracture stability on the time course of chondrogenesis, enchondral ossification and immigration of macrophages into the fracture callus. Using a fracture model of the rat's tibia, histological (Azan staining), immunohistological (antibodies directed against the macrophage-specific surface antigen ED2), and molecular biological techniques (expression of the mRNA of the cartilage-specific collagen IX, osteocalcin - a marker for mature osteoblasts - and the macrophage-specific macrosialin) were employed. In terms of histology and molecular biology (collagen IX mRNA expression) chondrogenesis in the fracture gap continued for longer in less stable fractures. In more stable fractures bone formation - identified by osteocalcin mRNA expression - increased from day 12 onwards. The expression of the macrophage-specific surface antigen ED2 and the mRNA of macrosialin was more pronounced but of shorter duration in the more stable fractures. This study shows that differing degrees of fracture stability not only influence the interplay between osteogenesis and chondrogenesis but also alter the kinetics of macrophage immigration into the fracture callus. These findings could aid in better understanding the cytobiologic mechanisms of callus formation and may suggest that macrophages are an important factor not only in soft tissue healing but also in bone healing.
authors.affiliation: Department of Trauma and Hand Surgery, Westfaelische Wilhelms-University, Muenster, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Hankemeier
authors.forename: S
authors.initials: S
authors.lastname: Grässel
authors.forename: G
authors.initials: G
authors.lastname: Plenz
authors.forename: H U
authors.initials: HU
authors.lastname: Spiegel
authors.forename: P
authors.initials: P
authors.lastname: Bruckner
authors.forename: A
authors.initials: A
authors.lastname: Probst
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000235:genetics; D015214:Antigens, Differentiation, Myelomonocytic / Q000235:genetics; D000954:Antigens, Surface / Q000032:analysis; D002465:Cell Movement / Q000276:immunology; D020219:Chondrogenesis / Q000502:physiology*; D003094:Collagen / Q000235:genetics; D017102:Fracture Healing / Q000502:physiology; D015870:Gene Expression / Q000502:physiology; D007150:Immunohistochemistry; D008264:Macrophages / Q000737:chemistry / Q000166:cytology / Q000276:immunology*; D008297:Male; D015675:Osteocalcin / Q000235:genetics; D010012:Osteogenesis / Q000502:physiology*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013977:Tibia / Q000502:physiology; D013978:Tibial Fractures / Q000276:immunology / Q000503:physiopathology*; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000954:Antigens, Surface; D003094:Collagen; D015675:Osteocalcin; D012333:RNA, Messenger; C081026:CD68 protein, mouse; D000097382:CD68 Molecule