Periosteal new bone formation in a canine neuropathic model of osteoarthritis

1997 ◽  
Vol 40 (10) ◽  
pp. 1756-1759 ◽  
Author(s):  
Stephen L. Myers ◽  
Kenneth D. Brandt ◽  
Brian O'Connor ◽  
William R. Widmer ◽  
Marjorie Albrecht
2008 ◽  
Vol 1 ◽  
pp. CMAMD.S442
Author(s):  
Meredith A. Lakey ◽  
Michael J. Klein ◽  
Ona M. Faye-Petersen

Periosteal new bone formation (PNBF) is the means by which appositional bone growth normally takes place on the surfaces of compact bone. Alterations in the periosteal microenvironment trigger complex interactions between osteoblasts and endothelial cells to promote PNBF. Physiologic processes like mechanical stress result in normal PNBF; but, a variety of pathologic processes result in excessive PNBF. The production of sufficient bone to be detectable by conventional radiography is a common feature of diverse etiologies, including infection; inflammation; prostaglandin E2 administration for ductal-dependent congenital heart disease; metabolic and hormonal abnormalities; neoplasms; fracture repair; systemic hypoxia; and hypertrophic osteoarthropathy. While the clinical settings and distribution of affected bone sites in these conditions are different, the histopathology of the PNBF is essentially identical; so, it seems logical that a common pathway might mediate them all. By combining the observations and insights gained from osseous research and studying the clinical pathology of these diverse conditions, we constructed a comprehensive pathway to explain PNBF. In doing so, it seems likely that Vascular Endothelial Growth Factor (VEGF) is the most likely common mediator of the pathways that lead to PNBF.


2011 ◽  
Vol 56 (No. 12) ◽  
pp. 595-601 ◽  
Author(s):  
MA Cetinkaya ◽  
B. Yardimci ◽  
C. Yardimci

This paper reviews hypertrophic osteopathy and describes one case report. Hypertrophic osteopathy is a rare pathologic disease process and is observed secondary to a mass in the thorax. In response to the presence of a mass(es), nonoedematous soft tissue swellings and a diffuse periosteal new bone formation develop in all four limbs. The result is mild to severe lameness. A twelve-year-old sexually intact female Cocker spaniel had undergone radical mastectomy on both sides in another veterinary hospital about two years before presentation in our hospital with lameness of both hind limbs. Pain and soft tissue swelling on the distal parts of extremities were determined in clinical examinations. Radiographs revealed periosteal new bone formation on all the long bones of all four limbs, pelvis and sternum; additionally, intrathoracic masses were observed. Euthanasia was performed five months later. Macroscopic examinations of the lungs revealed diffuse and exuberant masses with grizzled whitish cross-sectional colour and with necrotic and haemorrhagic foci. The radius-ulna, tibia, metacarpal and metatarsal bones of both limbs were examined and collected after the necropsy examination. Bone specimens were thicker and the outer surfaces seemed to be rough. At the histopathologic examination of the lung tissue, ovoid or round shaped and hyperchromatic nucleated diffuse anaplastic mammary gland epithelial cells were observed. According to these findings, these masses were diagnosed as the metastasis of malignant mixed tumours.  


1989 ◽  
Vol 40 (5) ◽  
pp. 490-493 ◽  
Author(s):  
A.P. Parnell ◽  
W. Simpson ◽  
M.K. Ward

2001 ◽  
Vol 121 (10) ◽  
pp. 549-553 ◽  
Author(s):  
T. Goto ◽  
T. Kojima ◽  
T. Iijima ◽  
S. Yokokura ◽  
H. Kawano ◽  
...  

2000 ◽  
Vol 19 (7) ◽  
pp. 55-57
Author(s):  
Barbara Carey

PROSTAGLANDIN THERAPY FOR neonates with ductal-dependent heart defects is a lifesaving intervention that permits optimal stabilization, diagnostic imaging, and timing of surgery. However, this therapy is not without complications (Table 1).1–3 When longterm (weeks or months) prostaglandin therapy is required because of neonatal immaturity or for optimal timing of procedures, one complication that may occur is bone changes: cortical hyperostosis/ periosteal new-bone formation.2,4


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