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The investigation involved a search for a model of atrophic nonunion. Fifty-two mature, adult, mongrel dogs were used to study the repair after creating a 0.5-cm bone defect in the mid-diaphysis of the radius. In addition, a 2-cm wide strip of periosteum was circumferentially resected from each osteotomy extremity. No immobilization was used thereafter. The reparative process was assessed by X-rays, histology, vascular injection, and scintigraphy. The dogs we distributed into three groups according to the time of follow-up (1, 3, and 6 months). Two kinds of repair were recognized after 3 months and were well-established after 6 months: disturbed healing with much callus (54%) and disturbed healing with absent or scanty callus (46%). In the first instance, the periosteum had regenerated and produced the external callus. The bone ends were capped with fibrocartilage; the vascularization around the defect was increased and displayed a well-defined vascular picture. In the healing pattern with absent external callus (atrophic nonunion), the bone defect was enlarged and filled with fibrous tissue, but there was no deficient vascularization in and around the osteotomy. Radioactivity counting showed an increased uptake around the osteotomy site in both types of repair, which persisted over time but was higher in the 1-month group. It was concluded that the present model yields a consistent pattern of a disturbed reparative process that mimics human cases of atrophic or hypertrophic nonunion. The differences between the two kinds of repair seemed to be related to the periosteal capacity of regeneration.
The investigation involved a search for a model of atrophic nonunion. Fifty-two mature, adult, mongrel dogs were used to study the repair after creating a 0.5-cm bone defect in the mid-diaphysis of the radius. In addition, a 2-cm wide strip of periosteum was circumferentially resected from each osteotomy extremity. No immobilization was used thereafter. The reparative process was assessed by X-rays, histology, vascular injection, and scintigraphy. The dogs we distributed into three groups according to the time of follow-up (1, 3, and 6 months). Two kinds of repair were recognized after 3 months and were well-established after 6 months: disturbed healing with much callus (54%) and disturbed healing with absent or scanty callus (46%). In the first instance, the periosteum had regenerated and produced the external callus. The bone ends were capped with fibrocartilage; the vascularization around the defect was increased and displayed a well-defined vascular picture. In the healing pattern with absent external callus (atrophic nonunion), the bone defect was enlarged and filled with fibrous tissue, but there was no deficient vascularization in and around the osteotomy. Radioactivity counting showed an increased uptake around the osteotomy site in both types of repair, which persisted over time but was higher in the 1-month group. It was concluded that the present model yields a consistent pattern of a disturbed reparative process that mimics human cases of atrophic or hypertrophic nonunion. The differences between the two kinds of repair seemed to be related to the periosteal capacity of regeneration.
We studied tissue samples of noninfected delayed union or nonunion of diaphyseal bones in 10 patients immunopathologically and neuroimmunologically 4 to 25 months after the primary injury. Samples mostly consisted of vascularized connective tissue of varying density with the proline-4-hydroxylase-containing fibroblast as the major cell type. Most inflammatory cells were CD4 T-lymphocytes and their number was always twice that of the CD8 positive cells. Staining for CD11b positive monocyte/macrophages showed in all samples positive cells scattered in the connective tissue stroma with perivascular enrichments. Mast cells were absent or very rare. Our findings suggest that delayed union and nonunion tissue consists of vascularized connective tissue, which mostly contains 5B5 fibroblasts, CD11b macrophages and vascular endothelial cells with only few immigrant recently recruited monocytes or lymphoid cells. Almost all resident cells seem to be involved in tissue remodeling as suggested by their content of fibroblast-type MMP-1 and its proteolytic activator MMP-3 or stromelysin. The most striking finding was the paucity or total lack of peripheral innervation, which may have to do with the nonunion of the fracture.
lowe a debt of deep gratitude to Dr. Meyer for the part he has taken in my studies, for numerous discussions, oral and in writing, through the years, and for his never failing and ever vivid interest in the job. For access to the files of case notes and X-ray films in the Refsn~s Hospital I am greatly indebted also to its present Head, Hans Bohr, M.D., who displayed a constant interest in the progress and results of the study and contributed by instructive discussions. Thanks are due, moreover, to the staff of the Refsn~s Hospital for extensive obligingness and help as well as for hospitality during my visits to collect data. . The investigations were continued while I was working in the Orthopaedic Department run by the Society and Home for the Disabled in Odense. Thanks are due to my chiefs in that Department, K. Harry S¢rensen, M.D., and A. Randl¢v, for their interest and for the access to that part of the Thomas caliper series which had been treated in Odense. The normal material too was collected in Odense. During my appointment as research assistant to the Anatomy Department of the Odense University I had ideal working conditions for combining and writing up all the data. I am thankful to Professor F. Bierring, Head of the Department, who also took an intense interest in the investigation of the vascularization of child hips which I carried out during that period. My thanks are due also to members of the Department staff who rendered help in various ways and took part in the studies. For careful typing of the book I would like to thank Jonna Madsen, medical secretary. The statistical calculations were performed by H. K. Kvist, M.Sc., to whom I am indebted for incredibly speedy help in a part of the study which I had no possibilities of solving myself.Last, but not least, I want to thank my wife, Hanne, for her great practical help, at many late hours, in recording the numerous data on punch cards (Karlo Hansen system), and for her enormous patience during all the years that this study took so much of the spare time which I ought .to have spent with my family. It is, therefore, a great pleasure to dedicate this book to my wife and children.
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